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The American Journal of Orthopedics is an Index Medicus publication that is valued by orthopedic surgeons for its peer-reviewed, practice-oriented clinical information. Most articles are written by specialists at leading teaching institutions and help incorporate the latest technology into everyday practice.
Special Considerations for Pediatric Patellar Instability
ABSTRACT
Patellar instability in children and adolescents is a challenging subset to treat. Varied forms of instability, ranging from episodic dislocation to fixed dislocation, have been recognized. It is of utmost importance for the treating physician to recognize these different patterns of instability and their associated risk factors, as more complex patterns of instability would require more extensive surgical procedures. Medial patellofemoral ligament (MPFL) reconstruction, by itself, may not suffice or may not be appropriate for the more complex instability patterns. Appropriate and early treatment of such instability in children would allow for functional progression and possible remodeling of the trochlea. However, early treatment has the associated risk of growth disturbances when surgical procedures are performed around open physis or if adult-type bony procedures are performed in children. Recent knowledge about the relationship between trochlea, MPFL femoral attachment, and distal femoral physis could help to advance safe surgical care for these patients. This article reviews the pathophysiology, risk factors, and the existing classification systems for patellar instability in children and adolescents. It focuses on varied surgical techniques, which are unique to the pediatric population, and summarizes the outcomes of these surgical techniques.
Continue to: EPIDEMIOLOGY
EPIDEMIOLOGY
In a prospective 2-year study of Finnish children, the annual incidence rate of patellar instability was 43/100,000 pediatric population.1 In patients 9 to 15 years of age, the incidence was approximately 1/1000.1 In another study, patients at highest risk for a first-time patellar dislocation were females aged 10 to 17 years.2 In a study in patients with traumatic hemarthrosis, 36% in the younger age group (10-14 years) and 28% in the older age group (15-18 years) had sustained patellar dislocation. In contrast, 22% in the younger age group and 40% in the older age group had sustained an anterior cruciate ligament tear.3
Approximately one-half of patients who dislocate their patella suffer from long-term complications.4,5 These complications include recurrent instability, patellofemoral pain, osteochondral lesions, and eventual arthritis.1,4,5 Young, active individuals are more prone to these issues.6 Also, 39% or more of patellar dislocation patients have an associated osteochondral fracture that might influence the management.1 Thus, patellar instability in young patients is an area of concern.
DEVELOPMENTAL ANATOMY
At 4-week gestation, the patellofemoral joint is an ectodermal sac filled with mesenchyme of the somatic mesoderm.7 Mesenchymal condensations then appear at 4 to 5 weeks gestation, followed by chondrification of both the femur and patella.7 The joint space is present by 6 weeks, and the patellar and distal femoral condyles are present at 7 weeks gestation.7 By 8 weeks gestation, the basic knee anatomy resembles that of an adult with the chondroepiphysis forming the articular surfaces of the femur, tibia, and patella.7 By this time, the extensor mechanism is formed, and active joint motion has begun, facilitating the development of the trochlear sulcus.7 The secondary ossification center in the distal femoral epiphysis forms around 36 weeks gestation.8 Postnatally, both the patella and distal femur grow through endochondral ossification.9,10
The patella is the largest sesamoid bone in the human body.11 The patella begins as a dense consolidation of cells that differentiate as the quadriceps mechanisms develop.12,13 The patellar anlage becomes distinguishable within the quadriceps tendon around 7.5-week gestation.12 The morphology of the patella conforms to the distal femur.12 The patella molds or re-models as the knee begins to move in response to mechanical stresses.7 The patella increases in relative size during the first 6 months of gestation, then enlarges proportionately to the rest of the bones.7 Ossification begins around 3 years of age for females and 4 to 5 years of age for males.8,14 The ossification center may appear irregular as it rapidly expands.14 Ossification proceeds in a proximal to distal direction, thus giving a spurious estimation of patellar height on radiographs in children. The overall morphology of the cartilaginous patella during development is comparable to the final mature shape.14 Abnormal contact stresses on the articular surface of the patella during skeletal immaturity can lead to deformation.7
Ultrasonographic measurements in normal patients show that trochlear groove (TG) morphology is present early and becomes more radiographically apparent as distal femoral ossification is completed.15 Anatomic dissections of aborted fetuses have verified the morphology of the TG as it remains constant during growth and the groove morphology is the same for both fetuses and adults.16 An ultrasound study performed on patients aged 12 to 18 years showed the cartilaginous sulcus angle (CSA) remained constant throughout all age groups (146°).17 The CSA however, differed in patients who suffered a patellar dislocation (average, 164°; range, 154°-195°) compared with normal knees (average CSA, 145°; range, 131°-158°).15,17,18 The osseous sulcus angle, on the other hand, appears flat at birth and the TG deepens with age. This increase in depth is more of a reflection of progressive ossification of a well-formed cartilaginous trochlea, rather than a true deepening of the sulcus.17 Thus, the axial radiographic view of the patella provides misleading information about the sulcus angle in children and should not be used to define trochlear morphology.
Continue to: MEDIAL PATELLOFEMORAL LIGAMENT ANATOMY
MEDIAL PATELLOFEMORAL LIGAMENT ANATOMY
The medial patellofemoral ligament (MPFL) functions to limit the lateral translation of the patella.19 The attachment sites on the femur and patella for the MPFL have been studied in children.20-23 Cadaveric dissections in specimens aged 2 to 11 years have noted the patellar attachment to be an average of 12 mm in length with the midpoint approximately 5 mm superior to the mid-pole of the patella.22 The patellar footprint of the MPFL insertion was a mean 41% of the entire patellar length.22
It is important to be aware of the characteristic anatomy of the MPFL, as fixation points should mimic the anatomic insertion as best as possible while also avoiding violation of the nearby physis. The MPFL originates between the adductor tubercle and the medial femoral epicondyle just distal to the distal femoral physis and attaches to the superomedial aspect of the patella.20-25 In relation to the physis in pediatric patients, the midpoint of MPFL insertion has been measured to be 4 mm to 9 mm distal to the femoral physis.21,24,25 These measurements represent averages as cadaveric studies have reported that some part of MPFL femoral insertion extends proximal to the distal femoral physis.21 A recent report of physeal injury to the posterior distal femoral physis during MPFL reconstruction leading to femoral flexion deformity highlights the importance of physeal-respecting surgery.26
TROCHLEA AND ANTERIOR DISTAL FEMORAL PHYSIS
The relationship between the proximal aspect of the trochlea and the anterior distal femoral physis has been recently studied in 175 knees with dysplastic trochlea.27 Based on magnetic resonance imaging evaluation, the lateral aspect of the trochlea extended proximal to the anterior distal femoral physis in 13% of patients and was at the level of the anterior physis in another 13% of patients (Figure 1).27 Hence, a cautious approach is recommended for any surgery to address trochlear dysplasia or trochlear bump in younger patients to prevent iatrogenic injury to anterior distal femoral physis and resultant genu recurvatum. The distance between the trochlea and the physis increased with increasing age.
LIMB ALIGNMENT
Physiologically, the quadriceps angle (Q angle) changes through the course of growth. As children begin standing and walking, they stand with their feet wider apart and in genu varum.28 Physiologic genu varum can reach 15°.28 This degree lessens during the first 1.5 to 2 years of life, transitioning to physiologic valgus of nearly 12° by 3 years of age.28 Genu valgum, thereafter, gradually decreases to reach the adult value of around 7° to 8° by age 7 years.28 Increased genu valgum is a risk factor for patellar instability. In skeletally immature patients, correction of genu valgum through guided growth may be desirable in patients undergoing patellar stabilization surgery (Figures 2A, 2B).29
PATHOPHYSIOLOGY OF PEDIATRIC PATELLAR DISLOCATION
TROCHLEAR DYSPLASIA
Trochlear dysplasia is an abnormal shape and depth of the TG.30 Up to 96% of patients with patellar dislocation have trochlear dysplasia.30-33 In a study of patellar instability in children, at least 1 of the 3 signs of trochlear dysplasia (the crossing sign, supratrochlear bump, and double contour sign) was present on lateral radiographs.34 In another study on the growth of trochlear dysplasia in children and adolescents, all grades of trochlear dysplasia were present at all ages (ie, the dysplasia was most likely present at birth and did not necessarily worsen with age and growth).35 The linear dimensions of lateral and medial condylar height as well as trochlear bump increased with age but both the sulcus angle and shape of the trochlea did not change significantly.35 Remodeling of a dysplastic trochlea can happen if the patella is stabilized and appropriately located at a younger age, preferably before 10 years of age.36,37
Continue to: PATELLAR HEIGHT
PATELLAR HEIGHT
The role of patellar height in patellar instability has been well established.38 In patients with patella alta, the patella remains proximal to the TG during the greater arc of knee motion, which predisposes it to patellar instability. Calculation of patellar height in children could be challenging due to incomplete ossification, as well as asymmetric ossification of the patella and the tibial tubercle (TT). Since the patella ossifies from proximal to distal, most radiographic methods that measure the patellar height from the distal aspect of the patella provide a spurious elevation of the measurement.
The Caton-Deschamps (CD) method measures the length of the patellar articular surface and the distance from the inferior edge of the articular surface to the anterosuperior corner of the tibial plateau.39 A ratio >1.3 signifies patella alta. The CD ratio has been verified as a simple and reliable index for measuring patellar height in children.40 Two other methods have been described for determining patellar height in children.41,42 Based on anteroposterior (AP) radiographs of the knee in full extension, Micheli and colleagues41 calculated the difference between the distance from the superior pole of the patella to the tibial plateau and the length of the patella. A positive difference signified patella alta. The Koshino method involves the ratio between a reference line from the midpoint of the patella to the midpoint of the proximal tibial physis and a second distance from the midpoint of the distal femoral physis to the midpoint of the proximal tibial physis on lateral knee radiographs.42 Normal values range from 0.99 to 1.20 with the knee in >30° flexion, in children 3 to 18 years of age.
HYPERLAXITY
In contrast to adults, children have increased levels of collagen III compared with collagen I, which is responsible for tissue elasticity.43 Tissue elasticity leads to increased joint mobility, which is more common in children. Joint hypermobility or hyperlaxity has to be differentiated from symptomatic instability. The traditional Beighton score identifies individuals as having joint hypermobility with a score of 5/9 or higher in school-aged children.44-46 Smits-Engelsman and colleagues44 suggested using stricter criteria with scores of 7/9 or higher being indicative of hyperlaxity in school-aged children. A study of 1845 Swedish school children noted that females have a higher degree of joint laxity.45 Maximal laxity was noted in females at 15 years of age.45 Hyperlaxity has been demonstrated to be greater on the left side of the body44 and can be part of generalized syndromes including Down’s syndrome, Marfan’s syndrome, or Ehlers-Danlos syndrome.
LIMB TORSION
Staheli and colleagues47 described the normative values of a lower extremity rotational profile, including femoral anteversion and tibial torsion. Children normally have increased femoral anteversion, which decreases with growth. Miserable malalignment is a term used to denote increased femoral anteversion and increased external tibial torsion.48,49 These rotational abnormalities can increase the Q angle and the lateral forces on the patella. Femoral anteversion or internal rotation of the femur of 30° significantly increases strain in all areas of the MPFL.48 This increased strain may lead to MPFL failure and patellar instability.48 Increased internal rotation of the femur also increases contact pressure on the lateral aspect of the patellofemoral joint.48 Miserable malalignment frequently manifests following a pubertal growth spurt and may require femoral and tibial osteotomy.50
SYNDROMIC ASSOCIATIONS
Several syndromes have patellar instability as a part of their manifestation. The more common syndromes include nail-patella syndrome, Kabuki syndrome, Down’s syndrome, and Rubinstein-Taybi syndrome.51-54 Other syndromes less commonly associated with patellar instability include Turner syndrome, patella aplasia, or absent patella syndrome. Since many patients with syndromic patellar instability are functionally limited, they may not require an aggressive approach to treatment. When treating these patients, it is important to recognize the unique features of a specific syndrome, which may affect the anesthesia risk profile, management decisions, rehabilitation, and prognosis.
Continue to: MPFL TEAR PATTERN
MPFL TEAR PATTERN
The MPFL serves as an important constraint to the patella to prevent lateral dislocation, primarily during the first 20° to 30° of knee flexion.55,56 Injury to the MPFL is noted in over 90% of patients who suffer a patellar dislocation.57 The location of MPFL tears in pediatric patients is variably reported at the patellar attachment (10%-61%), femoral attachment (12%-73%), both (12%-35%) or mid-substance (2.5%-15%).25,57 The most common tear patterns in pediatric patients are tears at the patellar attachment.25,57 This tear pattern may be accompanied by an avulsion fracture of the medial rim of the patella, though this fracture, being extra-articular, seldom needs treatment.
CLASSIFICATION
While several authors have established extensive classification systems of patellar dislocation based on both clinical and radiographic presentation and reviews of the literature, a single classification system has not been recognized as the gold standard. In this section, in addition to presenting our preferred methods of classification, we will review some of the more recent and extensive classification systems for patellar dislocation and patellar instability.
Dejour and colleagues31 initially used both the presence of patellofemoral anatomic abnormalities and pain to define 3 types of patellar instability: major, objective, and potential patellar instability. Major patellar instability indicates that the patient has experienced more than 1 documented dislocation, objective instability involves one dislocation in addition to an associated anatomic abnormality, and potential patellar instability refers to cases in which the patient has radiographic abnormalities and patellar pain.31 Garin and colleagues58 more simplistically divided patellar dislocation patients into 2 groups: major (permanent or habitual) dislocation of the patella and recurrent dislocation. Sillanpaa59 stressed the distinction between first-time dislocation and recurrent dislocation specifically in the context of acute injuries. These classification systems were formulated with adults as the most relevant population; however, classifications targeted specifically to pediatric patients have recently been presented in the literature.
Historically, pediatric patella dislocations were simply categorized as traumatic or congenital.60 In 2014, Chotel and colleagues61 focused on classifying patellar dislocation by extensively reviewing anatomic, biomechanical, pathophysiological, and clinical patterns seen most commonly in children. They included 5 categories: congenital dislocation, permanent dislocation, habitual dislocation during knee flexion, habitual dislocation during knee extension, and recurrent dislocation; however, they did not address traumatic dislocations.61 Congenital dislocation is a rare condition, typically presenting at birth, which produces a pattern of functional genu valgum.62 Permanent dislocation typically presents after the child has started walking, but before the age of 5 years.61 The 2 variations of habitual dislocation typically present between ages 5 and 8 years.61 The final category is the most common and typically occurs during pre-adolescence or adolescence as a result of an atraumatic or trivial traumatic event or sports injury.1 Using more specific terminology, Hiemstra and colleagues63 modeled a classification system based on the traumatic, unilateral, bankart lesion, surgery (TUBS)/atraumatic, multidirectional, bilateral, rehabilitation, inferior shift (AMBRI) for shoulder dislocation classifications. The patellar dislocation system is used to identify 2 distinct subsets of patients in the patellofemoral instability population. One subset is defined by the acronym WARPS (weak, atraumatic, risky anatomy, pain, and subluxation), the other is STAID (strong, traumatic, anatomy normal, instability, and dislocation).64 Patients categorized by the WARPS acronym tend to experience atraumatic onsets of patellofemoral instability and demonstrate anatomic issues that increase this instability. These underlying anatomic issues include valgus alignment, ligamentous laxity, rotational abnormalities, shallow and short TG, and patella alta. On the other hand, STAID patients describe a traumatic dislocation event and do not have underlying anatomic abnormalities that predispose them to instability.64
Taking into account these previous classifications, Frosch and colleagues65 added specific pathologies including “instability,” “maltracking,” and “loss of patellar tracking,” in addition to both clinical and radiographic factors to define 5 types of patellar dislocation and their specific treatment recommendations.65 Type 1 involves simple dislocation with neither maltracking nor instability and a low risk of redislocation.65 Type 2 is defined as primary dislocation followed by subsequent high risk of dislocation and no maltracking.65 Type 3 is divided into 5 subcategories of instability and maltracking issues involving soft tissue contracture, patella alta, pathological tibial tuberosity, and TG distance.65 Type 4 is defined as the highly unstable “floating patella,” and type 5 involves patellar maltracking without instability 65. In terms of treatment, conservative rehabilitation is recommended for type 1 whereas MPFL reconstruction tends to show positive outcomes for both types 2 and 3.66-70
Continue to: Parikh and Lykissas recently published...
Parikh and Lykissas recently published a comprehensive classification system of 4 defined types of patellar dislocation in addition to voluntary patellar instability and syndromic patellar instability (Table).60 The 4 types are Type 1, first-time patellar dislocation; Type 2, recurrent patellar instability; Type 3, dislocatable; and Type 4, dislocated. Type 2 is further subdivided into Type 2A, which presents with positive apprehension signs, and Type 2B, which involves instabilities related to anatomic abnormalities.60 A distinction is also made between Type 3A or passive patellar dislocation and Type 3B habitual patellar dislocation.60
The classification system proposed by Green and colleagues is more simplified with 3 main categories (Table) of pediatric patellar dislocation: traumatic (acute or recurrent), obligatory (either in flexion or extension), and fixed laterally.71,72 The acute traumatic categorization refers to patients who experienced an initial dislocation event due to trauma whereas recurrent traumatic involves repeated patella dislocations following an initial incident. Studies report that between 60% to 70% of these acute traumatic dislocations occur as a result of a sports-related incident.2,33,73 Obligatory dislocations occur with every episode of either knee flexion or extension, depending on the subtype. Obligatory patella dislocation in flexion typically cannot be manipulated or relocated into the trochlea while the knee is fixed but does reduce into the trochlea in full extension. Fixed lateral dislocations are rare, irreducible dislocations in which the patella stays dislocated laterally in flexion and extension. These dislocations often present with other congenital abnormalities. Each of these categories can be further specified as syndromic if the dislocation is associated with genetic or congenital conditions including skeletal dysplasia, Ehlers-Danlos syndrome, cerebral palsy, Marfan disease, nail-patella syndrome, Down syndrome, Rubenstein-Taybi syndrome, and Kabuki syndrome.51-54,61,74-76
SURGICAL TECHNIQUES IN SKELETALLY IMMATURE PATIENTS
While nonsurgical, conservative treatment involving physical therapy and activity modification is recommended for most patients who experience first-time traumatic patellar dislocations, many patients experience complicating factors that indicate them for surgery. These factors include recurrent dislocation, risk factors for patellofemoral instability, underlying malalignment issues, and congenital deformities. When evaluating these factors, particularly patellofemoral instability, the authors recommend assessing osteochondral lesions, age, skeletal maturity, number of previous dislocations, family history, and anatomic risk factors.2,5,77-79 Extra care should be taken when considering surgical treatment for skeletally immature patients at elevated risk for recurrent instability as the risk of cartilage damage in these cases is high.80-82
Recently, there has been a reported increase in surgical treatment for patellar instability in the skeletally immature.83 This finding may be attributed to heightened awareness of factors that indicate patients for surgical treatment and increased familiarity of surgeons with newer techniques.83 Many surgical techniques have been described to address patellar instability involving both soft-tissue procedures and bony corrections.84 In this article, we discuss the various surgical techniques for MPFL reconstruction, quadricepsplasty, and distal realignment. These procedures can be paired with any number of additional procedures including, but not limited to, lateral retinacular release or lengthening, chondroplasty, TT osteotomy (in skeletally mature patients), and removal of loose bodies.83
There is a need for more comprehensive studies, particularly randomized controlled trials, to evaluate the outcomes for both surgical and nonsurgical treatments for first-time dislocations. In the current literature, only very recently have surgical treatments shown outcomes that are more positive. In 2009, Nietosvaara and colleagues85 conducted a randomized controlled trial of nonoperative and operative treatment of primary acute patellar dislocation in both children and adolescents. After a long-term mean follow-up of 14 years, there was not a significant difference between the groups in recurrent dislocation and instability, subjective outcome, or activity scores.85 In a subsequent review of 5 studies including 339 knees, Hing and colleagues86 also found similar results in both the operative and nonoperative cohorts at risk of recurrent dislocations, Kujala scores, and reoperations. However, a recent systematic review comparing redislocation rates and clinical outcomes between surgical and conservative management of acute patellar dislocation reported more positive outcomes for the surgical cohort.87 This review included 627 knees, 470 of which received conservative management, 157 of which received operative treatment. The conservative cohort was followed for an average of 3.9 years and had a 31% rate of recurrent dislocation while the surgical group was followed for a mean 4.7 years and experienced a 22% redislocation rate.87 This study indicates that operative management for acute first-time dislocations may be the preferred treatment option.
Continue to: A potential reason some of these studies...
A potential reason some of these studies did not show any significant difference between the operative and nonoperative cohort could be that the surgical cohorts included a wide range of procedures including lateral releases and MPFL repairs. Recent publications have indicated that these techniques do not produce overall positive outcomes. While each surgical treatment plan is unique depending on the patient; recently, MPFL reconstruction has been shown to have better outcomes than both nonoperative management and simple medial repair and/or lateral
release.67,88-90
MPFL RECONSTRUCTION
INDICATIONS/OVERVIEW
The MPFL is an important stabilizer for the knee that primarily resists lateral translation of the patella. Damage to the MPFL is very common in acute patellar dislocations with up to 90% of first-time dislocations resulting in injury to the MPFL.91,92 Historically, simple medial and/or lateral MPFL repairs have not been shown to improve patellofemoral kinematics significantly and often result in recurrence.90,93 To address this issue, during the past few decades, numerous MPFL reconstruction techniques have been developed to reconstruct a stronger ligament with the same kinematics as the anatomic MPFL.2,19,69,81,94-106 The ultimate goal of MPFL reconstruction is to reestablish the anatomic “checkrein” to guide the patella into the trochlea between 0° and 30° of knee flexion.107,108 An essential secondary surgical goal in skeletally immature patients is to avoid damaging the distal femoral physis.
There are many variations in both the grafts used to replace the MPFL and the means by which to secure them. The ones discussed below include free semitendinosus or gracilis autografts or grafts constructed from a pedicled adductor, patellar, or quadriceps tendon.69,105,109 While not used as frequently, allografts have also been used.110 Methods to secure these grafts in osseous tunnels include suture anchors or tenodesis screws. Incomplete osseous sockets or medial-sided bone tunnels have also been used as a method to decrease patellar fractures as they preserve the lateral patellar cortex.111-114
DOUBLE-BUNDLE HAMSTRING AUTOGRAFT
The technique most often used by the author is a double-bundle hamstring autograft harvested from either the semitendinosus or the gracilis secured by short patellar and femoral sockets (Figure 3). After harvesting the hamstring graft from a posteromedial incision, an approximately 90-mm graft is prepared with Krackow stitches to secure 15 mm of the tendon in each socket.115 Lateral radiographs are used intraoperatively to ensure the guidewire for the femoral drill hole falls along the posterior cortex of the diaphysis of the femur while AP radiographs confirm placement distal to the physis. It is important to take both AP and lateral radiographs intraoperatively due to the concave curvature of the distal femoral physis. This unique anatomy can make a point that is located distally to the physis on the AP view appear on or proximal to it on the lateral cross reference view.24,116 For the patellar socket, 2 short sockets are made in the superior half of the patella. Once the sockets have been drilled, the graft is adjusted so that the patella stays seated in the center of the trochlea between 20° and 30° of flexion. This anchoring is accomplished by securing the graft while the knee is kept at 30° of flexion. Proper tension is confirmed by ensuring that the graft does not allow lateral patella movement over one-fourth the width of the patella in extension while crepitation must not appear throughout the ROM.92
QUADRICPETS TENDON TRANSFER
A combination of techniques by Steensen and colleagues,105 Goyal,109 Noyes and Albright,117 and Pinkowsky and Hennrikus118 describe an MPFL reconstruction in which the proximal end of a small medial portion of the quadriceps tendon is released and then attached to the medial epicondyle through a subcutaneous tunnel (Figure 4). This technique is particularly useful for cases in which the extra strength provided by the bone-quadriceps tendon is necessary to correct more severe dysplasia. Leaving the distal end of the quadriceps tendon intact at its patellar insertion, a graft of about 8 mm x 70 mm thickness is harvested from the tendon. The free distal end of the tendon is then run anatomically through the synovium and retinaculum to be either sutured to the medial intermuscular septum at the medial femoral epicondyle or fixed in femoral tunnel using interference screw.105,109,118 The placement of the femoral fixation point is essential to ensure positive surgical outcomes. If the graft is secured too anteriorly, it may be too loose in extension and too tight in flexion, both of which can lead to postoperative pain, loss of normal kinematics, and overload of the medial patellofemoral cartilage.119-121 Once the ideal placement of the femoral fixation point has been confirmed by intraoperative radiographs, the graft is secured with a small absorbable suture.122,123 While this technique has good clinical results, the longitudinal scar that results from graft harvesting is cosmetically unappealing, and it is technically challenging to harvest a consistent strip of the quadriceps tendon. To address some of these concerns, Fink and colleagues124 described a new harvesting technique that produces more consistent grafts and requires a smaller incision.
Continue to: ADDUCTOR MAGNUS TENDON TRANSFER
ADDUCTOR MAGNUS TENDON TRANSFER
This technique is a double-bundle MPFL reconstruction that uses a pedicled graft of the distal adductor magnus tendon and suture anchors or incomplete osseous sockets to recreate the MPFL anatomically (Figure 5). Avikainen and colleagues96 and Sillanpää and colleagues125 described this procedure as a progression from the original single-strand adductor magnus transfer technique. First, maintaining the distal insertion, a graft of approximately 14 cm to 18 cm is harvested from the adductor tendon and then passed through a subcutaneous tunnel between the distal vastus medialis obliquus and the superficial joint capsule. The graft is then looped at the medial patella so that the distal bundle runs back to the adductor tubercle.125 With the knee at 30° of flexion to assure proper tension, the graft is secured at both the patella and near the adductor tubercle with suture anchors.125 Hambridge and colleagues126 compared a similar adductor magnus transfer with other pedicled techniques including bone-quadriceps tendon autograft and bone-patellar tendon allograft and found positive results for all 3 methods of reconstruction.
HEMI-PATELLA TENDON TRANSFER
In a similar technique to the adductor tendon transfer, the medial section of the patellar tendon is harvested from the TT and run from its proximal insertion at the medial patella to the medial femoral attachment via a subcutaneous tunnel. The free end of the graft is then secured with suture anchors or incomplete osseous sockets with the knee at 30° of flexion.127
HAMSTRING GRAFT WITH ADDUCTOR TENDON AS A PULLEY
Several techniques opt to use a more dynamic model of MPFL reconstruction in which the adductor tendon or medial collateral ligament (MCL) is used as a pulley for the hamstring graft (Figure 6).128,129 The site of the pulley approximates the normal attachment of the MPFL to the femur and so acts as an effective anatomic replica of the MPFL origin. A semitendinosus graft is harvested and is prepared with continuous sutures, and 2 tunnels to secure the graft are drilled into the patella. The graft is then run subcutaneously from the medial side of the patella to the adductor magnus tubercle into which an osteoperiosteal tunnel is drilled at its distal femoral insertion. The graft is looped through the adductor tunnel and secured with sutures. Proper knee kinematics was ensured by placing the knee at 30° of flexion as the ends of the tendon are secured to the patella.114,130
HAMSTRING GRAFT WITH MCL AS A PULLEY
The MCL can also be used as a pulley rather than the adductor tendon. The semitendinosus graft is harvested and prepared and the patella drilled as it is in the previous technique. The MCL was fashioned into a pulley by making a slit in its posterior one-third. The semitendinosus graft is looped through this slit, and both ends of the graft are held in place with suture anchors on the surface of the patella.129
ADDITIONAL PROCEDURAL COMBINATIONS
Depending on the needs of the individual patient, MPFL reconstruction, and other patellar stabilization techniques can also be combined with additional procedures. Arshi and colleagues83 conducted a review of 6190 adolescents surgically treated for patellar instability and reported the most common additional procedures performed at the time of the stabilization. They found 43.7% of the population underwent lateral retinacular release, which while not effective as an isolated technique to treat patellar instability, has often been used in combination with MPFL reconstruction.131-133 There is currently a lack of consensus regarding the success of adding a lateral release to the reconstruction. Some studies report no difference while others report a decrease in stability after lateral release.90,134-136 While lateral retinacular release has been shown to decrease the force required to displace the patella, it can be surgically indicated in certain patients undergoing MPFL reconstruction.131 The authors advocate that if the lateral retinaculum is tight such that centralized patellar tracking is inhibited following the reconstruction, or if the patella cannot be pushed passively from a laterally tilted position to the neutral horizontal position, lateral retinacular lengthening should be performed to improve kinematics.132
Continue to: Arshi and colleagues...
Arshi and colleagues83 also reported a high rate of cartilage procedures, with chondroplasty performed in 31.1% and chondral fragment/loose body removal in 10.2%. These statistics suggest that a significant level of cartilage damage has occurred by the time of surgery.83
COMPLICATIONS
As MPFL reconstruction techniques have only recently been popularized and developed, there are not many comprehensive studies evaluating the outcomes and complications associated with these procedures. However, in the current literature, there is a general consensus that patients usually experience positive short-term clinical outcomes and relatively low complication rates.68,77 In one of the largest retrospective cohort studies of pediatric patients undergoing MPFL reconstruction, Parikh and colleagues114 reported both the type and rate of complications. They found complications occurred in 16.2% of patients, and the most common complications were recurrent patellar instability, patellar fractures, patellofemoral arthrosis, motion deficits, and stiffness with over half classified as avoidable. Most of these complications were due to technical errors with episodes of recurrent instability only reported in 4.5% of patients.114 In a comprehensive meta-analysis of MPFL reconstruction studies, Shah and colleagues137 reported a complication rate of 26% in both pediatric and adult patients. The cohort was not stratified by age, yet complications were similar to those reported by Parikh and colleagues,114 including pain, loss of knee flexion, wound complications, and patellar fracture.137
As indicated by the frequency of technical complications reported by Parikh and colleagues,114 extra caution should be taken in the operating room to minimize potential errors. In techniques that require drilling of femoral sockets, proper length for and placement of the graft is essential to reestablish proper kinematics. Studies have reported that placing the femoral socket too proximally can result in loss of ROM during flexion and increased compressive forces across the patella.138 A graft that is too short can have similar negative outcomes, and a graft that is too long can result in recurrent instability. Positioning the graft while the knee is in 30° of flexion can help ensure the proper length and tension is achieved. Once the graft is in place, it is important to ensure the ROM and isometry before completing the fixation.72 It is also essential to be vigilant about potential violation of the physes and subsequent growth disturbances. To establish the safest angles for drilling the distal femoral epiphysis for graft placement, Nguyen and colleagues139 conducted a study using high-resolution 3-dimensional images of cadaveric distal femoral epiphyses. By recording which tunnels disrupted the physis before reaching 20 mm of depth, the authors concluded that it is safest to drill distally and anteriorly at an angle between 15° and 20°.139 This technique should minimize damage to the physis, notch, and distal femoral cartilage and decrease potential complications.139
OUTCOMES
In general, the literature reports positive outcomes for MPFL reconstruction—in both studies that address a specific technique and all-encompassing studies. Outcomes are typically reported as Kujala and Tegner scores, results from clinical examinations, and rates of subsequence recurrences. Several recent studies have also evaluated the ability of MPFL reconstruction to restore proper kinematics. Edmonds and colleagues140 evaluated the difference in patellofemoral joint reaction forces and load experienced by 3 groups of adolescents: a cohort treated with MPFL reconstruction, a cohort treated with soft-tissue realignment of the extensor mechanism (the Insall method), and controls. While both surgical techniques were able to restore medial constraints to the patella, the study showed that only the MPFL reconstruction cohort experienced joint reaction forces that were analogous to the control group. In comparison, the cohort that was treated with soft-tissue realignment alone experienced higher patellofemoral joint reaction forces and did not regain normal joint mechanics.140 These results can be used to advocate for the further use of MPFL reconstruction as an effective anatomic replacement of the native ligament. Radiographic studies have similarly reported MPFL reconstruction as an effective means to restore anatomic normality. Fabricant and colleagues141 conducted a radiographic study in which patella alta was corrected to normal childhood ranges in patients who underwent MPFL reconstruction technique using a hamstring autograft. Lykissas and colleagues142 corroborated these results with another radiographic study that reported small but significant decreases in the Blackburne-Peel index and CD index following MPFL reconstruction in 25 adolescents. As correction of patella alta allows the patella to rest in a deeper, more secure position in the TG, these results indicate that effective early MPFL reconstruction can correct for patellar anatomic abnormalities that could be future risk factors.143,144 Several studies have also reported outcomes addressing specific MPFL techniques; these are reported and discussed in this article.
OUTCOMES BY TECHNIQUE
HAMSTRING AUTOGRAFT
Reports on outcomes following MPFL reconstructions using hamstring autografts have been particularly promising. A cohort of 21 skeletally immature patients who underwent MPFL reconstruction was evaluated pre- and postoperatively with an average of a 2.8-year follow-up. The authors of the study reported no redislocation events and significant improvement in the Kujala scores, and patients were able to return to athletic activities safely.145 Previous studies report similar positive increases in Kujala scores, subjective patient reports, and lack of subsequent redislocation for patients who underwent either semitendinosus or gracilis autograft MPFL reconstructions. One such study further documented an average patellar inclination angle decrease from 34.3° to 18.6° following MPFL reconstruction.146 However, while the literature typically reports positive Kujala scores and subjective outcomes for the hamstring autograft procedure, a study arthroscopically evaluating patellar tracking immediately following surgery and then at 6 to 26 months follow-up found that patellar tracking correction was not maintained for all patients who underwent this type of MPFL reconstruction.147
Continue to: QUADRICEPS TENDON TRANSFER OUTCOMES
QUADRICEPS TENDON TRANSFER OUTCOMES
Studies specifically evaluating the quadriceps tendon transfer technique for MPFL reconstruction in children are sparse, but authors have reported positive clinical outcomes and low complication rates in adults. After following 32 young adults who underwent this MPFL reconstruction technique for 3 years, Goyal109 reported a significant increase in mean Kujala scores from 49.31 to 91.25 and no complications or redislocation. He argues this type of quadriceps graft has a high success rate because it is anatomically more similar to the MPFL than other grafts and does not require additional patellar fixation.101,109 Similar positive Kujala scores and minimal complications have been reported in adult patient populations.148 Abouelsoud and colleagues149 conducted one of the few studies in skeletally immature patients and reported similarly positive results with no redislocations and significantly improved Kujala scores at a mean follow-up of 29.25 months in their 16-patient cohorts.
ADDUCTOR MAGNUS TENDON TRANSFER
After initially describing this technique in 14 adult patients, Avikainen and colleagues96 followed this cohort and reported positive subjective results and only 1 redislocation. In a more recent study in which the adductor tendon transfer technique was compared with the quadriceps tendon transfer described above and the bone-patellar tendon allograft, Steiner and colleagues69 reported similarly significant improvement in all cohorts in Lysholm, Kujala, and Tegner scores with no redislocations. Additionally, Malecki and colleagues150 followed a cohort of 33 children with 39 knees diagnosed with recurrent patellar dislocation, who underwent MPFL reconstruction using the adductor magnus tendon. After evaluating this cohort functionally and radiographically, the authors reported improvements in Lysholm and Kujala scores, patellar tilt and congruence angles, and peak torque of the quadriceps muscle and flexor.150 However, this cohort did report postoperative redislocations in 36.4% of patients (4 of 11).150
HEMI-PATELLA TENDON TRANSFER
In 2012, in the first randomized controlled trial, Bitar and colleagues67 compared the outcomes of patients who underwent MPFL reconstruction via the hemi-patellar tendon technique with those who were managed nonoperatively with immobilization and physiotherapy after first-time patellar dislocation. At 2-year follow-up, the surgical cohort presented positive results with a significantly higher mean Kujala score (88.9 to 70.8) and no redislocations or subluxations. In contrast, 35% of nonoperative cases presented with recurrences and subluxations over the 2-year period.67
MCL OR ADDUCTOR TENDON AS A PULLEY
Studies have reported good postoperative results and low complication rates for these dynamic techniques.128,129 In terms of kinematics, while hypermobility and patellar height were not fully corrected, improvements in patellar tilt and lateral shift were reported in a cohort of 6 patients with a minimum 4-year follow-up.129 To further evaluate whether the more dynamic pulley reconstruction technique resulted in better outcomes, Gomes and colleagues128 compared the subjective reports, clinical evaluations, and complication rates of patients who underwent MPFL reconstruction with a rigid adductor magnus fixation vs a semitendinosus tendon dynamic femoral fixation. One case in the rigid cohort experienced a subsequent subluxation, while patients in the semitendinosus group had better subjective reports and a higher rate of return to sport.128 More recently, Kumahashi and colleagues151 specifically studied the outcomes of the MCL tendon as a pulley in 5 patients aged 14 to 15 years. They reported similar successful results as no patients experienced recurrence, and all patients exhibited improvement in radiographic measures of patellar tilt and congruence angle, lateral shift ratio, and both Kujala and Lysholm scores.151
While there has yet to be a randomized controlled trial comparing all of these different techniques, there is a general consensus in the literature that patients tend to perform better following MPFL reconstruction vs MPFL repair.
OTHER STABILIZATION PROCEDURES, INCLUDING DISTAL REALIGNMENT
Patients with additional underlying deficits and malalignment issues such as significant trochlear dysplasia, increased TT-TG distance, patella alta, increased Q angle, and/or positive J sign may require stabilization procedures beyond MPFL reconstruction.152,153 TT osteotomies are often used to correct alignment issues in the adult patient population; however, these procedures are typically contraindicated in skeletally immature patients. Alternative realignment procedures for the pediatric population include both proximal and distal realignment, with proximal realignment performed primarily in children under the age of 12 years.153 Many variations on these procedures exist, some of which are no longer regularly performed due to poor reported outcomes. In this article, we discuss several of the techniques, focusing primarily on those that have demonstrated higher success rates.
Continue to: GALEAZZI TECHNIQUE
GALEAZZI TECHNIQUE
One of the first and most famous soft-tissue techniques to address patellar instability was the semitendinosus tenodesis, published by Galeazzi154 in 1922 (Figure 7). This technique stabilizes the patella without altering the TT. In the original technique, a portion of the semitendinosus tendon is harvested with its tibial insertion left intact. The free end of the tendon is then secured with sutures at the periosteal groove of the medial patella.154,155 Fiume156 modified this technique by adding a lateral release and medial retinacular reefing. The most recent addition to this procedure was introduced by Baker and colleagues,157 in which a tunnel is drilled from the medial to the lateral border of the patella. Tension placed on the grafted tendon is used to reposition the patella medially and draw it downward. Preliminary literature on this modified procedure reported fair clinical results with success rates of approximately 75%.155,158-160 A recent study evaluating both the clinical and radiographic outcomes of this technique also indicated that while clinical results were excellent in 62.5% of patients, this technique alone was unsuccessful in fully addressing patellar instability in patients with underlying anatomic abnormalities such as patellar alta.161 In light of these less than ideal reports, the authors no longer recommend this technique for patellofemoral instability cases.
ROUX-GOLDTHWAIT PROCEDURE
The Roux-Goldthwait procedure, first described by both Roux162 and Goldthwait163 in 1888 and 1895 respectively, was later modified in 1985 to involve a lateral release, plication of the medial retinaculum, medial transfer of the lateral patellar tendon without advancement, and advancement of the vastus medialis (Figure 8).164 More recently, Marsh and colleagues152 introduced an addition to aligning the extensor mechanism with the femoral shaft better. In this technique modification, the patellar tendon is split longitudinally, and its lateral half is detached and transferred distally beneath its medial half. The free end is then sutured to the periosteum on the medial side of the tibia.152 With a mean long-term follow-up of 6.2 years, Marsh and colleagues152 reported excellent results in 65%, good in 11%, and fair in 3% of the knees operated on with this modified technique. Of the patients in this cohort whose strength was evaluated, 80% had their strength returned to 90% of preoperative levels in the operated leg.152 While this study and others report improved outcomes, an increasing body of literature has found high rates of recurrence, patella infera, and other complications following the modified Roux-Goldthwait procedure.36,165-171 Also, a study comparing MPFL reconstruction using adductus magnus transfer with the Roux-Goldthwait procedure reported that patients in the MPFL cohort reported less pain postoperatively.150 In addition, whereas the Kujala and Lysholm scores, recurrence rates, patellofemoral angles, and apprehension test results did not demonstrate significant differences between these 2 groups, the MPFL group had significantly fewer abnormal congruence angles, better patellar medialization, and higher peak torque of the hamstring.150
COMBINED MPFL AND MEDIAL PATELLOTIBIAL LIGAMENT RECONSTRUCTION
While the medial patellotibial ligament (MPTL) has not received much attention with regard to patellar stability, recent studies have indicated its role during higher degrees of both flexion and extension.172 The MPTL acts as a secondary restrictor ligament which helps release stress on the MPFL by decreasing the Q angle and further normalizing patellar kinematics.173 Patients who present with hyperlaxity or knee hyperextension combined with extension subluxation and flexion instability could be indicated for this additional stabilizing procedure. Both Nietosvaara and colleagues85 and Brown and Ahmad174 have described a dual MPTL and MPFL reconstruction technique using a semitendinosus hamstring graft. More recently Hinckel and colleagues172 described a combined MPFL and MPTL reconstruction, using a graft from the quadriceps tendon to reconstruct the MPFL and one from the patellar tendon to reconstruct the MPTL. In this technique, once the respective grafts have been harvested, a femoral insertion for the graft recreating the MPFL is fluoroscopically established so that an anchor can be inserted distal to the femoral physeal growth plate. For the MPTL insertion, attachment to the tibia below the joint line and 2 cm medial to the patellar tendon is established fluoroscopically just above the physeal growth plate on the proximal epiphysis.19,175 The MPTL graft is sutured first with the knee at 90° of flexion to establish tension similar to that of the patellar tendon.176 Then, the knee is placed in 30° of flexion to fix the MPFL graft to the medial patella to prevent excessive lateral translation of the patella.
PATELLAR TENDON TRANSFER
Patellar tendon transfer with proximal realignment is a technique used in particularly young patients to address cases of patellofemoral instability involving concomitant bony or anatomic abnormalities. This procedure is effective for young children with substantial amounts of remaining growth as it better mimics native anatomy than other realignment procedures and does not require bony remodeling.152-154 It is important to familiarize with surgical techniques to address malalignment issues in young patients as neglected alignment issues can lead to worsening of trochlear dysplasia and instability, which are very difficult to treat later on when patients are older.153
The patellar tendon transfer technique (Figure 9), as described by Gordon and Schoenecker,177 starts with an extensive lateral retinacular release. The patellar tendon is then released from its distal insertion at the TT so that it can be moved medially without moving it inferiorly. After confirming patellar tracking and alignment by flexing the knee from 0° to 90° with the graft in place, the patellar tendon graft is secured with multiple nonabsorbable horizontal sutures.177 Of note, in skeletally mature patients, a TT osteotomy is used to accomplish the same goal. This osteotomy has been shown to improve both patellar height and TT-TG distance in skeletally mature patients, but is contraindicated in skeletally immature patients.92,178
Continue to: Initial studies conducted on patellar tendon...
Initial studies conducted on patellar tendon transfer have positive outcomes.179 At a mean follow-up of 5.1 years, patients reported a decrease in pain and increased the ROM and activity, and only 1 reported a postoperative redislocation.179 In more recent studies, both Benoit and colleagues36 and Garin and colleagues58 reviewed cases of patellar instability treated with patellar tendon transfer to address concomitant patellar alignment and anatomic abnormalities. They reported good functional, clinical, and radiographic outcomes with 12.5% and 16% recurrence rates, respectively.36,58 They also noted radiographic improvements in femoral sulcus angle, particularly in younger patients, which indicate this procedure is effective in addressing bony abnormalities that can result from neglected malalignment issues.36,58,154
QUADRICEPSPLASTY
Quadricepsplasty is a lengthening and remodeling technique not frequently used in the pediatric population. The goal of this procedure in patients with significant amounts of growth remaining is to reposition the patella to ameliorate trochlear remodeling and prevent worsening symptoms and anatomic abnormalities.36 A quadricepsplasty accomplishes this by de-rotating and/or lengthening the extensor mechanism and may or may not involve a concomitant MPFL reconstruction. This procedure is particularly effective in young patients who experience obligatory dislocation.60,72 Several quadricepsplasty techniques have been described including Thompson, Curtis and Fisher, Judet, Stanisavljevic, and V-Y technique.180-186 Most techniques initially involve sharp dissection of the vastus medialis and lateralis from the rectus femoral tendon. A tongue is then fashioned out of the rectus femoral tendon. Once the vastus medialis and lateralis are detached from the margins of the patella, the knee is extended, and the distal ends of the vasti are sutured to the tongue of the rectus tendon. Effective extension facilitates flexion to 90°.184 The authors recommend a modification of this technique in which a Z lengthening of the quadriceps tendon is performed after the vastus lateralis is removed distally from the patella and the quadriceps tendon.
Several series and case reports evaluating quadricepsplasty in adult patients report positive outcomes with most patients achieving good or excellent flexion with minimal complications.183,185,187-189 Reports on quadricepsplasty used to treat conditions other than patellofemoral instability in children have reported similar positive outcomes.190-192 As quadricepsplasty for patellar instability is relatively rare in pediatric patients, there is not much relevant literature. However, Kocon and colleagues193 reported results of quadricepsplasty and quadricepsplasty combined with the modified Galeazzi procedure in 8 children (10 knees) with a mean follow-up of 3.25 years. Seventy percent of cases resulted in stabilization and correction of patellar position, and only 2 postoperative redislocations were noted.193 Additionally, in a study evaluating 6 patients suffering from patellar instability, 2 of whom were obligate dislocators, quadricepsplasty resulted in patellar stability, satisfaction, and near normal gait patterns.194
Figure 10 shows the surgical algorithm used for patellar instability characteristics.
CONCLUSION
Patellofemoral joint stability relies on a complex interplay of musculotendinous units, ligaments and the osteocartilaginous morphology of the patellofemoral joint. Patellar instability in pediatric patients is different from adults. Having an in-depth understanding of the remodeling potential, the insertion sites for the MPFL and its relationship to the physis are of utmost importance when planning surgery. Reducing and maintaining the patella within the patellofemoral joint early enough can allow for remodeling of the patella and/or the trochlea to provide for lasting stability. Appropriate surgical principles, such as tensioning, can help both prevent continued pain and minimize future complications.
1. Nietosvaara Y, Aalto K, Kallio PE. Acute patellar dislocation in children: incidence and associated osteochondral fractures. J Pediatr Orthop. 1994;14(4):513-515.
2. Fithian DC, Paxton EW, Stone ML, et al. Epidemiology and natural history of acute patellar dislocation. Am J Sports Med. 2004;32(5):1114-1121. doi:10.1177/0363546503260788.
3. Abbasi D, May MM, Wall EJ, Chan G, Parikh SN. MRI findings in adolescent patients with acute traumatic knee hemarthrosis. J Pediatr Orthop. 2012;32(8):760-764. doi:10.1097/BPO.0b013e3182648d45.
4. Mäenpää H, Lehto MU. Patellar dislocation. The long-term results of nonoperative management in 100 patients. Am J Sports Med. 1997;25(2):213-217. doi:10.1177/036354659702500213.
5. Hawkins RJ, Bell RH, Anisette G. Acute patellar dislocations. The natural history. Am J Sports Med. 1986;14(2):117-120. doi:10.1177/036354658601400204.
6. Cofield RH, Bryan RS. Acute dislocation of the patella: results of conservative treatment. J Trauma. 1977;17(7):526-531.
7. Wasserlauf BL, Paletta GA. Developmental anatomy of the pediatric and adolescent knee. In: Micheli LJ, Kocher MS, eds. The Pediatric and Adolescent Knee. 1st ed. Elsevier; 2006:27-32.
8. Birch JG. Growth and development. In: Herring J, ed. Tachdjian’s Pediatric Orthopedics. 4th ed. Saunders/Elsevier; 2007:3-22.
9. Sarin VK, Carter DR. Mechanobiology and joint conformity regulate endochondral ossification of sesamoids. J Orthop Res. 2000;18(5):706-712. doi:10.1002/jor.1100180505.
10. Maes C, Kronenberg HM. Postnatal bone growth: growth plate biology, bone formation, and remodeling. In: Pediatric Bone. Elsevier; 2012:55-82.
11. Tecklenburg K, Dejour D, Hoser C, Fink C. Bony and cartilaginous anatomy of the patellofemoral joint. Knee Surg Sports Traumatol Arthrosc. 2006;14(3):235-240. doi:10.1007/s00167-005-0683-0.
12. Walmsley R. The development of the patella. J Anat. 1940;74(Pt 3):360-368.3.
13. Fulkerson J, Hungerford D. Disorders of the patellofemoral Joint. In: Normal Anatomy. 2nd ed. Baltimore: Williams & Wilkins; 1990:1-24.
14. Ogden JA. Radiology of postnatal skeletal development. X. Patella and tibial tuberosity. Skeletal Radiol. 1984;11(4):246-257.
15. Nietosvaara Y, Aalto K. The cartilaginous femoral sulcus in children with patellar dislocation: an ultrasonographic study. J Pediatr Orthop. 1997;17(1):50-53.
16. Glard Y, Jouve JL, Garron E, Adalian P, Tardieu C, Bollini G. Anatomic study of femoral patellar groove in fetus. J Pediatr Orthop. 2005;25(3):305-308.
17. Nietosvaara Y. The femoral sulcus in children. An ultrasonographic study. J Bone Joint Surg Br. 1994;76(5):807-809.
18. Nietosvaara AY, Aalto KA. Ultrasonographic evaluation of patellar tracking in children. Clin Orthop Relat Res. 1993;(297):62-64.
19. Desio SM, Burks RT, Bachus KN. Soft tissue restraints to lateral patellar translation in the human knee. Am J Sports Med. 26(1):59-65. doi:10.1177/03635465980260012701.
20. Shea KG, Styhl AC, Jacobs JC, et al. The relationship of the femoral physis and the medial patellofemoral ligament in children: a cadaveric study. Am J Sports Med. 2016;44(11):2833-2837. doi:10.1177/0363546516656366.
21. Shea KG, Polousky JD, Jacobs JC, et al. The relationship of the femoral physis and the medial patellofemoral ligament in children. J Pediatr Orthop. 2014;34(8):808-813. doi:10.1097/BPO.0000000000000165.
22. Shea KG, Polousky JD, Jacobs JC, et al. The patellar insertion of the medial patellofemoral ligament in children. J Pediatr Orthop. 2015;35(4):e31-e35. doi:10.1097/BPO.0000000000000399.
23. Shea KG, Grimm NL, Belzer J, Burks RT, Pfeiffer R. The relation of the femoral physis and the medial patellofemoral ligament. Arthroscopy. 2010;26(8):1083-1087. doi:10.1016/j.arthro.2009.12.020.
24. Nelitz M, Dornacher D, Dreyhaupt J, Reichel H, Lippacher S. The relation of the distal femoral physis and the medial patellofemoral ligament. Knee Surg Sport Traumatol Arthrosc. 2011;19(12):2067-2071. doi:10.1007/s00167-011-1548-3.
25. Kepler CK, Bogner EA, Hammoud S, Malcolmson G, Potter HG, Green DW. Zone of injury of the medial patellofemoral ligament after acute patellar dislocation in children and adolescents. Am J Sports Med. 2011;39(7):1444-1449. doi:10.1177/0363546510397174.
26. Seitlinger G, Moroder P, Fink C, Wierer G. Acquired femoral flexion deformity due to physeal injury during medial patellofemoral ligament reconstruction. Knee. 2017;24(3):680-685. doi:10.1016/j.knee.2017.02.003.
27. Parikh SN, Rajdev N. Relationship between trochlear dysplasia and the anterior distal femoral physis in pediatric and adolescent patients with patellar instability. In: 36th Annual Meething AANA. Denver; 2017.
28. Salenius P, Vankka E. The development of the tibiofemoral angle in children. J Bone Joint Surg Am. 1975;57(2):259-261.
29. Parikh SN. Medial patellofemoral ligament reconstruction and simultaneous guided correction of genu valgum for patellar instability in skeletally immature patients. In: EPOSNA. 2017.
30. Brattstroem H. Shape of the intercondylar groove normally and in recurrent dislocation of patella. A clinical and X-ray-Anatomical investigation. Acta Orthop Scand Suppl. 1964;68(suppl 68):1-148.
31. Dejour H, Walch G, Nove-Josserand L, Guier C. Factors of patellar instability: an anatomic radiographic study. Knee Surg Sports Traumatol Arthrosc. 1994;2(1):19-26.
32. Lewallen LW, McIntosh AL, Dahm DL. Predictors of recurrent instability after acute patellofemoral dislocation in pediatric and adolescent patients. Am J Sports Med. 2013;41(3):575-581. doi:10.1177/0363546512472873.
33. Jaquith BP, Parikh SN. Predictors of recurrent patellar instability in children and adolescents after first-time dislocation. J Pediatr Orthop. 2017;37(7):484-490. doi:10.1097/BPO.0000000000000674.
34. Lippacher S, Reichel H, Nelitz M. Radiological criteria for trochlear dysplasia in children and adolescents. J Pediatr Orthop B. 2011;20(5):341-344. doi:10.1097/BPB.0b013e3283474c8b.
35. Parikh SN, Rajdev N, Sun Q. The growth of trochlear dysplasia during adolescence. J Pediatr Orthop. 2018. doi:10.1097/BPO.0000000000001168. [Epub ahead of print]
36. Benoit B, Laflamme GY, Laflamme GH, Rouleau D, Delisle J, Morin B. Long-term outcome of surgically-treated habitual patellar dislocation in children with coexistent patella alta. Minimum follow-up of 11 years. J Bone Joint Surg Br. 2007;89(9):1172-1177. doi:10.1302/0301-620X.89B9.19065.
37. Sugimoto D, Christino MA, Micheli LJ. Effects of surgical intervention on trochlear remodeling in pediatric patients with recurrent patella dislocation cases. J Pediatr Orthop B. 2016;25(4):349-353. doi:10.1097/BPB.0000000000000341.
38. Insall J, Goldberg V, Salvati E. Recurrent dislocation and the high-riding patella. Clin Orthop Relat Res. 1972;88:67-69.
39. Caton J. [Method of measuring the height of the patella]. Acta Orthop Belg. 1989;55(3):385-386.
40. Thévenin-Lemoine C, Ferrand M, Courvoisier A, Damsin JP, Ducou le Pointe H, Vialle R. Is the Caton-Deschamps index a valuable ratio to investigate patellar height in children? J Bone Joint Surg Am. 2011;93(8):e35. doi:10.2106/JBJS.J.00759.
41. Micheli LJ, Slater JA, Woods E, Gerbino PG. Patella alta and the adolescent growth spurt. Clin Orthop Relat Res. 1986;213:159-162.
42. Koshino T, Sugimoto K. New measurement of patellar height in the knees of children using the epiphyseal line midpoint. J Pediatr Orthop. 1989;9(2):216-218.
43. Mays PK, Bishop JE, Laurent GJ. Age-related changes in the proportion of types I and III collagen. Mech Ageing Dev. 1988;45(3):203-212.
44. Smits-Engelsman B, Klerks M, Kirby A. Beighton score: a valid measure for generalized hypermobility in children. J Pediatr. 2011;158(1):119-123. doi:10.1016/j.jpeds.2010.07.021.
45. Jansson A, Saartok T, Werner S, Renström P. General joint laxity in 1845 Swedish school children of different ages: age- and gender-specific distributions. Acta Paediatr. 2004;93(9):1202-1206.
46. Beighton P, Solomon L, Soskolnet CL. Articular mobility in an African population. Ann rheum Dis. 1973;32(5):413-418.
47. Staheli LT, Corbett M, Wyss C, King H. Lower-extremity rotational problems in children. Normal values to guide management. J Bone Joint Surg Am. 1985;67(1):39-47.
48. Kijowski R, Plagens D, Shaeh S, Teitge R. The effects of rotational deformities of the femur on contact pressure and contact area in the patellofemoral joint and on strain in the medial patellofemoral ligament. Annu Meet Int Patellofemoral Study Group, Napa Val San Fr CA. 1999.
49. Post W, Teitge R, Amis A. Patellofemoral malalignment: looking beyond the viewbox. Clin Sports Med. 2002;21(3):521-546.
50. Bruce WD, Stevens PM. Surgical correction of miserable malalignment syndrome. J Pediatr Orthop. 2004;24(4):392-396.
51. Kurosawa K, Kawame H, Ochiai Y, Nakashima M, Tohma T, Ohashi H. Patellar dislocation in Kabuki syndrome. Am J Med Genet. 2002;108(2):160-163.
52. Mik G, Gholve PA, Scher DM, Widmann RF, Green DW. Down syndrome: orthopedic issues. Curr Opin Pediatr. 2008;20(1):30-36. doi:10.1097/MOP.0b013e3282f35f19.
53. Sweeney E, Fryer A, Mountford R, Green A, McIntosh I. Nail patella syndrome: a review of the phenotype aided by developmental biology. J Med Genet. 2003;40(3):153-162.
54. Stevens CA. Patellar dislocation in Rubenstein-Taybi syndrome. Am J Med Genet. 1997;72(2):188-190.
55. Andrish J. The biomechanics of patellofemoral stability. J Knee Surg. 2004;17(1):35-39.
56. Conlan T, Garth WP, Lemons JE. Evaluation of the medial soft-tissue restraints of the extensor mechanism of the knee. J Bone Joint Surg Am. 1993;75(5):682-693.
57. Balcarek P, Ammon J, Frosch S, et al. Magnetic resonance imaging characteristics of the medial patellofemoral ligament lesion in acute lateral patellar dislocations considering trochlear dysplasia, patella alta, and tibial tuberosity-TG distance. Arthroscopy. 2010;26(7):926-935. doi:10.1016/j.arthro.2009.11.004.
58. Garin C, Chaker M, Dohin B, Kohler R. Permanent, habitual dislocation and recurrent dislocation of the patella in children: surgical management by patellar ligamentous transfer in 50 knees. Rev Chir Orthop Reparatrice Appar Mot. 2007;93(7):690-700.
59. Sillanpaa P. Terminology of patellar dislocation. In: Sillanpaa P, ed. Trauma. Saarbrucken, Germany: Lambert Academic Publishing; 2010:16-18.
60. Parikh SN, Lykissas MG. Classification of lateral patellar instability in children and adolescents. Orthop Clin North Am. 2016;47(1):145-152. doi:10.1016/j.ocl.2015.08.016.
61. Chotel F, Bérard J, Raux S. Patellar instability in children and adolescents. Orthop Traumatol Surg Res. 2014;100(suppl 1):125-137. doi:10.1016/j.otsr.2013.06.014.
62. Wada A, Fujii T, Takamura K, Yanagida H, Surijamorn P. Congenital dislocation of the patella. J Child Orthop. 2008;2(2):119-123. doi:10.1007/s11832-008-0090-4.
63. Südkamp NP, Granrath M, Hoffmann R, Haas NP. Instability of the shoulder joint in the athlete. Chirurg. 1994;65(11):901-909.
64. Hiemstra LA, Kerslake S, Lafave M, Heard SM, Buchko GML. Introduction of a classification system for patients with patellofemoral instability (WARPS and STAID). Knee Surg Sport Traumatol Arthrosc. 2014;22(11):2776-2782. doi:10.1007/s00167-013-2477-0.
65. Frosch KH, Schmeling A. A new classification system of patellar instability and patellar maltracking. Arch Orthop Trauma Surg. 2016;136(4):485-497. doi:10.1007/s00402-015-2381-9.
66. Balcarek P, Oberthür S, Hopfensitz S, et al. Which patellae are likely to redislocate? Knee Surg Sport Traumatol Arthrosc. 2014;22(10):2308-2314. doi:10.1007/s00167-013-2650-5.
67. Bitar AC, Demange MK, D’Elia CO, Camanho GL. Traumatic patellar dislocation: nonoperative treatment compared with mpfl reconstruction using patellar tendon. Am J Sports Med. 2012;40(1):114-122. doi:10.1177/0363546511423742.
68. Smith TO, Walker J, Russell N. Outcomes of medial patellofemoral ligament reconstruction for patellar instability: a systematic review. Knee Surg Sport Traumatol Arthrosc. 2007;15(11):1301-1314. doi:10.1007/s00167-007-0390-0.
69. Steiner TM, Torga-Spak R, Teitge RA. Medial patellofemoral ligament reconstruction in patients with lateral patellar instability and trochlear dysplasia. Am J Sports Med. 2006;34(8):1254-1261. doi:10.1177/0363546505285584.
70. Ma LF, Wang F, Chen BC, Wang CH, Zhou JW, Wang HY. Medial retinaculum plasty versus medial patellofemoral ligament reconstruction for recurrent patellar instability in adults: a randomized controlled trial. Arthrosc J Arthrosc Relat Surg. 2013;29(5):891-897. doi:10.1016/j.arthro.2013.01.030.
71. Weeks KD, Fabricant PD, Ladenhauf HN, Green DW. Surgical options for patellar stabilization in the skeletally immature patient. Sports Med Arthrosc Rev. 2012;20(3):194-202.
72. Green D. Surgical treatment of pediatric patella instability. Die Ther der Instabilen patella. 2016:80-89.
73. Lewallen L, McIntosh A, Dahm D. First-time patellofemoral dislocation: risk factors for recurrent instability. J Knee Surg. 2015;28(4):303-309. doi:10.1055/s-0034-1398373.
74. Ghanem I, Wattincourt L, Seringe R. Congenital dislocation of the patella. Part I: pathologic anatomy. J Pediatr Orthop. 2000;20(6):812-816.
75. Bongers E, Van Kampen A, Van Bokhoven H, Knoers N. Human syndromes with congenital patellar anomalies and the underlying gene defects. Clin Genet. 2005;68(4):302-319. doi:10.1111/j.1399-0004.2005.00508.x.
76. Beighton P, Horan F. Orthopaedic aspects of the Ehlers-Danlos syndrome. J Bone Joint Surg Br. 1969;51(3):444-453.
77. Gausden EB, Fabricant PD, Taylor SA, et al. Medial patellofemoral reconstruction in children and adolescents. JBJS Rev. 2015;3(10):1-11. doi:10.2106/JBJS.RVW.N.00091.
78. Palmu S, Kallio PE, Donell ST, Helenius I, Nietosvaara Y. Acute patellar dislocation in children and adolescents: a randomized clinical trial. J Bone Joint Surg Am. 2008;90(3):463-470. doi:10.2106/JBJS.G.00072.
79. Webb JE, Lewallen LW, Christophersen C, Krych AJ, McIntosh AL. Clinical outcome of internal fixation of unstable juvenile osteochondritis dissecans lesions of the knee. Orthopedics. 2013;36(11):e1444-e1449. doi:10.3928/01477447-20131021-30.
80. Hennrikus W, Pylawka T. Patellofemoral instability in skeletally immature athletes. Instr Course Lect. 2013;62:445-453.
81. Nomura E, Inoue M. Surgical technique and rationale for medial patellofemoral ligament reconstruction for recurrent patellar dislocation. Arthroscopy. 2003;19(5):e47. doi:10.1053/jars.2003.50167.
82. Nomura E, Inoue M, Kobayashi S. Long-term follow-up and knee osteoarthritis change after medial patellofemoral ligament reconstruction for recurrent patellar dislocation. Am J Sports Med. 2007;35(11):1851-1858. doi:10.1177/0363546507306161.
83. Arshi A, Cohen JR, Wang JC, Hame SL, McAllister DR, Jones KJ. Operative management of patellar instability in the United States. Orthop J Sport Med. 2016;4(8):2325967116662873. doi:10.1177/2325967116662873.
84. Servien E, Verdonk PC, Neyret P. Tibial tuberosity transfer for episodic patellar dislocation. Sports Med Arthrosc. 2007;15(2):61-67. doi:10.1097/JSA.0b013e3180479464.
85. Nietosvaara Y, Paukku R, Palmu S, Donell ST. Acute patellar dislocation in children and adolescents. Surgical technique. J Bone Joint Surg Am. 2009;91(suppl 2):139-145. doi:10.2106/JBJS.H.01289.
86. Hing CBC, Smith TO, Donell S, Song F. Surgical versus non-surgical interventions for treating patellar dislocation. In Hing CB, ed. Cochrane Database Syst Rev. 2011;(11):CD008106. doi:10.1002/14651858.CD008106.pub2.
87. Nwachukwu BU, So C, Schairer WW, Green DW, Dodwell ER. Surgical versus conservative management of acute patellar dislocation in children and adolescents: a systematic review. Knee Surgery, Sport Traumatol Arthrosc. 2016;24(3):760-767. doi:10.1007/s00167-015-3948-2.
88. Camp CL, Krych AJ, Dahm DL, Levy BA, Stuart MJ. Medial patellofemoral ligament repair for recurrent patellar dislocation. Am J Sports Med. 2010;38(11):2248-2254. doi:10.1177/0363546510376230.
89. Nikku R, Nietosvaara Y, Aalto K, Kallio PE. Operative treatment of primary patellar dislocation does not improve medium-term outcome: a 7-year follow-up report and risk analysis of 127 randomized patients. Acta Orthop. 2005;76(5):699-704. doi:10.1080/17453670510041790.
90. Ostermeier S, Holst M, Hurschler C, Windhagen H, Stukenborg-Colsman C. Dynamic measurement of patellofemoral kinematics and contact pressure after lateral retinacular release: an in vitro study. Knee Surg Sport Traumatol Arthrosc. 2007;15(5):547-554. doi:10.1007/s00167-006-0261-0.
91. Sallay PI, Poggi J, Speer KP, Garrett WE. Acute dislocation of the patella. A correlative pathoanatomic study. Am J Sports Med. 1996;24(1):52-60. doi: 10.1177/036354659602400110.
92. Arendt EA, Fithian DC, Cohen E. Current concepts of lateral patella dislocation. Clin Sports Med. 2002;21(3):499-519.
93. Arendt EA, Moeller A, Agel J. Clinical outcomes of medial patellofemoral ligament repair in recurrent (chronic) lateral patella dislocations. Knee Surg Sports Traumatol Arthrosc. 2011;19(11):1909-1914. doi:10.1007/s00167-011-1516-y.
94. Ellera Gomes JL. Medial patellofemoral ligament reconstruction for recurrent dislocation of the patella: a preliminary report. Arthroscopy. 1992;8(3):335-340.
95. Amis AA, Firer P, Mountney J, Senavongse W, Thomas NP. Anatomy and biomechanics of the medial patellofemoral ligament. Knee. 2003;10(3):215-220.
96. Avikainen VJ, Nikku RK, Seppänen-Lehmonen TK. Adductor magnus tenodesis for patellar dislocation. Technique and preliminary results. Clin Orthop Relat Res. 1993;(297):12-16.
97. Davis DK, Fithian DC. Techniques of medial retinacular repair and reconstruction. Clin Orthop Relat Res. 2002;(402):38-52.
98. Dhillon MS, Mohan P, Nagi ON. Does harvesting the medial third of the patellar tendon cause lateral shift of the patella after ACL reconstruction? Acta Orthop Belg. 2003;69(4):334-340.
99. Drez D, Edwards TB, Williams CS. Results of medial patellofemoral ligament reconstruction in the treatment of patellar dislocation. Arthrosc J Arthrosc Relat Surg. 2001;17(3):298-306. doi:10.1053/jars.2001.21490.
100. Ellera Gomes JL, Stigler Marczyk LR, César de César P, Jungblut CF. Medial patellofemoral ligament reconstruction with semitendinosus autograft for chronic patellar instability: a follow-up study. Arthrosc J Arthrosc Relat Surg. 2004;20(2):147-151. doi:10.1016/j.arthro.2003.11.006.
101. Feller JA, Amis AA, Andrish JT, Arendt EA, Erasmus PJ, Powers CM. Surgical biomechanics of the patellofemoral joint. Arthrosc J Arthrosc Relat Surg. 2007;23(5):542-553. doi:10.1016/j.arthro.2007.03.006.
102. Nomura E, Horiuchi Y, Kihara M. Medial patellofemoral ligament restraint in lateral patellar translation and reconstruction. Knee. 2000;7(2):121-127.
103. Ostermeier S, Stukenborg-Colsman C, Hurschler C, Wirth CJ. In vitro investigation of the effect of medial patellofemoral ligament reconstruction and medial tibial tuberosity transfer on lateral patellar stability. Arthrosc J Arthrosc Relat Surg. 2006;22(3):308-319. doi:10.1016/j.arthro.2005.09.024.
104. Smirk C, Morris H. The anatomy and reconstruction of the medial patellofemoral ligament. Knee. 2003;10(3):221-227.
105. Steensen RN, Dopirak RM, Maurus PB. A simple technique for reconstruction of the medial patellofemoral ligament using a quadriceps tendon graft. Arthroscopy. 2005;21(3):365-370. doi:10.1016/j.arthro.2004.10.007.
106. Steensen RN, Dopirak RM, McDonald WG. The anatomy and isometry of the medial patellofemoral ligament: implications for reconstruction. Am J Sports Med. 2004;32(6):1509-1513. doi:10.1177/0363546503261505.
107. Farahmand F, Tahmasbi MN, Amis AA. Lateral force–displacement behaviour of the human patella and its variation with knee flexion—a biomechanical study in vitro. J Biomech. 1998;31(12):1147-1152.
108. Heegaard J, Leyvraz PF, Van Kampen A, Rakotomanana L, Rubin PJ, Blankevoort L. Influence of soft structures on patellar 3-dimensional tracking. Clin Orthop Relat Res. 1994;(299):235-243.
109. Goyal D. Medial patellofemoral ligament reconstruction: the superficial quad technique. Am J Sports Med. 2013;41(5):1022-1029. doi:10.1177/0363546513477828.
110. Hohn E, Pandya NK. Does the utilization of allograft tissue in medial patellofemoral ligament reconstruction in pediatric and adolescent patients restore patellar stability? Clin Orthop Relat Res. 2017;475(6):1563-1569. doi:10.1007/s11999-016-5060-4.
111. Csintalan R, Latt L, Fornalski S, Raiszadeh K, Inacio M, Fithian D. Medial patellofemoral ligament (MPFL) reconstruction for the treatment of patellofemoral instability. J Knee Surg. 2013;27(2):139-146. doi:10.1055/s-0033-1360652.
112. Ahmad CS, Brown GD, Stein BS. The docking technique for medial patellofemoral ligament reconstruction: surgical technique and clinical outcome. Am J Sports Med. 2009;37(10):2021-2027. doi:10.1177/0363546509336261.
113. Fernandez E, Sala D, Castejon M. Reconstruction of the medial patellofemoral ligament for patellar instability using a semitendinosus autograft. Acta Orthop Belg. 2005;71(3):303-308.
114. Parikh SN, Nathan ST, Wall EJ, Eismann EA. Complications of medial patellofemoral ligament reconstruction in young patients. Am J Sports Med. 2013;41(5):1030-1038. doi:10.1177/0363546513482085.
115. Green D, Gausden E. Medial patellofemoral ligament reconstruction: hamstring technique. In: Green D, Cordasco F, eds. Pediatr. Adolesc. Knee Surg. New York, NY: Wolters Kluwer; 2015:150-157.
116. Craig JG, Cody DD, van Holsbeeck M. The distal femoral and proximal tibial growth plates: MR imaging, 3-dimensional modeling and estimation of area and volume. Skeletal Radiol. 2004;33(6):337-344.
117. Noyes FR, Albright JC. Reconstruction of the medial patellofemoral ligament with autologous quadriceps tendon. Arthroscopy. 2006;22(8):904.e1-e7. doi:10.1016/j.arthro.2005.12.058.
118. Pinkowsky G, Hennrikus. Technique: quad tendon medial patellofemoral ligament reconstruction. In: Green DW, Cordasco FA, eds. Pediatr. Adolesc. Knee Surg. New York, NY: Wolters Kluwer; 2015:133-139.
119. Bollier M, Fulkerson J, Cosgarea A, Tanaka M. Technical failure of medial patellofemoral ligament reconstruction. Arthroscopy. 2011;27(8):1153-1159. doi:10.1016/j.arthro.2011.02.014.
120. Elias JJ, Cosgarea AJ. Technical errors during medial patellofemoral ligament reconstruction could overload medial patellofemoral cartilage: a computational analysis. Am J Sports Med. 2006;34(9):1478-1485. doi:10.1177/0363546506287486.
121. Thaunat M, Erasmus PJ. Management of overtight medial patellofemoral ligament reconstruction. Knee Surg Sports Traumatol Arthrosc. 2009;17(5):480-483. doi:10.1007/s00167-008-0702-z.
122. Schöttle PB, Schmeling A, Rosenstiel N, Weiler A. Radiographic landmarks for femoral tunnel placement in medial patellofemoral ligament reconstruction. Am J Sports Med. 2007;35(5):801-804. doi:10.1177/0363546506296415.
123. Redfern J, Kamath G, Burks R. Anatomical confirmation of the use of radiographic landmarks in medial patellofemoral ligament reconstruction. Am J Sports Med. 2010;38(2):293-297. doi:10.1177/0363546509347602.
124. Fink C, Veselko M, Herbort M, Hoser C. Minimally invasive reconstruction of the medial patellofemoral ligament using quadriceps tendon. Arthrosc Tech. 2014;3(3):e325-e329. doi:10.1016/j.eats.2014.01.012.
125. Sillanpää PJ, Mäenpää HM, Mattila VM, Visuri T, Pihlajamäki H. A mini-invasive adductor magnus tendon transfer technique for medial patellofemoral ligament reconstruction: a technical note. Knee Surg Sports Traumatol Arthrosc. 2009;17(5):508-512. doi:10.1007/s00167-008-0713-9.
126. Hambidge SJ, Davidson AJ, Gonzales R, Steiner JF. Epidemiology of pediatric injury-related primary care office visits in the United States. Pediatrics. 2002;109(4):559-565.
127. Camanho GL, Bitar AC, Hernandez AJ, Olivi R. Medial patellofemoral ligament reconstruction: a novel technique using the patellar ligament. Arthroscopy. 2007;23(1):108.e1-e4. doi:10.1016/j.arthro.2006.07.008.
128. Gomes JE. Comparison between a static and a dynamic technique for medial patellofemoral ligament reconstruction. Arthroscopy. 2008;24(4):430-435. doi:10.1016/j.arthro.2007.11.005.
129. Deie M, Ochi M, Sumen Y, Yasumoto M, Kobayashi K, Kimura H. Reconstruction of the medial patellofemoral ligament for the treatment of habitual or recurrent dislocation of the patella in children. J Bone Joint Surg Br. 2003;85(6):887-890.
130. Ladenhauf HN, Berkes MB, Green DW. Medial patellofemoral ligament reconstruction using hamstring autograft in children and adolescents. Arthrosc Tech. 2013;2(2):e151-e154. doi:10.1016/j.eats.2013.01.006.
131. Bedi H, Marzo J. The biomechanics of medial patellofemoral ligament repair followed by lateral retinacular release. Am J Sports Med. 2010;38(7):1462-1467. doi:10.1177/0363546510373581.
132. Lattermann C, Toth J, Bach BR. The role of lateral retinacular release in the treatment of patellar instability. Sports Med Arthrosc Rev. 2007;15(2):57-60. doi:10.1097/JSA.0b013e318042af30
133. Ricchetti ET, Mehta S, Sennett BJ, Huffman GR. Comparison of lateral release versus lateral release with medial soft-tissue realignment for the treatment of recurrent patellar instability: a systematic review. Arthroscopy. 2007;23(5):463-468. doi:10.1016/j.arthro.2007.01.007.
134. Dainer RD, Barrack RL, Buckley SL, Alexander AH. Arthroscopic treatment of acute patellar dislocations. Arthroscopy. 1988;4(4):267-271.
135. Miller JR, Adamson GJ, Pink MM, Fraipont MJ, Durand P. Arthroscopically assisted medial reefing without routine lateral release for patellar instability. Am J Sports Med. 2007;35(4):622-629. doi:10.1177/0363546506296041.
136. Vainionpää S, Laasonen E, Silvennoinen T, Vasenius J, Rokkanen P. Acute dislocation of the patella. A prospective review of operative treatment. J Bone Joint Surg Br. 1990;72(3):366-369.
137. Shah JN, Howard JS, Flanigan DC, Brophy RH, Carey JL, Lattermann C. A systematic review of complications and failures associated with medial patellofemoral ligament reconstruction for recurrent patellar dislocation. Am J Sports Med. 2012;40(8):1916-1923. doi:10.1177/0363546512442330.
138. Tanaka MJ, Bollier MJ, Andrish JT, Fulkerson JP, Cosgarea AJ. Complications of medial patellofemoral ligament reconstruction: common technical errors and factors for success: AAOS exhibit selection. J Bone Joint Surg Am. 2012;94(12):e87. doi:10.2106/JBJS.K.01449.
139. Nguyen CV, Farrow LD, Liu RW, Gilmore A. Safe drilling paths in the distal femoral epiphysis for pediatric medial patellofemoral ligament reconstruction. Am J Sports Med. 2017;45(5):1085-1089. doi:10.1177/0363546516677795.
140. Edmonds EW, Glaser DA. Adolescent patella instability extensor mechanics. J Pediatr Orthop. 2016;36(3):262-267. doi:10.1097/BPO.0000000000000430.
141. Fabricant PD, Ladenhauf HN, Salvati EA, Green DW. Medial patellofemoral ligament (MPFL) reconstruction improves radiographic measures of patella alta in children. Knee. 2014;21(6):1180-1184. doi:10.1016/j.knee.2014.07.023.
142. Lykissas MG, Li T, Eismann EA, Parikh SN. Does medial patellofemoral ligament reconstruction decrease patellar height? A preliminary report. J Pediatr Orthop. 2014;34(1):78-85. doi:10.1097/BPO.0b013e3182a12102.
143. Magnussen RA, De Simone V, Lustig S, Neyret P, Flanigan DC. Treatment of patella alta in patients with episodic patellar dislocation: a systematic review. Knee Surgery, Sport Traumatol Arthrosc. 2014;22(10):2545-2550. doi:10.1007/s00167-013-2445-8.
144. Schöttle PB, Fucentese SF, Romero J. Clinical and radiological outcome of medial patellofemoral ligament reconstruction with a semitendinosus autograft for patella instability. Knee Surg Sports Traumatol Arthrosc. 2005;13(7):516-521. doi:10.1007/s00167-005-0659-0.
145. Nelitz M, Dreyhaupt J, Reichel H, Woelfle J, Lippacher S. Anatomic reconstruction of the medial patellofemoral ligament in children and adolescents with open growth plates: surgical technique and clinical outcome. Am J Sports Med. 2013;41(1):58-63. doi:10.1177/0363546512463683.
146. Raghuveer RK, Mishra CB. Reconstruction of medial patellofemoral ligament for chronic patellar instability. Indian J Orthop. 2012;46(4):447-454. doi:10.4103/0019-5413.97259.
147. Kita K, Horibe S, Toritsuka Y, et al. Effects of medial patellofemoral ligament reconstruction on patellar tracking. Knee Surg Sports Traumatol Arthrosc. 2012;20(5):829-837. doi:10.1007/s00167-011-1609-7.
148. Lenschow S, Herbort M, Fink C. Medial patellofemoral ligament reconstruction using quadriceps tendon. Oper Orthop Traumatol. 2015;27(6):474-483. doi:10.1007/s00064-015-0416-6.
149. Abouelsoud MM, Abdelhady A, Elshazly O. Anatomic physeal-sparing technique for medial patellofemoral ligament reconstruction in skeletally immature patients with ligamentous laxity. Eur J Orthop Surg Traumatol. 2015;25(5):921-926. doi:10.1007/s00590-015-1618-1.
150. Malecki K, Fabis J, Flont P, Niedzielski KR. The results of adductor magnus tenodesis in adolescents with recurrent patellar dislocation. Biomed Res Int. 2015;2015:1-7. doi:10.1155/2015/456858.
151. Kumahashi N, Kuwata S, Tadenuma T, Kadowaki M, Uchio Y. A “sandwich” method of reconstruction of the medial patellofemoral ligament using a titanium interference screw for patellar instability in skeletally immature patients. Arch Orthop Trauma Surg. 2012;132(8):1077-1083. doi:10.1007/s00402-012-1516-5.
152. Marsh JS, Daigneault JP, Sethi P, Polzhofer GK. Treatment of recurrent patellar instability with a modification of the Roux-Goldthwait technique. J Pediatr Orthop. 2006;26(4):461-465. doi:10.1097/01.bpo.0000217711.34492.48.
153. Nepple J, Luhmann S. Medial patellar tendon transfer with proximal realignment. In: Green D, Cordasco F, eds. Pediatric and Adolescent Knee Surgery. New York, NY: Wolters Kluwer; 2015:148-153.
154. Galeazzi R. Nuove applicazioni del trapianto musculare e tendineo. Ard Di Orthop Milano. 1922;38:315-323.
155. Grannatt K, Heyworth BE, Ogunwole O, Micheli LJ, Kocher MS. Galeazzi semitendinosus tenodesis for patellofemoral instability in skeletally immature patients. J Pediatr Orthop. 2012;32(6):621-625. doi:10.1097/BPO.0b013e318263a230.
156. Fiume M. La rotulopessi secondi Galeazzi nella lussazione recidivante di rotula [in Italian]. Minerva Ortop. 1954;5:171-174.
157. Baker RH, Carroll N, Dewar FP, Hall JE. The semitendinosus tenodesis for recurrent dislocation of the patella. J Bone Joint Surg Br. 1972;54(1):103-109.
158. Hall JE, Micheli LJ, McManama GB. Semitendinosus tenodesis for recurrent subluxation or dislocation of the patella. Clin Orthop Relat Res. 1979;(144):31-35.
159. Moyad TF, Blakemore L. Modified Galeazzi technique for recurrent patellar dislocation in children. Orthopedics. 2006;29(4):302-304.
160. Letts RM, Davidson D, Beaule P. Semitendinosus tenodesis for repair of recurrent dislocation of the patella in children. J Pediatr Orthop. 1999;19(6):742-747.
161. Aulisa AG, Falciglia F, Giordano M, Savignoni P, Guzzanti V. Galeazzi’s modified technique for recurrent patella dislocation in skeletally immature patients. J Orthop Sci. 2012;17(2):148-155. doi:10.1007/s00776-011-0189-1.
162. Roux C. Recurrent dislocation of the patella: operative treatment. 1888. Clin Orthop Relat Res. 2006;452:17-20.
163. Goldthwait J. Dislocation of the Patella. Trans Am Orthop Assn. 1895.
164. Fondren FB, Goldner JL, Bassett FH. Recurrent dislocation of the patella treated by the modified Roux-Goldthwait procedure. A prospective study of forty-seven knees. J Bone Joint Surg Am. 1985;67(7):993-1005.
165. Aärimaa V, Ranne J, Mattila K, Rahi K, Virolainen P, Hiltunen A. Patellar tendon shortening after treatment of patellar instability with a patellar tendon medialization procedure. Scand J Med Sci Sports. 2008;18(4):442-446. doi:10.1111/j.1600-0838.2007.00730.x.
166. Nelitz M, Reichel H, Dornacher D, Lippacher S. Anatomical reconstruction of the medial patellofemoral ligament in children with open growth-plates. Arch Orthop Trauma Surg. 2012;132(11):1647-1651. doi:10.1007/s00402-012-1593-5.
167. Vähäsarja V, Kinnunen P, Lanning P, Serlo W. Operative realignment of patellar malalignment in children. J Pediatr Orthop. 1995;15(3):281-285.
168. Abraham E, Washington E, Huang TL. Insall proximal realignment for disorders of the patella. Clin Orthop Relat Res. 1989;248:61-65.
169. Insall JN, Aglietti P, Tria AJ. Patellar pain and incongruence. II: Clinical application. Clin Orthop Relat Res. 1983;176:225-232.
170. Chrisman OD, Snook GA, Wilson TC. A long-term prospective study of the Hauser and Roux-Goldthwait procedures for recurrent patellar dislocation. Clin Orthop Relat Res. 1979;144:27-30.
171. Niedzielski KR, Malecki K, Flont P, Fabis J. The results of an extensive soft-tissue procedure in the treatment of obligatory patellar dislocation in children with ligamentous laxity: a post-operative isokinetic study. Bone Joint J. 2015;97-B(1):129-133. doi:10.1302/0301-620X.97B1.33941.
172. Hinckel BB, Gobbi RG, Demange MK, Bonadio MB, Pécora JR, Camanho GL. Combined reconstruction of the medial patellofemoral ligament with quadricipital tendon and the medial patellotibial ligament with patellar tendon. Arthrosc Tech. 2016;5(1):e79-e84. doi:10.1016/j.eats.2015.10.004.
173. Mani S, Kirkpatrick MS, Saranathan A, Smith LG, Cosgarea AJ, Elias JJ. Tibial tuberosity osteotomy for patellofemoral realignment alters tibiofemoral kinematics. Am J Sports Med. 2011;39(5):1024-1031. doi:10.1177/0363546510390188.
174. Brown GD, Ahmad CS. Combined medial patellofemoral ligament and medial patellotibial ligament reconstruction in skeletally immature patients. J Knee Surg. 2008;21(4):328-332.
175. Panagiotopoulos E, Strzelczyk P, Herrmann M, Scuderi G. Cadaveric study on static medial patellar stabilizers: the dynamizing role of the vastus medialis obliquus on medial patellofemoral ligament. Knee Surg Sports Traumatol Arthrosc. 2006;14(1):7-12. doi:10.1007/s00167-005-0631-z.
176. Philippot R, Boyer B, Testa R, Farizon F, Moyen B. The role of the medial ligamentous structures on patellar tracking during knee flexion. Knee Surg Sports Traumatol Arthrosc. 2012;20(2):331-336. doi:10.1007/s00167-011-1598-6.
177. Gordon JE, Schoenecker PL. Surgical treatment of congenital dislocation of the patella. J Pediatr Orthop. 1999;19(2):260-264.
178. Koh JL, Stewart C. Patellar instability. Orthop Clin North Am. 2015;46(1):147-157. doi:10.1016/j.ocl.2014.09.011.
179. Pal S, Besier TF, Draper CE, et al. Patellar tilt correlates with vastus lateralis: vastus medialis activation ratio in maltracking patellofemoral pain patients. J Orthop Res. 2012;30(6):927-933. doi:10.1002/jor.22008.
180. Thompson TC. Quadricepsplasty. Ann Surg. 1945;121(5):751-754.
181. Daoud H, O’Farrell T, Cruess RL. Quadricepsplasty. The Judet technique and results of six cases. J Bone Joint Surg Br. 1982;64(2):194-197.
182. Stanisavljevic S, Zemenick G, Miller D. Congenital, irreducible, permanent lateral dislocation of the patella. Clin Orthop Relat Res. 1976;(116):190-199.
183. Kundu Z, Sangwan S, Guliani G, Siwach R, Kamboj P, Singh R. Thompson’s quadricepsplasty for stiff knee. Indian J Orthop. 2007;41(4):390-394. doi:10.4103/0019-5413.37004.
184. Tercier S, Shah H, Joseph B. Quadricepsplasty for congenital dislocation of the knee and congenital quadriceps contracture. J Child Orthop. 2012;6(5):397-410. doi:10.1007/s11832-012-0437-8.
185. Rose RE. Judet quadricepsplasty for extension contracture of the knee. West Indian Med J. 2005;54(4):238-241.
186. Tsukamoto N, Miura H, Matsuda S, Mawatari T, Kato H, Iwamoto Y. Functional evaluation of four patients treated with V-Y quadricepsplasty in total knee arthroplasty. J Orthop Sci. 2006;11(4):394-400. doi:10.1007/s00776-006-1023-z.
187. Dao Q, Chen DB, Scott RD. Proximal patellar quadricepsplasty realignment during total knee arthroplasty for irreducible congenital dislocation of the patella. J Bone Joint Surg Am. 2010;92(14):2457-2461. doi:10.2106/JBJS.H.00812.
188. Judet R, Judet J, Lord G. Results of treatment of stiffness of the knee caused by arthrolysis and disinsertion of the quadriceps femoris. Mem Acad Chir. 1959;85:645-654.
189. Oliveira VG, D’Elia LF, Tirico LEP, et al. Judet quadricepsplasty in the treatment of posttraumatic knee rigidity: long-term outcomes of 45 cases. J Trauma Acute Care Surg. 2012;72(2):e77-e80.
190. Hahn SB, Choi YR, Kang HJ, Lee SH. Prognostic factors and long-term outcomes following a modified Thompson’s quadricepsplasty for severely stiff knees. J Bone Joint Surg Br. 2010;92(2):217-221. doi:10.1302/0301-620X.92B2.22936.
191. Hosalkar HS, Jones S, Chowdhury M, Hartley J, Hill RA. Quadricepsplasty for knee stiffness after femoral lengthening in congenital short femur. J Bone Joint Surg Br. 2003;85(2):261-264.
192. Massè A, Biasibetti A, Demangos J, Dutto E, Pazzano S, Gallinaro P. The judet quadricepsplasty: long-term outcome of 21 cases. J Trauma. 2006;61(2):358-362. doi:10.1097/01.ta.0000230281.31144.1d.
193. Kocon H, Kabacyj M, Zgoda M. The results of the operative treatment of patellar instability in children with Down’s syndrome. J Pediatr Orthop B. 2012;21(5):407-410. doi:10.1097/BPB.0b013e328354f684.
194. Martin BD, Cherkashin AM, Tulchin K, Samchukov M, Birch JG. Treatment of femoral lengthening-related knee stiffness with a novel quadricepsplasty. J Pediatr Orthop. 2013;33(4):446-452. doi:10.1097/BPO.0b013e3182784e5d.
ABSTRACT
Patellar instability in children and adolescents is a challenging subset to treat. Varied forms of instability, ranging from episodic dislocation to fixed dislocation, have been recognized. It is of utmost importance for the treating physician to recognize these different patterns of instability and their associated risk factors, as more complex patterns of instability would require more extensive surgical procedures. Medial patellofemoral ligament (MPFL) reconstruction, by itself, may not suffice or may not be appropriate for the more complex instability patterns. Appropriate and early treatment of such instability in children would allow for functional progression and possible remodeling of the trochlea. However, early treatment has the associated risk of growth disturbances when surgical procedures are performed around open physis or if adult-type bony procedures are performed in children. Recent knowledge about the relationship between trochlea, MPFL femoral attachment, and distal femoral physis could help to advance safe surgical care for these patients. This article reviews the pathophysiology, risk factors, and the existing classification systems for patellar instability in children and adolescents. It focuses on varied surgical techniques, which are unique to the pediatric population, and summarizes the outcomes of these surgical techniques.
Continue to: EPIDEMIOLOGY
EPIDEMIOLOGY
In a prospective 2-year study of Finnish children, the annual incidence rate of patellar instability was 43/100,000 pediatric population.1 In patients 9 to 15 years of age, the incidence was approximately 1/1000.1 In another study, patients at highest risk for a first-time patellar dislocation were females aged 10 to 17 years.2 In a study in patients with traumatic hemarthrosis, 36% in the younger age group (10-14 years) and 28% in the older age group (15-18 years) had sustained patellar dislocation. In contrast, 22% in the younger age group and 40% in the older age group had sustained an anterior cruciate ligament tear.3
Approximately one-half of patients who dislocate their patella suffer from long-term complications.4,5 These complications include recurrent instability, patellofemoral pain, osteochondral lesions, and eventual arthritis.1,4,5 Young, active individuals are more prone to these issues.6 Also, 39% or more of patellar dislocation patients have an associated osteochondral fracture that might influence the management.1 Thus, patellar instability in young patients is an area of concern.
DEVELOPMENTAL ANATOMY
At 4-week gestation, the patellofemoral joint is an ectodermal sac filled with mesenchyme of the somatic mesoderm.7 Mesenchymal condensations then appear at 4 to 5 weeks gestation, followed by chondrification of both the femur and patella.7 The joint space is present by 6 weeks, and the patellar and distal femoral condyles are present at 7 weeks gestation.7 By 8 weeks gestation, the basic knee anatomy resembles that of an adult with the chondroepiphysis forming the articular surfaces of the femur, tibia, and patella.7 By this time, the extensor mechanism is formed, and active joint motion has begun, facilitating the development of the trochlear sulcus.7 The secondary ossification center in the distal femoral epiphysis forms around 36 weeks gestation.8 Postnatally, both the patella and distal femur grow through endochondral ossification.9,10
The patella is the largest sesamoid bone in the human body.11 The patella begins as a dense consolidation of cells that differentiate as the quadriceps mechanisms develop.12,13 The patellar anlage becomes distinguishable within the quadriceps tendon around 7.5-week gestation.12 The morphology of the patella conforms to the distal femur.12 The patella molds or re-models as the knee begins to move in response to mechanical stresses.7 The patella increases in relative size during the first 6 months of gestation, then enlarges proportionately to the rest of the bones.7 Ossification begins around 3 years of age for females and 4 to 5 years of age for males.8,14 The ossification center may appear irregular as it rapidly expands.14 Ossification proceeds in a proximal to distal direction, thus giving a spurious estimation of patellar height on radiographs in children. The overall morphology of the cartilaginous patella during development is comparable to the final mature shape.14 Abnormal contact stresses on the articular surface of the patella during skeletal immaturity can lead to deformation.7
Ultrasonographic measurements in normal patients show that trochlear groove (TG) morphology is present early and becomes more radiographically apparent as distal femoral ossification is completed.15 Anatomic dissections of aborted fetuses have verified the morphology of the TG as it remains constant during growth and the groove morphology is the same for both fetuses and adults.16 An ultrasound study performed on patients aged 12 to 18 years showed the cartilaginous sulcus angle (CSA) remained constant throughout all age groups (146°).17 The CSA however, differed in patients who suffered a patellar dislocation (average, 164°; range, 154°-195°) compared with normal knees (average CSA, 145°; range, 131°-158°).15,17,18 The osseous sulcus angle, on the other hand, appears flat at birth and the TG deepens with age. This increase in depth is more of a reflection of progressive ossification of a well-formed cartilaginous trochlea, rather than a true deepening of the sulcus.17 Thus, the axial radiographic view of the patella provides misleading information about the sulcus angle in children and should not be used to define trochlear morphology.
Continue to: MEDIAL PATELLOFEMORAL LIGAMENT ANATOMY
MEDIAL PATELLOFEMORAL LIGAMENT ANATOMY
The medial patellofemoral ligament (MPFL) functions to limit the lateral translation of the patella.19 The attachment sites on the femur and patella for the MPFL have been studied in children.20-23 Cadaveric dissections in specimens aged 2 to 11 years have noted the patellar attachment to be an average of 12 mm in length with the midpoint approximately 5 mm superior to the mid-pole of the patella.22 The patellar footprint of the MPFL insertion was a mean 41% of the entire patellar length.22
It is important to be aware of the characteristic anatomy of the MPFL, as fixation points should mimic the anatomic insertion as best as possible while also avoiding violation of the nearby physis. The MPFL originates between the adductor tubercle and the medial femoral epicondyle just distal to the distal femoral physis and attaches to the superomedial aspect of the patella.20-25 In relation to the physis in pediatric patients, the midpoint of MPFL insertion has been measured to be 4 mm to 9 mm distal to the femoral physis.21,24,25 These measurements represent averages as cadaveric studies have reported that some part of MPFL femoral insertion extends proximal to the distal femoral physis.21 A recent report of physeal injury to the posterior distal femoral physis during MPFL reconstruction leading to femoral flexion deformity highlights the importance of physeal-respecting surgery.26
TROCHLEA AND ANTERIOR DISTAL FEMORAL PHYSIS
The relationship between the proximal aspect of the trochlea and the anterior distal femoral physis has been recently studied in 175 knees with dysplastic trochlea.27 Based on magnetic resonance imaging evaluation, the lateral aspect of the trochlea extended proximal to the anterior distal femoral physis in 13% of patients and was at the level of the anterior physis in another 13% of patients (Figure 1).27 Hence, a cautious approach is recommended for any surgery to address trochlear dysplasia or trochlear bump in younger patients to prevent iatrogenic injury to anterior distal femoral physis and resultant genu recurvatum. The distance between the trochlea and the physis increased with increasing age.
LIMB ALIGNMENT
Physiologically, the quadriceps angle (Q angle) changes through the course of growth. As children begin standing and walking, they stand with their feet wider apart and in genu varum.28 Physiologic genu varum can reach 15°.28 This degree lessens during the first 1.5 to 2 years of life, transitioning to physiologic valgus of nearly 12° by 3 years of age.28 Genu valgum, thereafter, gradually decreases to reach the adult value of around 7° to 8° by age 7 years.28 Increased genu valgum is a risk factor for patellar instability. In skeletally immature patients, correction of genu valgum through guided growth may be desirable in patients undergoing patellar stabilization surgery (Figures 2A, 2B).29
PATHOPHYSIOLOGY OF PEDIATRIC PATELLAR DISLOCATION
TROCHLEAR DYSPLASIA
Trochlear dysplasia is an abnormal shape and depth of the TG.30 Up to 96% of patients with patellar dislocation have trochlear dysplasia.30-33 In a study of patellar instability in children, at least 1 of the 3 signs of trochlear dysplasia (the crossing sign, supratrochlear bump, and double contour sign) was present on lateral radiographs.34 In another study on the growth of trochlear dysplasia in children and adolescents, all grades of trochlear dysplasia were present at all ages (ie, the dysplasia was most likely present at birth and did not necessarily worsen with age and growth).35 The linear dimensions of lateral and medial condylar height as well as trochlear bump increased with age but both the sulcus angle and shape of the trochlea did not change significantly.35 Remodeling of a dysplastic trochlea can happen if the patella is stabilized and appropriately located at a younger age, preferably before 10 years of age.36,37
Continue to: PATELLAR HEIGHT
PATELLAR HEIGHT
The role of patellar height in patellar instability has been well established.38 In patients with patella alta, the patella remains proximal to the TG during the greater arc of knee motion, which predisposes it to patellar instability. Calculation of patellar height in children could be challenging due to incomplete ossification, as well as asymmetric ossification of the patella and the tibial tubercle (TT). Since the patella ossifies from proximal to distal, most radiographic methods that measure the patellar height from the distal aspect of the patella provide a spurious elevation of the measurement.
The Caton-Deschamps (CD) method measures the length of the patellar articular surface and the distance from the inferior edge of the articular surface to the anterosuperior corner of the tibial plateau.39 A ratio >1.3 signifies patella alta. The CD ratio has been verified as a simple and reliable index for measuring patellar height in children.40 Two other methods have been described for determining patellar height in children.41,42 Based on anteroposterior (AP) radiographs of the knee in full extension, Micheli and colleagues41 calculated the difference between the distance from the superior pole of the patella to the tibial plateau and the length of the patella. A positive difference signified patella alta. The Koshino method involves the ratio between a reference line from the midpoint of the patella to the midpoint of the proximal tibial physis and a second distance from the midpoint of the distal femoral physis to the midpoint of the proximal tibial physis on lateral knee radiographs.42 Normal values range from 0.99 to 1.20 with the knee in >30° flexion, in children 3 to 18 years of age.
HYPERLAXITY
In contrast to adults, children have increased levels of collagen III compared with collagen I, which is responsible for tissue elasticity.43 Tissue elasticity leads to increased joint mobility, which is more common in children. Joint hypermobility or hyperlaxity has to be differentiated from symptomatic instability. The traditional Beighton score identifies individuals as having joint hypermobility with a score of 5/9 or higher in school-aged children.44-46 Smits-Engelsman and colleagues44 suggested using stricter criteria with scores of 7/9 or higher being indicative of hyperlaxity in school-aged children. A study of 1845 Swedish school children noted that females have a higher degree of joint laxity.45 Maximal laxity was noted in females at 15 years of age.45 Hyperlaxity has been demonstrated to be greater on the left side of the body44 and can be part of generalized syndromes including Down’s syndrome, Marfan’s syndrome, or Ehlers-Danlos syndrome.
LIMB TORSION
Staheli and colleagues47 described the normative values of a lower extremity rotational profile, including femoral anteversion and tibial torsion. Children normally have increased femoral anteversion, which decreases with growth. Miserable malalignment is a term used to denote increased femoral anteversion and increased external tibial torsion.48,49 These rotational abnormalities can increase the Q angle and the lateral forces on the patella. Femoral anteversion or internal rotation of the femur of 30° significantly increases strain in all areas of the MPFL.48 This increased strain may lead to MPFL failure and patellar instability.48 Increased internal rotation of the femur also increases contact pressure on the lateral aspect of the patellofemoral joint.48 Miserable malalignment frequently manifests following a pubertal growth spurt and may require femoral and tibial osteotomy.50
SYNDROMIC ASSOCIATIONS
Several syndromes have patellar instability as a part of their manifestation. The more common syndromes include nail-patella syndrome, Kabuki syndrome, Down’s syndrome, and Rubinstein-Taybi syndrome.51-54 Other syndromes less commonly associated with patellar instability include Turner syndrome, patella aplasia, or absent patella syndrome. Since many patients with syndromic patellar instability are functionally limited, they may not require an aggressive approach to treatment. When treating these patients, it is important to recognize the unique features of a specific syndrome, which may affect the anesthesia risk profile, management decisions, rehabilitation, and prognosis.
Continue to: MPFL TEAR PATTERN
MPFL TEAR PATTERN
The MPFL serves as an important constraint to the patella to prevent lateral dislocation, primarily during the first 20° to 30° of knee flexion.55,56 Injury to the MPFL is noted in over 90% of patients who suffer a patellar dislocation.57 The location of MPFL tears in pediatric patients is variably reported at the patellar attachment (10%-61%), femoral attachment (12%-73%), both (12%-35%) or mid-substance (2.5%-15%).25,57 The most common tear patterns in pediatric patients are tears at the patellar attachment.25,57 This tear pattern may be accompanied by an avulsion fracture of the medial rim of the patella, though this fracture, being extra-articular, seldom needs treatment.
CLASSIFICATION
While several authors have established extensive classification systems of patellar dislocation based on both clinical and radiographic presentation and reviews of the literature, a single classification system has not been recognized as the gold standard. In this section, in addition to presenting our preferred methods of classification, we will review some of the more recent and extensive classification systems for patellar dislocation and patellar instability.
Dejour and colleagues31 initially used both the presence of patellofemoral anatomic abnormalities and pain to define 3 types of patellar instability: major, objective, and potential patellar instability. Major patellar instability indicates that the patient has experienced more than 1 documented dislocation, objective instability involves one dislocation in addition to an associated anatomic abnormality, and potential patellar instability refers to cases in which the patient has radiographic abnormalities and patellar pain.31 Garin and colleagues58 more simplistically divided patellar dislocation patients into 2 groups: major (permanent or habitual) dislocation of the patella and recurrent dislocation. Sillanpaa59 stressed the distinction between first-time dislocation and recurrent dislocation specifically in the context of acute injuries. These classification systems were formulated with adults as the most relevant population; however, classifications targeted specifically to pediatric patients have recently been presented in the literature.
Historically, pediatric patella dislocations were simply categorized as traumatic or congenital.60 In 2014, Chotel and colleagues61 focused on classifying patellar dislocation by extensively reviewing anatomic, biomechanical, pathophysiological, and clinical patterns seen most commonly in children. They included 5 categories: congenital dislocation, permanent dislocation, habitual dislocation during knee flexion, habitual dislocation during knee extension, and recurrent dislocation; however, they did not address traumatic dislocations.61 Congenital dislocation is a rare condition, typically presenting at birth, which produces a pattern of functional genu valgum.62 Permanent dislocation typically presents after the child has started walking, but before the age of 5 years.61 The 2 variations of habitual dislocation typically present between ages 5 and 8 years.61 The final category is the most common and typically occurs during pre-adolescence or adolescence as a result of an atraumatic or trivial traumatic event or sports injury.1 Using more specific terminology, Hiemstra and colleagues63 modeled a classification system based on the traumatic, unilateral, bankart lesion, surgery (TUBS)/atraumatic, multidirectional, bilateral, rehabilitation, inferior shift (AMBRI) for shoulder dislocation classifications. The patellar dislocation system is used to identify 2 distinct subsets of patients in the patellofemoral instability population. One subset is defined by the acronym WARPS (weak, atraumatic, risky anatomy, pain, and subluxation), the other is STAID (strong, traumatic, anatomy normal, instability, and dislocation).64 Patients categorized by the WARPS acronym tend to experience atraumatic onsets of patellofemoral instability and demonstrate anatomic issues that increase this instability. These underlying anatomic issues include valgus alignment, ligamentous laxity, rotational abnormalities, shallow and short TG, and patella alta. On the other hand, STAID patients describe a traumatic dislocation event and do not have underlying anatomic abnormalities that predispose them to instability.64
Taking into account these previous classifications, Frosch and colleagues65 added specific pathologies including “instability,” “maltracking,” and “loss of patellar tracking,” in addition to both clinical and radiographic factors to define 5 types of patellar dislocation and their specific treatment recommendations.65 Type 1 involves simple dislocation with neither maltracking nor instability and a low risk of redislocation.65 Type 2 is defined as primary dislocation followed by subsequent high risk of dislocation and no maltracking.65 Type 3 is divided into 5 subcategories of instability and maltracking issues involving soft tissue contracture, patella alta, pathological tibial tuberosity, and TG distance.65 Type 4 is defined as the highly unstable “floating patella,” and type 5 involves patellar maltracking without instability 65. In terms of treatment, conservative rehabilitation is recommended for type 1 whereas MPFL reconstruction tends to show positive outcomes for both types 2 and 3.66-70
Continue to: Parikh and Lykissas recently published...
Parikh and Lykissas recently published a comprehensive classification system of 4 defined types of patellar dislocation in addition to voluntary patellar instability and syndromic patellar instability (Table).60 The 4 types are Type 1, first-time patellar dislocation; Type 2, recurrent patellar instability; Type 3, dislocatable; and Type 4, dislocated. Type 2 is further subdivided into Type 2A, which presents with positive apprehension signs, and Type 2B, which involves instabilities related to anatomic abnormalities.60 A distinction is also made between Type 3A or passive patellar dislocation and Type 3B habitual patellar dislocation.60
The classification system proposed by Green and colleagues is more simplified with 3 main categories (Table) of pediatric patellar dislocation: traumatic (acute or recurrent), obligatory (either in flexion or extension), and fixed laterally.71,72 The acute traumatic categorization refers to patients who experienced an initial dislocation event due to trauma whereas recurrent traumatic involves repeated patella dislocations following an initial incident. Studies report that between 60% to 70% of these acute traumatic dislocations occur as a result of a sports-related incident.2,33,73 Obligatory dislocations occur with every episode of either knee flexion or extension, depending on the subtype. Obligatory patella dislocation in flexion typically cannot be manipulated or relocated into the trochlea while the knee is fixed but does reduce into the trochlea in full extension. Fixed lateral dislocations are rare, irreducible dislocations in which the patella stays dislocated laterally in flexion and extension. These dislocations often present with other congenital abnormalities. Each of these categories can be further specified as syndromic if the dislocation is associated with genetic or congenital conditions including skeletal dysplasia, Ehlers-Danlos syndrome, cerebral palsy, Marfan disease, nail-patella syndrome, Down syndrome, Rubenstein-Taybi syndrome, and Kabuki syndrome.51-54,61,74-76
SURGICAL TECHNIQUES IN SKELETALLY IMMATURE PATIENTS
While nonsurgical, conservative treatment involving physical therapy and activity modification is recommended for most patients who experience first-time traumatic patellar dislocations, many patients experience complicating factors that indicate them for surgery. These factors include recurrent dislocation, risk factors for patellofemoral instability, underlying malalignment issues, and congenital deformities. When evaluating these factors, particularly patellofemoral instability, the authors recommend assessing osteochondral lesions, age, skeletal maturity, number of previous dislocations, family history, and anatomic risk factors.2,5,77-79 Extra care should be taken when considering surgical treatment for skeletally immature patients at elevated risk for recurrent instability as the risk of cartilage damage in these cases is high.80-82
Recently, there has been a reported increase in surgical treatment for patellar instability in the skeletally immature.83 This finding may be attributed to heightened awareness of factors that indicate patients for surgical treatment and increased familiarity of surgeons with newer techniques.83 Many surgical techniques have been described to address patellar instability involving both soft-tissue procedures and bony corrections.84 In this article, we discuss the various surgical techniques for MPFL reconstruction, quadricepsplasty, and distal realignment. These procedures can be paired with any number of additional procedures including, but not limited to, lateral retinacular release or lengthening, chondroplasty, TT osteotomy (in skeletally mature patients), and removal of loose bodies.83
There is a need for more comprehensive studies, particularly randomized controlled trials, to evaluate the outcomes for both surgical and nonsurgical treatments for first-time dislocations. In the current literature, only very recently have surgical treatments shown outcomes that are more positive. In 2009, Nietosvaara and colleagues85 conducted a randomized controlled trial of nonoperative and operative treatment of primary acute patellar dislocation in both children and adolescents. After a long-term mean follow-up of 14 years, there was not a significant difference between the groups in recurrent dislocation and instability, subjective outcome, or activity scores.85 In a subsequent review of 5 studies including 339 knees, Hing and colleagues86 also found similar results in both the operative and nonoperative cohorts at risk of recurrent dislocations, Kujala scores, and reoperations. However, a recent systematic review comparing redislocation rates and clinical outcomes between surgical and conservative management of acute patellar dislocation reported more positive outcomes for the surgical cohort.87 This review included 627 knees, 470 of which received conservative management, 157 of which received operative treatment. The conservative cohort was followed for an average of 3.9 years and had a 31% rate of recurrent dislocation while the surgical group was followed for a mean 4.7 years and experienced a 22% redislocation rate.87 This study indicates that operative management for acute first-time dislocations may be the preferred treatment option.
Continue to: A potential reason some of these studies...
A potential reason some of these studies did not show any significant difference between the operative and nonoperative cohort could be that the surgical cohorts included a wide range of procedures including lateral releases and MPFL repairs. Recent publications have indicated that these techniques do not produce overall positive outcomes. While each surgical treatment plan is unique depending on the patient; recently, MPFL reconstruction has been shown to have better outcomes than both nonoperative management and simple medial repair and/or lateral
release.67,88-90
MPFL RECONSTRUCTION
INDICATIONS/OVERVIEW
The MPFL is an important stabilizer for the knee that primarily resists lateral translation of the patella. Damage to the MPFL is very common in acute patellar dislocations with up to 90% of first-time dislocations resulting in injury to the MPFL.91,92 Historically, simple medial and/or lateral MPFL repairs have not been shown to improve patellofemoral kinematics significantly and often result in recurrence.90,93 To address this issue, during the past few decades, numerous MPFL reconstruction techniques have been developed to reconstruct a stronger ligament with the same kinematics as the anatomic MPFL.2,19,69,81,94-106 The ultimate goal of MPFL reconstruction is to reestablish the anatomic “checkrein” to guide the patella into the trochlea between 0° and 30° of knee flexion.107,108 An essential secondary surgical goal in skeletally immature patients is to avoid damaging the distal femoral physis.
There are many variations in both the grafts used to replace the MPFL and the means by which to secure them. The ones discussed below include free semitendinosus or gracilis autografts or grafts constructed from a pedicled adductor, patellar, or quadriceps tendon.69,105,109 While not used as frequently, allografts have also been used.110 Methods to secure these grafts in osseous tunnels include suture anchors or tenodesis screws. Incomplete osseous sockets or medial-sided bone tunnels have also been used as a method to decrease patellar fractures as they preserve the lateral patellar cortex.111-114
DOUBLE-BUNDLE HAMSTRING AUTOGRAFT
The technique most often used by the author is a double-bundle hamstring autograft harvested from either the semitendinosus or the gracilis secured by short patellar and femoral sockets (Figure 3). After harvesting the hamstring graft from a posteromedial incision, an approximately 90-mm graft is prepared with Krackow stitches to secure 15 mm of the tendon in each socket.115 Lateral radiographs are used intraoperatively to ensure the guidewire for the femoral drill hole falls along the posterior cortex of the diaphysis of the femur while AP radiographs confirm placement distal to the physis. It is important to take both AP and lateral radiographs intraoperatively due to the concave curvature of the distal femoral physis. This unique anatomy can make a point that is located distally to the physis on the AP view appear on or proximal to it on the lateral cross reference view.24,116 For the patellar socket, 2 short sockets are made in the superior half of the patella. Once the sockets have been drilled, the graft is adjusted so that the patella stays seated in the center of the trochlea between 20° and 30° of flexion. This anchoring is accomplished by securing the graft while the knee is kept at 30° of flexion. Proper tension is confirmed by ensuring that the graft does not allow lateral patella movement over one-fourth the width of the patella in extension while crepitation must not appear throughout the ROM.92
QUADRICPETS TENDON TRANSFER
A combination of techniques by Steensen and colleagues,105 Goyal,109 Noyes and Albright,117 and Pinkowsky and Hennrikus118 describe an MPFL reconstruction in which the proximal end of a small medial portion of the quadriceps tendon is released and then attached to the medial epicondyle through a subcutaneous tunnel (Figure 4). This technique is particularly useful for cases in which the extra strength provided by the bone-quadriceps tendon is necessary to correct more severe dysplasia. Leaving the distal end of the quadriceps tendon intact at its patellar insertion, a graft of about 8 mm x 70 mm thickness is harvested from the tendon. The free distal end of the tendon is then run anatomically through the synovium and retinaculum to be either sutured to the medial intermuscular septum at the medial femoral epicondyle or fixed in femoral tunnel using interference screw.105,109,118 The placement of the femoral fixation point is essential to ensure positive surgical outcomes. If the graft is secured too anteriorly, it may be too loose in extension and too tight in flexion, both of which can lead to postoperative pain, loss of normal kinematics, and overload of the medial patellofemoral cartilage.119-121 Once the ideal placement of the femoral fixation point has been confirmed by intraoperative radiographs, the graft is secured with a small absorbable suture.122,123 While this technique has good clinical results, the longitudinal scar that results from graft harvesting is cosmetically unappealing, and it is technically challenging to harvest a consistent strip of the quadriceps tendon. To address some of these concerns, Fink and colleagues124 described a new harvesting technique that produces more consistent grafts and requires a smaller incision.
Continue to: ADDUCTOR MAGNUS TENDON TRANSFER
ADDUCTOR MAGNUS TENDON TRANSFER
This technique is a double-bundle MPFL reconstruction that uses a pedicled graft of the distal adductor magnus tendon and suture anchors or incomplete osseous sockets to recreate the MPFL anatomically (Figure 5). Avikainen and colleagues96 and Sillanpää and colleagues125 described this procedure as a progression from the original single-strand adductor magnus transfer technique. First, maintaining the distal insertion, a graft of approximately 14 cm to 18 cm is harvested from the adductor tendon and then passed through a subcutaneous tunnel between the distal vastus medialis obliquus and the superficial joint capsule. The graft is then looped at the medial patella so that the distal bundle runs back to the adductor tubercle.125 With the knee at 30° of flexion to assure proper tension, the graft is secured at both the patella and near the adductor tubercle with suture anchors.125 Hambridge and colleagues126 compared a similar adductor magnus transfer with other pedicled techniques including bone-quadriceps tendon autograft and bone-patellar tendon allograft and found positive results for all 3 methods of reconstruction.
HEMI-PATELLA TENDON TRANSFER
In a similar technique to the adductor tendon transfer, the medial section of the patellar tendon is harvested from the TT and run from its proximal insertion at the medial patella to the medial femoral attachment via a subcutaneous tunnel. The free end of the graft is then secured with suture anchors or incomplete osseous sockets with the knee at 30° of flexion.127
HAMSTRING GRAFT WITH ADDUCTOR TENDON AS A PULLEY
Several techniques opt to use a more dynamic model of MPFL reconstruction in which the adductor tendon or medial collateral ligament (MCL) is used as a pulley for the hamstring graft (Figure 6).128,129 The site of the pulley approximates the normal attachment of the MPFL to the femur and so acts as an effective anatomic replica of the MPFL origin. A semitendinosus graft is harvested and is prepared with continuous sutures, and 2 tunnels to secure the graft are drilled into the patella. The graft is then run subcutaneously from the medial side of the patella to the adductor magnus tubercle into which an osteoperiosteal tunnel is drilled at its distal femoral insertion. The graft is looped through the adductor tunnel and secured with sutures. Proper knee kinematics was ensured by placing the knee at 30° of flexion as the ends of the tendon are secured to the patella.114,130
HAMSTRING GRAFT WITH MCL AS A PULLEY
The MCL can also be used as a pulley rather than the adductor tendon. The semitendinosus graft is harvested and prepared and the patella drilled as it is in the previous technique. The MCL was fashioned into a pulley by making a slit in its posterior one-third. The semitendinosus graft is looped through this slit, and both ends of the graft are held in place with suture anchors on the surface of the patella.129
ADDITIONAL PROCEDURAL COMBINATIONS
Depending on the needs of the individual patient, MPFL reconstruction, and other patellar stabilization techniques can also be combined with additional procedures. Arshi and colleagues83 conducted a review of 6190 adolescents surgically treated for patellar instability and reported the most common additional procedures performed at the time of the stabilization. They found 43.7% of the population underwent lateral retinacular release, which while not effective as an isolated technique to treat patellar instability, has often been used in combination with MPFL reconstruction.131-133 There is currently a lack of consensus regarding the success of adding a lateral release to the reconstruction. Some studies report no difference while others report a decrease in stability after lateral release.90,134-136 While lateral retinacular release has been shown to decrease the force required to displace the patella, it can be surgically indicated in certain patients undergoing MPFL reconstruction.131 The authors advocate that if the lateral retinaculum is tight such that centralized patellar tracking is inhibited following the reconstruction, or if the patella cannot be pushed passively from a laterally tilted position to the neutral horizontal position, lateral retinacular lengthening should be performed to improve kinematics.132
Continue to: Arshi and colleagues...
Arshi and colleagues83 also reported a high rate of cartilage procedures, with chondroplasty performed in 31.1% and chondral fragment/loose body removal in 10.2%. These statistics suggest that a significant level of cartilage damage has occurred by the time of surgery.83
COMPLICATIONS
As MPFL reconstruction techniques have only recently been popularized and developed, there are not many comprehensive studies evaluating the outcomes and complications associated with these procedures. However, in the current literature, there is a general consensus that patients usually experience positive short-term clinical outcomes and relatively low complication rates.68,77 In one of the largest retrospective cohort studies of pediatric patients undergoing MPFL reconstruction, Parikh and colleagues114 reported both the type and rate of complications. They found complications occurred in 16.2% of patients, and the most common complications were recurrent patellar instability, patellar fractures, patellofemoral arthrosis, motion deficits, and stiffness with over half classified as avoidable. Most of these complications were due to technical errors with episodes of recurrent instability only reported in 4.5% of patients.114 In a comprehensive meta-analysis of MPFL reconstruction studies, Shah and colleagues137 reported a complication rate of 26% in both pediatric and adult patients. The cohort was not stratified by age, yet complications were similar to those reported by Parikh and colleagues,114 including pain, loss of knee flexion, wound complications, and patellar fracture.137
As indicated by the frequency of technical complications reported by Parikh and colleagues,114 extra caution should be taken in the operating room to minimize potential errors. In techniques that require drilling of femoral sockets, proper length for and placement of the graft is essential to reestablish proper kinematics. Studies have reported that placing the femoral socket too proximally can result in loss of ROM during flexion and increased compressive forces across the patella.138 A graft that is too short can have similar negative outcomes, and a graft that is too long can result in recurrent instability. Positioning the graft while the knee is in 30° of flexion can help ensure the proper length and tension is achieved. Once the graft is in place, it is important to ensure the ROM and isometry before completing the fixation.72 It is also essential to be vigilant about potential violation of the physes and subsequent growth disturbances. To establish the safest angles for drilling the distal femoral epiphysis for graft placement, Nguyen and colleagues139 conducted a study using high-resolution 3-dimensional images of cadaveric distal femoral epiphyses. By recording which tunnels disrupted the physis before reaching 20 mm of depth, the authors concluded that it is safest to drill distally and anteriorly at an angle between 15° and 20°.139 This technique should minimize damage to the physis, notch, and distal femoral cartilage and decrease potential complications.139
OUTCOMES
In general, the literature reports positive outcomes for MPFL reconstruction—in both studies that address a specific technique and all-encompassing studies. Outcomes are typically reported as Kujala and Tegner scores, results from clinical examinations, and rates of subsequence recurrences. Several recent studies have also evaluated the ability of MPFL reconstruction to restore proper kinematics. Edmonds and colleagues140 evaluated the difference in patellofemoral joint reaction forces and load experienced by 3 groups of adolescents: a cohort treated with MPFL reconstruction, a cohort treated with soft-tissue realignment of the extensor mechanism (the Insall method), and controls. While both surgical techniques were able to restore medial constraints to the patella, the study showed that only the MPFL reconstruction cohort experienced joint reaction forces that were analogous to the control group. In comparison, the cohort that was treated with soft-tissue realignment alone experienced higher patellofemoral joint reaction forces and did not regain normal joint mechanics.140 These results can be used to advocate for the further use of MPFL reconstruction as an effective anatomic replacement of the native ligament. Radiographic studies have similarly reported MPFL reconstruction as an effective means to restore anatomic normality. Fabricant and colleagues141 conducted a radiographic study in which patella alta was corrected to normal childhood ranges in patients who underwent MPFL reconstruction technique using a hamstring autograft. Lykissas and colleagues142 corroborated these results with another radiographic study that reported small but significant decreases in the Blackburne-Peel index and CD index following MPFL reconstruction in 25 adolescents. As correction of patella alta allows the patella to rest in a deeper, more secure position in the TG, these results indicate that effective early MPFL reconstruction can correct for patellar anatomic abnormalities that could be future risk factors.143,144 Several studies have also reported outcomes addressing specific MPFL techniques; these are reported and discussed in this article.
OUTCOMES BY TECHNIQUE
HAMSTRING AUTOGRAFT
Reports on outcomes following MPFL reconstructions using hamstring autografts have been particularly promising. A cohort of 21 skeletally immature patients who underwent MPFL reconstruction was evaluated pre- and postoperatively with an average of a 2.8-year follow-up. The authors of the study reported no redislocation events and significant improvement in the Kujala scores, and patients were able to return to athletic activities safely.145 Previous studies report similar positive increases in Kujala scores, subjective patient reports, and lack of subsequent redislocation for patients who underwent either semitendinosus or gracilis autograft MPFL reconstructions. One such study further documented an average patellar inclination angle decrease from 34.3° to 18.6° following MPFL reconstruction.146 However, while the literature typically reports positive Kujala scores and subjective outcomes for the hamstring autograft procedure, a study arthroscopically evaluating patellar tracking immediately following surgery and then at 6 to 26 months follow-up found that patellar tracking correction was not maintained for all patients who underwent this type of MPFL reconstruction.147
Continue to: QUADRICEPS TENDON TRANSFER OUTCOMES
QUADRICEPS TENDON TRANSFER OUTCOMES
Studies specifically evaluating the quadriceps tendon transfer technique for MPFL reconstruction in children are sparse, but authors have reported positive clinical outcomes and low complication rates in adults. After following 32 young adults who underwent this MPFL reconstruction technique for 3 years, Goyal109 reported a significant increase in mean Kujala scores from 49.31 to 91.25 and no complications or redislocation. He argues this type of quadriceps graft has a high success rate because it is anatomically more similar to the MPFL than other grafts and does not require additional patellar fixation.101,109 Similar positive Kujala scores and minimal complications have been reported in adult patient populations.148 Abouelsoud and colleagues149 conducted one of the few studies in skeletally immature patients and reported similarly positive results with no redislocations and significantly improved Kujala scores at a mean follow-up of 29.25 months in their 16-patient cohorts.
ADDUCTOR MAGNUS TENDON TRANSFER
After initially describing this technique in 14 adult patients, Avikainen and colleagues96 followed this cohort and reported positive subjective results and only 1 redislocation. In a more recent study in which the adductor tendon transfer technique was compared with the quadriceps tendon transfer described above and the bone-patellar tendon allograft, Steiner and colleagues69 reported similarly significant improvement in all cohorts in Lysholm, Kujala, and Tegner scores with no redislocations. Additionally, Malecki and colleagues150 followed a cohort of 33 children with 39 knees diagnosed with recurrent patellar dislocation, who underwent MPFL reconstruction using the adductor magnus tendon. After evaluating this cohort functionally and radiographically, the authors reported improvements in Lysholm and Kujala scores, patellar tilt and congruence angles, and peak torque of the quadriceps muscle and flexor.150 However, this cohort did report postoperative redislocations in 36.4% of patients (4 of 11).150
HEMI-PATELLA TENDON TRANSFER
In 2012, in the first randomized controlled trial, Bitar and colleagues67 compared the outcomes of patients who underwent MPFL reconstruction via the hemi-patellar tendon technique with those who were managed nonoperatively with immobilization and physiotherapy after first-time patellar dislocation. At 2-year follow-up, the surgical cohort presented positive results with a significantly higher mean Kujala score (88.9 to 70.8) and no redislocations or subluxations. In contrast, 35% of nonoperative cases presented with recurrences and subluxations over the 2-year period.67
MCL OR ADDUCTOR TENDON AS A PULLEY
Studies have reported good postoperative results and low complication rates for these dynamic techniques.128,129 In terms of kinematics, while hypermobility and patellar height were not fully corrected, improvements in patellar tilt and lateral shift were reported in a cohort of 6 patients with a minimum 4-year follow-up.129 To further evaluate whether the more dynamic pulley reconstruction technique resulted in better outcomes, Gomes and colleagues128 compared the subjective reports, clinical evaluations, and complication rates of patients who underwent MPFL reconstruction with a rigid adductor magnus fixation vs a semitendinosus tendon dynamic femoral fixation. One case in the rigid cohort experienced a subsequent subluxation, while patients in the semitendinosus group had better subjective reports and a higher rate of return to sport.128 More recently, Kumahashi and colleagues151 specifically studied the outcomes of the MCL tendon as a pulley in 5 patients aged 14 to 15 years. They reported similar successful results as no patients experienced recurrence, and all patients exhibited improvement in radiographic measures of patellar tilt and congruence angle, lateral shift ratio, and both Kujala and Lysholm scores.151
While there has yet to be a randomized controlled trial comparing all of these different techniques, there is a general consensus in the literature that patients tend to perform better following MPFL reconstruction vs MPFL repair.
OTHER STABILIZATION PROCEDURES, INCLUDING DISTAL REALIGNMENT
Patients with additional underlying deficits and malalignment issues such as significant trochlear dysplasia, increased TT-TG distance, patella alta, increased Q angle, and/or positive J sign may require stabilization procedures beyond MPFL reconstruction.152,153 TT osteotomies are often used to correct alignment issues in the adult patient population; however, these procedures are typically contraindicated in skeletally immature patients. Alternative realignment procedures for the pediatric population include both proximal and distal realignment, with proximal realignment performed primarily in children under the age of 12 years.153 Many variations on these procedures exist, some of which are no longer regularly performed due to poor reported outcomes. In this article, we discuss several of the techniques, focusing primarily on those that have demonstrated higher success rates.
Continue to: GALEAZZI TECHNIQUE
GALEAZZI TECHNIQUE
One of the first and most famous soft-tissue techniques to address patellar instability was the semitendinosus tenodesis, published by Galeazzi154 in 1922 (Figure 7). This technique stabilizes the patella without altering the TT. In the original technique, a portion of the semitendinosus tendon is harvested with its tibial insertion left intact. The free end of the tendon is then secured with sutures at the periosteal groove of the medial patella.154,155 Fiume156 modified this technique by adding a lateral release and medial retinacular reefing. The most recent addition to this procedure was introduced by Baker and colleagues,157 in which a tunnel is drilled from the medial to the lateral border of the patella. Tension placed on the grafted tendon is used to reposition the patella medially and draw it downward. Preliminary literature on this modified procedure reported fair clinical results with success rates of approximately 75%.155,158-160 A recent study evaluating both the clinical and radiographic outcomes of this technique also indicated that while clinical results were excellent in 62.5% of patients, this technique alone was unsuccessful in fully addressing patellar instability in patients with underlying anatomic abnormalities such as patellar alta.161 In light of these less than ideal reports, the authors no longer recommend this technique for patellofemoral instability cases.
ROUX-GOLDTHWAIT PROCEDURE
The Roux-Goldthwait procedure, first described by both Roux162 and Goldthwait163 in 1888 and 1895 respectively, was later modified in 1985 to involve a lateral release, plication of the medial retinaculum, medial transfer of the lateral patellar tendon without advancement, and advancement of the vastus medialis (Figure 8).164 More recently, Marsh and colleagues152 introduced an addition to aligning the extensor mechanism with the femoral shaft better. In this technique modification, the patellar tendon is split longitudinally, and its lateral half is detached and transferred distally beneath its medial half. The free end is then sutured to the periosteum on the medial side of the tibia.152 With a mean long-term follow-up of 6.2 years, Marsh and colleagues152 reported excellent results in 65%, good in 11%, and fair in 3% of the knees operated on with this modified technique. Of the patients in this cohort whose strength was evaluated, 80% had their strength returned to 90% of preoperative levels in the operated leg.152 While this study and others report improved outcomes, an increasing body of literature has found high rates of recurrence, patella infera, and other complications following the modified Roux-Goldthwait procedure.36,165-171 Also, a study comparing MPFL reconstruction using adductus magnus transfer with the Roux-Goldthwait procedure reported that patients in the MPFL cohort reported less pain postoperatively.150 In addition, whereas the Kujala and Lysholm scores, recurrence rates, patellofemoral angles, and apprehension test results did not demonstrate significant differences between these 2 groups, the MPFL group had significantly fewer abnormal congruence angles, better patellar medialization, and higher peak torque of the hamstring.150
COMBINED MPFL AND MEDIAL PATELLOTIBIAL LIGAMENT RECONSTRUCTION
While the medial patellotibial ligament (MPTL) has not received much attention with regard to patellar stability, recent studies have indicated its role during higher degrees of both flexion and extension.172 The MPTL acts as a secondary restrictor ligament which helps release stress on the MPFL by decreasing the Q angle and further normalizing patellar kinematics.173 Patients who present with hyperlaxity or knee hyperextension combined with extension subluxation and flexion instability could be indicated for this additional stabilizing procedure. Both Nietosvaara and colleagues85 and Brown and Ahmad174 have described a dual MPTL and MPFL reconstruction technique using a semitendinosus hamstring graft. More recently Hinckel and colleagues172 described a combined MPFL and MPTL reconstruction, using a graft from the quadriceps tendon to reconstruct the MPFL and one from the patellar tendon to reconstruct the MPTL. In this technique, once the respective grafts have been harvested, a femoral insertion for the graft recreating the MPFL is fluoroscopically established so that an anchor can be inserted distal to the femoral physeal growth plate. For the MPTL insertion, attachment to the tibia below the joint line and 2 cm medial to the patellar tendon is established fluoroscopically just above the physeal growth plate on the proximal epiphysis.19,175 The MPTL graft is sutured first with the knee at 90° of flexion to establish tension similar to that of the patellar tendon.176 Then, the knee is placed in 30° of flexion to fix the MPFL graft to the medial patella to prevent excessive lateral translation of the patella.
PATELLAR TENDON TRANSFER
Patellar tendon transfer with proximal realignment is a technique used in particularly young patients to address cases of patellofemoral instability involving concomitant bony or anatomic abnormalities. This procedure is effective for young children with substantial amounts of remaining growth as it better mimics native anatomy than other realignment procedures and does not require bony remodeling.152-154 It is important to familiarize with surgical techniques to address malalignment issues in young patients as neglected alignment issues can lead to worsening of trochlear dysplasia and instability, which are very difficult to treat later on when patients are older.153
The patellar tendon transfer technique (Figure 9), as described by Gordon and Schoenecker,177 starts with an extensive lateral retinacular release. The patellar tendon is then released from its distal insertion at the TT so that it can be moved medially without moving it inferiorly. After confirming patellar tracking and alignment by flexing the knee from 0° to 90° with the graft in place, the patellar tendon graft is secured with multiple nonabsorbable horizontal sutures.177 Of note, in skeletally mature patients, a TT osteotomy is used to accomplish the same goal. This osteotomy has been shown to improve both patellar height and TT-TG distance in skeletally mature patients, but is contraindicated in skeletally immature patients.92,178
Continue to: Initial studies conducted on patellar tendon...
Initial studies conducted on patellar tendon transfer have positive outcomes.179 At a mean follow-up of 5.1 years, patients reported a decrease in pain and increased the ROM and activity, and only 1 reported a postoperative redislocation.179 In more recent studies, both Benoit and colleagues36 and Garin and colleagues58 reviewed cases of patellar instability treated with patellar tendon transfer to address concomitant patellar alignment and anatomic abnormalities. They reported good functional, clinical, and radiographic outcomes with 12.5% and 16% recurrence rates, respectively.36,58 They also noted radiographic improvements in femoral sulcus angle, particularly in younger patients, which indicate this procedure is effective in addressing bony abnormalities that can result from neglected malalignment issues.36,58,154
QUADRICEPSPLASTY
Quadricepsplasty is a lengthening and remodeling technique not frequently used in the pediatric population. The goal of this procedure in patients with significant amounts of growth remaining is to reposition the patella to ameliorate trochlear remodeling and prevent worsening symptoms and anatomic abnormalities.36 A quadricepsplasty accomplishes this by de-rotating and/or lengthening the extensor mechanism and may or may not involve a concomitant MPFL reconstruction. This procedure is particularly effective in young patients who experience obligatory dislocation.60,72 Several quadricepsplasty techniques have been described including Thompson, Curtis and Fisher, Judet, Stanisavljevic, and V-Y technique.180-186 Most techniques initially involve sharp dissection of the vastus medialis and lateralis from the rectus femoral tendon. A tongue is then fashioned out of the rectus femoral tendon. Once the vastus medialis and lateralis are detached from the margins of the patella, the knee is extended, and the distal ends of the vasti are sutured to the tongue of the rectus tendon. Effective extension facilitates flexion to 90°.184 The authors recommend a modification of this technique in which a Z lengthening of the quadriceps tendon is performed after the vastus lateralis is removed distally from the patella and the quadriceps tendon.
Several series and case reports evaluating quadricepsplasty in adult patients report positive outcomes with most patients achieving good or excellent flexion with minimal complications.183,185,187-189 Reports on quadricepsplasty used to treat conditions other than patellofemoral instability in children have reported similar positive outcomes.190-192 As quadricepsplasty for patellar instability is relatively rare in pediatric patients, there is not much relevant literature. However, Kocon and colleagues193 reported results of quadricepsplasty and quadricepsplasty combined with the modified Galeazzi procedure in 8 children (10 knees) with a mean follow-up of 3.25 years. Seventy percent of cases resulted in stabilization and correction of patellar position, and only 2 postoperative redislocations were noted.193 Additionally, in a study evaluating 6 patients suffering from patellar instability, 2 of whom were obligate dislocators, quadricepsplasty resulted in patellar stability, satisfaction, and near normal gait patterns.194
Figure 10 shows the surgical algorithm used for patellar instability characteristics.
CONCLUSION
Patellofemoral joint stability relies on a complex interplay of musculotendinous units, ligaments and the osteocartilaginous morphology of the patellofemoral joint. Patellar instability in pediatric patients is different from adults. Having an in-depth understanding of the remodeling potential, the insertion sites for the MPFL and its relationship to the physis are of utmost importance when planning surgery. Reducing and maintaining the patella within the patellofemoral joint early enough can allow for remodeling of the patella and/or the trochlea to provide for lasting stability. Appropriate surgical principles, such as tensioning, can help both prevent continued pain and minimize future complications.
ABSTRACT
Patellar instability in children and adolescents is a challenging subset to treat. Varied forms of instability, ranging from episodic dislocation to fixed dislocation, have been recognized. It is of utmost importance for the treating physician to recognize these different patterns of instability and their associated risk factors, as more complex patterns of instability would require more extensive surgical procedures. Medial patellofemoral ligament (MPFL) reconstruction, by itself, may not suffice or may not be appropriate for the more complex instability patterns. Appropriate and early treatment of such instability in children would allow for functional progression and possible remodeling of the trochlea. However, early treatment has the associated risk of growth disturbances when surgical procedures are performed around open physis or if adult-type bony procedures are performed in children. Recent knowledge about the relationship between trochlea, MPFL femoral attachment, and distal femoral physis could help to advance safe surgical care for these patients. This article reviews the pathophysiology, risk factors, and the existing classification systems for patellar instability in children and adolescents. It focuses on varied surgical techniques, which are unique to the pediatric population, and summarizes the outcomes of these surgical techniques.
Continue to: EPIDEMIOLOGY
EPIDEMIOLOGY
In a prospective 2-year study of Finnish children, the annual incidence rate of patellar instability was 43/100,000 pediatric population.1 In patients 9 to 15 years of age, the incidence was approximately 1/1000.1 In another study, patients at highest risk for a first-time patellar dislocation were females aged 10 to 17 years.2 In a study in patients with traumatic hemarthrosis, 36% in the younger age group (10-14 years) and 28% in the older age group (15-18 years) had sustained patellar dislocation. In contrast, 22% in the younger age group and 40% in the older age group had sustained an anterior cruciate ligament tear.3
Approximately one-half of patients who dislocate their patella suffer from long-term complications.4,5 These complications include recurrent instability, patellofemoral pain, osteochondral lesions, and eventual arthritis.1,4,5 Young, active individuals are more prone to these issues.6 Also, 39% or more of patellar dislocation patients have an associated osteochondral fracture that might influence the management.1 Thus, patellar instability in young patients is an area of concern.
DEVELOPMENTAL ANATOMY
At 4-week gestation, the patellofemoral joint is an ectodermal sac filled with mesenchyme of the somatic mesoderm.7 Mesenchymal condensations then appear at 4 to 5 weeks gestation, followed by chondrification of both the femur and patella.7 The joint space is present by 6 weeks, and the patellar and distal femoral condyles are present at 7 weeks gestation.7 By 8 weeks gestation, the basic knee anatomy resembles that of an adult with the chondroepiphysis forming the articular surfaces of the femur, tibia, and patella.7 By this time, the extensor mechanism is formed, and active joint motion has begun, facilitating the development of the trochlear sulcus.7 The secondary ossification center in the distal femoral epiphysis forms around 36 weeks gestation.8 Postnatally, both the patella and distal femur grow through endochondral ossification.9,10
The patella is the largest sesamoid bone in the human body.11 The patella begins as a dense consolidation of cells that differentiate as the quadriceps mechanisms develop.12,13 The patellar anlage becomes distinguishable within the quadriceps tendon around 7.5-week gestation.12 The morphology of the patella conforms to the distal femur.12 The patella molds or re-models as the knee begins to move in response to mechanical stresses.7 The patella increases in relative size during the first 6 months of gestation, then enlarges proportionately to the rest of the bones.7 Ossification begins around 3 years of age for females and 4 to 5 years of age for males.8,14 The ossification center may appear irregular as it rapidly expands.14 Ossification proceeds in a proximal to distal direction, thus giving a spurious estimation of patellar height on radiographs in children. The overall morphology of the cartilaginous patella during development is comparable to the final mature shape.14 Abnormal contact stresses on the articular surface of the patella during skeletal immaturity can lead to deformation.7
Ultrasonographic measurements in normal patients show that trochlear groove (TG) morphology is present early and becomes more radiographically apparent as distal femoral ossification is completed.15 Anatomic dissections of aborted fetuses have verified the morphology of the TG as it remains constant during growth and the groove morphology is the same for both fetuses and adults.16 An ultrasound study performed on patients aged 12 to 18 years showed the cartilaginous sulcus angle (CSA) remained constant throughout all age groups (146°).17 The CSA however, differed in patients who suffered a patellar dislocation (average, 164°; range, 154°-195°) compared with normal knees (average CSA, 145°; range, 131°-158°).15,17,18 The osseous sulcus angle, on the other hand, appears flat at birth and the TG deepens with age. This increase in depth is more of a reflection of progressive ossification of a well-formed cartilaginous trochlea, rather than a true deepening of the sulcus.17 Thus, the axial radiographic view of the patella provides misleading information about the sulcus angle in children and should not be used to define trochlear morphology.
Continue to: MEDIAL PATELLOFEMORAL LIGAMENT ANATOMY
MEDIAL PATELLOFEMORAL LIGAMENT ANATOMY
The medial patellofemoral ligament (MPFL) functions to limit the lateral translation of the patella.19 The attachment sites on the femur and patella for the MPFL have been studied in children.20-23 Cadaveric dissections in specimens aged 2 to 11 years have noted the patellar attachment to be an average of 12 mm in length with the midpoint approximately 5 mm superior to the mid-pole of the patella.22 The patellar footprint of the MPFL insertion was a mean 41% of the entire patellar length.22
It is important to be aware of the characteristic anatomy of the MPFL, as fixation points should mimic the anatomic insertion as best as possible while also avoiding violation of the nearby physis. The MPFL originates between the adductor tubercle and the medial femoral epicondyle just distal to the distal femoral physis and attaches to the superomedial aspect of the patella.20-25 In relation to the physis in pediatric patients, the midpoint of MPFL insertion has been measured to be 4 mm to 9 mm distal to the femoral physis.21,24,25 These measurements represent averages as cadaveric studies have reported that some part of MPFL femoral insertion extends proximal to the distal femoral physis.21 A recent report of physeal injury to the posterior distal femoral physis during MPFL reconstruction leading to femoral flexion deformity highlights the importance of physeal-respecting surgery.26
TROCHLEA AND ANTERIOR DISTAL FEMORAL PHYSIS
The relationship between the proximal aspect of the trochlea and the anterior distal femoral physis has been recently studied in 175 knees with dysplastic trochlea.27 Based on magnetic resonance imaging evaluation, the lateral aspect of the trochlea extended proximal to the anterior distal femoral physis in 13% of patients and was at the level of the anterior physis in another 13% of patients (Figure 1).27 Hence, a cautious approach is recommended for any surgery to address trochlear dysplasia or trochlear bump in younger patients to prevent iatrogenic injury to anterior distal femoral physis and resultant genu recurvatum. The distance between the trochlea and the physis increased with increasing age.
LIMB ALIGNMENT
Physiologically, the quadriceps angle (Q angle) changes through the course of growth. As children begin standing and walking, they stand with their feet wider apart and in genu varum.28 Physiologic genu varum can reach 15°.28 This degree lessens during the first 1.5 to 2 years of life, transitioning to physiologic valgus of nearly 12° by 3 years of age.28 Genu valgum, thereafter, gradually decreases to reach the adult value of around 7° to 8° by age 7 years.28 Increased genu valgum is a risk factor for patellar instability. In skeletally immature patients, correction of genu valgum through guided growth may be desirable in patients undergoing patellar stabilization surgery (Figures 2A, 2B).29
PATHOPHYSIOLOGY OF PEDIATRIC PATELLAR DISLOCATION
TROCHLEAR DYSPLASIA
Trochlear dysplasia is an abnormal shape and depth of the TG.30 Up to 96% of patients with patellar dislocation have trochlear dysplasia.30-33 In a study of patellar instability in children, at least 1 of the 3 signs of trochlear dysplasia (the crossing sign, supratrochlear bump, and double contour sign) was present on lateral radiographs.34 In another study on the growth of trochlear dysplasia in children and adolescents, all grades of trochlear dysplasia were present at all ages (ie, the dysplasia was most likely present at birth and did not necessarily worsen with age and growth).35 The linear dimensions of lateral and medial condylar height as well as trochlear bump increased with age but both the sulcus angle and shape of the trochlea did not change significantly.35 Remodeling of a dysplastic trochlea can happen if the patella is stabilized and appropriately located at a younger age, preferably before 10 years of age.36,37
Continue to: PATELLAR HEIGHT
PATELLAR HEIGHT
The role of patellar height in patellar instability has been well established.38 In patients with patella alta, the patella remains proximal to the TG during the greater arc of knee motion, which predisposes it to patellar instability. Calculation of patellar height in children could be challenging due to incomplete ossification, as well as asymmetric ossification of the patella and the tibial tubercle (TT). Since the patella ossifies from proximal to distal, most radiographic methods that measure the patellar height from the distal aspect of the patella provide a spurious elevation of the measurement.
The Caton-Deschamps (CD) method measures the length of the patellar articular surface and the distance from the inferior edge of the articular surface to the anterosuperior corner of the tibial plateau.39 A ratio >1.3 signifies patella alta. The CD ratio has been verified as a simple and reliable index for measuring patellar height in children.40 Two other methods have been described for determining patellar height in children.41,42 Based on anteroposterior (AP) radiographs of the knee in full extension, Micheli and colleagues41 calculated the difference between the distance from the superior pole of the patella to the tibial plateau and the length of the patella. A positive difference signified patella alta. The Koshino method involves the ratio between a reference line from the midpoint of the patella to the midpoint of the proximal tibial physis and a second distance from the midpoint of the distal femoral physis to the midpoint of the proximal tibial physis on lateral knee radiographs.42 Normal values range from 0.99 to 1.20 with the knee in >30° flexion, in children 3 to 18 years of age.
HYPERLAXITY
In contrast to adults, children have increased levels of collagen III compared with collagen I, which is responsible for tissue elasticity.43 Tissue elasticity leads to increased joint mobility, which is more common in children. Joint hypermobility or hyperlaxity has to be differentiated from symptomatic instability. The traditional Beighton score identifies individuals as having joint hypermobility with a score of 5/9 or higher in school-aged children.44-46 Smits-Engelsman and colleagues44 suggested using stricter criteria with scores of 7/9 or higher being indicative of hyperlaxity in school-aged children. A study of 1845 Swedish school children noted that females have a higher degree of joint laxity.45 Maximal laxity was noted in females at 15 years of age.45 Hyperlaxity has been demonstrated to be greater on the left side of the body44 and can be part of generalized syndromes including Down’s syndrome, Marfan’s syndrome, or Ehlers-Danlos syndrome.
LIMB TORSION
Staheli and colleagues47 described the normative values of a lower extremity rotational profile, including femoral anteversion and tibial torsion. Children normally have increased femoral anteversion, which decreases with growth. Miserable malalignment is a term used to denote increased femoral anteversion and increased external tibial torsion.48,49 These rotational abnormalities can increase the Q angle and the lateral forces on the patella. Femoral anteversion or internal rotation of the femur of 30° significantly increases strain in all areas of the MPFL.48 This increased strain may lead to MPFL failure and patellar instability.48 Increased internal rotation of the femur also increases contact pressure on the lateral aspect of the patellofemoral joint.48 Miserable malalignment frequently manifests following a pubertal growth spurt and may require femoral and tibial osteotomy.50
SYNDROMIC ASSOCIATIONS
Several syndromes have patellar instability as a part of their manifestation. The more common syndromes include nail-patella syndrome, Kabuki syndrome, Down’s syndrome, and Rubinstein-Taybi syndrome.51-54 Other syndromes less commonly associated with patellar instability include Turner syndrome, patella aplasia, or absent patella syndrome. Since many patients with syndromic patellar instability are functionally limited, they may not require an aggressive approach to treatment. When treating these patients, it is important to recognize the unique features of a specific syndrome, which may affect the anesthesia risk profile, management decisions, rehabilitation, and prognosis.
Continue to: MPFL TEAR PATTERN
MPFL TEAR PATTERN
The MPFL serves as an important constraint to the patella to prevent lateral dislocation, primarily during the first 20° to 30° of knee flexion.55,56 Injury to the MPFL is noted in over 90% of patients who suffer a patellar dislocation.57 The location of MPFL tears in pediatric patients is variably reported at the patellar attachment (10%-61%), femoral attachment (12%-73%), both (12%-35%) or mid-substance (2.5%-15%).25,57 The most common tear patterns in pediatric patients are tears at the patellar attachment.25,57 This tear pattern may be accompanied by an avulsion fracture of the medial rim of the patella, though this fracture, being extra-articular, seldom needs treatment.
CLASSIFICATION
While several authors have established extensive classification systems of patellar dislocation based on both clinical and radiographic presentation and reviews of the literature, a single classification system has not been recognized as the gold standard. In this section, in addition to presenting our preferred methods of classification, we will review some of the more recent and extensive classification systems for patellar dislocation and patellar instability.
Dejour and colleagues31 initially used both the presence of patellofemoral anatomic abnormalities and pain to define 3 types of patellar instability: major, objective, and potential patellar instability. Major patellar instability indicates that the patient has experienced more than 1 documented dislocation, objective instability involves one dislocation in addition to an associated anatomic abnormality, and potential patellar instability refers to cases in which the patient has radiographic abnormalities and patellar pain.31 Garin and colleagues58 more simplistically divided patellar dislocation patients into 2 groups: major (permanent or habitual) dislocation of the patella and recurrent dislocation. Sillanpaa59 stressed the distinction between first-time dislocation and recurrent dislocation specifically in the context of acute injuries. These classification systems were formulated with adults as the most relevant population; however, classifications targeted specifically to pediatric patients have recently been presented in the literature.
Historically, pediatric patella dislocations were simply categorized as traumatic or congenital.60 In 2014, Chotel and colleagues61 focused on classifying patellar dislocation by extensively reviewing anatomic, biomechanical, pathophysiological, and clinical patterns seen most commonly in children. They included 5 categories: congenital dislocation, permanent dislocation, habitual dislocation during knee flexion, habitual dislocation during knee extension, and recurrent dislocation; however, they did not address traumatic dislocations.61 Congenital dislocation is a rare condition, typically presenting at birth, which produces a pattern of functional genu valgum.62 Permanent dislocation typically presents after the child has started walking, but before the age of 5 years.61 The 2 variations of habitual dislocation typically present between ages 5 and 8 years.61 The final category is the most common and typically occurs during pre-adolescence or adolescence as a result of an atraumatic or trivial traumatic event or sports injury.1 Using more specific terminology, Hiemstra and colleagues63 modeled a classification system based on the traumatic, unilateral, bankart lesion, surgery (TUBS)/atraumatic, multidirectional, bilateral, rehabilitation, inferior shift (AMBRI) for shoulder dislocation classifications. The patellar dislocation system is used to identify 2 distinct subsets of patients in the patellofemoral instability population. One subset is defined by the acronym WARPS (weak, atraumatic, risky anatomy, pain, and subluxation), the other is STAID (strong, traumatic, anatomy normal, instability, and dislocation).64 Patients categorized by the WARPS acronym tend to experience atraumatic onsets of patellofemoral instability and demonstrate anatomic issues that increase this instability. These underlying anatomic issues include valgus alignment, ligamentous laxity, rotational abnormalities, shallow and short TG, and patella alta. On the other hand, STAID patients describe a traumatic dislocation event and do not have underlying anatomic abnormalities that predispose them to instability.64
Taking into account these previous classifications, Frosch and colleagues65 added specific pathologies including “instability,” “maltracking,” and “loss of patellar tracking,” in addition to both clinical and radiographic factors to define 5 types of patellar dislocation and their specific treatment recommendations.65 Type 1 involves simple dislocation with neither maltracking nor instability and a low risk of redislocation.65 Type 2 is defined as primary dislocation followed by subsequent high risk of dislocation and no maltracking.65 Type 3 is divided into 5 subcategories of instability and maltracking issues involving soft tissue contracture, patella alta, pathological tibial tuberosity, and TG distance.65 Type 4 is defined as the highly unstable “floating patella,” and type 5 involves patellar maltracking without instability 65. In terms of treatment, conservative rehabilitation is recommended for type 1 whereas MPFL reconstruction tends to show positive outcomes for both types 2 and 3.66-70
Continue to: Parikh and Lykissas recently published...
Parikh and Lykissas recently published a comprehensive classification system of 4 defined types of patellar dislocation in addition to voluntary patellar instability and syndromic patellar instability (Table).60 The 4 types are Type 1, first-time patellar dislocation; Type 2, recurrent patellar instability; Type 3, dislocatable; and Type 4, dislocated. Type 2 is further subdivided into Type 2A, which presents with positive apprehension signs, and Type 2B, which involves instabilities related to anatomic abnormalities.60 A distinction is also made between Type 3A or passive patellar dislocation and Type 3B habitual patellar dislocation.60
The classification system proposed by Green and colleagues is more simplified with 3 main categories (Table) of pediatric patellar dislocation: traumatic (acute or recurrent), obligatory (either in flexion or extension), and fixed laterally.71,72 The acute traumatic categorization refers to patients who experienced an initial dislocation event due to trauma whereas recurrent traumatic involves repeated patella dislocations following an initial incident. Studies report that between 60% to 70% of these acute traumatic dislocations occur as a result of a sports-related incident.2,33,73 Obligatory dislocations occur with every episode of either knee flexion or extension, depending on the subtype. Obligatory patella dislocation in flexion typically cannot be manipulated or relocated into the trochlea while the knee is fixed but does reduce into the trochlea in full extension. Fixed lateral dislocations are rare, irreducible dislocations in which the patella stays dislocated laterally in flexion and extension. These dislocations often present with other congenital abnormalities. Each of these categories can be further specified as syndromic if the dislocation is associated with genetic or congenital conditions including skeletal dysplasia, Ehlers-Danlos syndrome, cerebral palsy, Marfan disease, nail-patella syndrome, Down syndrome, Rubenstein-Taybi syndrome, and Kabuki syndrome.51-54,61,74-76
SURGICAL TECHNIQUES IN SKELETALLY IMMATURE PATIENTS
While nonsurgical, conservative treatment involving physical therapy and activity modification is recommended for most patients who experience first-time traumatic patellar dislocations, many patients experience complicating factors that indicate them for surgery. These factors include recurrent dislocation, risk factors for patellofemoral instability, underlying malalignment issues, and congenital deformities. When evaluating these factors, particularly patellofemoral instability, the authors recommend assessing osteochondral lesions, age, skeletal maturity, number of previous dislocations, family history, and anatomic risk factors.2,5,77-79 Extra care should be taken when considering surgical treatment for skeletally immature patients at elevated risk for recurrent instability as the risk of cartilage damage in these cases is high.80-82
Recently, there has been a reported increase in surgical treatment for patellar instability in the skeletally immature.83 This finding may be attributed to heightened awareness of factors that indicate patients for surgical treatment and increased familiarity of surgeons with newer techniques.83 Many surgical techniques have been described to address patellar instability involving both soft-tissue procedures and bony corrections.84 In this article, we discuss the various surgical techniques for MPFL reconstruction, quadricepsplasty, and distal realignment. These procedures can be paired with any number of additional procedures including, but not limited to, lateral retinacular release or lengthening, chondroplasty, TT osteotomy (in skeletally mature patients), and removal of loose bodies.83
There is a need for more comprehensive studies, particularly randomized controlled trials, to evaluate the outcomes for both surgical and nonsurgical treatments for first-time dislocations. In the current literature, only very recently have surgical treatments shown outcomes that are more positive. In 2009, Nietosvaara and colleagues85 conducted a randomized controlled trial of nonoperative and operative treatment of primary acute patellar dislocation in both children and adolescents. After a long-term mean follow-up of 14 years, there was not a significant difference between the groups in recurrent dislocation and instability, subjective outcome, or activity scores.85 In a subsequent review of 5 studies including 339 knees, Hing and colleagues86 also found similar results in both the operative and nonoperative cohorts at risk of recurrent dislocations, Kujala scores, and reoperations. However, a recent systematic review comparing redislocation rates and clinical outcomes between surgical and conservative management of acute patellar dislocation reported more positive outcomes for the surgical cohort.87 This review included 627 knees, 470 of which received conservative management, 157 of which received operative treatment. The conservative cohort was followed for an average of 3.9 years and had a 31% rate of recurrent dislocation while the surgical group was followed for a mean 4.7 years and experienced a 22% redislocation rate.87 This study indicates that operative management for acute first-time dislocations may be the preferred treatment option.
Continue to: A potential reason some of these studies...
A potential reason some of these studies did not show any significant difference between the operative and nonoperative cohort could be that the surgical cohorts included a wide range of procedures including lateral releases and MPFL repairs. Recent publications have indicated that these techniques do not produce overall positive outcomes. While each surgical treatment plan is unique depending on the patient; recently, MPFL reconstruction has been shown to have better outcomes than both nonoperative management and simple medial repair and/or lateral
release.67,88-90
MPFL RECONSTRUCTION
INDICATIONS/OVERVIEW
The MPFL is an important stabilizer for the knee that primarily resists lateral translation of the patella. Damage to the MPFL is very common in acute patellar dislocations with up to 90% of first-time dislocations resulting in injury to the MPFL.91,92 Historically, simple medial and/or lateral MPFL repairs have not been shown to improve patellofemoral kinematics significantly and often result in recurrence.90,93 To address this issue, during the past few decades, numerous MPFL reconstruction techniques have been developed to reconstruct a stronger ligament with the same kinematics as the anatomic MPFL.2,19,69,81,94-106 The ultimate goal of MPFL reconstruction is to reestablish the anatomic “checkrein” to guide the patella into the trochlea between 0° and 30° of knee flexion.107,108 An essential secondary surgical goal in skeletally immature patients is to avoid damaging the distal femoral physis.
There are many variations in both the grafts used to replace the MPFL and the means by which to secure them. The ones discussed below include free semitendinosus or gracilis autografts or grafts constructed from a pedicled adductor, patellar, or quadriceps tendon.69,105,109 While not used as frequently, allografts have also been used.110 Methods to secure these grafts in osseous tunnels include suture anchors or tenodesis screws. Incomplete osseous sockets or medial-sided bone tunnels have also been used as a method to decrease patellar fractures as they preserve the lateral patellar cortex.111-114
DOUBLE-BUNDLE HAMSTRING AUTOGRAFT
The technique most often used by the author is a double-bundle hamstring autograft harvested from either the semitendinosus or the gracilis secured by short patellar and femoral sockets (Figure 3). After harvesting the hamstring graft from a posteromedial incision, an approximately 90-mm graft is prepared with Krackow stitches to secure 15 mm of the tendon in each socket.115 Lateral radiographs are used intraoperatively to ensure the guidewire for the femoral drill hole falls along the posterior cortex of the diaphysis of the femur while AP radiographs confirm placement distal to the physis. It is important to take both AP and lateral radiographs intraoperatively due to the concave curvature of the distal femoral physis. This unique anatomy can make a point that is located distally to the physis on the AP view appear on or proximal to it on the lateral cross reference view.24,116 For the patellar socket, 2 short sockets are made in the superior half of the patella. Once the sockets have been drilled, the graft is adjusted so that the patella stays seated in the center of the trochlea between 20° and 30° of flexion. This anchoring is accomplished by securing the graft while the knee is kept at 30° of flexion. Proper tension is confirmed by ensuring that the graft does not allow lateral patella movement over one-fourth the width of the patella in extension while crepitation must not appear throughout the ROM.92
QUADRICPETS TENDON TRANSFER
A combination of techniques by Steensen and colleagues,105 Goyal,109 Noyes and Albright,117 and Pinkowsky and Hennrikus118 describe an MPFL reconstruction in which the proximal end of a small medial portion of the quadriceps tendon is released and then attached to the medial epicondyle through a subcutaneous tunnel (Figure 4). This technique is particularly useful for cases in which the extra strength provided by the bone-quadriceps tendon is necessary to correct more severe dysplasia. Leaving the distal end of the quadriceps tendon intact at its patellar insertion, a graft of about 8 mm x 70 mm thickness is harvested from the tendon. The free distal end of the tendon is then run anatomically through the synovium and retinaculum to be either sutured to the medial intermuscular septum at the medial femoral epicondyle or fixed in femoral tunnel using interference screw.105,109,118 The placement of the femoral fixation point is essential to ensure positive surgical outcomes. If the graft is secured too anteriorly, it may be too loose in extension and too tight in flexion, both of which can lead to postoperative pain, loss of normal kinematics, and overload of the medial patellofemoral cartilage.119-121 Once the ideal placement of the femoral fixation point has been confirmed by intraoperative radiographs, the graft is secured with a small absorbable suture.122,123 While this technique has good clinical results, the longitudinal scar that results from graft harvesting is cosmetically unappealing, and it is technically challenging to harvest a consistent strip of the quadriceps tendon. To address some of these concerns, Fink and colleagues124 described a new harvesting technique that produces more consistent grafts and requires a smaller incision.
Continue to: ADDUCTOR MAGNUS TENDON TRANSFER
ADDUCTOR MAGNUS TENDON TRANSFER
This technique is a double-bundle MPFL reconstruction that uses a pedicled graft of the distal adductor magnus tendon and suture anchors or incomplete osseous sockets to recreate the MPFL anatomically (Figure 5). Avikainen and colleagues96 and Sillanpää and colleagues125 described this procedure as a progression from the original single-strand adductor magnus transfer technique. First, maintaining the distal insertion, a graft of approximately 14 cm to 18 cm is harvested from the adductor tendon and then passed through a subcutaneous tunnel between the distal vastus medialis obliquus and the superficial joint capsule. The graft is then looped at the medial patella so that the distal bundle runs back to the adductor tubercle.125 With the knee at 30° of flexion to assure proper tension, the graft is secured at both the patella and near the adductor tubercle with suture anchors.125 Hambridge and colleagues126 compared a similar adductor magnus transfer with other pedicled techniques including bone-quadriceps tendon autograft and bone-patellar tendon allograft and found positive results for all 3 methods of reconstruction.
HEMI-PATELLA TENDON TRANSFER
In a similar technique to the adductor tendon transfer, the medial section of the patellar tendon is harvested from the TT and run from its proximal insertion at the medial patella to the medial femoral attachment via a subcutaneous tunnel. The free end of the graft is then secured with suture anchors or incomplete osseous sockets with the knee at 30° of flexion.127
HAMSTRING GRAFT WITH ADDUCTOR TENDON AS A PULLEY
Several techniques opt to use a more dynamic model of MPFL reconstruction in which the adductor tendon or medial collateral ligament (MCL) is used as a pulley for the hamstring graft (Figure 6).128,129 The site of the pulley approximates the normal attachment of the MPFL to the femur and so acts as an effective anatomic replica of the MPFL origin. A semitendinosus graft is harvested and is prepared with continuous sutures, and 2 tunnels to secure the graft are drilled into the patella. The graft is then run subcutaneously from the medial side of the patella to the adductor magnus tubercle into which an osteoperiosteal tunnel is drilled at its distal femoral insertion. The graft is looped through the adductor tunnel and secured with sutures. Proper knee kinematics was ensured by placing the knee at 30° of flexion as the ends of the tendon are secured to the patella.114,130
HAMSTRING GRAFT WITH MCL AS A PULLEY
The MCL can also be used as a pulley rather than the adductor tendon. The semitendinosus graft is harvested and prepared and the patella drilled as it is in the previous technique. The MCL was fashioned into a pulley by making a slit in its posterior one-third. The semitendinosus graft is looped through this slit, and both ends of the graft are held in place with suture anchors on the surface of the patella.129
ADDITIONAL PROCEDURAL COMBINATIONS
Depending on the needs of the individual patient, MPFL reconstruction, and other patellar stabilization techniques can also be combined with additional procedures. Arshi and colleagues83 conducted a review of 6190 adolescents surgically treated for patellar instability and reported the most common additional procedures performed at the time of the stabilization. They found 43.7% of the population underwent lateral retinacular release, which while not effective as an isolated technique to treat patellar instability, has often been used in combination with MPFL reconstruction.131-133 There is currently a lack of consensus regarding the success of adding a lateral release to the reconstruction. Some studies report no difference while others report a decrease in stability after lateral release.90,134-136 While lateral retinacular release has been shown to decrease the force required to displace the patella, it can be surgically indicated in certain patients undergoing MPFL reconstruction.131 The authors advocate that if the lateral retinaculum is tight such that centralized patellar tracking is inhibited following the reconstruction, or if the patella cannot be pushed passively from a laterally tilted position to the neutral horizontal position, lateral retinacular lengthening should be performed to improve kinematics.132
Continue to: Arshi and colleagues...
Arshi and colleagues83 also reported a high rate of cartilage procedures, with chondroplasty performed in 31.1% and chondral fragment/loose body removal in 10.2%. These statistics suggest that a significant level of cartilage damage has occurred by the time of surgery.83
COMPLICATIONS
As MPFL reconstruction techniques have only recently been popularized and developed, there are not many comprehensive studies evaluating the outcomes and complications associated with these procedures. However, in the current literature, there is a general consensus that patients usually experience positive short-term clinical outcomes and relatively low complication rates.68,77 In one of the largest retrospective cohort studies of pediatric patients undergoing MPFL reconstruction, Parikh and colleagues114 reported both the type and rate of complications. They found complications occurred in 16.2% of patients, and the most common complications were recurrent patellar instability, patellar fractures, patellofemoral arthrosis, motion deficits, and stiffness with over half classified as avoidable. Most of these complications were due to technical errors with episodes of recurrent instability only reported in 4.5% of patients.114 In a comprehensive meta-analysis of MPFL reconstruction studies, Shah and colleagues137 reported a complication rate of 26% in both pediatric and adult patients. The cohort was not stratified by age, yet complications were similar to those reported by Parikh and colleagues,114 including pain, loss of knee flexion, wound complications, and patellar fracture.137
As indicated by the frequency of technical complications reported by Parikh and colleagues,114 extra caution should be taken in the operating room to minimize potential errors. In techniques that require drilling of femoral sockets, proper length for and placement of the graft is essential to reestablish proper kinematics. Studies have reported that placing the femoral socket too proximally can result in loss of ROM during flexion and increased compressive forces across the patella.138 A graft that is too short can have similar negative outcomes, and a graft that is too long can result in recurrent instability. Positioning the graft while the knee is in 30° of flexion can help ensure the proper length and tension is achieved. Once the graft is in place, it is important to ensure the ROM and isometry before completing the fixation.72 It is also essential to be vigilant about potential violation of the physes and subsequent growth disturbances. To establish the safest angles for drilling the distal femoral epiphysis for graft placement, Nguyen and colleagues139 conducted a study using high-resolution 3-dimensional images of cadaveric distal femoral epiphyses. By recording which tunnels disrupted the physis before reaching 20 mm of depth, the authors concluded that it is safest to drill distally and anteriorly at an angle between 15° and 20°.139 This technique should minimize damage to the physis, notch, and distal femoral cartilage and decrease potential complications.139
OUTCOMES
In general, the literature reports positive outcomes for MPFL reconstruction—in both studies that address a specific technique and all-encompassing studies. Outcomes are typically reported as Kujala and Tegner scores, results from clinical examinations, and rates of subsequence recurrences. Several recent studies have also evaluated the ability of MPFL reconstruction to restore proper kinematics. Edmonds and colleagues140 evaluated the difference in patellofemoral joint reaction forces and load experienced by 3 groups of adolescents: a cohort treated with MPFL reconstruction, a cohort treated with soft-tissue realignment of the extensor mechanism (the Insall method), and controls. While both surgical techniques were able to restore medial constraints to the patella, the study showed that only the MPFL reconstruction cohort experienced joint reaction forces that were analogous to the control group. In comparison, the cohort that was treated with soft-tissue realignment alone experienced higher patellofemoral joint reaction forces and did not regain normal joint mechanics.140 These results can be used to advocate for the further use of MPFL reconstruction as an effective anatomic replacement of the native ligament. Radiographic studies have similarly reported MPFL reconstruction as an effective means to restore anatomic normality. Fabricant and colleagues141 conducted a radiographic study in which patella alta was corrected to normal childhood ranges in patients who underwent MPFL reconstruction technique using a hamstring autograft. Lykissas and colleagues142 corroborated these results with another radiographic study that reported small but significant decreases in the Blackburne-Peel index and CD index following MPFL reconstruction in 25 adolescents. As correction of patella alta allows the patella to rest in a deeper, more secure position in the TG, these results indicate that effective early MPFL reconstruction can correct for patellar anatomic abnormalities that could be future risk factors.143,144 Several studies have also reported outcomes addressing specific MPFL techniques; these are reported and discussed in this article.
OUTCOMES BY TECHNIQUE
HAMSTRING AUTOGRAFT
Reports on outcomes following MPFL reconstructions using hamstring autografts have been particularly promising. A cohort of 21 skeletally immature patients who underwent MPFL reconstruction was evaluated pre- and postoperatively with an average of a 2.8-year follow-up. The authors of the study reported no redislocation events and significant improvement in the Kujala scores, and patients were able to return to athletic activities safely.145 Previous studies report similar positive increases in Kujala scores, subjective patient reports, and lack of subsequent redislocation for patients who underwent either semitendinosus or gracilis autograft MPFL reconstructions. One such study further documented an average patellar inclination angle decrease from 34.3° to 18.6° following MPFL reconstruction.146 However, while the literature typically reports positive Kujala scores and subjective outcomes for the hamstring autograft procedure, a study arthroscopically evaluating patellar tracking immediately following surgery and then at 6 to 26 months follow-up found that patellar tracking correction was not maintained for all patients who underwent this type of MPFL reconstruction.147
Continue to: QUADRICEPS TENDON TRANSFER OUTCOMES
QUADRICEPS TENDON TRANSFER OUTCOMES
Studies specifically evaluating the quadriceps tendon transfer technique for MPFL reconstruction in children are sparse, but authors have reported positive clinical outcomes and low complication rates in adults. After following 32 young adults who underwent this MPFL reconstruction technique for 3 years, Goyal109 reported a significant increase in mean Kujala scores from 49.31 to 91.25 and no complications or redislocation. He argues this type of quadriceps graft has a high success rate because it is anatomically more similar to the MPFL than other grafts and does not require additional patellar fixation.101,109 Similar positive Kujala scores and minimal complications have been reported in adult patient populations.148 Abouelsoud and colleagues149 conducted one of the few studies in skeletally immature patients and reported similarly positive results with no redislocations and significantly improved Kujala scores at a mean follow-up of 29.25 months in their 16-patient cohorts.
ADDUCTOR MAGNUS TENDON TRANSFER
After initially describing this technique in 14 adult patients, Avikainen and colleagues96 followed this cohort and reported positive subjective results and only 1 redislocation. In a more recent study in which the adductor tendon transfer technique was compared with the quadriceps tendon transfer described above and the bone-patellar tendon allograft, Steiner and colleagues69 reported similarly significant improvement in all cohorts in Lysholm, Kujala, and Tegner scores with no redislocations. Additionally, Malecki and colleagues150 followed a cohort of 33 children with 39 knees diagnosed with recurrent patellar dislocation, who underwent MPFL reconstruction using the adductor magnus tendon. After evaluating this cohort functionally and radiographically, the authors reported improvements in Lysholm and Kujala scores, patellar tilt and congruence angles, and peak torque of the quadriceps muscle and flexor.150 However, this cohort did report postoperative redislocations in 36.4% of patients (4 of 11).150
HEMI-PATELLA TENDON TRANSFER
In 2012, in the first randomized controlled trial, Bitar and colleagues67 compared the outcomes of patients who underwent MPFL reconstruction via the hemi-patellar tendon technique with those who were managed nonoperatively with immobilization and physiotherapy after first-time patellar dislocation. At 2-year follow-up, the surgical cohort presented positive results with a significantly higher mean Kujala score (88.9 to 70.8) and no redislocations or subluxations. In contrast, 35% of nonoperative cases presented with recurrences and subluxations over the 2-year period.67
MCL OR ADDUCTOR TENDON AS A PULLEY
Studies have reported good postoperative results and low complication rates for these dynamic techniques.128,129 In terms of kinematics, while hypermobility and patellar height were not fully corrected, improvements in patellar tilt and lateral shift were reported in a cohort of 6 patients with a minimum 4-year follow-up.129 To further evaluate whether the more dynamic pulley reconstruction technique resulted in better outcomes, Gomes and colleagues128 compared the subjective reports, clinical evaluations, and complication rates of patients who underwent MPFL reconstruction with a rigid adductor magnus fixation vs a semitendinosus tendon dynamic femoral fixation. One case in the rigid cohort experienced a subsequent subluxation, while patients in the semitendinosus group had better subjective reports and a higher rate of return to sport.128 More recently, Kumahashi and colleagues151 specifically studied the outcomes of the MCL tendon as a pulley in 5 patients aged 14 to 15 years. They reported similar successful results as no patients experienced recurrence, and all patients exhibited improvement in radiographic measures of patellar tilt and congruence angle, lateral shift ratio, and both Kujala and Lysholm scores.151
While there has yet to be a randomized controlled trial comparing all of these different techniques, there is a general consensus in the literature that patients tend to perform better following MPFL reconstruction vs MPFL repair.
OTHER STABILIZATION PROCEDURES, INCLUDING DISTAL REALIGNMENT
Patients with additional underlying deficits and malalignment issues such as significant trochlear dysplasia, increased TT-TG distance, patella alta, increased Q angle, and/or positive J sign may require stabilization procedures beyond MPFL reconstruction.152,153 TT osteotomies are often used to correct alignment issues in the adult patient population; however, these procedures are typically contraindicated in skeletally immature patients. Alternative realignment procedures for the pediatric population include both proximal and distal realignment, with proximal realignment performed primarily in children under the age of 12 years.153 Many variations on these procedures exist, some of which are no longer regularly performed due to poor reported outcomes. In this article, we discuss several of the techniques, focusing primarily on those that have demonstrated higher success rates.
Continue to: GALEAZZI TECHNIQUE
GALEAZZI TECHNIQUE
One of the first and most famous soft-tissue techniques to address patellar instability was the semitendinosus tenodesis, published by Galeazzi154 in 1922 (Figure 7). This technique stabilizes the patella without altering the TT. In the original technique, a portion of the semitendinosus tendon is harvested with its tibial insertion left intact. The free end of the tendon is then secured with sutures at the periosteal groove of the medial patella.154,155 Fiume156 modified this technique by adding a lateral release and medial retinacular reefing. The most recent addition to this procedure was introduced by Baker and colleagues,157 in which a tunnel is drilled from the medial to the lateral border of the patella. Tension placed on the grafted tendon is used to reposition the patella medially and draw it downward. Preliminary literature on this modified procedure reported fair clinical results with success rates of approximately 75%.155,158-160 A recent study evaluating both the clinical and radiographic outcomes of this technique also indicated that while clinical results were excellent in 62.5% of patients, this technique alone was unsuccessful in fully addressing patellar instability in patients with underlying anatomic abnormalities such as patellar alta.161 In light of these less than ideal reports, the authors no longer recommend this technique for patellofemoral instability cases.
ROUX-GOLDTHWAIT PROCEDURE
The Roux-Goldthwait procedure, first described by both Roux162 and Goldthwait163 in 1888 and 1895 respectively, was later modified in 1985 to involve a lateral release, plication of the medial retinaculum, medial transfer of the lateral patellar tendon without advancement, and advancement of the vastus medialis (Figure 8).164 More recently, Marsh and colleagues152 introduced an addition to aligning the extensor mechanism with the femoral shaft better. In this technique modification, the patellar tendon is split longitudinally, and its lateral half is detached and transferred distally beneath its medial half. The free end is then sutured to the periosteum on the medial side of the tibia.152 With a mean long-term follow-up of 6.2 years, Marsh and colleagues152 reported excellent results in 65%, good in 11%, and fair in 3% of the knees operated on with this modified technique. Of the patients in this cohort whose strength was evaluated, 80% had their strength returned to 90% of preoperative levels in the operated leg.152 While this study and others report improved outcomes, an increasing body of literature has found high rates of recurrence, patella infera, and other complications following the modified Roux-Goldthwait procedure.36,165-171 Also, a study comparing MPFL reconstruction using adductus magnus transfer with the Roux-Goldthwait procedure reported that patients in the MPFL cohort reported less pain postoperatively.150 In addition, whereas the Kujala and Lysholm scores, recurrence rates, patellofemoral angles, and apprehension test results did not demonstrate significant differences between these 2 groups, the MPFL group had significantly fewer abnormal congruence angles, better patellar medialization, and higher peak torque of the hamstring.150
COMBINED MPFL AND MEDIAL PATELLOTIBIAL LIGAMENT RECONSTRUCTION
While the medial patellotibial ligament (MPTL) has not received much attention with regard to patellar stability, recent studies have indicated its role during higher degrees of both flexion and extension.172 The MPTL acts as a secondary restrictor ligament which helps release stress on the MPFL by decreasing the Q angle and further normalizing patellar kinematics.173 Patients who present with hyperlaxity or knee hyperextension combined with extension subluxation and flexion instability could be indicated for this additional stabilizing procedure. Both Nietosvaara and colleagues85 and Brown and Ahmad174 have described a dual MPTL and MPFL reconstruction technique using a semitendinosus hamstring graft. More recently Hinckel and colleagues172 described a combined MPFL and MPTL reconstruction, using a graft from the quadriceps tendon to reconstruct the MPFL and one from the patellar tendon to reconstruct the MPTL. In this technique, once the respective grafts have been harvested, a femoral insertion for the graft recreating the MPFL is fluoroscopically established so that an anchor can be inserted distal to the femoral physeal growth plate. For the MPTL insertion, attachment to the tibia below the joint line and 2 cm medial to the patellar tendon is established fluoroscopically just above the physeal growth plate on the proximal epiphysis.19,175 The MPTL graft is sutured first with the knee at 90° of flexion to establish tension similar to that of the patellar tendon.176 Then, the knee is placed in 30° of flexion to fix the MPFL graft to the medial patella to prevent excessive lateral translation of the patella.
PATELLAR TENDON TRANSFER
Patellar tendon transfer with proximal realignment is a technique used in particularly young patients to address cases of patellofemoral instability involving concomitant bony or anatomic abnormalities. This procedure is effective for young children with substantial amounts of remaining growth as it better mimics native anatomy than other realignment procedures and does not require bony remodeling.152-154 It is important to familiarize with surgical techniques to address malalignment issues in young patients as neglected alignment issues can lead to worsening of trochlear dysplasia and instability, which are very difficult to treat later on when patients are older.153
The patellar tendon transfer technique (Figure 9), as described by Gordon and Schoenecker,177 starts with an extensive lateral retinacular release. The patellar tendon is then released from its distal insertion at the TT so that it can be moved medially without moving it inferiorly. After confirming patellar tracking and alignment by flexing the knee from 0° to 90° with the graft in place, the patellar tendon graft is secured with multiple nonabsorbable horizontal sutures.177 Of note, in skeletally mature patients, a TT osteotomy is used to accomplish the same goal. This osteotomy has been shown to improve both patellar height and TT-TG distance in skeletally mature patients, but is contraindicated in skeletally immature patients.92,178
Continue to: Initial studies conducted on patellar tendon...
Initial studies conducted on patellar tendon transfer have positive outcomes.179 At a mean follow-up of 5.1 years, patients reported a decrease in pain and increased the ROM and activity, and only 1 reported a postoperative redislocation.179 In more recent studies, both Benoit and colleagues36 and Garin and colleagues58 reviewed cases of patellar instability treated with patellar tendon transfer to address concomitant patellar alignment and anatomic abnormalities. They reported good functional, clinical, and radiographic outcomes with 12.5% and 16% recurrence rates, respectively.36,58 They also noted radiographic improvements in femoral sulcus angle, particularly in younger patients, which indicate this procedure is effective in addressing bony abnormalities that can result from neglected malalignment issues.36,58,154
QUADRICEPSPLASTY
Quadricepsplasty is a lengthening and remodeling technique not frequently used in the pediatric population. The goal of this procedure in patients with significant amounts of growth remaining is to reposition the patella to ameliorate trochlear remodeling and prevent worsening symptoms and anatomic abnormalities.36 A quadricepsplasty accomplishes this by de-rotating and/or lengthening the extensor mechanism and may or may not involve a concomitant MPFL reconstruction. This procedure is particularly effective in young patients who experience obligatory dislocation.60,72 Several quadricepsplasty techniques have been described including Thompson, Curtis and Fisher, Judet, Stanisavljevic, and V-Y technique.180-186 Most techniques initially involve sharp dissection of the vastus medialis and lateralis from the rectus femoral tendon. A tongue is then fashioned out of the rectus femoral tendon. Once the vastus medialis and lateralis are detached from the margins of the patella, the knee is extended, and the distal ends of the vasti are sutured to the tongue of the rectus tendon. Effective extension facilitates flexion to 90°.184 The authors recommend a modification of this technique in which a Z lengthening of the quadriceps tendon is performed after the vastus lateralis is removed distally from the patella and the quadriceps tendon.
Several series and case reports evaluating quadricepsplasty in adult patients report positive outcomes with most patients achieving good or excellent flexion with minimal complications.183,185,187-189 Reports on quadricepsplasty used to treat conditions other than patellofemoral instability in children have reported similar positive outcomes.190-192 As quadricepsplasty for patellar instability is relatively rare in pediatric patients, there is not much relevant literature. However, Kocon and colleagues193 reported results of quadricepsplasty and quadricepsplasty combined with the modified Galeazzi procedure in 8 children (10 knees) with a mean follow-up of 3.25 years. Seventy percent of cases resulted in stabilization and correction of patellar position, and only 2 postoperative redislocations were noted.193 Additionally, in a study evaluating 6 patients suffering from patellar instability, 2 of whom were obligate dislocators, quadricepsplasty resulted in patellar stability, satisfaction, and near normal gait patterns.194
Figure 10 shows the surgical algorithm used for patellar instability characteristics.
CONCLUSION
Patellofemoral joint stability relies on a complex interplay of musculotendinous units, ligaments and the osteocartilaginous morphology of the patellofemoral joint. Patellar instability in pediatric patients is different from adults. Having an in-depth understanding of the remodeling potential, the insertion sites for the MPFL and its relationship to the physis are of utmost importance when planning surgery. Reducing and maintaining the patella within the patellofemoral joint early enough can allow for remodeling of the patella and/or the trochlea to provide for lasting stability. Appropriate surgical principles, such as tensioning, can help both prevent continued pain and minimize future complications.
1. Nietosvaara Y, Aalto K, Kallio PE. Acute patellar dislocation in children: incidence and associated osteochondral fractures. J Pediatr Orthop. 1994;14(4):513-515.
2. Fithian DC, Paxton EW, Stone ML, et al. Epidemiology and natural history of acute patellar dislocation. Am J Sports Med. 2004;32(5):1114-1121. doi:10.1177/0363546503260788.
3. Abbasi D, May MM, Wall EJ, Chan G, Parikh SN. MRI findings in adolescent patients with acute traumatic knee hemarthrosis. J Pediatr Orthop. 2012;32(8):760-764. doi:10.1097/BPO.0b013e3182648d45.
4. Mäenpää H, Lehto MU. Patellar dislocation. The long-term results of nonoperative management in 100 patients. Am J Sports Med. 1997;25(2):213-217. doi:10.1177/036354659702500213.
5. Hawkins RJ, Bell RH, Anisette G. Acute patellar dislocations. The natural history. Am J Sports Med. 1986;14(2):117-120. doi:10.1177/036354658601400204.
6. Cofield RH, Bryan RS. Acute dislocation of the patella: results of conservative treatment. J Trauma. 1977;17(7):526-531.
7. Wasserlauf BL, Paletta GA. Developmental anatomy of the pediatric and adolescent knee. In: Micheli LJ, Kocher MS, eds. The Pediatric and Adolescent Knee. 1st ed. Elsevier; 2006:27-32.
8. Birch JG. Growth and development. In: Herring J, ed. Tachdjian’s Pediatric Orthopedics. 4th ed. Saunders/Elsevier; 2007:3-22.
9. Sarin VK, Carter DR. Mechanobiology and joint conformity regulate endochondral ossification of sesamoids. J Orthop Res. 2000;18(5):706-712. doi:10.1002/jor.1100180505.
10. Maes C, Kronenberg HM. Postnatal bone growth: growth plate biology, bone formation, and remodeling. In: Pediatric Bone. Elsevier; 2012:55-82.
11. Tecklenburg K, Dejour D, Hoser C, Fink C. Bony and cartilaginous anatomy of the patellofemoral joint. Knee Surg Sports Traumatol Arthrosc. 2006;14(3):235-240. doi:10.1007/s00167-005-0683-0.
12. Walmsley R. The development of the patella. J Anat. 1940;74(Pt 3):360-368.3.
13. Fulkerson J, Hungerford D. Disorders of the patellofemoral Joint. In: Normal Anatomy. 2nd ed. Baltimore: Williams & Wilkins; 1990:1-24.
14. Ogden JA. Radiology of postnatal skeletal development. X. Patella and tibial tuberosity. Skeletal Radiol. 1984;11(4):246-257.
15. Nietosvaara Y, Aalto K. The cartilaginous femoral sulcus in children with patellar dislocation: an ultrasonographic study. J Pediatr Orthop. 1997;17(1):50-53.
16. Glard Y, Jouve JL, Garron E, Adalian P, Tardieu C, Bollini G. Anatomic study of femoral patellar groove in fetus. J Pediatr Orthop. 2005;25(3):305-308.
17. Nietosvaara Y. The femoral sulcus in children. An ultrasonographic study. J Bone Joint Surg Br. 1994;76(5):807-809.
18. Nietosvaara AY, Aalto KA. Ultrasonographic evaluation of patellar tracking in children. Clin Orthop Relat Res. 1993;(297):62-64.
19. Desio SM, Burks RT, Bachus KN. Soft tissue restraints to lateral patellar translation in the human knee. Am J Sports Med. 26(1):59-65. doi:10.1177/03635465980260012701.
20. Shea KG, Styhl AC, Jacobs JC, et al. The relationship of the femoral physis and the medial patellofemoral ligament in children: a cadaveric study. Am J Sports Med. 2016;44(11):2833-2837. doi:10.1177/0363546516656366.
21. Shea KG, Polousky JD, Jacobs JC, et al. The relationship of the femoral physis and the medial patellofemoral ligament in children. J Pediatr Orthop. 2014;34(8):808-813. doi:10.1097/BPO.0000000000000165.
22. Shea KG, Polousky JD, Jacobs JC, et al. The patellar insertion of the medial patellofemoral ligament in children. J Pediatr Orthop. 2015;35(4):e31-e35. doi:10.1097/BPO.0000000000000399.
23. Shea KG, Grimm NL, Belzer J, Burks RT, Pfeiffer R. The relation of the femoral physis and the medial patellofemoral ligament. Arthroscopy. 2010;26(8):1083-1087. doi:10.1016/j.arthro.2009.12.020.
24. Nelitz M, Dornacher D, Dreyhaupt J, Reichel H, Lippacher S. The relation of the distal femoral physis and the medial patellofemoral ligament. Knee Surg Sport Traumatol Arthrosc. 2011;19(12):2067-2071. doi:10.1007/s00167-011-1548-3.
25. Kepler CK, Bogner EA, Hammoud S, Malcolmson G, Potter HG, Green DW. Zone of injury of the medial patellofemoral ligament after acute patellar dislocation in children and adolescents. Am J Sports Med. 2011;39(7):1444-1449. doi:10.1177/0363546510397174.
26. Seitlinger G, Moroder P, Fink C, Wierer G. Acquired femoral flexion deformity due to physeal injury during medial patellofemoral ligament reconstruction. Knee. 2017;24(3):680-685. doi:10.1016/j.knee.2017.02.003.
27. Parikh SN, Rajdev N. Relationship between trochlear dysplasia and the anterior distal femoral physis in pediatric and adolescent patients with patellar instability. In: 36th Annual Meething AANA. Denver; 2017.
28. Salenius P, Vankka E. The development of the tibiofemoral angle in children. J Bone Joint Surg Am. 1975;57(2):259-261.
29. Parikh SN. Medial patellofemoral ligament reconstruction and simultaneous guided correction of genu valgum for patellar instability in skeletally immature patients. In: EPOSNA. 2017.
30. Brattstroem H. Shape of the intercondylar groove normally and in recurrent dislocation of patella. A clinical and X-ray-Anatomical investigation. Acta Orthop Scand Suppl. 1964;68(suppl 68):1-148.
31. Dejour H, Walch G, Nove-Josserand L, Guier C. Factors of patellar instability: an anatomic radiographic study. Knee Surg Sports Traumatol Arthrosc. 1994;2(1):19-26.
32. Lewallen LW, McIntosh AL, Dahm DL. Predictors of recurrent instability after acute patellofemoral dislocation in pediatric and adolescent patients. Am J Sports Med. 2013;41(3):575-581. doi:10.1177/0363546512472873.
33. Jaquith BP, Parikh SN. Predictors of recurrent patellar instability in children and adolescents after first-time dislocation. J Pediatr Orthop. 2017;37(7):484-490. doi:10.1097/BPO.0000000000000674.
34. Lippacher S, Reichel H, Nelitz M. Radiological criteria for trochlear dysplasia in children and adolescents. J Pediatr Orthop B. 2011;20(5):341-344. doi:10.1097/BPB.0b013e3283474c8b.
35. Parikh SN, Rajdev N, Sun Q. The growth of trochlear dysplasia during adolescence. J Pediatr Orthop. 2018. doi:10.1097/BPO.0000000000001168. [Epub ahead of print]
36. Benoit B, Laflamme GY, Laflamme GH, Rouleau D, Delisle J, Morin B. Long-term outcome of surgically-treated habitual patellar dislocation in children with coexistent patella alta. Minimum follow-up of 11 years. J Bone Joint Surg Br. 2007;89(9):1172-1177. doi:10.1302/0301-620X.89B9.19065.
37. Sugimoto D, Christino MA, Micheli LJ. Effects of surgical intervention on trochlear remodeling in pediatric patients with recurrent patella dislocation cases. J Pediatr Orthop B. 2016;25(4):349-353. doi:10.1097/BPB.0000000000000341.
38. Insall J, Goldberg V, Salvati E. Recurrent dislocation and the high-riding patella. Clin Orthop Relat Res. 1972;88:67-69.
39. Caton J. [Method of measuring the height of the patella]. Acta Orthop Belg. 1989;55(3):385-386.
40. Thévenin-Lemoine C, Ferrand M, Courvoisier A, Damsin JP, Ducou le Pointe H, Vialle R. Is the Caton-Deschamps index a valuable ratio to investigate patellar height in children? J Bone Joint Surg Am. 2011;93(8):e35. doi:10.2106/JBJS.J.00759.
41. Micheli LJ, Slater JA, Woods E, Gerbino PG. Patella alta and the adolescent growth spurt. Clin Orthop Relat Res. 1986;213:159-162.
42. Koshino T, Sugimoto K. New measurement of patellar height in the knees of children using the epiphyseal line midpoint. J Pediatr Orthop. 1989;9(2):216-218.
43. Mays PK, Bishop JE, Laurent GJ. Age-related changes in the proportion of types I and III collagen. Mech Ageing Dev. 1988;45(3):203-212.
44. Smits-Engelsman B, Klerks M, Kirby A. Beighton score: a valid measure for generalized hypermobility in children. J Pediatr. 2011;158(1):119-123. doi:10.1016/j.jpeds.2010.07.021.
45. Jansson A, Saartok T, Werner S, Renström P. General joint laxity in 1845 Swedish school children of different ages: age- and gender-specific distributions. Acta Paediatr. 2004;93(9):1202-1206.
46. Beighton P, Solomon L, Soskolnet CL. Articular mobility in an African population. Ann rheum Dis. 1973;32(5):413-418.
47. Staheli LT, Corbett M, Wyss C, King H. Lower-extremity rotational problems in children. Normal values to guide management. J Bone Joint Surg Am. 1985;67(1):39-47.
48. Kijowski R, Plagens D, Shaeh S, Teitge R. The effects of rotational deformities of the femur on contact pressure and contact area in the patellofemoral joint and on strain in the medial patellofemoral ligament. Annu Meet Int Patellofemoral Study Group, Napa Val San Fr CA. 1999.
49. Post W, Teitge R, Amis A. Patellofemoral malalignment: looking beyond the viewbox. Clin Sports Med. 2002;21(3):521-546.
50. Bruce WD, Stevens PM. Surgical correction of miserable malalignment syndrome. J Pediatr Orthop. 2004;24(4):392-396.
51. Kurosawa K, Kawame H, Ochiai Y, Nakashima M, Tohma T, Ohashi H. Patellar dislocation in Kabuki syndrome. Am J Med Genet. 2002;108(2):160-163.
52. Mik G, Gholve PA, Scher DM, Widmann RF, Green DW. Down syndrome: orthopedic issues. Curr Opin Pediatr. 2008;20(1):30-36. doi:10.1097/MOP.0b013e3282f35f19.
53. Sweeney E, Fryer A, Mountford R, Green A, McIntosh I. Nail patella syndrome: a review of the phenotype aided by developmental biology. J Med Genet. 2003;40(3):153-162.
54. Stevens CA. Patellar dislocation in Rubenstein-Taybi syndrome. Am J Med Genet. 1997;72(2):188-190.
55. Andrish J. The biomechanics of patellofemoral stability. J Knee Surg. 2004;17(1):35-39.
56. Conlan T, Garth WP, Lemons JE. Evaluation of the medial soft-tissue restraints of the extensor mechanism of the knee. J Bone Joint Surg Am. 1993;75(5):682-693.
57. Balcarek P, Ammon J, Frosch S, et al. Magnetic resonance imaging characteristics of the medial patellofemoral ligament lesion in acute lateral patellar dislocations considering trochlear dysplasia, patella alta, and tibial tuberosity-TG distance. Arthroscopy. 2010;26(7):926-935. doi:10.1016/j.arthro.2009.11.004.
58. Garin C, Chaker M, Dohin B, Kohler R. Permanent, habitual dislocation and recurrent dislocation of the patella in children: surgical management by patellar ligamentous transfer in 50 knees. Rev Chir Orthop Reparatrice Appar Mot. 2007;93(7):690-700.
59. Sillanpaa P. Terminology of patellar dislocation. In: Sillanpaa P, ed. Trauma. Saarbrucken, Germany: Lambert Academic Publishing; 2010:16-18.
60. Parikh SN, Lykissas MG. Classification of lateral patellar instability in children and adolescents. Orthop Clin North Am. 2016;47(1):145-152. doi:10.1016/j.ocl.2015.08.016.
61. Chotel F, Bérard J, Raux S. Patellar instability in children and adolescents. Orthop Traumatol Surg Res. 2014;100(suppl 1):125-137. doi:10.1016/j.otsr.2013.06.014.
62. Wada A, Fujii T, Takamura K, Yanagida H, Surijamorn P. Congenital dislocation of the patella. J Child Orthop. 2008;2(2):119-123. doi:10.1007/s11832-008-0090-4.
63. Südkamp NP, Granrath M, Hoffmann R, Haas NP. Instability of the shoulder joint in the athlete. Chirurg. 1994;65(11):901-909.
64. Hiemstra LA, Kerslake S, Lafave M, Heard SM, Buchko GML. Introduction of a classification system for patients with patellofemoral instability (WARPS and STAID). Knee Surg Sport Traumatol Arthrosc. 2014;22(11):2776-2782. doi:10.1007/s00167-013-2477-0.
65. Frosch KH, Schmeling A. A new classification system of patellar instability and patellar maltracking. Arch Orthop Trauma Surg. 2016;136(4):485-497. doi:10.1007/s00402-015-2381-9.
66. Balcarek P, Oberthür S, Hopfensitz S, et al. Which patellae are likely to redislocate? Knee Surg Sport Traumatol Arthrosc. 2014;22(10):2308-2314. doi:10.1007/s00167-013-2650-5.
67. Bitar AC, Demange MK, D’Elia CO, Camanho GL. Traumatic patellar dislocation: nonoperative treatment compared with mpfl reconstruction using patellar tendon. Am J Sports Med. 2012;40(1):114-122. doi:10.1177/0363546511423742.
68. Smith TO, Walker J, Russell N. Outcomes of medial patellofemoral ligament reconstruction for patellar instability: a systematic review. Knee Surg Sport Traumatol Arthrosc. 2007;15(11):1301-1314. doi:10.1007/s00167-007-0390-0.
69. Steiner TM, Torga-Spak R, Teitge RA. Medial patellofemoral ligament reconstruction in patients with lateral patellar instability and trochlear dysplasia. Am J Sports Med. 2006;34(8):1254-1261. doi:10.1177/0363546505285584.
70. Ma LF, Wang F, Chen BC, Wang CH, Zhou JW, Wang HY. Medial retinaculum plasty versus medial patellofemoral ligament reconstruction for recurrent patellar instability in adults: a randomized controlled trial. Arthrosc J Arthrosc Relat Surg. 2013;29(5):891-897. doi:10.1016/j.arthro.2013.01.030.
71. Weeks KD, Fabricant PD, Ladenhauf HN, Green DW. Surgical options for patellar stabilization in the skeletally immature patient. Sports Med Arthrosc Rev. 2012;20(3):194-202.
72. Green D. Surgical treatment of pediatric patella instability. Die Ther der Instabilen patella. 2016:80-89.
73. Lewallen L, McIntosh A, Dahm D. First-time patellofemoral dislocation: risk factors for recurrent instability. J Knee Surg. 2015;28(4):303-309. doi:10.1055/s-0034-1398373.
74. Ghanem I, Wattincourt L, Seringe R. Congenital dislocation of the patella. Part I: pathologic anatomy. J Pediatr Orthop. 2000;20(6):812-816.
75. Bongers E, Van Kampen A, Van Bokhoven H, Knoers N. Human syndromes with congenital patellar anomalies and the underlying gene defects. Clin Genet. 2005;68(4):302-319. doi:10.1111/j.1399-0004.2005.00508.x.
76. Beighton P, Horan F. Orthopaedic aspects of the Ehlers-Danlos syndrome. J Bone Joint Surg Br. 1969;51(3):444-453.
77. Gausden EB, Fabricant PD, Taylor SA, et al. Medial patellofemoral reconstruction in children and adolescents. JBJS Rev. 2015;3(10):1-11. doi:10.2106/JBJS.RVW.N.00091.
78. Palmu S, Kallio PE, Donell ST, Helenius I, Nietosvaara Y. Acute patellar dislocation in children and adolescents: a randomized clinical trial. J Bone Joint Surg Am. 2008;90(3):463-470. doi:10.2106/JBJS.G.00072.
79. Webb JE, Lewallen LW, Christophersen C, Krych AJ, McIntosh AL. Clinical outcome of internal fixation of unstable juvenile osteochondritis dissecans lesions of the knee. Orthopedics. 2013;36(11):e1444-e1449. doi:10.3928/01477447-20131021-30.
80. Hennrikus W, Pylawka T. Patellofemoral instability in skeletally immature athletes. Instr Course Lect. 2013;62:445-453.
81. Nomura E, Inoue M. Surgical technique and rationale for medial patellofemoral ligament reconstruction for recurrent patellar dislocation. Arthroscopy. 2003;19(5):e47. doi:10.1053/jars.2003.50167.
82. Nomura E, Inoue M, Kobayashi S. Long-term follow-up and knee osteoarthritis change after medial patellofemoral ligament reconstruction for recurrent patellar dislocation. Am J Sports Med. 2007;35(11):1851-1858. doi:10.1177/0363546507306161.
83. Arshi A, Cohen JR, Wang JC, Hame SL, McAllister DR, Jones KJ. Operative management of patellar instability in the United States. Orthop J Sport Med. 2016;4(8):2325967116662873. doi:10.1177/2325967116662873.
84. Servien E, Verdonk PC, Neyret P. Tibial tuberosity transfer for episodic patellar dislocation. Sports Med Arthrosc. 2007;15(2):61-67. doi:10.1097/JSA.0b013e3180479464.
85. Nietosvaara Y, Paukku R, Palmu S, Donell ST. Acute patellar dislocation in children and adolescents. Surgical technique. J Bone Joint Surg Am. 2009;91(suppl 2):139-145. doi:10.2106/JBJS.H.01289.
86. Hing CBC, Smith TO, Donell S, Song F. Surgical versus non-surgical interventions for treating patellar dislocation. In Hing CB, ed. Cochrane Database Syst Rev. 2011;(11):CD008106. doi:10.1002/14651858.CD008106.pub2.
87. Nwachukwu BU, So C, Schairer WW, Green DW, Dodwell ER. Surgical versus conservative management of acute patellar dislocation in children and adolescents: a systematic review. Knee Surgery, Sport Traumatol Arthrosc. 2016;24(3):760-767. doi:10.1007/s00167-015-3948-2.
88. Camp CL, Krych AJ, Dahm DL, Levy BA, Stuart MJ. Medial patellofemoral ligament repair for recurrent patellar dislocation. Am J Sports Med. 2010;38(11):2248-2254. doi:10.1177/0363546510376230.
89. Nikku R, Nietosvaara Y, Aalto K, Kallio PE. Operative treatment of primary patellar dislocation does not improve medium-term outcome: a 7-year follow-up report and risk analysis of 127 randomized patients. Acta Orthop. 2005;76(5):699-704. doi:10.1080/17453670510041790.
90. Ostermeier S, Holst M, Hurschler C, Windhagen H, Stukenborg-Colsman C. Dynamic measurement of patellofemoral kinematics and contact pressure after lateral retinacular release: an in vitro study. Knee Surg Sport Traumatol Arthrosc. 2007;15(5):547-554. doi:10.1007/s00167-006-0261-0.
91. Sallay PI, Poggi J, Speer KP, Garrett WE. Acute dislocation of the patella. A correlative pathoanatomic study. Am J Sports Med. 1996;24(1):52-60. doi: 10.1177/036354659602400110.
92. Arendt EA, Fithian DC, Cohen E. Current concepts of lateral patella dislocation. Clin Sports Med. 2002;21(3):499-519.
93. Arendt EA, Moeller A, Agel J. Clinical outcomes of medial patellofemoral ligament repair in recurrent (chronic) lateral patella dislocations. Knee Surg Sports Traumatol Arthrosc. 2011;19(11):1909-1914. doi:10.1007/s00167-011-1516-y.
94. Ellera Gomes JL. Medial patellofemoral ligament reconstruction for recurrent dislocation of the patella: a preliminary report. Arthroscopy. 1992;8(3):335-340.
95. Amis AA, Firer P, Mountney J, Senavongse W, Thomas NP. Anatomy and biomechanics of the medial patellofemoral ligament. Knee. 2003;10(3):215-220.
96. Avikainen VJ, Nikku RK, Seppänen-Lehmonen TK. Adductor magnus tenodesis for patellar dislocation. Technique and preliminary results. Clin Orthop Relat Res. 1993;(297):12-16.
97. Davis DK, Fithian DC. Techniques of medial retinacular repair and reconstruction. Clin Orthop Relat Res. 2002;(402):38-52.
98. Dhillon MS, Mohan P, Nagi ON. Does harvesting the medial third of the patellar tendon cause lateral shift of the patella after ACL reconstruction? Acta Orthop Belg. 2003;69(4):334-340.
99. Drez D, Edwards TB, Williams CS. Results of medial patellofemoral ligament reconstruction in the treatment of patellar dislocation. Arthrosc J Arthrosc Relat Surg. 2001;17(3):298-306. doi:10.1053/jars.2001.21490.
100. Ellera Gomes JL, Stigler Marczyk LR, César de César P, Jungblut CF. Medial patellofemoral ligament reconstruction with semitendinosus autograft for chronic patellar instability: a follow-up study. Arthrosc J Arthrosc Relat Surg. 2004;20(2):147-151. doi:10.1016/j.arthro.2003.11.006.
101. Feller JA, Amis AA, Andrish JT, Arendt EA, Erasmus PJ, Powers CM. Surgical biomechanics of the patellofemoral joint. Arthrosc J Arthrosc Relat Surg. 2007;23(5):542-553. doi:10.1016/j.arthro.2007.03.006.
102. Nomura E, Horiuchi Y, Kihara M. Medial patellofemoral ligament restraint in lateral patellar translation and reconstruction. Knee. 2000;7(2):121-127.
103. Ostermeier S, Stukenborg-Colsman C, Hurschler C, Wirth CJ. In vitro investigation of the effect of medial patellofemoral ligament reconstruction and medial tibial tuberosity transfer on lateral patellar stability. Arthrosc J Arthrosc Relat Surg. 2006;22(3):308-319. doi:10.1016/j.arthro.2005.09.024.
104. Smirk C, Morris H. The anatomy and reconstruction of the medial patellofemoral ligament. Knee. 2003;10(3):221-227.
105. Steensen RN, Dopirak RM, Maurus PB. A simple technique for reconstruction of the medial patellofemoral ligament using a quadriceps tendon graft. Arthroscopy. 2005;21(3):365-370. doi:10.1016/j.arthro.2004.10.007.
106. Steensen RN, Dopirak RM, McDonald WG. The anatomy and isometry of the medial patellofemoral ligament: implications for reconstruction. Am J Sports Med. 2004;32(6):1509-1513. doi:10.1177/0363546503261505.
107. Farahmand F, Tahmasbi MN, Amis AA. Lateral force–displacement behaviour of the human patella and its variation with knee flexion—a biomechanical study in vitro. J Biomech. 1998;31(12):1147-1152.
108. Heegaard J, Leyvraz PF, Van Kampen A, Rakotomanana L, Rubin PJ, Blankevoort L. Influence of soft structures on patellar 3-dimensional tracking. Clin Orthop Relat Res. 1994;(299):235-243.
109. Goyal D. Medial patellofemoral ligament reconstruction: the superficial quad technique. Am J Sports Med. 2013;41(5):1022-1029. doi:10.1177/0363546513477828.
110. Hohn E, Pandya NK. Does the utilization of allograft tissue in medial patellofemoral ligament reconstruction in pediatric and adolescent patients restore patellar stability? Clin Orthop Relat Res. 2017;475(6):1563-1569. doi:10.1007/s11999-016-5060-4.
111. Csintalan R, Latt L, Fornalski S, Raiszadeh K, Inacio M, Fithian D. Medial patellofemoral ligament (MPFL) reconstruction for the treatment of patellofemoral instability. J Knee Surg. 2013;27(2):139-146. doi:10.1055/s-0033-1360652.
112. Ahmad CS, Brown GD, Stein BS. The docking technique for medial patellofemoral ligament reconstruction: surgical technique and clinical outcome. Am J Sports Med. 2009;37(10):2021-2027. doi:10.1177/0363546509336261.
113. Fernandez E, Sala D, Castejon M. Reconstruction of the medial patellofemoral ligament for patellar instability using a semitendinosus autograft. Acta Orthop Belg. 2005;71(3):303-308.
114. Parikh SN, Nathan ST, Wall EJ, Eismann EA. Complications of medial patellofemoral ligament reconstruction in young patients. Am J Sports Med. 2013;41(5):1030-1038. doi:10.1177/0363546513482085.
115. Green D, Gausden E. Medial patellofemoral ligament reconstruction: hamstring technique. In: Green D, Cordasco F, eds. Pediatr. Adolesc. Knee Surg. New York, NY: Wolters Kluwer; 2015:150-157.
116. Craig JG, Cody DD, van Holsbeeck M. The distal femoral and proximal tibial growth plates: MR imaging, 3-dimensional modeling and estimation of area and volume. Skeletal Radiol. 2004;33(6):337-344.
117. Noyes FR, Albright JC. Reconstruction of the medial patellofemoral ligament with autologous quadriceps tendon. Arthroscopy. 2006;22(8):904.e1-e7. doi:10.1016/j.arthro.2005.12.058.
118. Pinkowsky G, Hennrikus. Technique: quad tendon medial patellofemoral ligament reconstruction. In: Green DW, Cordasco FA, eds. Pediatr. Adolesc. Knee Surg. New York, NY: Wolters Kluwer; 2015:133-139.
119. Bollier M, Fulkerson J, Cosgarea A, Tanaka M. Technical failure of medial patellofemoral ligament reconstruction. Arthroscopy. 2011;27(8):1153-1159. doi:10.1016/j.arthro.2011.02.014.
120. Elias JJ, Cosgarea AJ. Technical errors during medial patellofemoral ligament reconstruction could overload medial patellofemoral cartilage: a computational analysis. Am J Sports Med. 2006;34(9):1478-1485. doi:10.1177/0363546506287486.
121. Thaunat M, Erasmus PJ. Management of overtight medial patellofemoral ligament reconstruction. Knee Surg Sports Traumatol Arthrosc. 2009;17(5):480-483. doi:10.1007/s00167-008-0702-z.
122. Schöttle PB, Schmeling A, Rosenstiel N, Weiler A. Radiographic landmarks for femoral tunnel placement in medial patellofemoral ligament reconstruction. Am J Sports Med. 2007;35(5):801-804. doi:10.1177/0363546506296415.
123. Redfern J, Kamath G, Burks R. Anatomical confirmation of the use of radiographic landmarks in medial patellofemoral ligament reconstruction. Am J Sports Med. 2010;38(2):293-297. doi:10.1177/0363546509347602.
124. Fink C, Veselko M, Herbort M, Hoser C. Minimally invasive reconstruction of the medial patellofemoral ligament using quadriceps tendon. Arthrosc Tech. 2014;3(3):e325-e329. doi:10.1016/j.eats.2014.01.012.
125. Sillanpää PJ, Mäenpää HM, Mattila VM, Visuri T, Pihlajamäki H. A mini-invasive adductor magnus tendon transfer technique for medial patellofemoral ligament reconstruction: a technical note. Knee Surg Sports Traumatol Arthrosc. 2009;17(5):508-512. doi:10.1007/s00167-008-0713-9.
126. Hambidge SJ, Davidson AJ, Gonzales R, Steiner JF. Epidemiology of pediatric injury-related primary care office visits in the United States. Pediatrics. 2002;109(4):559-565.
127. Camanho GL, Bitar AC, Hernandez AJ, Olivi R. Medial patellofemoral ligament reconstruction: a novel technique using the patellar ligament. Arthroscopy. 2007;23(1):108.e1-e4. doi:10.1016/j.arthro.2006.07.008.
128. Gomes JE. Comparison between a static and a dynamic technique for medial patellofemoral ligament reconstruction. Arthroscopy. 2008;24(4):430-435. doi:10.1016/j.arthro.2007.11.005.
129. Deie M, Ochi M, Sumen Y, Yasumoto M, Kobayashi K, Kimura H. Reconstruction of the medial patellofemoral ligament for the treatment of habitual or recurrent dislocation of the patella in children. J Bone Joint Surg Br. 2003;85(6):887-890.
130. Ladenhauf HN, Berkes MB, Green DW. Medial patellofemoral ligament reconstruction using hamstring autograft in children and adolescents. Arthrosc Tech. 2013;2(2):e151-e154. doi:10.1016/j.eats.2013.01.006.
131. Bedi H, Marzo J. The biomechanics of medial patellofemoral ligament repair followed by lateral retinacular release. Am J Sports Med. 2010;38(7):1462-1467. doi:10.1177/0363546510373581.
132. Lattermann C, Toth J, Bach BR. The role of lateral retinacular release in the treatment of patellar instability. Sports Med Arthrosc Rev. 2007;15(2):57-60. doi:10.1097/JSA.0b013e318042af30
133. Ricchetti ET, Mehta S, Sennett BJ, Huffman GR. Comparison of lateral release versus lateral release with medial soft-tissue realignment for the treatment of recurrent patellar instability: a systematic review. Arthroscopy. 2007;23(5):463-468. doi:10.1016/j.arthro.2007.01.007.
134. Dainer RD, Barrack RL, Buckley SL, Alexander AH. Arthroscopic treatment of acute patellar dislocations. Arthroscopy. 1988;4(4):267-271.
135. Miller JR, Adamson GJ, Pink MM, Fraipont MJ, Durand P. Arthroscopically assisted medial reefing without routine lateral release for patellar instability. Am J Sports Med. 2007;35(4):622-629. doi:10.1177/0363546506296041.
136. Vainionpää S, Laasonen E, Silvennoinen T, Vasenius J, Rokkanen P. Acute dislocation of the patella. A prospective review of operative treatment. J Bone Joint Surg Br. 1990;72(3):366-369.
137. Shah JN, Howard JS, Flanigan DC, Brophy RH, Carey JL, Lattermann C. A systematic review of complications and failures associated with medial patellofemoral ligament reconstruction for recurrent patellar dislocation. Am J Sports Med. 2012;40(8):1916-1923. doi:10.1177/0363546512442330.
138. Tanaka MJ, Bollier MJ, Andrish JT, Fulkerson JP, Cosgarea AJ. Complications of medial patellofemoral ligament reconstruction: common technical errors and factors for success: AAOS exhibit selection. J Bone Joint Surg Am. 2012;94(12):e87. doi:10.2106/JBJS.K.01449.
139. Nguyen CV, Farrow LD, Liu RW, Gilmore A. Safe drilling paths in the distal femoral epiphysis for pediatric medial patellofemoral ligament reconstruction. Am J Sports Med. 2017;45(5):1085-1089. doi:10.1177/0363546516677795.
140. Edmonds EW, Glaser DA. Adolescent patella instability extensor mechanics. J Pediatr Orthop. 2016;36(3):262-267. doi:10.1097/BPO.0000000000000430.
141. Fabricant PD, Ladenhauf HN, Salvati EA, Green DW. Medial patellofemoral ligament (MPFL) reconstruction improves radiographic measures of patella alta in children. Knee. 2014;21(6):1180-1184. doi:10.1016/j.knee.2014.07.023.
142. Lykissas MG, Li T, Eismann EA, Parikh SN. Does medial patellofemoral ligament reconstruction decrease patellar height? A preliminary report. J Pediatr Orthop. 2014;34(1):78-85. doi:10.1097/BPO.0b013e3182a12102.
143. Magnussen RA, De Simone V, Lustig S, Neyret P, Flanigan DC. Treatment of patella alta in patients with episodic patellar dislocation: a systematic review. Knee Surgery, Sport Traumatol Arthrosc. 2014;22(10):2545-2550. doi:10.1007/s00167-013-2445-8.
144. Schöttle PB, Fucentese SF, Romero J. Clinical and radiological outcome of medial patellofemoral ligament reconstruction with a semitendinosus autograft for patella instability. Knee Surg Sports Traumatol Arthrosc. 2005;13(7):516-521. doi:10.1007/s00167-005-0659-0.
145. Nelitz M, Dreyhaupt J, Reichel H, Woelfle J, Lippacher S. Anatomic reconstruction of the medial patellofemoral ligament in children and adolescents with open growth plates: surgical technique and clinical outcome. Am J Sports Med. 2013;41(1):58-63. doi:10.1177/0363546512463683.
146. Raghuveer RK, Mishra CB. Reconstruction of medial patellofemoral ligament for chronic patellar instability. Indian J Orthop. 2012;46(4):447-454. doi:10.4103/0019-5413.97259.
147. Kita K, Horibe S, Toritsuka Y, et al. Effects of medial patellofemoral ligament reconstruction on patellar tracking. Knee Surg Sports Traumatol Arthrosc. 2012;20(5):829-837. doi:10.1007/s00167-011-1609-7.
148. Lenschow S, Herbort M, Fink C. Medial patellofemoral ligament reconstruction using quadriceps tendon. Oper Orthop Traumatol. 2015;27(6):474-483. doi:10.1007/s00064-015-0416-6.
149. Abouelsoud MM, Abdelhady A, Elshazly O. Anatomic physeal-sparing technique for medial patellofemoral ligament reconstruction in skeletally immature patients with ligamentous laxity. Eur J Orthop Surg Traumatol. 2015;25(5):921-926. doi:10.1007/s00590-015-1618-1.
150. Malecki K, Fabis J, Flont P, Niedzielski KR. The results of adductor magnus tenodesis in adolescents with recurrent patellar dislocation. Biomed Res Int. 2015;2015:1-7. doi:10.1155/2015/456858.
151. Kumahashi N, Kuwata S, Tadenuma T, Kadowaki M, Uchio Y. A “sandwich” method of reconstruction of the medial patellofemoral ligament using a titanium interference screw for patellar instability in skeletally immature patients. Arch Orthop Trauma Surg. 2012;132(8):1077-1083. doi:10.1007/s00402-012-1516-5.
152. Marsh JS, Daigneault JP, Sethi P, Polzhofer GK. Treatment of recurrent patellar instability with a modification of the Roux-Goldthwait technique. J Pediatr Orthop. 2006;26(4):461-465. doi:10.1097/01.bpo.0000217711.34492.48.
153. Nepple J, Luhmann S. Medial patellar tendon transfer with proximal realignment. In: Green D, Cordasco F, eds. Pediatric and Adolescent Knee Surgery. New York, NY: Wolters Kluwer; 2015:148-153.
154. Galeazzi R. Nuove applicazioni del trapianto musculare e tendineo. Ard Di Orthop Milano. 1922;38:315-323.
155. Grannatt K, Heyworth BE, Ogunwole O, Micheli LJ, Kocher MS. Galeazzi semitendinosus tenodesis for patellofemoral instability in skeletally immature patients. J Pediatr Orthop. 2012;32(6):621-625. doi:10.1097/BPO.0b013e318263a230.
156. Fiume M. La rotulopessi secondi Galeazzi nella lussazione recidivante di rotula [in Italian]. Minerva Ortop. 1954;5:171-174.
157. Baker RH, Carroll N, Dewar FP, Hall JE. The semitendinosus tenodesis for recurrent dislocation of the patella. J Bone Joint Surg Br. 1972;54(1):103-109.
158. Hall JE, Micheli LJ, McManama GB. Semitendinosus tenodesis for recurrent subluxation or dislocation of the patella. Clin Orthop Relat Res. 1979;(144):31-35.
159. Moyad TF, Blakemore L. Modified Galeazzi technique for recurrent patellar dislocation in children. Orthopedics. 2006;29(4):302-304.
160. Letts RM, Davidson D, Beaule P. Semitendinosus tenodesis for repair of recurrent dislocation of the patella in children. J Pediatr Orthop. 1999;19(6):742-747.
161. Aulisa AG, Falciglia F, Giordano M, Savignoni P, Guzzanti V. Galeazzi’s modified technique for recurrent patella dislocation in skeletally immature patients. J Orthop Sci. 2012;17(2):148-155. doi:10.1007/s00776-011-0189-1.
162. Roux C. Recurrent dislocation of the patella: operative treatment. 1888. Clin Orthop Relat Res. 2006;452:17-20.
163. Goldthwait J. Dislocation of the Patella. Trans Am Orthop Assn. 1895.
164. Fondren FB, Goldner JL, Bassett FH. Recurrent dislocation of the patella treated by the modified Roux-Goldthwait procedure. A prospective study of forty-seven knees. J Bone Joint Surg Am. 1985;67(7):993-1005.
165. Aärimaa V, Ranne J, Mattila K, Rahi K, Virolainen P, Hiltunen A. Patellar tendon shortening after treatment of patellar instability with a patellar tendon medialization procedure. Scand J Med Sci Sports. 2008;18(4):442-446. doi:10.1111/j.1600-0838.2007.00730.x.
166. Nelitz M, Reichel H, Dornacher D, Lippacher S. Anatomical reconstruction of the medial patellofemoral ligament in children with open growth-plates. Arch Orthop Trauma Surg. 2012;132(11):1647-1651. doi:10.1007/s00402-012-1593-5.
167. Vähäsarja V, Kinnunen P, Lanning P, Serlo W. Operative realignment of patellar malalignment in children. J Pediatr Orthop. 1995;15(3):281-285.
168. Abraham E, Washington E, Huang TL. Insall proximal realignment for disorders of the patella. Clin Orthop Relat Res. 1989;248:61-65.
169. Insall JN, Aglietti P, Tria AJ. Patellar pain and incongruence. II: Clinical application. Clin Orthop Relat Res. 1983;176:225-232.
170. Chrisman OD, Snook GA, Wilson TC. A long-term prospective study of the Hauser and Roux-Goldthwait procedures for recurrent patellar dislocation. Clin Orthop Relat Res. 1979;144:27-30.
171. Niedzielski KR, Malecki K, Flont P, Fabis J. The results of an extensive soft-tissue procedure in the treatment of obligatory patellar dislocation in children with ligamentous laxity: a post-operative isokinetic study. Bone Joint J. 2015;97-B(1):129-133. doi:10.1302/0301-620X.97B1.33941.
172. Hinckel BB, Gobbi RG, Demange MK, Bonadio MB, Pécora JR, Camanho GL. Combined reconstruction of the medial patellofemoral ligament with quadricipital tendon and the medial patellotibial ligament with patellar tendon. Arthrosc Tech. 2016;5(1):e79-e84. doi:10.1016/j.eats.2015.10.004.
173. Mani S, Kirkpatrick MS, Saranathan A, Smith LG, Cosgarea AJ, Elias JJ. Tibial tuberosity osteotomy for patellofemoral realignment alters tibiofemoral kinematics. Am J Sports Med. 2011;39(5):1024-1031. doi:10.1177/0363546510390188.
174. Brown GD, Ahmad CS. Combined medial patellofemoral ligament and medial patellotibial ligament reconstruction in skeletally immature patients. J Knee Surg. 2008;21(4):328-332.
175. Panagiotopoulos E, Strzelczyk P, Herrmann M, Scuderi G. Cadaveric study on static medial patellar stabilizers: the dynamizing role of the vastus medialis obliquus on medial patellofemoral ligament. Knee Surg Sports Traumatol Arthrosc. 2006;14(1):7-12. doi:10.1007/s00167-005-0631-z.
176. Philippot R, Boyer B, Testa R, Farizon F, Moyen B. The role of the medial ligamentous structures on patellar tracking during knee flexion. Knee Surg Sports Traumatol Arthrosc. 2012;20(2):331-336. doi:10.1007/s00167-011-1598-6.
177. Gordon JE, Schoenecker PL. Surgical treatment of congenital dislocation of the patella. J Pediatr Orthop. 1999;19(2):260-264.
178. Koh JL, Stewart C. Patellar instability. Orthop Clin North Am. 2015;46(1):147-157. doi:10.1016/j.ocl.2014.09.011.
179. Pal S, Besier TF, Draper CE, et al. Patellar tilt correlates with vastus lateralis: vastus medialis activation ratio in maltracking patellofemoral pain patients. J Orthop Res. 2012;30(6):927-933. doi:10.1002/jor.22008.
180. Thompson TC. Quadricepsplasty. Ann Surg. 1945;121(5):751-754.
181. Daoud H, O’Farrell T, Cruess RL. Quadricepsplasty. The Judet technique and results of six cases. J Bone Joint Surg Br. 1982;64(2):194-197.
182. Stanisavljevic S, Zemenick G, Miller D. Congenital, irreducible, permanent lateral dislocation of the patella. Clin Orthop Relat Res. 1976;(116):190-199.
183. Kundu Z, Sangwan S, Guliani G, Siwach R, Kamboj P, Singh R. Thompson’s quadricepsplasty for stiff knee. Indian J Orthop. 2007;41(4):390-394. doi:10.4103/0019-5413.37004.
184. Tercier S, Shah H, Joseph B. Quadricepsplasty for congenital dislocation of the knee and congenital quadriceps contracture. J Child Orthop. 2012;6(5):397-410. doi:10.1007/s11832-012-0437-8.
185. Rose RE. Judet quadricepsplasty for extension contracture of the knee. West Indian Med J. 2005;54(4):238-241.
186. Tsukamoto N, Miura H, Matsuda S, Mawatari T, Kato H, Iwamoto Y. Functional evaluation of four patients treated with V-Y quadricepsplasty in total knee arthroplasty. J Orthop Sci. 2006;11(4):394-400. doi:10.1007/s00776-006-1023-z.
187. Dao Q, Chen DB, Scott RD. Proximal patellar quadricepsplasty realignment during total knee arthroplasty for irreducible congenital dislocation of the patella. J Bone Joint Surg Am. 2010;92(14):2457-2461. doi:10.2106/JBJS.H.00812.
188. Judet R, Judet J, Lord G. Results of treatment of stiffness of the knee caused by arthrolysis and disinsertion of the quadriceps femoris. Mem Acad Chir. 1959;85:645-654.
189. Oliveira VG, D’Elia LF, Tirico LEP, et al. Judet quadricepsplasty in the treatment of posttraumatic knee rigidity: long-term outcomes of 45 cases. J Trauma Acute Care Surg. 2012;72(2):e77-e80.
190. Hahn SB, Choi YR, Kang HJ, Lee SH. Prognostic factors and long-term outcomes following a modified Thompson’s quadricepsplasty for severely stiff knees. J Bone Joint Surg Br. 2010;92(2):217-221. doi:10.1302/0301-620X.92B2.22936.
191. Hosalkar HS, Jones S, Chowdhury M, Hartley J, Hill RA. Quadricepsplasty for knee stiffness after femoral lengthening in congenital short femur. J Bone Joint Surg Br. 2003;85(2):261-264.
192. Massè A, Biasibetti A, Demangos J, Dutto E, Pazzano S, Gallinaro P. The judet quadricepsplasty: long-term outcome of 21 cases. J Trauma. 2006;61(2):358-362. doi:10.1097/01.ta.0000230281.31144.1d.
193. Kocon H, Kabacyj M, Zgoda M. The results of the operative treatment of patellar instability in children with Down’s syndrome. J Pediatr Orthop B. 2012;21(5):407-410. doi:10.1097/BPB.0b013e328354f684.
194. Martin BD, Cherkashin AM, Tulchin K, Samchukov M, Birch JG. Treatment of femoral lengthening-related knee stiffness with a novel quadricepsplasty. J Pediatr Orthop. 2013;33(4):446-452. doi:10.1097/BPO.0b013e3182784e5d.
1. Nietosvaara Y, Aalto K, Kallio PE. Acute patellar dislocation in children: incidence and associated osteochondral fractures. J Pediatr Orthop. 1994;14(4):513-515.
2. Fithian DC, Paxton EW, Stone ML, et al. Epidemiology and natural history of acute patellar dislocation. Am J Sports Med. 2004;32(5):1114-1121. doi:10.1177/0363546503260788.
3. Abbasi D, May MM, Wall EJ, Chan G, Parikh SN. MRI findings in adolescent patients with acute traumatic knee hemarthrosis. J Pediatr Orthop. 2012;32(8):760-764. doi:10.1097/BPO.0b013e3182648d45.
4. Mäenpää H, Lehto MU. Patellar dislocation. The long-term results of nonoperative management in 100 patients. Am J Sports Med. 1997;25(2):213-217. doi:10.1177/036354659702500213.
5. Hawkins RJ, Bell RH, Anisette G. Acute patellar dislocations. The natural history. Am J Sports Med. 1986;14(2):117-120. doi:10.1177/036354658601400204.
6. Cofield RH, Bryan RS. Acute dislocation of the patella: results of conservative treatment. J Trauma. 1977;17(7):526-531.
7. Wasserlauf BL, Paletta GA. Developmental anatomy of the pediatric and adolescent knee. In: Micheli LJ, Kocher MS, eds. The Pediatric and Adolescent Knee. 1st ed. Elsevier; 2006:27-32.
8. Birch JG. Growth and development. In: Herring J, ed. Tachdjian’s Pediatric Orthopedics. 4th ed. Saunders/Elsevier; 2007:3-22.
9. Sarin VK, Carter DR. Mechanobiology and joint conformity regulate endochondral ossification of sesamoids. J Orthop Res. 2000;18(5):706-712. doi:10.1002/jor.1100180505.
10. Maes C, Kronenberg HM. Postnatal bone growth: growth plate biology, bone formation, and remodeling. In: Pediatric Bone. Elsevier; 2012:55-82.
11. Tecklenburg K, Dejour D, Hoser C, Fink C. Bony and cartilaginous anatomy of the patellofemoral joint. Knee Surg Sports Traumatol Arthrosc. 2006;14(3):235-240. doi:10.1007/s00167-005-0683-0.
12. Walmsley R. The development of the patella. J Anat. 1940;74(Pt 3):360-368.3.
13. Fulkerson J, Hungerford D. Disorders of the patellofemoral Joint. In: Normal Anatomy. 2nd ed. Baltimore: Williams & Wilkins; 1990:1-24.
14. Ogden JA. Radiology of postnatal skeletal development. X. Patella and tibial tuberosity. Skeletal Radiol. 1984;11(4):246-257.
15. Nietosvaara Y, Aalto K. The cartilaginous femoral sulcus in children with patellar dislocation: an ultrasonographic study. J Pediatr Orthop. 1997;17(1):50-53.
16. Glard Y, Jouve JL, Garron E, Adalian P, Tardieu C, Bollini G. Anatomic study of femoral patellar groove in fetus. J Pediatr Orthop. 2005;25(3):305-308.
17. Nietosvaara Y. The femoral sulcus in children. An ultrasonographic study. J Bone Joint Surg Br. 1994;76(5):807-809.
18. Nietosvaara AY, Aalto KA. Ultrasonographic evaluation of patellar tracking in children. Clin Orthop Relat Res. 1993;(297):62-64.
19. Desio SM, Burks RT, Bachus KN. Soft tissue restraints to lateral patellar translation in the human knee. Am J Sports Med. 26(1):59-65. doi:10.1177/03635465980260012701.
20. Shea KG, Styhl AC, Jacobs JC, et al. The relationship of the femoral physis and the medial patellofemoral ligament in children: a cadaveric study. Am J Sports Med. 2016;44(11):2833-2837. doi:10.1177/0363546516656366.
21. Shea KG, Polousky JD, Jacobs JC, et al. The relationship of the femoral physis and the medial patellofemoral ligament in children. J Pediatr Orthop. 2014;34(8):808-813. doi:10.1097/BPO.0000000000000165.
22. Shea KG, Polousky JD, Jacobs JC, et al. The patellar insertion of the medial patellofemoral ligament in children. J Pediatr Orthop. 2015;35(4):e31-e35. doi:10.1097/BPO.0000000000000399.
23. Shea KG, Grimm NL, Belzer J, Burks RT, Pfeiffer R. The relation of the femoral physis and the medial patellofemoral ligament. Arthroscopy. 2010;26(8):1083-1087. doi:10.1016/j.arthro.2009.12.020.
24. Nelitz M, Dornacher D, Dreyhaupt J, Reichel H, Lippacher S. The relation of the distal femoral physis and the medial patellofemoral ligament. Knee Surg Sport Traumatol Arthrosc. 2011;19(12):2067-2071. doi:10.1007/s00167-011-1548-3.
25. Kepler CK, Bogner EA, Hammoud S, Malcolmson G, Potter HG, Green DW. Zone of injury of the medial patellofemoral ligament after acute patellar dislocation in children and adolescents. Am J Sports Med. 2011;39(7):1444-1449. doi:10.1177/0363546510397174.
26. Seitlinger G, Moroder P, Fink C, Wierer G. Acquired femoral flexion deformity due to physeal injury during medial patellofemoral ligament reconstruction. Knee. 2017;24(3):680-685. doi:10.1016/j.knee.2017.02.003.
27. Parikh SN, Rajdev N. Relationship between trochlear dysplasia and the anterior distal femoral physis in pediatric and adolescent patients with patellar instability. In: 36th Annual Meething AANA. Denver; 2017.
28. Salenius P, Vankka E. The development of the tibiofemoral angle in children. J Bone Joint Surg Am. 1975;57(2):259-261.
29. Parikh SN. Medial patellofemoral ligament reconstruction and simultaneous guided correction of genu valgum for patellar instability in skeletally immature patients. In: EPOSNA. 2017.
30. Brattstroem H. Shape of the intercondylar groove normally and in recurrent dislocation of patella. A clinical and X-ray-Anatomical investigation. Acta Orthop Scand Suppl. 1964;68(suppl 68):1-148.
31. Dejour H, Walch G, Nove-Josserand L, Guier C. Factors of patellar instability: an anatomic radiographic study. Knee Surg Sports Traumatol Arthrosc. 1994;2(1):19-26.
32. Lewallen LW, McIntosh AL, Dahm DL. Predictors of recurrent instability after acute patellofemoral dislocation in pediatric and adolescent patients. Am J Sports Med. 2013;41(3):575-581. doi:10.1177/0363546512472873.
33. Jaquith BP, Parikh SN. Predictors of recurrent patellar instability in children and adolescents after first-time dislocation. J Pediatr Orthop. 2017;37(7):484-490. doi:10.1097/BPO.0000000000000674.
34. Lippacher S, Reichel H, Nelitz M. Radiological criteria for trochlear dysplasia in children and adolescents. J Pediatr Orthop B. 2011;20(5):341-344. doi:10.1097/BPB.0b013e3283474c8b.
35. Parikh SN, Rajdev N, Sun Q. The growth of trochlear dysplasia during adolescence. J Pediatr Orthop. 2018. doi:10.1097/BPO.0000000000001168. [Epub ahead of print]
36. Benoit B, Laflamme GY, Laflamme GH, Rouleau D, Delisle J, Morin B. Long-term outcome of surgically-treated habitual patellar dislocation in children with coexistent patella alta. Minimum follow-up of 11 years. J Bone Joint Surg Br. 2007;89(9):1172-1177. doi:10.1302/0301-620X.89B9.19065.
37. Sugimoto D, Christino MA, Micheli LJ. Effects of surgical intervention on trochlear remodeling in pediatric patients with recurrent patella dislocation cases. J Pediatr Orthop B. 2016;25(4):349-353. doi:10.1097/BPB.0000000000000341.
38. Insall J, Goldberg V, Salvati E. Recurrent dislocation and the high-riding patella. Clin Orthop Relat Res. 1972;88:67-69.
39. Caton J. [Method of measuring the height of the patella]. Acta Orthop Belg. 1989;55(3):385-386.
40. Thévenin-Lemoine C, Ferrand M, Courvoisier A, Damsin JP, Ducou le Pointe H, Vialle R. Is the Caton-Deschamps index a valuable ratio to investigate patellar height in children? J Bone Joint Surg Am. 2011;93(8):e35. doi:10.2106/JBJS.J.00759.
41. Micheli LJ, Slater JA, Woods E, Gerbino PG. Patella alta and the adolescent growth spurt. Clin Orthop Relat Res. 1986;213:159-162.
42. Koshino T, Sugimoto K. New measurement of patellar height in the knees of children using the epiphyseal line midpoint. J Pediatr Orthop. 1989;9(2):216-218.
43. Mays PK, Bishop JE, Laurent GJ. Age-related changes in the proportion of types I and III collagen. Mech Ageing Dev. 1988;45(3):203-212.
44. Smits-Engelsman B, Klerks M, Kirby A. Beighton score: a valid measure for generalized hypermobility in children. J Pediatr. 2011;158(1):119-123. doi:10.1016/j.jpeds.2010.07.021.
45. Jansson A, Saartok T, Werner S, Renström P. General joint laxity in 1845 Swedish school children of different ages: age- and gender-specific distributions. Acta Paediatr. 2004;93(9):1202-1206.
46. Beighton P, Solomon L, Soskolnet CL. Articular mobility in an African population. Ann rheum Dis. 1973;32(5):413-418.
47. Staheli LT, Corbett M, Wyss C, King H. Lower-extremity rotational problems in children. Normal values to guide management. J Bone Joint Surg Am. 1985;67(1):39-47.
48. Kijowski R, Plagens D, Shaeh S, Teitge R. The effects of rotational deformities of the femur on contact pressure and contact area in the patellofemoral joint and on strain in the medial patellofemoral ligament. Annu Meet Int Patellofemoral Study Group, Napa Val San Fr CA. 1999.
49. Post W, Teitge R, Amis A. Patellofemoral malalignment: looking beyond the viewbox. Clin Sports Med. 2002;21(3):521-546.
50. Bruce WD, Stevens PM. Surgical correction of miserable malalignment syndrome. J Pediatr Orthop. 2004;24(4):392-396.
51. Kurosawa K, Kawame H, Ochiai Y, Nakashima M, Tohma T, Ohashi H. Patellar dislocation in Kabuki syndrome. Am J Med Genet. 2002;108(2):160-163.
52. Mik G, Gholve PA, Scher DM, Widmann RF, Green DW. Down syndrome: orthopedic issues. Curr Opin Pediatr. 2008;20(1):30-36. doi:10.1097/MOP.0b013e3282f35f19.
53. Sweeney E, Fryer A, Mountford R, Green A, McIntosh I. Nail patella syndrome: a review of the phenotype aided by developmental biology. J Med Genet. 2003;40(3):153-162.
54. Stevens CA. Patellar dislocation in Rubenstein-Taybi syndrome. Am J Med Genet. 1997;72(2):188-190.
55. Andrish J. The biomechanics of patellofemoral stability. J Knee Surg. 2004;17(1):35-39.
56. Conlan T, Garth WP, Lemons JE. Evaluation of the medial soft-tissue restraints of the extensor mechanism of the knee. J Bone Joint Surg Am. 1993;75(5):682-693.
57. Balcarek P, Ammon J, Frosch S, et al. Magnetic resonance imaging characteristics of the medial patellofemoral ligament lesion in acute lateral patellar dislocations considering trochlear dysplasia, patella alta, and tibial tuberosity-TG distance. Arthroscopy. 2010;26(7):926-935. doi:10.1016/j.arthro.2009.11.004.
58. Garin C, Chaker M, Dohin B, Kohler R. Permanent, habitual dislocation and recurrent dislocation of the patella in children: surgical management by patellar ligamentous transfer in 50 knees. Rev Chir Orthop Reparatrice Appar Mot. 2007;93(7):690-700.
59. Sillanpaa P. Terminology of patellar dislocation. In: Sillanpaa P, ed. Trauma. Saarbrucken, Germany: Lambert Academic Publishing; 2010:16-18.
60. Parikh SN, Lykissas MG. Classification of lateral patellar instability in children and adolescents. Orthop Clin North Am. 2016;47(1):145-152. doi:10.1016/j.ocl.2015.08.016.
61. Chotel F, Bérard J, Raux S. Patellar instability in children and adolescents. Orthop Traumatol Surg Res. 2014;100(suppl 1):125-137. doi:10.1016/j.otsr.2013.06.014.
62. Wada A, Fujii T, Takamura K, Yanagida H, Surijamorn P. Congenital dislocation of the patella. J Child Orthop. 2008;2(2):119-123. doi:10.1007/s11832-008-0090-4.
63. Südkamp NP, Granrath M, Hoffmann R, Haas NP. Instability of the shoulder joint in the athlete. Chirurg. 1994;65(11):901-909.
64. Hiemstra LA, Kerslake S, Lafave M, Heard SM, Buchko GML. Introduction of a classification system for patients with patellofemoral instability (WARPS and STAID). Knee Surg Sport Traumatol Arthrosc. 2014;22(11):2776-2782. doi:10.1007/s00167-013-2477-0.
65. Frosch KH, Schmeling A. A new classification system of patellar instability and patellar maltracking. Arch Orthop Trauma Surg. 2016;136(4):485-497. doi:10.1007/s00402-015-2381-9.
66. Balcarek P, Oberthür S, Hopfensitz S, et al. Which patellae are likely to redislocate? Knee Surg Sport Traumatol Arthrosc. 2014;22(10):2308-2314. doi:10.1007/s00167-013-2650-5.
67. Bitar AC, Demange MK, D’Elia CO, Camanho GL. Traumatic patellar dislocation: nonoperative treatment compared with mpfl reconstruction using patellar tendon. Am J Sports Med. 2012;40(1):114-122. doi:10.1177/0363546511423742.
68. Smith TO, Walker J, Russell N. Outcomes of medial patellofemoral ligament reconstruction for patellar instability: a systematic review. Knee Surg Sport Traumatol Arthrosc. 2007;15(11):1301-1314. doi:10.1007/s00167-007-0390-0.
69. Steiner TM, Torga-Spak R, Teitge RA. Medial patellofemoral ligament reconstruction in patients with lateral patellar instability and trochlear dysplasia. Am J Sports Med. 2006;34(8):1254-1261. doi:10.1177/0363546505285584.
70. Ma LF, Wang F, Chen BC, Wang CH, Zhou JW, Wang HY. Medial retinaculum plasty versus medial patellofemoral ligament reconstruction for recurrent patellar instability in adults: a randomized controlled trial. Arthrosc J Arthrosc Relat Surg. 2013;29(5):891-897. doi:10.1016/j.arthro.2013.01.030.
71. Weeks KD, Fabricant PD, Ladenhauf HN, Green DW. Surgical options for patellar stabilization in the skeletally immature patient. Sports Med Arthrosc Rev. 2012;20(3):194-202.
72. Green D. Surgical treatment of pediatric patella instability. Die Ther der Instabilen patella. 2016:80-89.
73. Lewallen L, McIntosh A, Dahm D. First-time patellofemoral dislocation: risk factors for recurrent instability. J Knee Surg. 2015;28(4):303-309. doi:10.1055/s-0034-1398373.
74. Ghanem I, Wattincourt L, Seringe R. Congenital dislocation of the patella. Part I: pathologic anatomy. J Pediatr Orthop. 2000;20(6):812-816.
75. Bongers E, Van Kampen A, Van Bokhoven H, Knoers N. Human syndromes with congenital patellar anomalies and the underlying gene defects. Clin Genet. 2005;68(4):302-319. doi:10.1111/j.1399-0004.2005.00508.x.
76. Beighton P, Horan F. Orthopaedic aspects of the Ehlers-Danlos syndrome. J Bone Joint Surg Br. 1969;51(3):444-453.
77. Gausden EB, Fabricant PD, Taylor SA, et al. Medial patellofemoral reconstruction in children and adolescents. JBJS Rev. 2015;3(10):1-11. doi:10.2106/JBJS.RVW.N.00091.
78. Palmu S, Kallio PE, Donell ST, Helenius I, Nietosvaara Y. Acute patellar dislocation in children and adolescents: a randomized clinical trial. J Bone Joint Surg Am. 2008;90(3):463-470. doi:10.2106/JBJS.G.00072.
79. Webb JE, Lewallen LW, Christophersen C, Krych AJ, McIntosh AL. Clinical outcome of internal fixation of unstable juvenile osteochondritis dissecans lesions of the knee. Orthopedics. 2013;36(11):e1444-e1449. doi:10.3928/01477447-20131021-30.
80. Hennrikus W, Pylawka T. Patellofemoral instability in skeletally immature athletes. Instr Course Lect. 2013;62:445-453.
81. Nomura E, Inoue M. Surgical technique and rationale for medial patellofemoral ligament reconstruction for recurrent patellar dislocation. Arthroscopy. 2003;19(5):e47. doi:10.1053/jars.2003.50167.
82. Nomura E, Inoue M, Kobayashi S. Long-term follow-up and knee osteoarthritis change after medial patellofemoral ligament reconstruction for recurrent patellar dislocation. Am J Sports Med. 2007;35(11):1851-1858. doi:10.1177/0363546507306161.
83. Arshi A, Cohen JR, Wang JC, Hame SL, McAllister DR, Jones KJ. Operative management of patellar instability in the United States. Orthop J Sport Med. 2016;4(8):2325967116662873. doi:10.1177/2325967116662873.
84. Servien E, Verdonk PC, Neyret P. Tibial tuberosity transfer for episodic patellar dislocation. Sports Med Arthrosc. 2007;15(2):61-67. doi:10.1097/JSA.0b013e3180479464.
85. Nietosvaara Y, Paukku R, Palmu S, Donell ST. Acute patellar dislocation in children and adolescents. Surgical technique. J Bone Joint Surg Am. 2009;91(suppl 2):139-145. doi:10.2106/JBJS.H.01289.
86. Hing CBC, Smith TO, Donell S, Song F. Surgical versus non-surgical interventions for treating patellar dislocation. In Hing CB, ed. Cochrane Database Syst Rev. 2011;(11):CD008106. doi:10.1002/14651858.CD008106.pub2.
87. Nwachukwu BU, So C, Schairer WW, Green DW, Dodwell ER. Surgical versus conservative management of acute patellar dislocation in children and adolescents: a systematic review. Knee Surgery, Sport Traumatol Arthrosc. 2016;24(3):760-767. doi:10.1007/s00167-015-3948-2.
88. Camp CL, Krych AJ, Dahm DL, Levy BA, Stuart MJ. Medial patellofemoral ligament repair for recurrent patellar dislocation. Am J Sports Med. 2010;38(11):2248-2254. doi:10.1177/0363546510376230.
89. Nikku R, Nietosvaara Y, Aalto K, Kallio PE. Operative treatment of primary patellar dislocation does not improve medium-term outcome: a 7-year follow-up report and risk analysis of 127 randomized patients. Acta Orthop. 2005;76(5):699-704. doi:10.1080/17453670510041790.
90. Ostermeier S, Holst M, Hurschler C, Windhagen H, Stukenborg-Colsman C. Dynamic measurement of patellofemoral kinematics and contact pressure after lateral retinacular release: an in vitro study. Knee Surg Sport Traumatol Arthrosc. 2007;15(5):547-554. doi:10.1007/s00167-006-0261-0.
91. Sallay PI, Poggi J, Speer KP, Garrett WE. Acute dislocation of the patella. A correlative pathoanatomic study. Am J Sports Med. 1996;24(1):52-60. doi: 10.1177/036354659602400110.
92. Arendt EA, Fithian DC, Cohen E. Current concepts of lateral patella dislocation. Clin Sports Med. 2002;21(3):499-519.
93. Arendt EA, Moeller A, Agel J. Clinical outcomes of medial patellofemoral ligament repair in recurrent (chronic) lateral patella dislocations. Knee Surg Sports Traumatol Arthrosc. 2011;19(11):1909-1914. doi:10.1007/s00167-011-1516-y.
94. Ellera Gomes JL. Medial patellofemoral ligament reconstruction for recurrent dislocation of the patella: a preliminary report. Arthroscopy. 1992;8(3):335-340.
95. Amis AA, Firer P, Mountney J, Senavongse W, Thomas NP. Anatomy and biomechanics of the medial patellofemoral ligament. Knee. 2003;10(3):215-220.
96. Avikainen VJ, Nikku RK, Seppänen-Lehmonen TK. Adductor magnus tenodesis for patellar dislocation. Technique and preliminary results. Clin Orthop Relat Res. 1993;(297):12-16.
97. Davis DK, Fithian DC. Techniques of medial retinacular repair and reconstruction. Clin Orthop Relat Res. 2002;(402):38-52.
98. Dhillon MS, Mohan P, Nagi ON. Does harvesting the medial third of the patellar tendon cause lateral shift of the patella after ACL reconstruction? Acta Orthop Belg. 2003;69(4):334-340.
99. Drez D, Edwards TB, Williams CS. Results of medial patellofemoral ligament reconstruction in the treatment of patellar dislocation. Arthrosc J Arthrosc Relat Surg. 2001;17(3):298-306. doi:10.1053/jars.2001.21490.
100. Ellera Gomes JL, Stigler Marczyk LR, César de César P, Jungblut CF. Medial patellofemoral ligament reconstruction with semitendinosus autograft for chronic patellar instability: a follow-up study. Arthrosc J Arthrosc Relat Surg. 2004;20(2):147-151. doi:10.1016/j.arthro.2003.11.006.
101. Feller JA, Amis AA, Andrish JT, Arendt EA, Erasmus PJ, Powers CM. Surgical biomechanics of the patellofemoral joint. Arthrosc J Arthrosc Relat Surg. 2007;23(5):542-553. doi:10.1016/j.arthro.2007.03.006.
102. Nomura E, Horiuchi Y, Kihara M. Medial patellofemoral ligament restraint in lateral patellar translation and reconstruction. Knee. 2000;7(2):121-127.
103. Ostermeier S, Stukenborg-Colsman C, Hurschler C, Wirth CJ. In vitro investigation of the effect of medial patellofemoral ligament reconstruction and medial tibial tuberosity transfer on lateral patellar stability. Arthrosc J Arthrosc Relat Surg. 2006;22(3):308-319. doi:10.1016/j.arthro.2005.09.024.
104. Smirk C, Morris H. The anatomy and reconstruction of the medial patellofemoral ligament. Knee. 2003;10(3):221-227.
105. Steensen RN, Dopirak RM, Maurus PB. A simple technique for reconstruction of the medial patellofemoral ligament using a quadriceps tendon graft. Arthroscopy. 2005;21(3):365-370. doi:10.1016/j.arthro.2004.10.007.
106. Steensen RN, Dopirak RM, McDonald WG. The anatomy and isometry of the medial patellofemoral ligament: implications for reconstruction. Am J Sports Med. 2004;32(6):1509-1513. doi:10.1177/0363546503261505.
107. Farahmand F, Tahmasbi MN, Amis AA. Lateral force–displacement behaviour of the human patella and its variation with knee flexion—a biomechanical study in vitro. J Biomech. 1998;31(12):1147-1152.
108. Heegaard J, Leyvraz PF, Van Kampen A, Rakotomanana L, Rubin PJ, Blankevoort L. Influence of soft structures on patellar 3-dimensional tracking. Clin Orthop Relat Res. 1994;(299):235-243.
109. Goyal D. Medial patellofemoral ligament reconstruction: the superficial quad technique. Am J Sports Med. 2013;41(5):1022-1029. doi:10.1177/0363546513477828.
110. Hohn E, Pandya NK. Does the utilization of allograft tissue in medial patellofemoral ligament reconstruction in pediatric and adolescent patients restore patellar stability? Clin Orthop Relat Res. 2017;475(6):1563-1569. doi:10.1007/s11999-016-5060-4.
111. Csintalan R, Latt L, Fornalski S, Raiszadeh K, Inacio M, Fithian D. Medial patellofemoral ligament (MPFL) reconstruction for the treatment of patellofemoral instability. J Knee Surg. 2013;27(2):139-146. doi:10.1055/s-0033-1360652.
112. Ahmad CS, Brown GD, Stein BS. The docking technique for medial patellofemoral ligament reconstruction: surgical technique and clinical outcome. Am J Sports Med. 2009;37(10):2021-2027. doi:10.1177/0363546509336261.
113. Fernandez E, Sala D, Castejon M. Reconstruction of the medial patellofemoral ligament for patellar instability using a semitendinosus autograft. Acta Orthop Belg. 2005;71(3):303-308.
114. Parikh SN, Nathan ST, Wall EJ, Eismann EA. Complications of medial patellofemoral ligament reconstruction in young patients. Am J Sports Med. 2013;41(5):1030-1038. doi:10.1177/0363546513482085.
115. Green D, Gausden E. Medial patellofemoral ligament reconstruction: hamstring technique. In: Green D, Cordasco F, eds. Pediatr. Adolesc. Knee Surg. New York, NY: Wolters Kluwer; 2015:150-157.
116. Craig JG, Cody DD, van Holsbeeck M. The distal femoral and proximal tibial growth plates: MR imaging, 3-dimensional modeling and estimation of area and volume. Skeletal Radiol. 2004;33(6):337-344.
117. Noyes FR, Albright JC. Reconstruction of the medial patellofemoral ligament with autologous quadriceps tendon. Arthroscopy. 2006;22(8):904.e1-e7. doi:10.1016/j.arthro.2005.12.058.
118. Pinkowsky G, Hennrikus. Technique: quad tendon medial patellofemoral ligament reconstruction. In: Green DW, Cordasco FA, eds. Pediatr. Adolesc. Knee Surg. New York, NY: Wolters Kluwer; 2015:133-139.
119. Bollier M, Fulkerson J, Cosgarea A, Tanaka M. Technical failure of medial patellofemoral ligament reconstruction. Arthroscopy. 2011;27(8):1153-1159. doi:10.1016/j.arthro.2011.02.014.
120. Elias JJ, Cosgarea AJ. Technical errors during medial patellofemoral ligament reconstruction could overload medial patellofemoral cartilage: a computational analysis. Am J Sports Med. 2006;34(9):1478-1485. doi:10.1177/0363546506287486.
121. Thaunat M, Erasmus PJ. Management of overtight medial patellofemoral ligament reconstruction. Knee Surg Sports Traumatol Arthrosc. 2009;17(5):480-483. doi:10.1007/s00167-008-0702-z.
122. Schöttle PB, Schmeling A, Rosenstiel N, Weiler A. Radiographic landmarks for femoral tunnel placement in medial patellofemoral ligament reconstruction. Am J Sports Med. 2007;35(5):801-804. doi:10.1177/0363546506296415.
123. Redfern J, Kamath G, Burks R. Anatomical confirmation of the use of radiographic landmarks in medial patellofemoral ligament reconstruction. Am J Sports Med. 2010;38(2):293-297. doi:10.1177/0363546509347602.
124. Fink C, Veselko M, Herbort M, Hoser C. Minimally invasive reconstruction of the medial patellofemoral ligament using quadriceps tendon. Arthrosc Tech. 2014;3(3):e325-e329. doi:10.1016/j.eats.2014.01.012.
125. Sillanpää PJ, Mäenpää HM, Mattila VM, Visuri T, Pihlajamäki H. A mini-invasive adductor magnus tendon transfer technique for medial patellofemoral ligament reconstruction: a technical note. Knee Surg Sports Traumatol Arthrosc. 2009;17(5):508-512. doi:10.1007/s00167-008-0713-9.
126. Hambidge SJ, Davidson AJ, Gonzales R, Steiner JF. Epidemiology of pediatric injury-related primary care office visits in the United States. Pediatrics. 2002;109(4):559-565.
127. Camanho GL, Bitar AC, Hernandez AJ, Olivi R. Medial patellofemoral ligament reconstruction: a novel technique using the patellar ligament. Arthroscopy. 2007;23(1):108.e1-e4. doi:10.1016/j.arthro.2006.07.008.
128. Gomes JE. Comparison between a static and a dynamic technique for medial patellofemoral ligament reconstruction. Arthroscopy. 2008;24(4):430-435. doi:10.1016/j.arthro.2007.11.005.
129. Deie M, Ochi M, Sumen Y, Yasumoto M, Kobayashi K, Kimura H. Reconstruction of the medial patellofemoral ligament for the treatment of habitual or recurrent dislocation of the patella in children. J Bone Joint Surg Br. 2003;85(6):887-890.
130. Ladenhauf HN, Berkes MB, Green DW. Medial patellofemoral ligament reconstruction using hamstring autograft in children and adolescents. Arthrosc Tech. 2013;2(2):e151-e154. doi:10.1016/j.eats.2013.01.006.
131. Bedi H, Marzo J. The biomechanics of medial patellofemoral ligament repair followed by lateral retinacular release. Am J Sports Med. 2010;38(7):1462-1467. doi:10.1177/0363546510373581.
132. Lattermann C, Toth J, Bach BR. The role of lateral retinacular release in the treatment of patellar instability. Sports Med Arthrosc Rev. 2007;15(2):57-60. doi:10.1097/JSA.0b013e318042af30
133. Ricchetti ET, Mehta S, Sennett BJ, Huffman GR. Comparison of lateral release versus lateral release with medial soft-tissue realignment for the treatment of recurrent patellar instability: a systematic review. Arthroscopy. 2007;23(5):463-468. doi:10.1016/j.arthro.2007.01.007.
134. Dainer RD, Barrack RL, Buckley SL, Alexander AH. Arthroscopic treatment of acute patellar dislocations. Arthroscopy. 1988;4(4):267-271.
135. Miller JR, Adamson GJ, Pink MM, Fraipont MJ, Durand P. Arthroscopically assisted medial reefing without routine lateral release for patellar instability. Am J Sports Med. 2007;35(4):622-629. doi:10.1177/0363546506296041.
136. Vainionpää S, Laasonen E, Silvennoinen T, Vasenius J, Rokkanen P. Acute dislocation of the patella. A prospective review of operative treatment. J Bone Joint Surg Br. 1990;72(3):366-369.
137. Shah JN, Howard JS, Flanigan DC, Brophy RH, Carey JL, Lattermann C. A systematic review of complications and failures associated with medial patellofemoral ligament reconstruction for recurrent patellar dislocation. Am J Sports Med. 2012;40(8):1916-1923. doi:10.1177/0363546512442330.
138. Tanaka MJ, Bollier MJ, Andrish JT, Fulkerson JP, Cosgarea AJ. Complications of medial patellofemoral ligament reconstruction: common technical errors and factors for success: AAOS exhibit selection. J Bone Joint Surg Am. 2012;94(12):e87. doi:10.2106/JBJS.K.01449.
139. Nguyen CV, Farrow LD, Liu RW, Gilmore A. Safe drilling paths in the distal femoral epiphysis for pediatric medial patellofemoral ligament reconstruction. Am J Sports Med. 2017;45(5):1085-1089. doi:10.1177/0363546516677795.
140. Edmonds EW, Glaser DA. Adolescent patella instability extensor mechanics. J Pediatr Orthop. 2016;36(3):262-267. doi:10.1097/BPO.0000000000000430.
141. Fabricant PD, Ladenhauf HN, Salvati EA, Green DW. Medial patellofemoral ligament (MPFL) reconstruction improves radiographic measures of patella alta in children. Knee. 2014;21(6):1180-1184. doi:10.1016/j.knee.2014.07.023.
142. Lykissas MG, Li T, Eismann EA, Parikh SN. Does medial patellofemoral ligament reconstruction decrease patellar height? A preliminary report. J Pediatr Orthop. 2014;34(1):78-85. doi:10.1097/BPO.0b013e3182a12102.
143. Magnussen RA, De Simone V, Lustig S, Neyret P, Flanigan DC. Treatment of patella alta in patients with episodic patellar dislocation: a systematic review. Knee Surgery, Sport Traumatol Arthrosc. 2014;22(10):2545-2550. doi:10.1007/s00167-013-2445-8.
144. Schöttle PB, Fucentese SF, Romero J. Clinical and radiological outcome of medial patellofemoral ligament reconstruction with a semitendinosus autograft for patella instability. Knee Surg Sports Traumatol Arthrosc. 2005;13(7):516-521. doi:10.1007/s00167-005-0659-0.
145. Nelitz M, Dreyhaupt J, Reichel H, Woelfle J, Lippacher S. Anatomic reconstruction of the medial patellofemoral ligament in children and adolescents with open growth plates: surgical technique and clinical outcome. Am J Sports Med. 2013;41(1):58-63. doi:10.1177/0363546512463683.
146. Raghuveer RK, Mishra CB. Reconstruction of medial patellofemoral ligament for chronic patellar instability. Indian J Orthop. 2012;46(4):447-454. doi:10.4103/0019-5413.97259.
147. Kita K, Horibe S, Toritsuka Y, et al. Effects of medial patellofemoral ligament reconstruction on patellar tracking. Knee Surg Sports Traumatol Arthrosc. 2012;20(5):829-837. doi:10.1007/s00167-011-1609-7.
148. Lenschow S, Herbort M, Fink C. Medial patellofemoral ligament reconstruction using quadriceps tendon. Oper Orthop Traumatol. 2015;27(6):474-483. doi:10.1007/s00064-015-0416-6.
149. Abouelsoud MM, Abdelhady A, Elshazly O. Anatomic physeal-sparing technique for medial patellofemoral ligament reconstruction in skeletally immature patients with ligamentous laxity. Eur J Orthop Surg Traumatol. 2015;25(5):921-926. doi:10.1007/s00590-015-1618-1.
150. Malecki K, Fabis J, Flont P, Niedzielski KR. The results of adductor magnus tenodesis in adolescents with recurrent patellar dislocation. Biomed Res Int. 2015;2015:1-7. doi:10.1155/2015/456858.
151. Kumahashi N, Kuwata S, Tadenuma T, Kadowaki M, Uchio Y. A “sandwich” method of reconstruction of the medial patellofemoral ligament using a titanium interference screw for patellar instability in skeletally immature patients. Arch Orthop Trauma Surg. 2012;132(8):1077-1083. doi:10.1007/s00402-012-1516-5.
152. Marsh JS, Daigneault JP, Sethi P, Polzhofer GK. Treatment of recurrent patellar instability with a modification of the Roux-Goldthwait technique. J Pediatr Orthop. 2006;26(4):461-465. doi:10.1097/01.bpo.0000217711.34492.48.
153. Nepple J, Luhmann S. Medial patellar tendon transfer with proximal realignment. In: Green D, Cordasco F, eds. Pediatric and Adolescent Knee Surgery. New York, NY: Wolters Kluwer; 2015:148-153.
154. Galeazzi R. Nuove applicazioni del trapianto musculare e tendineo. Ard Di Orthop Milano. 1922;38:315-323.
155. Grannatt K, Heyworth BE, Ogunwole O, Micheli LJ, Kocher MS. Galeazzi semitendinosus tenodesis for patellofemoral instability in skeletally immature patients. J Pediatr Orthop. 2012;32(6):621-625. doi:10.1097/BPO.0b013e318263a230.
156. Fiume M. La rotulopessi secondi Galeazzi nella lussazione recidivante di rotula [in Italian]. Minerva Ortop. 1954;5:171-174.
157. Baker RH, Carroll N, Dewar FP, Hall JE. The semitendinosus tenodesis for recurrent dislocation of the patella. J Bone Joint Surg Br. 1972;54(1):103-109.
158. Hall JE, Micheli LJ, McManama GB. Semitendinosus tenodesis for recurrent subluxation or dislocation of the patella. Clin Orthop Relat Res. 1979;(144):31-35.
159. Moyad TF, Blakemore L. Modified Galeazzi technique for recurrent patellar dislocation in children. Orthopedics. 2006;29(4):302-304.
160. Letts RM, Davidson D, Beaule P. Semitendinosus tenodesis for repair of recurrent dislocation of the patella in children. J Pediatr Orthop. 1999;19(6):742-747.
161. Aulisa AG, Falciglia F, Giordano M, Savignoni P, Guzzanti V. Galeazzi’s modified technique for recurrent patella dislocation in skeletally immature patients. J Orthop Sci. 2012;17(2):148-155. doi:10.1007/s00776-011-0189-1.
162. Roux C. Recurrent dislocation of the patella: operative treatment. 1888. Clin Orthop Relat Res. 2006;452:17-20.
163. Goldthwait J. Dislocation of the Patella. Trans Am Orthop Assn. 1895.
164. Fondren FB, Goldner JL, Bassett FH. Recurrent dislocation of the patella treated by the modified Roux-Goldthwait procedure. A prospective study of forty-seven knees. J Bone Joint Surg Am. 1985;67(7):993-1005.
165. Aärimaa V, Ranne J, Mattila K, Rahi K, Virolainen P, Hiltunen A. Patellar tendon shortening after treatment of patellar instability with a patellar tendon medialization procedure. Scand J Med Sci Sports. 2008;18(4):442-446. doi:10.1111/j.1600-0838.2007.00730.x.
166. Nelitz M, Reichel H, Dornacher D, Lippacher S. Anatomical reconstruction of the medial patellofemoral ligament in children with open growth-plates. Arch Orthop Trauma Surg. 2012;132(11):1647-1651. doi:10.1007/s00402-012-1593-5.
167. Vähäsarja V, Kinnunen P, Lanning P, Serlo W. Operative realignment of patellar malalignment in children. J Pediatr Orthop. 1995;15(3):281-285.
168. Abraham E, Washington E, Huang TL. Insall proximal realignment for disorders of the patella. Clin Orthop Relat Res. 1989;248:61-65.
169. Insall JN, Aglietti P, Tria AJ. Patellar pain and incongruence. II: Clinical application. Clin Orthop Relat Res. 1983;176:225-232.
170. Chrisman OD, Snook GA, Wilson TC. A long-term prospective study of the Hauser and Roux-Goldthwait procedures for recurrent patellar dislocation. Clin Orthop Relat Res. 1979;144:27-30.
171. Niedzielski KR, Malecki K, Flont P, Fabis J. The results of an extensive soft-tissue procedure in the treatment of obligatory patellar dislocation in children with ligamentous laxity: a post-operative isokinetic study. Bone Joint J. 2015;97-B(1):129-133. doi:10.1302/0301-620X.97B1.33941.
172. Hinckel BB, Gobbi RG, Demange MK, Bonadio MB, Pécora JR, Camanho GL. Combined reconstruction of the medial patellofemoral ligament with quadricipital tendon and the medial patellotibial ligament with patellar tendon. Arthrosc Tech. 2016;5(1):e79-e84. doi:10.1016/j.eats.2015.10.004.
173. Mani S, Kirkpatrick MS, Saranathan A, Smith LG, Cosgarea AJ, Elias JJ. Tibial tuberosity osteotomy for patellofemoral realignment alters tibiofemoral kinematics. Am J Sports Med. 2011;39(5):1024-1031. doi:10.1177/0363546510390188.
174. Brown GD, Ahmad CS. Combined medial patellofemoral ligament and medial patellotibial ligament reconstruction in skeletally immature patients. J Knee Surg. 2008;21(4):328-332.
175. Panagiotopoulos E, Strzelczyk P, Herrmann M, Scuderi G. Cadaveric study on static medial patellar stabilizers: the dynamizing role of the vastus medialis obliquus on medial patellofemoral ligament. Knee Surg Sports Traumatol Arthrosc. 2006;14(1):7-12. doi:10.1007/s00167-005-0631-z.
176. Philippot R, Boyer B, Testa R, Farizon F, Moyen B. The role of the medial ligamentous structures on patellar tracking during knee flexion. Knee Surg Sports Traumatol Arthrosc. 2012;20(2):331-336. doi:10.1007/s00167-011-1598-6.
177. Gordon JE, Schoenecker PL. Surgical treatment of congenital dislocation of the patella. J Pediatr Orthop. 1999;19(2):260-264.
178. Koh JL, Stewart C. Patellar instability. Orthop Clin North Am. 2015;46(1):147-157. doi:10.1016/j.ocl.2014.09.011.
179. Pal S, Besier TF, Draper CE, et al. Patellar tilt correlates with vastus lateralis: vastus medialis activation ratio in maltracking patellofemoral pain patients. J Orthop Res. 2012;30(6):927-933. doi:10.1002/jor.22008.
180. Thompson TC. Quadricepsplasty. Ann Surg. 1945;121(5):751-754.
181. Daoud H, O’Farrell T, Cruess RL. Quadricepsplasty. The Judet technique and results of six cases. J Bone Joint Surg Br. 1982;64(2):194-197.
182. Stanisavljevic S, Zemenick G, Miller D. Congenital, irreducible, permanent lateral dislocation of the patella. Clin Orthop Relat Res. 1976;(116):190-199.
183. Kundu Z, Sangwan S, Guliani G, Siwach R, Kamboj P, Singh R. Thompson’s quadricepsplasty for stiff knee. Indian J Orthop. 2007;41(4):390-394. doi:10.4103/0019-5413.37004.
184. Tercier S, Shah H, Joseph B. Quadricepsplasty for congenital dislocation of the knee and congenital quadriceps contracture. J Child Orthop. 2012;6(5):397-410. doi:10.1007/s11832-012-0437-8.
185. Rose RE. Judet quadricepsplasty for extension contracture of the knee. West Indian Med J. 2005;54(4):238-241.
186. Tsukamoto N, Miura H, Matsuda S, Mawatari T, Kato H, Iwamoto Y. Functional evaluation of four patients treated with V-Y quadricepsplasty in total knee arthroplasty. J Orthop Sci. 2006;11(4):394-400. doi:10.1007/s00776-006-1023-z.
187. Dao Q, Chen DB, Scott RD. Proximal patellar quadricepsplasty realignment during total knee arthroplasty for irreducible congenital dislocation of the patella. J Bone Joint Surg Am. 2010;92(14):2457-2461. doi:10.2106/JBJS.H.00812.
188. Judet R, Judet J, Lord G. Results of treatment of stiffness of the knee caused by arthrolysis and disinsertion of the quadriceps femoris. Mem Acad Chir. 1959;85:645-654.
189. Oliveira VG, D’Elia LF, Tirico LEP, et al. Judet quadricepsplasty in the treatment of posttraumatic knee rigidity: long-term outcomes of 45 cases. J Trauma Acute Care Surg. 2012;72(2):e77-e80.
190. Hahn SB, Choi YR, Kang HJ, Lee SH. Prognostic factors and long-term outcomes following a modified Thompson’s quadricepsplasty for severely stiff knees. J Bone Joint Surg Br. 2010;92(2):217-221. doi:10.1302/0301-620X.92B2.22936.
191. Hosalkar HS, Jones S, Chowdhury M, Hartley J, Hill RA. Quadricepsplasty for knee stiffness after femoral lengthening in congenital short femur. J Bone Joint Surg Br. 2003;85(2):261-264.
192. Massè A, Biasibetti A, Demangos J, Dutto E, Pazzano S, Gallinaro P. The judet quadricepsplasty: long-term outcome of 21 cases. J Trauma. 2006;61(2):358-362. doi:10.1097/01.ta.0000230281.31144.1d.
193. Kocon H, Kabacyj M, Zgoda M. The results of the operative treatment of patellar instability in children with Down’s syndrome. J Pediatr Orthop B. 2012;21(5):407-410. doi:10.1097/BPB.0b013e328354f684.
194. Martin BD, Cherkashin AM, Tulchin K, Samchukov M, Birch JG. Treatment of femoral lengthening-related knee stiffness with a novel quadricepsplasty. J Pediatr Orthop. 2013;33(4):446-452. doi:10.1097/BPO.0b013e3182784e5d.
TAKE-HOME POINTS
- Patellofemoral joint stability is dependent on a complex interplay of musculotendinous units, ligaments, and the osteocartilaginous morphology of the patellofemoral joint.
- Varied patterns of patellar instability in the pediatric population should be recognized. Habitual dislocation in flexion and permanent dislocation are the more severe types.
- Assessment of major risk factors and, if required, their correction would influence management decisions and would have prognostic value related to outcomes.
- Physeal-sparing MPFL reconstruction can suffice for most children and adolescents with recurrent patellar dislocation.
- Distal stabilization techniques and quadricepsplasty are an important part of surgical armamentarium, especially for the more complex patellar instability patterns.
Glenoid Bone Loss in Reverse Shoulder Arthroplasty Treated with Bone Graft Techniques
ABSTRACT
The reverse shoulder arthroplasty facilitates surgical treatment of primary and revision shoulder with rotator cuff and bone deficiencies. Wear pattern classifications and a logical treatment approach for glenoid bone loss enable the surgeon to address a difficult series of problems in the reconstructions where the glenoid might not otherwise be able to support the implants. Bone grafting using the native humeral head in primary cases, and in revision cases, iliac crest are the most reliable sources for structural grafts for the worn or deficient glenoid vault.
Continue to: The reverse shoulder arthroplasty...
The reverse shoulder arthroplasty (RSA) technique was approved by the US Food and Drug Administration and introduced to the US market in 2004. It has been a successful addition to the treatment of shoulder pathologies with bone and rotator cuff loss. Its indications have expanded from treatment of very elderly patients with rotator cuff deficiencies to now include younger patients with humeral and glenoid bone loss, arthritis, soft-tissue losses, fractures, instability, and revision arthroplasty. Many of these conditions, when not adequately addressed with anatomic arthroplasty, now have viable treatment options for newer complex and successful reconstructions.
Glenoid bone deficiencies offer unique challenges for successful arthroplasty management. Basing treatment on bone loss classifications permits meaningful evaluation of these surgical options and whether they might be carried out in 1- or 2-stage reconstructions. An underlying premise is that restoration of the glenoid joint line and version assist in final stability, power, and functional results. For this purpose, bone graft options, or augmented implants are beneficial. This review covers the bone grafting options for autografts and allografts for deficient glenoids in reverse shoulder arthroplasty reconstructions.
OPERATIVE TECHNIQUES
For patients without prior arthroplasty, the humeral head is available for bone grafting the glenoid bone deficits. Favard and Hamada have described vertical glenoid classifications for uneven glenoid bone loss applicable to cuff tear arthropathy and inflammatory arthritis patients.1,2 The more severe E3 superior and medial bone loss is ideally addressed with the humeral head. An early example in 2004 confirmed that this was a good indication for glenoid bone grafting and using the reverse shoulder in these advanced cases (Figures 1A-1E).
In this case, it was noted that with bone grafts the base plate post did not engage the native scapula glenoid vault. Given that the on-growth central post was the strongest part of the fixation, it was fortunate that this healed. The need for a longer post with bone grafts was recognized. Laurent Comtat with the Wright Medical company accommodated the author’s request to develop the first 25- and 30-mm-long posts to allow better fixation and on-growth potential when used with bone grafts.
Gilles Walch’s classification addresses arthritic central and horizontal bone loss.3,4 Considerations relevant in RSA include the severe A2 central bone loss found in inflammatory arthritis and the B2, B3, and C patterns with posterior bone loss seen in osteoarthritis, rheumatoid arthritis, and congenital dysplasia5,6 as seen in Figures 2A, 2B. The 3-dimensional (3-D) computed tomography (CT) scan is considered the most accurate method of assessment when compared with axial radiographs.7 The glenoid vault model as a measurement of glenoid bone loss has great promise in designing prosthetic replacements and bone graft techniques.8
Continue to: Modern methods for determining glenoid version...
Modern methods for determining glenoid version, medialization, and eccentric bone wear include 3-D reconstruction and patient-specific instruments. For many years, version determination has been confirmed at surgery with subscapularis elevation, palpating the glenoid center point along Friedman’s line, and then inserting a Steinmann pin as a guide to restore version and the lateral joint line at the time of bone grafting. An example of this is demonstrated in Figures 3A-3E.9
All grafts are harvested with a hole saw from the humeral head. The inner diameter is 29 mm, the same as that of the base plate. Originally, the hole saw and mandrel were obtained from the hardware store, but Pascal Boileau upgraded the hole saw quality when he had industry develop a stainless-steel hole saw and published his results with the BIO-RSA (Wright Medical).10 In an unpublished study, Harmsen reviewed our 220 consecutive humeral head bone grafts for use of this technique with successful and reproducible results. In a separate evaluation, 29 shaped humeral head bone grafts for B2, B3, and C glenoid bone deficits showed 100% healing.11 This technique has good reproducibility when performed with an autogenous bone graft from a local donor source.
The more challenging cases involve glenoid bone loss from polyethylene osteolysis and, in some revision cases, concomitant sepsis.12 The humeral head is no longer available, and the distal clavicle or humeral metaphysis are often insufficient to restore the glenoid vault and joint line. Gunther and associates at the UC Berkeley biomaterials laboratory have made many contributions to our understanding of polyethylene wear and the factors leading to its loosening that result in massive glenoid bone loss.13
Antuna and colleagues14 classified these cases as having a central vault cavitary defect, or one combined with a peripheral glenoid wall bone loss of either the anterior or posterior glenoid. Newton and colleagues15 described the structural tricortical iliac crest bone graft as a 2-stage reconstruction. The second stage could be performed 4 to 6 months later after graft incorporation. With the excellent Association for Osteosynthesis (AO) type fixation using the base plate with compression and locking screws, it was reasonable to perform this in 1 stage, assuming that adequate fixation could be obtained with the iliac bone graft to the glenoid.16 This worked well with the cavitary glenoid defects and those in which either the anterior or posterior wall was absent.17-19
EXCEPTIONS TO THE 1-STAGE FIXATION TECHNIQUE
Fixation could still be obtained medially, but more severe cases were encountered with loss of both the anterior and posterior walls. In these more advanced cases, the vault was no longer present after removal of the polyethylene, cement, and rubbery osteolytic tissue that replaced the bone. To account for this, a simplified 3-stage classification was proposed.20 The cavitary vault defect is designated as type 1 bone loss. Type 2A includes the cavitary central defect plus loss of the anterior glenoid wall, and 2B is similar with loss of the posterior wall (Figures 4A-4F). Type 3 involves loss of the glenoid vault and both anterior and posterior walls with erosion down to the medial juncture of the base of the scapular spine, coracoid, and pillar of the scapula.
Continue to: The tricortical iliac crest bone graft...
The tricortical iliac crest bone graft (TICBG) offered a structural graft that worked well for these cases of bone loss. When the graft is performed in 1 stage, the glenoid is exposed, and the defect measured after removing the osteolytic, polyethylene-laden tissue from the glenoid. The iliac graft is harvested and placed with the long post base plate engaging the native scapula medially (Figures 5A-5C).
This technique worked well with the type 1 and 2 defects, but when attempted with the type 3 glenoid defect with global glenoid bone loss, adequate fixation for a single-stage reconstruction could not be predictably obtained with type 3 loss of the vault and both walls. In this situation, the base plate post is wider than the remaining medialized glenoid vault (Figures 6A-6C). The iliac crest provides better bone for this global loss when harvested sideways, fixed with screws, and after secure healing, the second-stage base plate is placed (Figures 7A-7F).
An alternative to the iliac crest as a bone graft donor site is the femoral neck allograft.21 It avoids the additional surgery and pain at the donor site, but healing is less assured. Scalise and Iannotti22 have had good clinical results but noted substantial graft resorption when revising a total shoulder to a humeral head arthroplasty. In a recent report by Ozgur and colleagues,23 64% of femoral neck allografts were still intact at 1-year follow-up. The technique involved harvesting the graft with a hole saw, shaping and affixing it to the deficient glenoid, and gaining central fixation with a threaded or solid post base plate and peripheral screws. Poor results were obtained with the use of the femoral shaft, as it is brittle. Angled peripheral screws caused the allograft shaft to fracture. Low-grade sepsis remained an unanswered problem in the patient group, which averaged 6 prior procedures, and often led to another revision. Less favorable results were found using the 1-piece threaded post base plate with grafts.24 It is assumed that the allograft has less healing potential, and micro motion plays a role when the long central screw has no on-growth healing potential in the native scapula. This graft choice is the author’s least favorite, but is available in desperate situations. Jones and colleagues25 report promising results with bulk allografts and autografts for large glenoid defects with good clinical results. The results in the graft cohort were inferior to those in a matched group not requiring grafts. Their complications were consistent with the revision setting for shoulders having multiple operations. It is well known that preoperative factors are strong predictors of postoperative outcomes.26
CONCLUSION
The author’s current technique is to use the native humeral head when available, or iliac crest for structural support to the base plate and glenosphere. Secure fixation to the native scapula is necessary if the operation is to be done in 1-stage. Incorporation with calcium orthophosphate bone substitution does not replace the need for structural support as shown in Figures 8A-8D.
For the type 2 vault and 1 wall glenoid bone loss defects, the TICBG is still the most useful option. For the type 3 global bone loss defects, a 2-stage approach is the safer option. Additional options that may replace some of these grafting techniques are the introduction of the metallic augmented ingrowth base plates to correct for superior, anterior, and posterior glenoid bone losses. The early unpublished experiences by Wright and colleagues are very promising. All of the above options should be available in the operating room for a busy arthroplasty surgeon.
1. Hamada K, Fukuda H, Mikasa M, Kobay Y. Roentgenographic findings in massive rotator cuff tears. A long-term observation. Clin Orthop Relat Res. 1990;254:92-96.
2. Favard L, Alami G. The glenoid in the frontal plane: The Favard and Hamada radiographic classifications of cuff tear osteoarthritis. In: Walch G, Boileau P, Favard ML, Lévigne C, Sirveaux F, eds. Shoulder Concepts 2010: The Glenoid. Paris, France: Sauramps Medical; 2010:53-58.
3. Rouleau DM, Kidder JF, Pons-Villanueva J, Dynamidis S, Walch G. The glenoid in the horizontal plane: Walch classification revisited humeral subluxation and glenoid retroversion. In: Walch G, Boileau P, Favard ML, Lévigne C, Sirveaux F, eds. Shoulder Concepts 2010: The Glenoid. Paris, France: Sauramps Medical; 2010:45-51.
4. Walch G, Badet R, Boulahia A, Khoury A. Morphological study of the glenoid in primary glenohumeral osteoarthritis. J Arthroplasty. 1999;14(6):756-760.
5. Iannotti JP, Ricchetti E. Walch classification: adding two new glenoid types. Orthopaedic Insights Cleveland Clinic. 2017:6-7.
6. Mizuno N, Denard PJ, Raiss P, Walch G. Reverse shoulder arthroplasty for primary glenohumeral osteoarthritis with a biconcave glenoid. J Bone Joint Surg Am. 2013;95(14):1297-1304.
7. Nyffeler RW, Jost B, Pfirrmann CW, Gerber C. Measurement of glenoid version: conventional radiographs verses computed tomography scans. J Shoulder Elbow Surg. 2003;12(5):493-496.
8. Scalise JJ, Bryan J, Polster J, Brems JJ, Iannotti JP. Quantitative analysis of glenoid bone loss in osteoarthritis using three-dimensional compute tomography scans. [published online ahead of print January 22, 2008]. J Shoulder Elbow Surg. 2008;17(2):328-335.
9. Friedman RJ, Hawthorne KB, Genez BM. The use of computerized tomography in the measurement of glenoid version. J Bone Joint Surg Am. 1992;74(7):1032-1037.
10. Boileau P, Moineau G, Roussanne Y, O’Shea K. Bony increased-offset reverse shoulder arthroplasty: minimizing scapular impingement while maximizing glenoid fixation. Clin Orthop Relat Res. 2011;469(9):2558-2567.
11. Harmsen S, Casagrande D, Norris T: “Shaped” humeral head autograft reverse shoulder arthroplasty: Treatment for primary glenohumeral osteoarthritis with significant posterior glenoid bone loss (B2, B3, and C-type). Orthopade. 2017;46(12):1045-1054.
12. Norris TR, Phipatanakul WP. Treatment of glenoid loosening and bone loss due to osteolysis with glenoid bone grafting. J Shoulder Elbow Surg. 2006;15(1):84-87.
13. Farzana F, Lee T, Malito L, et al. Analysis of severely fractured glenoid components: clinical consequences of biomechanics, design, and materials selection on implant performance. J Shoulder Elbow Surg. 2016;25(7):1041-1050.
14. Antuña SA, Sperling JW, Cofield RH, Rowland CM. Glenoid revision surgery after total shoulder arthroplasty. J Shoulder Elbow Surg. 2001;10(3):217-224.
15. Newton L, Walch G, Nove-Josserand L, Edwards TB. Glenoid cortical cancellous bone grafting after glenoid component removal in the treatment of glenoid loosening. J Shoulder Elbow Surg. 2006;15(2):173-179.
16. Norris TR, Kelly JD, Humphrey CS. Management of glenoid bone defects in revision shoulder arthroplasty: a new application of the reverse total shoulder prosthesis. Techniques Shoulder Elbow Surgery. 2007;8(1):37-46.
17. Kelly JD II, Zhao JX, Hobgood ER, Norris TR. Clinical results of revision shoulder arthroplasty using the reverse prosthesis. J Shoulder Elbow Surg. 2012;21(11):1516-1525.
18. Norris TR. Reconstruction of glenoid bone loss in total shoulder arthroplasty. In: Boileau P, ed. Shoulder Concepts 2008-Arthroscopy and Arthroplasty. Paris, France: Sauramps Medical; 2008:397-404.
19. Humphrey CS, Kelly JD, Norris TR. Management of glenoid deficiency in reverse shoulder arthroplasty. In: Fealy S, Warren RF, Craig EV, Sperling JW, eds. Shoulder Arthroplasty. New York, NY: Thieme; 2006.
20. Norris TR, Abdus-Salaam S. Lessons learned from the Hylamer experience and technical salvage for glenoid reconstruction. In: Walch G, Boileau P, Favard ML, Lévigne C, Sirveaux F, eds. Shoulder Concepts 2010: The Glenoid. Paris, France: Sauramps Medical; 2010:265-278.
21. Bateman E, Donald SM. Reconstruction of massive uncontained glenoid defects using a combined autograft-allograft construct with reverse shoulder arthroplasty: preliminary results. J Shoulder Elbow Surg. 2012;21(7):925-934.
22. Scalise JJ, Iannotti JP. Bone grafting severe glenoid defects in revision shoulder arthroplasty. Clin Orthop. 2008;466(1):139-145.
23. Ozgur S, Sadeghpour R, Norris TR. Revision shoulder arthroplasty with a reverse shoulder prosthesis. Use of structural allograft for glenoid bone loss. Orthopade. 2017;46(12):1055-1062.
24. Sadeghpour R, Ozgur S, Norris TR. Threaded post baseplate failures in RSA. In: Hardy PH, Valenti PH, Scheibel M, eds. Shoulder Arthroplasty, Current Concepts. Paris International Shoulder Course 2017. 2017:148-157.
25. Jones RB, Wright TW, Zuckerman JD. Reverse total shoulder arthroplasty with structural bone grafting of large glenoid defects. J Shoulder Elbow Surg. 2016;25(9):1425-1432.
26. Iannotti JP, Norris TR. Influence of preoperative factors on outcome of shoulder arthroplasty for glenohumeral osteoarthritis. J Bone Joint Surg. 2003;85(2):251-258.
ABSTRACT
The reverse shoulder arthroplasty facilitates surgical treatment of primary and revision shoulder with rotator cuff and bone deficiencies. Wear pattern classifications and a logical treatment approach for glenoid bone loss enable the surgeon to address a difficult series of problems in the reconstructions where the glenoid might not otherwise be able to support the implants. Bone grafting using the native humeral head in primary cases, and in revision cases, iliac crest are the most reliable sources for structural grafts for the worn or deficient glenoid vault.
Continue to: The reverse shoulder arthroplasty...
The reverse shoulder arthroplasty (RSA) technique was approved by the US Food and Drug Administration and introduced to the US market in 2004. It has been a successful addition to the treatment of shoulder pathologies with bone and rotator cuff loss. Its indications have expanded from treatment of very elderly patients with rotator cuff deficiencies to now include younger patients with humeral and glenoid bone loss, arthritis, soft-tissue losses, fractures, instability, and revision arthroplasty. Many of these conditions, when not adequately addressed with anatomic arthroplasty, now have viable treatment options for newer complex and successful reconstructions.
Glenoid bone deficiencies offer unique challenges for successful arthroplasty management. Basing treatment on bone loss classifications permits meaningful evaluation of these surgical options and whether they might be carried out in 1- or 2-stage reconstructions. An underlying premise is that restoration of the glenoid joint line and version assist in final stability, power, and functional results. For this purpose, bone graft options, or augmented implants are beneficial. This review covers the bone grafting options for autografts and allografts for deficient glenoids in reverse shoulder arthroplasty reconstructions.
OPERATIVE TECHNIQUES
For patients without prior arthroplasty, the humeral head is available for bone grafting the glenoid bone deficits. Favard and Hamada have described vertical glenoid classifications for uneven glenoid bone loss applicable to cuff tear arthropathy and inflammatory arthritis patients.1,2 The more severe E3 superior and medial bone loss is ideally addressed with the humeral head. An early example in 2004 confirmed that this was a good indication for glenoid bone grafting and using the reverse shoulder in these advanced cases (Figures 1A-1E).
In this case, it was noted that with bone grafts the base plate post did not engage the native scapula glenoid vault. Given that the on-growth central post was the strongest part of the fixation, it was fortunate that this healed. The need for a longer post with bone grafts was recognized. Laurent Comtat with the Wright Medical company accommodated the author’s request to develop the first 25- and 30-mm-long posts to allow better fixation and on-growth potential when used with bone grafts.
Gilles Walch’s classification addresses arthritic central and horizontal bone loss.3,4 Considerations relevant in RSA include the severe A2 central bone loss found in inflammatory arthritis and the B2, B3, and C patterns with posterior bone loss seen in osteoarthritis, rheumatoid arthritis, and congenital dysplasia5,6 as seen in Figures 2A, 2B. The 3-dimensional (3-D) computed tomography (CT) scan is considered the most accurate method of assessment when compared with axial radiographs.7 The glenoid vault model as a measurement of glenoid bone loss has great promise in designing prosthetic replacements and bone graft techniques.8
Continue to: Modern methods for determining glenoid version...
Modern methods for determining glenoid version, medialization, and eccentric bone wear include 3-D reconstruction and patient-specific instruments. For many years, version determination has been confirmed at surgery with subscapularis elevation, palpating the glenoid center point along Friedman’s line, and then inserting a Steinmann pin as a guide to restore version and the lateral joint line at the time of bone grafting. An example of this is demonstrated in Figures 3A-3E.9
All grafts are harvested with a hole saw from the humeral head. The inner diameter is 29 mm, the same as that of the base plate. Originally, the hole saw and mandrel were obtained from the hardware store, but Pascal Boileau upgraded the hole saw quality when he had industry develop a stainless-steel hole saw and published his results with the BIO-RSA (Wright Medical).10 In an unpublished study, Harmsen reviewed our 220 consecutive humeral head bone grafts for use of this technique with successful and reproducible results. In a separate evaluation, 29 shaped humeral head bone grafts for B2, B3, and C glenoid bone deficits showed 100% healing.11 This technique has good reproducibility when performed with an autogenous bone graft from a local donor source.
The more challenging cases involve glenoid bone loss from polyethylene osteolysis and, in some revision cases, concomitant sepsis.12 The humeral head is no longer available, and the distal clavicle or humeral metaphysis are often insufficient to restore the glenoid vault and joint line. Gunther and associates at the UC Berkeley biomaterials laboratory have made many contributions to our understanding of polyethylene wear and the factors leading to its loosening that result in massive glenoid bone loss.13
Antuna and colleagues14 classified these cases as having a central vault cavitary defect, or one combined with a peripheral glenoid wall bone loss of either the anterior or posterior glenoid. Newton and colleagues15 described the structural tricortical iliac crest bone graft as a 2-stage reconstruction. The second stage could be performed 4 to 6 months later after graft incorporation. With the excellent Association for Osteosynthesis (AO) type fixation using the base plate with compression and locking screws, it was reasonable to perform this in 1 stage, assuming that adequate fixation could be obtained with the iliac bone graft to the glenoid.16 This worked well with the cavitary glenoid defects and those in which either the anterior or posterior wall was absent.17-19
EXCEPTIONS TO THE 1-STAGE FIXATION TECHNIQUE
Fixation could still be obtained medially, but more severe cases were encountered with loss of both the anterior and posterior walls. In these more advanced cases, the vault was no longer present after removal of the polyethylene, cement, and rubbery osteolytic tissue that replaced the bone. To account for this, a simplified 3-stage classification was proposed.20 The cavitary vault defect is designated as type 1 bone loss. Type 2A includes the cavitary central defect plus loss of the anterior glenoid wall, and 2B is similar with loss of the posterior wall (Figures 4A-4F). Type 3 involves loss of the glenoid vault and both anterior and posterior walls with erosion down to the medial juncture of the base of the scapular spine, coracoid, and pillar of the scapula.
Continue to: The tricortical iliac crest bone graft...
The tricortical iliac crest bone graft (TICBG) offered a structural graft that worked well for these cases of bone loss. When the graft is performed in 1 stage, the glenoid is exposed, and the defect measured after removing the osteolytic, polyethylene-laden tissue from the glenoid. The iliac graft is harvested and placed with the long post base plate engaging the native scapula medially (Figures 5A-5C).
This technique worked well with the type 1 and 2 defects, but when attempted with the type 3 glenoid defect with global glenoid bone loss, adequate fixation for a single-stage reconstruction could not be predictably obtained with type 3 loss of the vault and both walls. In this situation, the base plate post is wider than the remaining medialized glenoid vault (Figures 6A-6C). The iliac crest provides better bone for this global loss when harvested sideways, fixed with screws, and after secure healing, the second-stage base plate is placed (Figures 7A-7F).
An alternative to the iliac crest as a bone graft donor site is the femoral neck allograft.21 It avoids the additional surgery and pain at the donor site, but healing is less assured. Scalise and Iannotti22 have had good clinical results but noted substantial graft resorption when revising a total shoulder to a humeral head arthroplasty. In a recent report by Ozgur and colleagues,23 64% of femoral neck allografts were still intact at 1-year follow-up. The technique involved harvesting the graft with a hole saw, shaping and affixing it to the deficient glenoid, and gaining central fixation with a threaded or solid post base plate and peripheral screws. Poor results were obtained with the use of the femoral shaft, as it is brittle. Angled peripheral screws caused the allograft shaft to fracture. Low-grade sepsis remained an unanswered problem in the patient group, which averaged 6 prior procedures, and often led to another revision. Less favorable results were found using the 1-piece threaded post base plate with grafts.24 It is assumed that the allograft has less healing potential, and micro motion plays a role when the long central screw has no on-growth healing potential in the native scapula. This graft choice is the author’s least favorite, but is available in desperate situations. Jones and colleagues25 report promising results with bulk allografts and autografts for large glenoid defects with good clinical results. The results in the graft cohort were inferior to those in a matched group not requiring grafts. Their complications were consistent with the revision setting for shoulders having multiple operations. It is well known that preoperative factors are strong predictors of postoperative outcomes.26
CONCLUSION
The author’s current technique is to use the native humeral head when available, or iliac crest for structural support to the base plate and glenosphere. Secure fixation to the native scapula is necessary if the operation is to be done in 1-stage. Incorporation with calcium orthophosphate bone substitution does not replace the need for structural support as shown in Figures 8A-8D.
For the type 2 vault and 1 wall glenoid bone loss defects, the TICBG is still the most useful option. For the type 3 global bone loss defects, a 2-stage approach is the safer option. Additional options that may replace some of these grafting techniques are the introduction of the metallic augmented ingrowth base plates to correct for superior, anterior, and posterior glenoid bone losses. The early unpublished experiences by Wright and colleagues are very promising. All of the above options should be available in the operating room for a busy arthroplasty surgeon.
ABSTRACT
The reverse shoulder arthroplasty facilitates surgical treatment of primary and revision shoulder with rotator cuff and bone deficiencies. Wear pattern classifications and a logical treatment approach for glenoid bone loss enable the surgeon to address a difficult series of problems in the reconstructions where the glenoid might not otherwise be able to support the implants. Bone grafting using the native humeral head in primary cases, and in revision cases, iliac crest are the most reliable sources for structural grafts for the worn or deficient glenoid vault.
Continue to: The reverse shoulder arthroplasty...
The reverse shoulder arthroplasty (RSA) technique was approved by the US Food and Drug Administration and introduced to the US market in 2004. It has been a successful addition to the treatment of shoulder pathologies with bone and rotator cuff loss. Its indications have expanded from treatment of very elderly patients with rotator cuff deficiencies to now include younger patients with humeral and glenoid bone loss, arthritis, soft-tissue losses, fractures, instability, and revision arthroplasty. Many of these conditions, when not adequately addressed with anatomic arthroplasty, now have viable treatment options for newer complex and successful reconstructions.
Glenoid bone deficiencies offer unique challenges for successful arthroplasty management. Basing treatment on bone loss classifications permits meaningful evaluation of these surgical options and whether they might be carried out in 1- or 2-stage reconstructions. An underlying premise is that restoration of the glenoid joint line and version assist in final stability, power, and functional results. For this purpose, bone graft options, or augmented implants are beneficial. This review covers the bone grafting options for autografts and allografts for deficient glenoids in reverse shoulder arthroplasty reconstructions.
OPERATIVE TECHNIQUES
For patients without prior arthroplasty, the humeral head is available for bone grafting the glenoid bone deficits. Favard and Hamada have described vertical glenoid classifications for uneven glenoid bone loss applicable to cuff tear arthropathy and inflammatory arthritis patients.1,2 The more severe E3 superior and medial bone loss is ideally addressed with the humeral head. An early example in 2004 confirmed that this was a good indication for glenoid bone grafting and using the reverse shoulder in these advanced cases (Figures 1A-1E).
In this case, it was noted that with bone grafts the base plate post did not engage the native scapula glenoid vault. Given that the on-growth central post was the strongest part of the fixation, it was fortunate that this healed. The need for a longer post with bone grafts was recognized. Laurent Comtat with the Wright Medical company accommodated the author’s request to develop the first 25- and 30-mm-long posts to allow better fixation and on-growth potential when used with bone grafts.
Gilles Walch’s classification addresses arthritic central and horizontal bone loss.3,4 Considerations relevant in RSA include the severe A2 central bone loss found in inflammatory arthritis and the B2, B3, and C patterns with posterior bone loss seen in osteoarthritis, rheumatoid arthritis, and congenital dysplasia5,6 as seen in Figures 2A, 2B. The 3-dimensional (3-D) computed tomography (CT) scan is considered the most accurate method of assessment when compared with axial radiographs.7 The glenoid vault model as a measurement of glenoid bone loss has great promise in designing prosthetic replacements and bone graft techniques.8
Continue to: Modern methods for determining glenoid version...
Modern methods for determining glenoid version, medialization, and eccentric bone wear include 3-D reconstruction and patient-specific instruments. For many years, version determination has been confirmed at surgery with subscapularis elevation, palpating the glenoid center point along Friedman’s line, and then inserting a Steinmann pin as a guide to restore version and the lateral joint line at the time of bone grafting. An example of this is demonstrated in Figures 3A-3E.9
All grafts are harvested with a hole saw from the humeral head. The inner diameter is 29 mm, the same as that of the base plate. Originally, the hole saw and mandrel were obtained from the hardware store, but Pascal Boileau upgraded the hole saw quality when he had industry develop a stainless-steel hole saw and published his results with the BIO-RSA (Wright Medical).10 In an unpublished study, Harmsen reviewed our 220 consecutive humeral head bone grafts for use of this technique with successful and reproducible results. In a separate evaluation, 29 shaped humeral head bone grafts for B2, B3, and C glenoid bone deficits showed 100% healing.11 This technique has good reproducibility when performed with an autogenous bone graft from a local donor source.
The more challenging cases involve glenoid bone loss from polyethylene osteolysis and, in some revision cases, concomitant sepsis.12 The humeral head is no longer available, and the distal clavicle or humeral metaphysis are often insufficient to restore the glenoid vault and joint line. Gunther and associates at the UC Berkeley biomaterials laboratory have made many contributions to our understanding of polyethylene wear and the factors leading to its loosening that result in massive glenoid bone loss.13
Antuna and colleagues14 classified these cases as having a central vault cavitary defect, or one combined with a peripheral glenoid wall bone loss of either the anterior or posterior glenoid. Newton and colleagues15 described the structural tricortical iliac crest bone graft as a 2-stage reconstruction. The second stage could be performed 4 to 6 months later after graft incorporation. With the excellent Association for Osteosynthesis (AO) type fixation using the base plate with compression and locking screws, it was reasonable to perform this in 1 stage, assuming that adequate fixation could be obtained with the iliac bone graft to the glenoid.16 This worked well with the cavitary glenoid defects and those in which either the anterior or posterior wall was absent.17-19
EXCEPTIONS TO THE 1-STAGE FIXATION TECHNIQUE
Fixation could still be obtained medially, but more severe cases were encountered with loss of both the anterior and posterior walls. In these more advanced cases, the vault was no longer present after removal of the polyethylene, cement, and rubbery osteolytic tissue that replaced the bone. To account for this, a simplified 3-stage classification was proposed.20 The cavitary vault defect is designated as type 1 bone loss. Type 2A includes the cavitary central defect plus loss of the anterior glenoid wall, and 2B is similar with loss of the posterior wall (Figures 4A-4F). Type 3 involves loss of the glenoid vault and both anterior and posterior walls with erosion down to the medial juncture of the base of the scapular spine, coracoid, and pillar of the scapula.
Continue to: The tricortical iliac crest bone graft...
The tricortical iliac crest bone graft (TICBG) offered a structural graft that worked well for these cases of bone loss. When the graft is performed in 1 stage, the glenoid is exposed, and the defect measured after removing the osteolytic, polyethylene-laden tissue from the glenoid. The iliac graft is harvested and placed with the long post base plate engaging the native scapula medially (Figures 5A-5C).
This technique worked well with the type 1 and 2 defects, but when attempted with the type 3 glenoid defect with global glenoid bone loss, adequate fixation for a single-stage reconstruction could not be predictably obtained with type 3 loss of the vault and both walls. In this situation, the base plate post is wider than the remaining medialized glenoid vault (Figures 6A-6C). The iliac crest provides better bone for this global loss when harvested sideways, fixed with screws, and after secure healing, the second-stage base plate is placed (Figures 7A-7F).
An alternative to the iliac crest as a bone graft donor site is the femoral neck allograft.21 It avoids the additional surgery and pain at the donor site, but healing is less assured. Scalise and Iannotti22 have had good clinical results but noted substantial graft resorption when revising a total shoulder to a humeral head arthroplasty. In a recent report by Ozgur and colleagues,23 64% of femoral neck allografts were still intact at 1-year follow-up. The technique involved harvesting the graft with a hole saw, shaping and affixing it to the deficient glenoid, and gaining central fixation with a threaded or solid post base plate and peripheral screws. Poor results were obtained with the use of the femoral shaft, as it is brittle. Angled peripheral screws caused the allograft shaft to fracture. Low-grade sepsis remained an unanswered problem in the patient group, which averaged 6 prior procedures, and often led to another revision. Less favorable results were found using the 1-piece threaded post base plate with grafts.24 It is assumed that the allograft has less healing potential, and micro motion plays a role when the long central screw has no on-growth healing potential in the native scapula. This graft choice is the author’s least favorite, but is available in desperate situations. Jones and colleagues25 report promising results with bulk allografts and autografts for large glenoid defects with good clinical results. The results in the graft cohort were inferior to those in a matched group not requiring grafts. Their complications were consistent with the revision setting for shoulders having multiple operations. It is well known that preoperative factors are strong predictors of postoperative outcomes.26
CONCLUSION
The author’s current technique is to use the native humeral head when available, or iliac crest for structural support to the base plate and glenosphere. Secure fixation to the native scapula is necessary if the operation is to be done in 1-stage. Incorporation with calcium orthophosphate bone substitution does not replace the need for structural support as shown in Figures 8A-8D.
For the type 2 vault and 1 wall glenoid bone loss defects, the TICBG is still the most useful option. For the type 3 global bone loss defects, a 2-stage approach is the safer option. Additional options that may replace some of these grafting techniques are the introduction of the metallic augmented ingrowth base plates to correct for superior, anterior, and posterior glenoid bone losses. The early unpublished experiences by Wright and colleagues are very promising. All of the above options should be available in the operating room for a busy arthroplasty surgeon.
1. Hamada K, Fukuda H, Mikasa M, Kobay Y. Roentgenographic findings in massive rotator cuff tears. A long-term observation. Clin Orthop Relat Res. 1990;254:92-96.
2. Favard L, Alami G. The glenoid in the frontal plane: The Favard and Hamada radiographic classifications of cuff tear osteoarthritis. In: Walch G, Boileau P, Favard ML, Lévigne C, Sirveaux F, eds. Shoulder Concepts 2010: The Glenoid. Paris, France: Sauramps Medical; 2010:53-58.
3. Rouleau DM, Kidder JF, Pons-Villanueva J, Dynamidis S, Walch G. The glenoid in the horizontal plane: Walch classification revisited humeral subluxation and glenoid retroversion. In: Walch G, Boileau P, Favard ML, Lévigne C, Sirveaux F, eds. Shoulder Concepts 2010: The Glenoid. Paris, France: Sauramps Medical; 2010:45-51.
4. Walch G, Badet R, Boulahia A, Khoury A. Morphological study of the glenoid in primary glenohumeral osteoarthritis. J Arthroplasty. 1999;14(6):756-760.
5. Iannotti JP, Ricchetti E. Walch classification: adding two new glenoid types. Orthopaedic Insights Cleveland Clinic. 2017:6-7.
6. Mizuno N, Denard PJ, Raiss P, Walch G. Reverse shoulder arthroplasty for primary glenohumeral osteoarthritis with a biconcave glenoid. J Bone Joint Surg Am. 2013;95(14):1297-1304.
7. Nyffeler RW, Jost B, Pfirrmann CW, Gerber C. Measurement of glenoid version: conventional radiographs verses computed tomography scans. J Shoulder Elbow Surg. 2003;12(5):493-496.
8. Scalise JJ, Bryan J, Polster J, Brems JJ, Iannotti JP. Quantitative analysis of glenoid bone loss in osteoarthritis using three-dimensional compute tomography scans. [published online ahead of print January 22, 2008]. J Shoulder Elbow Surg. 2008;17(2):328-335.
9. Friedman RJ, Hawthorne KB, Genez BM. The use of computerized tomography in the measurement of glenoid version. J Bone Joint Surg Am. 1992;74(7):1032-1037.
10. Boileau P, Moineau G, Roussanne Y, O’Shea K. Bony increased-offset reverse shoulder arthroplasty: minimizing scapular impingement while maximizing glenoid fixation. Clin Orthop Relat Res. 2011;469(9):2558-2567.
11. Harmsen S, Casagrande D, Norris T: “Shaped” humeral head autograft reverse shoulder arthroplasty: Treatment for primary glenohumeral osteoarthritis with significant posterior glenoid bone loss (B2, B3, and C-type). Orthopade. 2017;46(12):1045-1054.
12. Norris TR, Phipatanakul WP. Treatment of glenoid loosening and bone loss due to osteolysis with glenoid bone grafting. J Shoulder Elbow Surg. 2006;15(1):84-87.
13. Farzana F, Lee T, Malito L, et al. Analysis of severely fractured glenoid components: clinical consequences of biomechanics, design, and materials selection on implant performance. J Shoulder Elbow Surg. 2016;25(7):1041-1050.
14. Antuña SA, Sperling JW, Cofield RH, Rowland CM. Glenoid revision surgery after total shoulder arthroplasty. J Shoulder Elbow Surg. 2001;10(3):217-224.
15. Newton L, Walch G, Nove-Josserand L, Edwards TB. Glenoid cortical cancellous bone grafting after glenoid component removal in the treatment of glenoid loosening. J Shoulder Elbow Surg. 2006;15(2):173-179.
16. Norris TR, Kelly JD, Humphrey CS. Management of glenoid bone defects in revision shoulder arthroplasty: a new application of the reverse total shoulder prosthesis. Techniques Shoulder Elbow Surgery. 2007;8(1):37-46.
17. Kelly JD II, Zhao JX, Hobgood ER, Norris TR. Clinical results of revision shoulder arthroplasty using the reverse prosthesis. J Shoulder Elbow Surg. 2012;21(11):1516-1525.
18. Norris TR. Reconstruction of glenoid bone loss in total shoulder arthroplasty. In: Boileau P, ed. Shoulder Concepts 2008-Arthroscopy and Arthroplasty. Paris, France: Sauramps Medical; 2008:397-404.
19. Humphrey CS, Kelly JD, Norris TR. Management of glenoid deficiency in reverse shoulder arthroplasty. In: Fealy S, Warren RF, Craig EV, Sperling JW, eds. Shoulder Arthroplasty. New York, NY: Thieme; 2006.
20. Norris TR, Abdus-Salaam S. Lessons learned from the Hylamer experience and technical salvage for glenoid reconstruction. In: Walch G, Boileau P, Favard ML, Lévigne C, Sirveaux F, eds. Shoulder Concepts 2010: The Glenoid. Paris, France: Sauramps Medical; 2010:265-278.
21. Bateman E, Donald SM. Reconstruction of massive uncontained glenoid defects using a combined autograft-allograft construct with reverse shoulder arthroplasty: preliminary results. J Shoulder Elbow Surg. 2012;21(7):925-934.
22. Scalise JJ, Iannotti JP. Bone grafting severe glenoid defects in revision shoulder arthroplasty. Clin Orthop. 2008;466(1):139-145.
23. Ozgur S, Sadeghpour R, Norris TR. Revision shoulder arthroplasty with a reverse shoulder prosthesis. Use of structural allograft for glenoid bone loss. Orthopade. 2017;46(12):1055-1062.
24. Sadeghpour R, Ozgur S, Norris TR. Threaded post baseplate failures in RSA. In: Hardy PH, Valenti PH, Scheibel M, eds. Shoulder Arthroplasty, Current Concepts. Paris International Shoulder Course 2017. 2017:148-157.
25. Jones RB, Wright TW, Zuckerman JD. Reverse total shoulder arthroplasty with structural bone grafting of large glenoid defects. J Shoulder Elbow Surg. 2016;25(9):1425-1432.
26. Iannotti JP, Norris TR. Influence of preoperative factors on outcome of shoulder arthroplasty for glenohumeral osteoarthritis. J Bone Joint Surg. 2003;85(2):251-258.
1. Hamada K, Fukuda H, Mikasa M, Kobay Y. Roentgenographic findings in massive rotator cuff tears. A long-term observation. Clin Orthop Relat Res. 1990;254:92-96.
2. Favard L, Alami G. The glenoid in the frontal plane: The Favard and Hamada radiographic classifications of cuff tear osteoarthritis. In: Walch G, Boileau P, Favard ML, Lévigne C, Sirveaux F, eds. Shoulder Concepts 2010: The Glenoid. Paris, France: Sauramps Medical; 2010:53-58.
3. Rouleau DM, Kidder JF, Pons-Villanueva J, Dynamidis S, Walch G. The glenoid in the horizontal plane: Walch classification revisited humeral subluxation and glenoid retroversion. In: Walch G, Boileau P, Favard ML, Lévigne C, Sirveaux F, eds. Shoulder Concepts 2010: The Glenoid. Paris, France: Sauramps Medical; 2010:45-51.
4. Walch G, Badet R, Boulahia A, Khoury A. Morphological study of the glenoid in primary glenohumeral osteoarthritis. J Arthroplasty. 1999;14(6):756-760.
5. Iannotti JP, Ricchetti E. Walch classification: adding two new glenoid types. Orthopaedic Insights Cleveland Clinic. 2017:6-7.
6. Mizuno N, Denard PJ, Raiss P, Walch G. Reverse shoulder arthroplasty for primary glenohumeral osteoarthritis with a biconcave glenoid. J Bone Joint Surg Am. 2013;95(14):1297-1304.
7. Nyffeler RW, Jost B, Pfirrmann CW, Gerber C. Measurement of glenoid version: conventional radiographs verses computed tomography scans. J Shoulder Elbow Surg. 2003;12(5):493-496.
8. Scalise JJ, Bryan J, Polster J, Brems JJ, Iannotti JP. Quantitative analysis of glenoid bone loss in osteoarthritis using three-dimensional compute tomography scans. [published online ahead of print January 22, 2008]. J Shoulder Elbow Surg. 2008;17(2):328-335.
9. Friedman RJ, Hawthorne KB, Genez BM. The use of computerized tomography in the measurement of glenoid version. J Bone Joint Surg Am. 1992;74(7):1032-1037.
10. Boileau P, Moineau G, Roussanne Y, O’Shea K. Bony increased-offset reverse shoulder arthroplasty: minimizing scapular impingement while maximizing glenoid fixation. Clin Orthop Relat Res. 2011;469(9):2558-2567.
11. Harmsen S, Casagrande D, Norris T: “Shaped” humeral head autograft reverse shoulder arthroplasty: Treatment for primary glenohumeral osteoarthritis with significant posterior glenoid bone loss (B2, B3, and C-type). Orthopade. 2017;46(12):1045-1054.
12. Norris TR, Phipatanakul WP. Treatment of glenoid loosening and bone loss due to osteolysis with glenoid bone grafting. J Shoulder Elbow Surg. 2006;15(1):84-87.
13. Farzana F, Lee T, Malito L, et al. Analysis of severely fractured glenoid components: clinical consequences of biomechanics, design, and materials selection on implant performance. J Shoulder Elbow Surg. 2016;25(7):1041-1050.
14. Antuña SA, Sperling JW, Cofield RH, Rowland CM. Glenoid revision surgery after total shoulder arthroplasty. J Shoulder Elbow Surg. 2001;10(3):217-224.
15. Newton L, Walch G, Nove-Josserand L, Edwards TB. Glenoid cortical cancellous bone grafting after glenoid component removal in the treatment of glenoid loosening. J Shoulder Elbow Surg. 2006;15(2):173-179.
16. Norris TR, Kelly JD, Humphrey CS. Management of glenoid bone defects in revision shoulder arthroplasty: a new application of the reverse total shoulder prosthesis. Techniques Shoulder Elbow Surgery. 2007;8(1):37-46.
17. Kelly JD II, Zhao JX, Hobgood ER, Norris TR. Clinical results of revision shoulder arthroplasty using the reverse prosthesis. J Shoulder Elbow Surg. 2012;21(11):1516-1525.
18. Norris TR. Reconstruction of glenoid bone loss in total shoulder arthroplasty. In: Boileau P, ed. Shoulder Concepts 2008-Arthroscopy and Arthroplasty. Paris, France: Sauramps Medical; 2008:397-404.
19. Humphrey CS, Kelly JD, Norris TR. Management of glenoid deficiency in reverse shoulder arthroplasty. In: Fealy S, Warren RF, Craig EV, Sperling JW, eds. Shoulder Arthroplasty. New York, NY: Thieme; 2006.
20. Norris TR, Abdus-Salaam S. Lessons learned from the Hylamer experience and technical salvage for glenoid reconstruction. In: Walch G, Boileau P, Favard ML, Lévigne C, Sirveaux F, eds. Shoulder Concepts 2010: The Glenoid. Paris, France: Sauramps Medical; 2010:265-278.
21. Bateman E, Donald SM. Reconstruction of massive uncontained glenoid defects using a combined autograft-allograft construct with reverse shoulder arthroplasty: preliminary results. J Shoulder Elbow Surg. 2012;21(7):925-934.
22. Scalise JJ, Iannotti JP. Bone grafting severe glenoid defects in revision shoulder arthroplasty. Clin Orthop. 2008;466(1):139-145.
23. Ozgur S, Sadeghpour R, Norris TR. Revision shoulder arthroplasty with a reverse shoulder prosthesis. Use of structural allograft for glenoid bone loss. Orthopade. 2017;46(12):1055-1062.
24. Sadeghpour R, Ozgur S, Norris TR. Threaded post baseplate failures in RSA. In: Hardy PH, Valenti PH, Scheibel M, eds. Shoulder Arthroplasty, Current Concepts. Paris International Shoulder Course 2017. 2017:148-157.
25. Jones RB, Wright TW, Zuckerman JD. Reverse total shoulder arthroplasty with structural bone grafting of large glenoid defects. J Shoulder Elbow Surg. 2016;25(9):1425-1432.
26. Iannotti JP, Norris TR. Influence of preoperative factors on outcome of shoulder arthroplasty for glenohumeral osteoarthritis. J Bone Joint Surg. 2003;85(2):251-258.
TAKE-HOME POINTS
- Glenoid deficiencies that occur from dysplasia, arthritis, or polyethylene osteolysis may be successfully addressed with bone grafting techniques and reverse shoulder arthroplasty.
- The intact humeral head in a primary case is ideal graft to be shaped to fit the glenoid deficits.
- The reverse shoulder with a long post base plate that is fixed securely to the native scapula is the author’s preferred technique.
- As the native humeral head is not available in revision cases, the tricortical iliac crest bone graft may be fixed as a structural graft in 1-stage.
- When the scapular walls are deficient and medial fixation is not secure, 2 stages 4 months to 6 months apart will be necessary before loading the construct.
Prevalence and Impact of Self-Citation in Academic Orthopedic Surgery
ABSTRACT
The h-index is a commonly utilized metric for academic productivity. Previous studies have proposed that self-citation may limit the utility of the h-index. The purpose of this study is to evaluate the impact of self-citation on the h-index among orthopedic investigators. The study cohort consisted of program directors, chairpersons, and faculty at orthopedic surgery residency programs in the United States. The Scopus database was used to determine the h-index and number of citations ± self-citations. The total number of publications was correlated with the change in the h-index via self-citation. A total of 463 researchers were included (198 National Institutes of Health-funded faculty, 147 chairpersons, 118 program directors). Of these researchers, 83.8% cited previous work at least once (mean, 123.9 ± 277.6). Self-citations accounted for 5.8% of all citations. Including these citations increased the author h-index from 18.5 ± 14.9 to 19.2 ± 15.6 (P < .001). A minority of researchers (36.3%, P < .001) had increased their h-index via self-citation (range, 0-11). The proportional increase in the h-index via self-citation was positively related to the number of publications (P < .001). While the practice of self-citation is prevalent in orthopedics, its impact on the h-index is minimal for most researchers. With more publications, researchers can increase their h-index to a greater degree via self-citation.
Continue to: The competitive nature of academic research...
The competitive nature of academic research requires objective metrics to define career end points, such as promotion and funding procurement. While various criteria are used to assess performance in academia, publications and research funding are particularly regarded.1 Quantifying research dollars is relatively straightforward, but measuring research productivity is more complex. Not all articles are created equal, and disparities exist regarding effort and the ultimate impact of articles. In 2005, a physicist created the h-index to measure both research impact and productivity.2 As a bibliometric, the h-index equals the number of publications h that have been cited at least h times. Given its simplicity, the h-index has gained wide popularity in diverse medical specialties, including orthopedic surgery.3 Other recent studies have applied the h-index to hand surgery and spine surgery.4,5
Importantly, some authors have raised concerns regarding potential limitations of the h-index. One potentially significant limitation is the ability of authors to artificially inflate their h-index via self-citation. The impact of this practice is of particular interest as the h-index becomes widely adopted as a metric for promotion at many academic institutions.6-7 Furthermore, scholarly productivity has remained a critical component of successful grant funding procurement, and future grant funding applications may evaluate the h-index.8-10
The purpose of this study is to determine the prevalence and impact of self-citation on the h-index in a large cohort of orthopedic investigators. Given their high level of investment in academic orthopedic surgery, we focused on program directors, chairpersons, and National Institutes of Health (NIH)-funded research faculty at orthopedic surgery residency programs.
METHODS
INCLUSION CRITERIA
This study qualified as non-human and non-animal research and received exemption per the standing policy of the Institutional Review Board. The Fellowship and Residency Electronic Interactive Database (FREIDA) was accessed to generate a list of orthopedic residency program directors.11 This database was also used to generate a list of allopathic orthopedic surgery residency programs. Official program websites were accessed to generate a list of orthopedic chairpersons. Lastly, the NIH RePORTER was used to generate a list of basic science orthopedic investigators who received funding anytime during 2011 to 2014.12 This methodology was used due to the lack of reporting of basic science investigators on program websites. A list of NIH-funded orthopedic investigators was cross-referenced via an online search to isolate a cohort of PhD investigators.
Orthopedic faculty were defined as chairpersons, program directors, or NIH-funded investigators. In cases of overlap, preference was given in that order. Orthopedic investigators who had not published an article after 1995 were excluded (6 chairpersons, 1 program director).
BIBLIOMETRIC ANALYSIS
While several resources exist to calculate the h-index, the Scopus database (Elsevier) is one of the easiest programs to use.13 Author entries are created via institutional affiliations, thereby alleviating the need for manual reconciliations. Investigators were identified on Scopus via “author last name” and “first name, middle initial.” For each author, publications were screened for relevance to the field of orthopedics. Affiliated institutions were cross-referenced with information obtained from individual program websites. The “view h-graph” feature was used to calculate the number of publications, h-index, and number of citations. Then, the “Exclude self-citations” feature was used to calculate the number of corrected citations and the h-index excluding self-citations. Metrics were calculated over a 2-day period.
Continue to: STATISTICAL ANALYSIS
STATISTICAL ANALYSIS
Bibliometric analyses were presented descriptively with means ± standard deviation. After testing for normality, differences in the h-index between groups were assessed via analysis of variance tests. The proportional increase in the number of citations and the h-index were calculated by dividing the difference between the before and after exclusion of self-citations by the total number of citations before exclusion. The relationship between the number of publications and the proportional change in the h-index was assessed via calculation of the Spearman correlation coefficient. The independent variable was the number of publications, and the proportional increase in the h-index via self-citation was the dependent variable. Statistical tests were performed on STATA 13 (StataCorp) and the results considered significant if P < .05. Figures were created using GraphPad Prism 6.02 Software.
RESULTS
A total of 463 orthopedic investigators were included (147 chairpersons, 118 program directors, and 198 NIH-funded faculty) (Table 1). On average, these researchers produced 72.3 ± 83.0 articles and referenced 2139 ± 3222 articles (mean, 29.6 references per article). The cumulative h-index was 19.2 ± 15.6, and was the highest among NIH-funded researchers (24.3 ± 17.0) (P < .001). In all, 83.8% of orthopedic investigators self-cited their previous work at least once, and the total number of self-citations was highest among NIH-funded investigators (221 ± 355) (P < .001). After these self-citations were excluded, the h-index changed by 0.6 ± 1.1 for all investigators, and this change was greatest among NIH-funded researchers (1.1 ± 1.3) (P < .001).
Table 1. Effect of Self-Citation on NIH-funded Investigators, Chairpersons, and Program Directors in Orthopedics
| Investigator | N (%) | Articles, n (mean ± SD) |
Total Citations (mean ± SD)
| h-index | Self-Citations (mean ± SD) | Corrected h-index | ∆ h-index |
| NIH-funded | 198 (42.8) | 87.6 ± 84.9 | 3086 ± 3799 | 24.3 ± 17.0 | 221 ± 355 | 23.2 ± 16.3 | 1.1 ± 1.3 |
| Chairperson | 147 (31.7) | 85.3 ± 95.5 | 2151 ± 3098 | 19.9 ± 15.0 | 85.2 ± 221 | 19.5 ± 14.5 | 0.4 ± 0.8 |
| Program Director | 118 (25.5) | 30.5 ± 35.9 | 536.8 ± 785 | 9.6 ± 7.2 | 8.8 ± 19.9 | 9.5 ± 7.1 | 0.1 ± 0.3 |
| Total | 463 (100) | 72.3 ± 83.0 | 2139 ± 3222 | 19.2 ± 15.6 | 123.9 ± 277.6 | 18.5 ± 14.9 | 0.6 ± 1.1 |
Abbreviation: NIH, National Institutes of Health.
Most orthopedic investigators did not increase their h-index via self-citation (63.7%, P < .001). Table 2 categorizes investigators by changes in their h-index after excluding self-citations (range, 0-11). The maximal change in the h-index was seen in the most prolific group of investigators, who produced 261.0 ± 149.3 articles. In this group, the h-index increased by 11.1% ± 5.2%. The Figure investigates the relationship between the number of articles and the proportional increase in the h-index. The number of publications was positively correlated with the change in h-index after self-citations were excluded (r = 0.448, P < .001).
Table 2. Stratification of Orthopedic Researcher Investigators by Change in h-index After Self-Citation
∆ h-index
| N (%) |
Articles (mean ± SD)
| Self-Citations (mean ± SD) |
h-index (mean ± SD) | % Increase in h-index |
| 0 | 295 (63.7) | 43.8 ± 51.3 | 27.6 ± 58.4 | 13.1 ± 10.7 | 0 |
| 1 | 101 (21.8) | 87.9 ± 68.3 | 126.0 ± 130.6 | 24.0 ± 13.3 | 5.9 ± 4.1 |
| 2 | 42 (9.1) | 141.9 ± 111.1 | 331.6 ± 318.0 | 32.4 ± 16.6 | 8.4 ± 5.5 |
| 3 | 14 (3.0) | 203.1 ± 92.6 | 611.6 ± 332.9 | 45.4 ± 14.9 | 7.6 ± 3.6 |
| 4+ | 11 (2.4) | 261.0 ± 149.3 | 1277.1 ± 692.4 | 53.1 ± 18.9 | 11.1 ± 5.2 |
DISCUSSION
The practice of self-citation is widely prevalent among experienced orthopedic investigators. However, this practice seems to have minimal impact on the h-index for most investigators. Self-citation had a measurable impact on the h-index only after an investigator had many publications. At a mean of 87.9 ± 68.3 articles, investigators had a ∆h-index of 1. This represented a mean 5.9% increase. Overall, these findings underscore the utility of the h-index in assessing scholarly impact and ameliorate concerns over bibliometric manipulation.
Among a large group of experienced orthopedic investigators, self-citation has minimal effect on the h-index. Importantly, most investigators (63.7%) did not experience a full integer increase in their h-index. At a threshold of ∆ h-index increase of 1, investigators had impressive h-indices (24.0 ± 13.3), which eclipsed those of recent studies of hand surgeons (10.2 ± 9.9) and spine surgeons (13.6 ± 8.7).4,5 This finding suggests that committees for academic promotion in orthopedic surgery may disregard the impact of self-citation on the h-index. While the thresholds for promotion have not been defined in the orthopedic literature, a study in plastic surgery established an h-index threshold of 14.5 for promotion from associate to full professor.14 It may be, however, that h-indices are higher among orthopedic surgeons, as a previous study reported an h-index of 20 among full professors.15 Future research is needed to determine thresholds for promotion within orthopedic surgery, as the h-index varies by specialty according to unique citation patterns.
Continue to: It is worth highlighting...
It is worth highlighting the academic performance of NIH-funded PhD researchers in orthopedics. Even including training grant awardees in this group, this cohort exceeded the academic productivity of their orthopedic chairpersons, as measured by the h-index. Previous studies in urology, neurosurgery, and otolaryngology have demonstrated the impact of NIH-funding on academic productivity.8-10 Ultimately, orthopedic departments could increase academic productivity by recruiting more PhD investigators with NIH funding.
In contrast to academic radiology,16 this study demonstrated a correlation between the number of publications and the increase in h-index via self-citation. Several reasons may help explain this disparity. The first reason is a technical one, as at the time of this study, the Scopus database had been updated to include citations before 1996. Considering that the h-index increases over time as older publications are cited, the exclusion of older articles is a significant limitation of previous h-index studies. Applying the same logic, the mean h-index for chairpersons of 19.9 quoted in this study contradicts a recent study, which quoted a mean h-index of 15.3.3 This previous study utilized citations that were limited to articles published after 1996.
Previous work on self-citation in the field of orthopedics has been limited to its influence on journal impact factors. Our results build on this literature in several important ways. Firstly, the calculation of a journal’s impact factor is a highly scrutinized process, and authors have criticized the mechanisms employed by editors to inflate impact factors.17 One study reported that 20% of authors have been encouraged to cite a journal during the revision process.18 Self-citation practices have been demonstrated in journals of cardiology,19 diabetes,20 anesthesia,21 and medicine.22 A study using a hypothetical model to assess the maximum potential for h-index increase by self-citation demonstrated an h-index inflation of 5 points over 20 years (5/14, 35.7%) by publishing 3 papers per year with 3 self-citations each.23 This study highlights a potential limitation of the h-index, but our study observed an h-index inflation of ≥4 in only 11 researchers (2.4%). Thus, results from our study ameliorate self-citation concerns in academic orthopedic surgery.
There are several limitations to this study that offer future areas of research. First, the validity of the h-index academic promotion in orthopedic surgery has not been evaluated. This was a motivation for the present study, and the authors have ongoing efforts to characterize the h-index in a larger cohort of orthopedic investigators. Importantly, an appropriate amount of self-citation was not established. It may be necessary for orthopedic researchers to cite their works as they become experts on a specific topic. Lastly, our analyses are prone to limitations inherent in the h-index, which does not account for author contribution or journal impact factors. Despite these limitations, we show that for most orthopedic researchers, the practice of self-citation does not impact the h-index.
In summary, self-citation is a widely prevalent practice among orthopedic investigators, but this practice has minimal impact on an author’s h-index. Approximately one third of orthopedic faculty in our study had a higher h-index due to self-citation. Greater h-index inflation through self-citation correlated with more publications. For the majority of orthopedic faculty, however, self-citation did not inflate the h-index, suggesting that promotional committees may disregard this concern when using the h-index as an adjunct measure for career advancement.
1. Atasoylu AA, Wright SM, Beasley BW, et al. Promotion criteria for clinician-educators. J Gen Intern Med. 2003;18(9):711-716.
2. Hirsch JE. An index to quantify an individual's scientific research output. Proc Natl Acad Sci U S A. 2005;102(46):16569-16572.
3. Stavrakis AI, Patel AD, Burke ZD, et al. The role of chairman and research director in influencing scholarly productivity and research funding in academic orthopaedic surgery. J Orthop Res. 2015;33(10)1407-1411. doi:10.1002/jor.22919.
4. Lopez J, Susarla SM, Swanson EW, Calotta N, Lifchez SD. The association of the H-index and academic rank among full-time academic hand surgeons affiliated with fellowship programs. J Hand Surg Am. 2015;40(7):1434-1441. doi:10.1016/j.jhsa.2015.03.026.
5. Schoenfeld AJ, Bhalla A, George J, Harris MB, Bono CM. Academic productivity and contributions to the literature among spine surgery fellowship faculty. Spine J. 2015;15(10)2126-2131. doi:10.1016/j.spinee.2015.03.026.
6. Jackson JB. Promotion at the Johns Hopkins School of Medicine. Johns Hopkins Medicine. https://www.hopkinsmedicine.org/gim/useful_links/PPC%20Promotion.pdf. Accessed February 1, 2015.
7. Appointments, promotion, and tenure. The Ohio State University School of Medicine. https://oaa.osu.edu/sites/default/files/uploads/governance-documents/college-of-medicine/surgery/Surgery_APT_5-20-14.pdf. Accessed February 1, 2015.
8. Colaco M, Svider PF, Mauro KM, Eloy JA, Jackson-Rosario I. Is there a relationship between National Institutes of Health funding and research impact on academic urology? J Urol .2013;190(3):999-1003. doi:10.1016/j.juro.2013.02.3186.
9. Svider PF, Husain Q, Folbe AJ, Couldwell WT, Liu JK, Eloy JA. Assessing National Institutes of Health funding and scholarly impact in neurological surgery. J Neurosurg. 2014;120(1):191-196. doi:10.3171/2013.8.JNS13938.
10. Svider PF, Mauro KM, Sanghvi S, Setzen M, Baredes S, Eloy JA. Is NIH funding predictive of greater research productivity and impact among academic otolaryngologists? Laryngoscope. 2013;123(1):118-122. doi:10.1002/lary.23659.
11. American Medical Association. FREIDA Online. http://www.ama-assn.org/ama/pub/education-careers/graduate-medical-education/freida-online.page? Accessed February 1, 2015.
12. NIH. Research Portfolio Online Reporting Tools. https://projectreporter.nih.gov/reporter.cfm. Accessed February 1, 2015.
13. Falagas ME, Pitsouni EI, Malietzis GA, Pappas G. Comparison of PubMed, Scopus, Web of Science, and Google Scholar: strengths and weaknesses. FASEB Journal. 2008;22(2):338-342. doi:10.1096/fj.07-9492LSF.
14. Gast KM, Kuzon WM Jr, Waljee JF. Bibliometric indices and academic promotion within plastic surgery. Plast Reconstr Surg. 2014;134(5):838e-844e. doi:10.1097/PRS.0000000000000594.
15. Svider PF, Pashkova AA, Choudhry Z, et al. Comparison of scholarly impact among surgical specialties: an examination of 2429 academic surgeons. Laryngoscope. 2013;123(4):884-889. doi:10.1002/lary.23951.
16. Rad AE, Shahgholi L, Kallmes D. Impact of self-citation on the H index in the field of academic radiology. Acad Radiol. 2012;19(4):455-457. doi:10.1016/j.acra.2011.11.013.
17. Hakkalamani S, Rawal A, Hennessy MS, Parkinson RW. The impact factor of seven orthopaedic journals: factors influencing it. J Bone Joint Surg Br. 2006;88(2):159-162. doi:10.1302/0301-620X.88B2.16983.
18. Foley JA, Della Sala S. The impact of self-citation. Cortex. 2010;46(6):802-810. doi:10.1016/j.cortex.2010.01.004.
19. Opthof T. Inflation of impact factors by journal self-citation in cardiovascular science. Neth Heart J. 2013;21(4):163-165. doi:10.1007/s12471-013-0384-0.
20. Gami AS, Montori VM, Wilczynski NL, Haynes RB. Author self-citation in the diabetes literature. CMAJ. 2004;170(13):1925-1927.
21. Fassoulaki A, Paraskeva A, Papilas K, Karabinis G. Self-citations in six anaesthesia journals and their significance in determining the impact factor. Br J Anaesth. 2000;84(2):266-269.
22. Kulkarni AV, Aziz B, Shams I, Busse JW. Author self-citation in the general medicine literature. PloS One. 2011;6(6): e20885. doi:10.1371/journal.pone.0020885.
23. Bartneck C, Kokkelmans S. Detecting h-index manipulation through self-citation analysis. Scientometrics. 2011;87(1):85-98. doi:10.1007/s11192-010-0306-5.
ABSTRACT
The h-index is a commonly utilized metric for academic productivity. Previous studies have proposed that self-citation may limit the utility of the h-index. The purpose of this study is to evaluate the impact of self-citation on the h-index among orthopedic investigators. The study cohort consisted of program directors, chairpersons, and faculty at orthopedic surgery residency programs in the United States. The Scopus database was used to determine the h-index and number of citations ± self-citations. The total number of publications was correlated with the change in the h-index via self-citation. A total of 463 researchers were included (198 National Institutes of Health-funded faculty, 147 chairpersons, 118 program directors). Of these researchers, 83.8% cited previous work at least once (mean, 123.9 ± 277.6). Self-citations accounted for 5.8% of all citations. Including these citations increased the author h-index from 18.5 ± 14.9 to 19.2 ± 15.6 (P < .001). A minority of researchers (36.3%, P < .001) had increased their h-index via self-citation (range, 0-11). The proportional increase in the h-index via self-citation was positively related to the number of publications (P < .001). While the practice of self-citation is prevalent in orthopedics, its impact on the h-index is minimal for most researchers. With more publications, researchers can increase their h-index to a greater degree via self-citation.
Continue to: The competitive nature of academic research...
The competitive nature of academic research requires objective metrics to define career end points, such as promotion and funding procurement. While various criteria are used to assess performance in academia, publications and research funding are particularly regarded.1 Quantifying research dollars is relatively straightforward, but measuring research productivity is more complex. Not all articles are created equal, and disparities exist regarding effort and the ultimate impact of articles. In 2005, a physicist created the h-index to measure both research impact and productivity.2 As a bibliometric, the h-index equals the number of publications h that have been cited at least h times. Given its simplicity, the h-index has gained wide popularity in diverse medical specialties, including orthopedic surgery.3 Other recent studies have applied the h-index to hand surgery and spine surgery.4,5
Importantly, some authors have raised concerns regarding potential limitations of the h-index. One potentially significant limitation is the ability of authors to artificially inflate their h-index via self-citation. The impact of this practice is of particular interest as the h-index becomes widely adopted as a metric for promotion at many academic institutions.6-7 Furthermore, scholarly productivity has remained a critical component of successful grant funding procurement, and future grant funding applications may evaluate the h-index.8-10
The purpose of this study is to determine the prevalence and impact of self-citation on the h-index in a large cohort of orthopedic investigators. Given their high level of investment in academic orthopedic surgery, we focused on program directors, chairpersons, and National Institutes of Health (NIH)-funded research faculty at orthopedic surgery residency programs.
METHODS
INCLUSION CRITERIA
This study qualified as non-human and non-animal research and received exemption per the standing policy of the Institutional Review Board. The Fellowship and Residency Electronic Interactive Database (FREIDA) was accessed to generate a list of orthopedic residency program directors.11 This database was also used to generate a list of allopathic orthopedic surgery residency programs. Official program websites were accessed to generate a list of orthopedic chairpersons. Lastly, the NIH RePORTER was used to generate a list of basic science orthopedic investigators who received funding anytime during 2011 to 2014.12 This methodology was used due to the lack of reporting of basic science investigators on program websites. A list of NIH-funded orthopedic investigators was cross-referenced via an online search to isolate a cohort of PhD investigators.
Orthopedic faculty were defined as chairpersons, program directors, or NIH-funded investigators. In cases of overlap, preference was given in that order. Orthopedic investigators who had not published an article after 1995 were excluded (6 chairpersons, 1 program director).
BIBLIOMETRIC ANALYSIS
While several resources exist to calculate the h-index, the Scopus database (Elsevier) is one of the easiest programs to use.13 Author entries are created via institutional affiliations, thereby alleviating the need for manual reconciliations. Investigators were identified on Scopus via “author last name” and “first name, middle initial.” For each author, publications were screened for relevance to the field of orthopedics. Affiliated institutions were cross-referenced with information obtained from individual program websites. The “view h-graph” feature was used to calculate the number of publications, h-index, and number of citations. Then, the “Exclude self-citations” feature was used to calculate the number of corrected citations and the h-index excluding self-citations. Metrics were calculated over a 2-day period.
Continue to: STATISTICAL ANALYSIS
STATISTICAL ANALYSIS
Bibliometric analyses were presented descriptively with means ± standard deviation. After testing for normality, differences in the h-index between groups were assessed via analysis of variance tests. The proportional increase in the number of citations and the h-index were calculated by dividing the difference between the before and after exclusion of self-citations by the total number of citations before exclusion. The relationship between the number of publications and the proportional change in the h-index was assessed via calculation of the Spearman correlation coefficient. The independent variable was the number of publications, and the proportional increase in the h-index via self-citation was the dependent variable. Statistical tests were performed on STATA 13 (StataCorp) and the results considered significant if P < .05. Figures were created using GraphPad Prism 6.02 Software.
RESULTS
A total of 463 orthopedic investigators were included (147 chairpersons, 118 program directors, and 198 NIH-funded faculty) (Table 1). On average, these researchers produced 72.3 ± 83.0 articles and referenced 2139 ± 3222 articles (mean, 29.6 references per article). The cumulative h-index was 19.2 ± 15.6, and was the highest among NIH-funded researchers (24.3 ± 17.0) (P < .001). In all, 83.8% of orthopedic investigators self-cited their previous work at least once, and the total number of self-citations was highest among NIH-funded investigators (221 ± 355) (P < .001). After these self-citations were excluded, the h-index changed by 0.6 ± 1.1 for all investigators, and this change was greatest among NIH-funded researchers (1.1 ± 1.3) (P < .001).
Table 1. Effect of Self-Citation on NIH-funded Investigators, Chairpersons, and Program Directors in Orthopedics
| Investigator | N (%) | Articles, n (mean ± SD) |
Total Citations (mean ± SD)
| h-index | Self-Citations (mean ± SD) | Corrected h-index | ∆ h-index |
| NIH-funded | 198 (42.8) | 87.6 ± 84.9 | 3086 ± 3799 | 24.3 ± 17.0 | 221 ± 355 | 23.2 ± 16.3 | 1.1 ± 1.3 |
| Chairperson | 147 (31.7) | 85.3 ± 95.5 | 2151 ± 3098 | 19.9 ± 15.0 | 85.2 ± 221 | 19.5 ± 14.5 | 0.4 ± 0.8 |
| Program Director | 118 (25.5) | 30.5 ± 35.9 | 536.8 ± 785 | 9.6 ± 7.2 | 8.8 ± 19.9 | 9.5 ± 7.1 | 0.1 ± 0.3 |
| Total | 463 (100) | 72.3 ± 83.0 | 2139 ± 3222 | 19.2 ± 15.6 | 123.9 ± 277.6 | 18.5 ± 14.9 | 0.6 ± 1.1 |
Abbreviation: NIH, National Institutes of Health.
Most orthopedic investigators did not increase their h-index via self-citation (63.7%, P < .001). Table 2 categorizes investigators by changes in their h-index after excluding self-citations (range, 0-11). The maximal change in the h-index was seen in the most prolific group of investigators, who produced 261.0 ± 149.3 articles. In this group, the h-index increased by 11.1% ± 5.2%. The Figure investigates the relationship between the number of articles and the proportional increase in the h-index. The number of publications was positively correlated with the change in h-index after self-citations were excluded (r = 0.448, P < .001).
Table 2. Stratification of Orthopedic Researcher Investigators by Change in h-index After Self-Citation
∆ h-index
| N (%) |
Articles (mean ± SD)
| Self-Citations (mean ± SD) |
h-index (mean ± SD) | % Increase in h-index |
| 0 | 295 (63.7) | 43.8 ± 51.3 | 27.6 ± 58.4 | 13.1 ± 10.7 | 0 |
| 1 | 101 (21.8) | 87.9 ± 68.3 | 126.0 ± 130.6 | 24.0 ± 13.3 | 5.9 ± 4.1 |
| 2 | 42 (9.1) | 141.9 ± 111.1 | 331.6 ± 318.0 | 32.4 ± 16.6 | 8.4 ± 5.5 |
| 3 | 14 (3.0) | 203.1 ± 92.6 | 611.6 ± 332.9 | 45.4 ± 14.9 | 7.6 ± 3.6 |
| 4+ | 11 (2.4) | 261.0 ± 149.3 | 1277.1 ± 692.4 | 53.1 ± 18.9 | 11.1 ± 5.2 |
DISCUSSION
The practice of self-citation is widely prevalent among experienced orthopedic investigators. However, this practice seems to have minimal impact on the h-index for most investigators. Self-citation had a measurable impact on the h-index only after an investigator had many publications. At a mean of 87.9 ± 68.3 articles, investigators had a ∆h-index of 1. This represented a mean 5.9% increase. Overall, these findings underscore the utility of the h-index in assessing scholarly impact and ameliorate concerns over bibliometric manipulation.
Among a large group of experienced orthopedic investigators, self-citation has minimal effect on the h-index. Importantly, most investigators (63.7%) did not experience a full integer increase in their h-index. At a threshold of ∆ h-index increase of 1, investigators had impressive h-indices (24.0 ± 13.3), which eclipsed those of recent studies of hand surgeons (10.2 ± 9.9) and spine surgeons (13.6 ± 8.7).4,5 This finding suggests that committees for academic promotion in orthopedic surgery may disregard the impact of self-citation on the h-index. While the thresholds for promotion have not been defined in the orthopedic literature, a study in plastic surgery established an h-index threshold of 14.5 for promotion from associate to full professor.14 It may be, however, that h-indices are higher among orthopedic surgeons, as a previous study reported an h-index of 20 among full professors.15 Future research is needed to determine thresholds for promotion within orthopedic surgery, as the h-index varies by specialty according to unique citation patterns.
Continue to: It is worth highlighting...
It is worth highlighting the academic performance of NIH-funded PhD researchers in orthopedics. Even including training grant awardees in this group, this cohort exceeded the academic productivity of their orthopedic chairpersons, as measured by the h-index. Previous studies in urology, neurosurgery, and otolaryngology have demonstrated the impact of NIH-funding on academic productivity.8-10 Ultimately, orthopedic departments could increase academic productivity by recruiting more PhD investigators with NIH funding.
In contrast to academic radiology,16 this study demonstrated a correlation between the number of publications and the increase in h-index via self-citation. Several reasons may help explain this disparity. The first reason is a technical one, as at the time of this study, the Scopus database had been updated to include citations before 1996. Considering that the h-index increases over time as older publications are cited, the exclusion of older articles is a significant limitation of previous h-index studies. Applying the same logic, the mean h-index for chairpersons of 19.9 quoted in this study contradicts a recent study, which quoted a mean h-index of 15.3.3 This previous study utilized citations that were limited to articles published after 1996.
Previous work on self-citation in the field of orthopedics has been limited to its influence on journal impact factors. Our results build on this literature in several important ways. Firstly, the calculation of a journal’s impact factor is a highly scrutinized process, and authors have criticized the mechanisms employed by editors to inflate impact factors.17 One study reported that 20% of authors have been encouraged to cite a journal during the revision process.18 Self-citation practices have been demonstrated in journals of cardiology,19 diabetes,20 anesthesia,21 and medicine.22 A study using a hypothetical model to assess the maximum potential for h-index increase by self-citation demonstrated an h-index inflation of 5 points over 20 years (5/14, 35.7%) by publishing 3 papers per year with 3 self-citations each.23 This study highlights a potential limitation of the h-index, but our study observed an h-index inflation of ≥4 in only 11 researchers (2.4%). Thus, results from our study ameliorate self-citation concerns in academic orthopedic surgery.
There are several limitations to this study that offer future areas of research. First, the validity of the h-index academic promotion in orthopedic surgery has not been evaluated. This was a motivation for the present study, and the authors have ongoing efforts to characterize the h-index in a larger cohort of orthopedic investigators. Importantly, an appropriate amount of self-citation was not established. It may be necessary for orthopedic researchers to cite their works as they become experts on a specific topic. Lastly, our analyses are prone to limitations inherent in the h-index, which does not account for author contribution or journal impact factors. Despite these limitations, we show that for most orthopedic researchers, the practice of self-citation does not impact the h-index.
In summary, self-citation is a widely prevalent practice among orthopedic investigators, but this practice has minimal impact on an author’s h-index. Approximately one third of orthopedic faculty in our study had a higher h-index due to self-citation. Greater h-index inflation through self-citation correlated with more publications. For the majority of orthopedic faculty, however, self-citation did not inflate the h-index, suggesting that promotional committees may disregard this concern when using the h-index as an adjunct measure for career advancement.
ABSTRACT
The h-index is a commonly utilized metric for academic productivity. Previous studies have proposed that self-citation may limit the utility of the h-index. The purpose of this study is to evaluate the impact of self-citation on the h-index among orthopedic investigators. The study cohort consisted of program directors, chairpersons, and faculty at orthopedic surgery residency programs in the United States. The Scopus database was used to determine the h-index and number of citations ± self-citations. The total number of publications was correlated with the change in the h-index via self-citation. A total of 463 researchers were included (198 National Institutes of Health-funded faculty, 147 chairpersons, 118 program directors). Of these researchers, 83.8% cited previous work at least once (mean, 123.9 ± 277.6). Self-citations accounted for 5.8% of all citations. Including these citations increased the author h-index from 18.5 ± 14.9 to 19.2 ± 15.6 (P < .001). A minority of researchers (36.3%, P < .001) had increased their h-index via self-citation (range, 0-11). The proportional increase in the h-index via self-citation was positively related to the number of publications (P < .001). While the practice of self-citation is prevalent in orthopedics, its impact on the h-index is minimal for most researchers. With more publications, researchers can increase their h-index to a greater degree via self-citation.
Continue to: The competitive nature of academic research...
The competitive nature of academic research requires objective metrics to define career end points, such as promotion and funding procurement. While various criteria are used to assess performance in academia, publications and research funding are particularly regarded.1 Quantifying research dollars is relatively straightforward, but measuring research productivity is more complex. Not all articles are created equal, and disparities exist regarding effort and the ultimate impact of articles. In 2005, a physicist created the h-index to measure both research impact and productivity.2 As a bibliometric, the h-index equals the number of publications h that have been cited at least h times. Given its simplicity, the h-index has gained wide popularity in diverse medical specialties, including orthopedic surgery.3 Other recent studies have applied the h-index to hand surgery and spine surgery.4,5
Importantly, some authors have raised concerns regarding potential limitations of the h-index. One potentially significant limitation is the ability of authors to artificially inflate their h-index via self-citation. The impact of this practice is of particular interest as the h-index becomes widely adopted as a metric for promotion at many academic institutions.6-7 Furthermore, scholarly productivity has remained a critical component of successful grant funding procurement, and future grant funding applications may evaluate the h-index.8-10
The purpose of this study is to determine the prevalence and impact of self-citation on the h-index in a large cohort of orthopedic investigators. Given their high level of investment in academic orthopedic surgery, we focused on program directors, chairpersons, and National Institutes of Health (NIH)-funded research faculty at orthopedic surgery residency programs.
METHODS
INCLUSION CRITERIA
This study qualified as non-human and non-animal research and received exemption per the standing policy of the Institutional Review Board. The Fellowship and Residency Electronic Interactive Database (FREIDA) was accessed to generate a list of orthopedic residency program directors.11 This database was also used to generate a list of allopathic orthopedic surgery residency programs. Official program websites were accessed to generate a list of orthopedic chairpersons. Lastly, the NIH RePORTER was used to generate a list of basic science orthopedic investigators who received funding anytime during 2011 to 2014.12 This methodology was used due to the lack of reporting of basic science investigators on program websites. A list of NIH-funded orthopedic investigators was cross-referenced via an online search to isolate a cohort of PhD investigators.
Orthopedic faculty were defined as chairpersons, program directors, or NIH-funded investigators. In cases of overlap, preference was given in that order. Orthopedic investigators who had not published an article after 1995 were excluded (6 chairpersons, 1 program director).
BIBLIOMETRIC ANALYSIS
While several resources exist to calculate the h-index, the Scopus database (Elsevier) is one of the easiest programs to use.13 Author entries are created via institutional affiliations, thereby alleviating the need for manual reconciliations. Investigators were identified on Scopus via “author last name” and “first name, middle initial.” For each author, publications were screened for relevance to the field of orthopedics. Affiliated institutions were cross-referenced with information obtained from individual program websites. The “view h-graph” feature was used to calculate the number of publications, h-index, and number of citations. Then, the “Exclude self-citations” feature was used to calculate the number of corrected citations and the h-index excluding self-citations. Metrics were calculated over a 2-day period.
Continue to: STATISTICAL ANALYSIS
STATISTICAL ANALYSIS
Bibliometric analyses were presented descriptively with means ± standard deviation. After testing for normality, differences in the h-index between groups were assessed via analysis of variance tests. The proportional increase in the number of citations and the h-index were calculated by dividing the difference between the before and after exclusion of self-citations by the total number of citations before exclusion. The relationship between the number of publications and the proportional change in the h-index was assessed via calculation of the Spearman correlation coefficient. The independent variable was the number of publications, and the proportional increase in the h-index via self-citation was the dependent variable. Statistical tests were performed on STATA 13 (StataCorp) and the results considered significant if P < .05. Figures were created using GraphPad Prism 6.02 Software.
RESULTS
A total of 463 orthopedic investigators were included (147 chairpersons, 118 program directors, and 198 NIH-funded faculty) (Table 1). On average, these researchers produced 72.3 ± 83.0 articles and referenced 2139 ± 3222 articles (mean, 29.6 references per article). The cumulative h-index was 19.2 ± 15.6, and was the highest among NIH-funded researchers (24.3 ± 17.0) (P < .001). In all, 83.8% of orthopedic investigators self-cited their previous work at least once, and the total number of self-citations was highest among NIH-funded investigators (221 ± 355) (P < .001). After these self-citations were excluded, the h-index changed by 0.6 ± 1.1 for all investigators, and this change was greatest among NIH-funded researchers (1.1 ± 1.3) (P < .001).
Table 1. Effect of Self-Citation on NIH-funded Investigators, Chairpersons, and Program Directors in Orthopedics
| Investigator | N (%) | Articles, n (mean ± SD) |
Total Citations (mean ± SD)
| h-index | Self-Citations (mean ± SD) | Corrected h-index | ∆ h-index |
| NIH-funded | 198 (42.8) | 87.6 ± 84.9 | 3086 ± 3799 | 24.3 ± 17.0 | 221 ± 355 | 23.2 ± 16.3 | 1.1 ± 1.3 |
| Chairperson | 147 (31.7) | 85.3 ± 95.5 | 2151 ± 3098 | 19.9 ± 15.0 | 85.2 ± 221 | 19.5 ± 14.5 | 0.4 ± 0.8 |
| Program Director | 118 (25.5) | 30.5 ± 35.9 | 536.8 ± 785 | 9.6 ± 7.2 | 8.8 ± 19.9 | 9.5 ± 7.1 | 0.1 ± 0.3 |
| Total | 463 (100) | 72.3 ± 83.0 | 2139 ± 3222 | 19.2 ± 15.6 | 123.9 ± 277.6 | 18.5 ± 14.9 | 0.6 ± 1.1 |
Abbreviation: NIH, National Institutes of Health.
Most orthopedic investigators did not increase their h-index via self-citation (63.7%, P < .001). Table 2 categorizes investigators by changes in their h-index after excluding self-citations (range, 0-11). The maximal change in the h-index was seen in the most prolific group of investigators, who produced 261.0 ± 149.3 articles. In this group, the h-index increased by 11.1% ± 5.2%. The Figure investigates the relationship between the number of articles and the proportional increase in the h-index. The number of publications was positively correlated with the change in h-index after self-citations were excluded (r = 0.448, P < .001).
Table 2. Stratification of Orthopedic Researcher Investigators by Change in h-index After Self-Citation
∆ h-index
| N (%) |
Articles (mean ± SD)
| Self-Citations (mean ± SD) |
h-index (mean ± SD) | % Increase in h-index |
| 0 | 295 (63.7) | 43.8 ± 51.3 | 27.6 ± 58.4 | 13.1 ± 10.7 | 0 |
| 1 | 101 (21.8) | 87.9 ± 68.3 | 126.0 ± 130.6 | 24.0 ± 13.3 | 5.9 ± 4.1 |
| 2 | 42 (9.1) | 141.9 ± 111.1 | 331.6 ± 318.0 | 32.4 ± 16.6 | 8.4 ± 5.5 |
| 3 | 14 (3.0) | 203.1 ± 92.6 | 611.6 ± 332.9 | 45.4 ± 14.9 | 7.6 ± 3.6 |
| 4+ | 11 (2.4) | 261.0 ± 149.3 | 1277.1 ± 692.4 | 53.1 ± 18.9 | 11.1 ± 5.2 |
DISCUSSION
The practice of self-citation is widely prevalent among experienced orthopedic investigators. However, this practice seems to have minimal impact on the h-index for most investigators. Self-citation had a measurable impact on the h-index only after an investigator had many publications. At a mean of 87.9 ± 68.3 articles, investigators had a ∆h-index of 1. This represented a mean 5.9% increase. Overall, these findings underscore the utility of the h-index in assessing scholarly impact and ameliorate concerns over bibliometric manipulation.
Among a large group of experienced orthopedic investigators, self-citation has minimal effect on the h-index. Importantly, most investigators (63.7%) did not experience a full integer increase in their h-index. At a threshold of ∆ h-index increase of 1, investigators had impressive h-indices (24.0 ± 13.3), which eclipsed those of recent studies of hand surgeons (10.2 ± 9.9) and spine surgeons (13.6 ± 8.7).4,5 This finding suggests that committees for academic promotion in orthopedic surgery may disregard the impact of self-citation on the h-index. While the thresholds for promotion have not been defined in the orthopedic literature, a study in plastic surgery established an h-index threshold of 14.5 for promotion from associate to full professor.14 It may be, however, that h-indices are higher among orthopedic surgeons, as a previous study reported an h-index of 20 among full professors.15 Future research is needed to determine thresholds for promotion within orthopedic surgery, as the h-index varies by specialty according to unique citation patterns.
Continue to: It is worth highlighting...
It is worth highlighting the academic performance of NIH-funded PhD researchers in orthopedics. Even including training grant awardees in this group, this cohort exceeded the academic productivity of their orthopedic chairpersons, as measured by the h-index. Previous studies in urology, neurosurgery, and otolaryngology have demonstrated the impact of NIH-funding on academic productivity.8-10 Ultimately, orthopedic departments could increase academic productivity by recruiting more PhD investigators with NIH funding.
In contrast to academic radiology,16 this study demonstrated a correlation between the number of publications and the increase in h-index via self-citation. Several reasons may help explain this disparity. The first reason is a technical one, as at the time of this study, the Scopus database had been updated to include citations before 1996. Considering that the h-index increases over time as older publications are cited, the exclusion of older articles is a significant limitation of previous h-index studies. Applying the same logic, the mean h-index for chairpersons of 19.9 quoted in this study contradicts a recent study, which quoted a mean h-index of 15.3.3 This previous study utilized citations that were limited to articles published after 1996.
Previous work on self-citation in the field of orthopedics has been limited to its influence on journal impact factors. Our results build on this literature in several important ways. Firstly, the calculation of a journal’s impact factor is a highly scrutinized process, and authors have criticized the mechanisms employed by editors to inflate impact factors.17 One study reported that 20% of authors have been encouraged to cite a journal during the revision process.18 Self-citation practices have been demonstrated in journals of cardiology,19 diabetes,20 anesthesia,21 and medicine.22 A study using a hypothetical model to assess the maximum potential for h-index increase by self-citation demonstrated an h-index inflation of 5 points over 20 years (5/14, 35.7%) by publishing 3 papers per year with 3 self-citations each.23 This study highlights a potential limitation of the h-index, but our study observed an h-index inflation of ≥4 in only 11 researchers (2.4%). Thus, results from our study ameliorate self-citation concerns in academic orthopedic surgery.
There are several limitations to this study that offer future areas of research. First, the validity of the h-index academic promotion in orthopedic surgery has not been evaluated. This was a motivation for the present study, and the authors have ongoing efforts to characterize the h-index in a larger cohort of orthopedic investigators. Importantly, an appropriate amount of self-citation was not established. It may be necessary for orthopedic researchers to cite their works as they become experts on a specific topic. Lastly, our analyses are prone to limitations inherent in the h-index, which does not account for author contribution or journal impact factors. Despite these limitations, we show that for most orthopedic researchers, the practice of self-citation does not impact the h-index.
In summary, self-citation is a widely prevalent practice among orthopedic investigators, but this practice has minimal impact on an author’s h-index. Approximately one third of orthopedic faculty in our study had a higher h-index due to self-citation. Greater h-index inflation through self-citation correlated with more publications. For the majority of orthopedic faculty, however, self-citation did not inflate the h-index, suggesting that promotional committees may disregard this concern when using the h-index as an adjunct measure for career advancement.
1. Atasoylu AA, Wright SM, Beasley BW, et al. Promotion criteria for clinician-educators. J Gen Intern Med. 2003;18(9):711-716.
2. Hirsch JE. An index to quantify an individual's scientific research output. Proc Natl Acad Sci U S A. 2005;102(46):16569-16572.
3. Stavrakis AI, Patel AD, Burke ZD, et al. The role of chairman and research director in influencing scholarly productivity and research funding in academic orthopaedic surgery. J Orthop Res. 2015;33(10)1407-1411. doi:10.1002/jor.22919.
4. Lopez J, Susarla SM, Swanson EW, Calotta N, Lifchez SD. The association of the H-index and academic rank among full-time academic hand surgeons affiliated with fellowship programs. J Hand Surg Am. 2015;40(7):1434-1441. doi:10.1016/j.jhsa.2015.03.026.
5. Schoenfeld AJ, Bhalla A, George J, Harris MB, Bono CM. Academic productivity and contributions to the literature among spine surgery fellowship faculty. Spine J. 2015;15(10)2126-2131. doi:10.1016/j.spinee.2015.03.026.
6. Jackson JB. Promotion at the Johns Hopkins School of Medicine. Johns Hopkins Medicine. https://www.hopkinsmedicine.org/gim/useful_links/PPC%20Promotion.pdf. Accessed February 1, 2015.
7. Appointments, promotion, and tenure. The Ohio State University School of Medicine. https://oaa.osu.edu/sites/default/files/uploads/governance-documents/college-of-medicine/surgery/Surgery_APT_5-20-14.pdf. Accessed February 1, 2015.
8. Colaco M, Svider PF, Mauro KM, Eloy JA, Jackson-Rosario I. Is there a relationship between National Institutes of Health funding and research impact on academic urology? J Urol .2013;190(3):999-1003. doi:10.1016/j.juro.2013.02.3186.
9. Svider PF, Husain Q, Folbe AJ, Couldwell WT, Liu JK, Eloy JA. Assessing National Institutes of Health funding and scholarly impact in neurological surgery. J Neurosurg. 2014;120(1):191-196. doi:10.3171/2013.8.JNS13938.
10. Svider PF, Mauro KM, Sanghvi S, Setzen M, Baredes S, Eloy JA. Is NIH funding predictive of greater research productivity and impact among academic otolaryngologists? Laryngoscope. 2013;123(1):118-122. doi:10.1002/lary.23659.
11. American Medical Association. FREIDA Online. http://www.ama-assn.org/ama/pub/education-careers/graduate-medical-education/freida-online.page? Accessed February 1, 2015.
12. NIH. Research Portfolio Online Reporting Tools. https://projectreporter.nih.gov/reporter.cfm. Accessed February 1, 2015.
13. Falagas ME, Pitsouni EI, Malietzis GA, Pappas G. Comparison of PubMed, Scopus, Web of Science, and Google Scholar: strengths and weaknesses. FASEB Journal. 2008;22(2):338-342. doi:10.1096/fj.07-9492LSF.
14. Gast KM, Kuzon WM Jr, Waljee JF. Bibliometric indices and academic promotion within plastic surgery. Plast Reconstr Surg. 2014;134(5):838e-844e. doi:10.1097/PRS.0000000000000594.
15. Svider PF, Pashkova AA, Choudhry Z, et al. Comparison of scholarly impact among surgical specialties: an examination of 2429 academic surgeons. Laryngoscope. 2013;123(4):884-889. doi:10.1002/lary.23951.
16. Rad AE, Shahgholi L, Kallmes D. Impact of self-citation on the H index in the field of academic radiology. Acad Radiol. 2012;19(4):455-457. doi:10.1016/j.acra.2011.11.013.
17. Hakkalamani S, Rawal A, Hennessy MS, Parkinson RW. The impact factor of seven orthopaedic journals: factors influencing it. J Bone Joint Surg Br. 2006;88(2):159-162. doi:10.1302/0301-620X.88B2.16983.
18. Foley JA, Della Sala S. The impact of self-citation. Cortex. 2010;46(6):802-810. doi:10.1016/j.cortex.2010.01.004.
19. Opthof T. Inflation of impact factors by journal self-citation in cardiovascular science. Neth Heart J. 2013;21(4):163-165. doi:10.1007/s12471-013-0384-0.
20. Gami AS, Montori VM, Wilczynski NL, Haynes RB. Author self-citation in the diabetes literature. CMAJ. 2004;170(13):1925-1927.
21. Fassoulaki A, Paraskeva A, Papilas K, Karabinis G. Self-citations in six anaesthesia journals and their significance in determining the impact factor. Br J Anaesth. 2000;84(2):266-269.
22. Kulkarni AV, Aziz B, Shams I, Busse JW. Author self-citation in the general medicine literature. PloS One. 2011;6(6): e20885. doi:10.1371/journal.pone.0020885.
23. Bartneck C, Kokkelmans S. Detecting h-index manipulation through self-citation analysis. Scientometrics. 2011;87(1):85-98. doi:10.1007/s11192-010-0306-5.
1. Atasoylu AA, Wright SM, Beasley BW, et al. Promotion criteria for clinician-educators. J Gen Intern Med. 2003;18(9):711-716.
2. Hirsch JE. An index to quantify an individual's scientific research output. Proc Natl Acad Sci U S A. 2005;102(46):16569-16572.
3. Stavrakis AI, Patel AD, Burke ZD, et al. The role of chairman and research director in influencing scholarly productivity and research funding in academic orthopaedic surgery. J Orthop Res. 2015;33(10)1407-1411. doi:10.1002/jor.22919.
4. Lopez J, Susarla SM, Swanson EW, Calotta N, Lifchez SD. The association of the H-index and academic rank among full-time academic hand surgeons affiliated with fellowship programs. J Hand Surg Am. 2015;40(7):1434-1441. doi:10.1016/j.jhsa.2015.03.026.
5. Schoenfeld AJ, Bhalla A, George J, Harris MB, Bono CM. Academic productivity and contributions to the literature among spine surgery fellowship faculty. Spine J. 2015;15(10)2126-2131. doi:10.1016/j.spinee.2015.03.026.
6. Jackson JB. Promotion at the Johns Hopkins School of Medicine. Johns Hopkins Medicine. https://www.hopkinsmedicine.org/gim/useful_links/PPC%20Promotion.pdf. Accessed February 1, 2015.
7. Appointments, promotion, and tenure. The Ohio State University School of Medicine. https://oaa.osu.edu/sites/default/files/uploads/governance-documents/college-of-medicine/surgery/Surgery_APT_5-20-14.pdf. Accessed February 1, 2015.
8. Colaco M, Svider PF, Mauro KM, Eloy JA, Jackson-Rosario I. Is there a relationship between National Institutes of Health funding and research impact on academic urology? J Urol .2013;190(3):999-1003. doi:10.1016/j.juro.2013.02.3186.
9. Svider PF, Husain Q, Folbe AJ, Couldwell WT, Liu JK, Eloy JA. Assessing National Institutes of Health funding and scholarly impact in neurological surgery. J Neurosurg. 2014;120(1):191-196. doi:10.3171/2013.8.JNS13938.
10. Svider PF, Mauro KM, Sanghvi S, Setzen M, Baredes S, Eloy JA. Is NIH funding predictive of greater research productivity and impact among academic otolaryngologists? Laryngoscope. 2013;123(1):118-122. doi:10.1002/lary.23659.
11. American Medical Association. FREIDA Online. http://www.ama-assn.org/ama/pub/education-careers/graduate-medical-education/freida-online.page? Accessed February 1, 2015.
12. NIH. Research Portfolio Online Reporting Tools. https://projectreporter.nih.gov/reporter.cfm. Accessed February 1, 2015.
13. Falagas ME, Pitsouni EI, Malietzis GA, Pappas G. Comparison of PubMed, Scopus, Web of Science, and Google Scholar: strengths and weaknesses. FASEB Journal. 2008;22(2):338-342. doi:10.1096/fj.07-9492LSF.
14. Gast KM, Kuzon WM Jr, Waljee JF. Bibliometric indices and academic promotion within plastic surgery. Plast Reconstr Surg. 2014;134(5):838e-844e. doi:10.1097/PRS.0000000000000594.
15. Svider PF, Pashkova AA, Choudhry Z, et al. Comparison of scholarly impact among surgical specialties: an examination of 2429 academic surgeons. Laryngoscope. 2013;123(4):884-889. doi:10.1002/lary.23951.
16. Rad AE, Shahgholi L, Kallmes D. Impact of self-citation on the H index in the field of academic radiology. Acad Radiol. 2012;19(4):455-457. doi:10.1016/j.acra.2011.11.013.
17. Hakkalamani S, Rawal A, Hennessy MS, Parkinson RW. The impact factor of seven orthopaedic journals: factors influencing it. J Bone Joint Surg Br. 2006;88(2):159-162. doi:10.1302/0301-620X.88B2.16983.
18. Foley JA, Della Sala S. The impact of self-citation. Cortex. 2010;46(6):802-810. doi:10.1016/j.cortex.2010.01.004.
19. Opthof T. Inflation of impact factors by journal self-citation in cardiovascular science. Neth Heart J. 2013;21(4):163-165. doi:10.1007/s12471-013-0384-0.
20. Gami AS, Montori VM, Wilczynski NL, Haynes RB. Author self-citation in the diabetes literature. CMAJ. 2004;170(13):1925-1927.
21. Fassoulaki A, Paraskeva A, Papilas K, Karabinis G. Self-citations in six anaesthesia journals and their significance in determining the impact factor. Br J Anaesth. 2000;84(2):266-269.
22. Kulkarni AV, Aziz B, Shams I, Busse JW. Author self-citation in the general medicine literature. PloS One. 2011;6(6): e20885. doi:10.1371/journal.pone.0020885.
23. Bartneck C, Kokkelmans S. Detecting h-index manipulation through self-citation analysis. Scientometrics. 2011;87(1):85-98. doi:10.1007/s11192-010-0306-5.
TAKE-HOME POINTS
- In all, 83.8% of orthopedic surgeons cite previous work at least once.
- Self-citations account for only 5.8% of all citations.
- Including self-citations increases the mean h-index from 18.5 ± 14.9 to 19.2 ± 15.6 (P < .001).
- The magnitude of increase in h-index via self-citation is proportional to the career number of publications.
- Overall, while prevalent, the practice of self-citation has minimal impact on an academic orthopedic surgeon’s h-index.
Managing Glenoid Bone Deficiency—The Augment Experience in Anatomic and Reverse Shoulder Arthroplasty
ABSTRACT
Glenoid bone deficiency in the setting of shoulder replacement surgery is far more common than originally reported. The frequency and severity of the glenoid defects are noted to be more common and severe with the advent of computer-assisted surgery. The results of an anatomic total shoulder arthroplasty (aTSA) with glenoid deficiency have been reported to be inferior to aTSA patients without a glenoid deficiency. Options for treating the glenoid deficiency include eccentric reaming, bone grafting, and the use of augmented glenoid components. The purpose of this article is to present the indications, technique, and results of augmented glenoids for both aTSA and reverse TSA (RTSA).
Augments for both aTSA and RTSA are viable options. They preserve subchondral bone at the same time as optimizing the joint line without the need for bone grafts. Complications, revisions and results are as good as compared to shoulder arthroplasties without glenoid wear.
Continue to: Glenoid bone deficiency...
Glenoid bone deficiency in arthritic or cuff-deficient shoulder has been reported in up to 50% of shoulder defect cases.1,2 The type and severity of glenoid deformities vary depending on the underlying pathology and time of manifestation. Osteoarthritis with bone loss typically results in posterior or posterior inferior glenoid wear and is commonly classified as Walch types B1 or B2 (biconcave). In cases of severe erosion, B3 classification has been proposed; in this classification, bone loss becomes extremely severe, progressing to resemble a type C glenoid. Unlike primary osteoarthritis, inflammatory arthropathy more commonly causes central loss of glenoid bone (Walch A2). With the rotator cuff insufficiency, superior migration of the humeral head occurs. As these conditions progress, cuff tear arthropathy (CTA) changes result in superior or posterior-superior bone loss.1 Anterior bone loss (type D) will be rarely encountered due to recurrent anterior instability.3
Classically, with anatomic total shoulder arthroplasty (aTSA), the surgeon considers several options for managing glenoid deficiencies. The most commonly employed technique involves eccentrically reaming the glenoid and correcting the deformity. This procedure is relatively easy but features significant drawbacks, such as sacrificing the subchondral bone, medializing the glenohumeral joint line, and secondarily shrinking the glenoid surface area. Other options include structural bone grafting behind the glenoid component. Most anatomic prosthetic glenoids prove to be unsuitable for fixation of structural bone graft. Therefore, the graft is first internally fixed, followed by placement of the glenoid component. Cement, which is commonly used for glenoid fixation, may potentially inhibit bone-graft healing. Reports using this technique documented high radiographic failure rate of up to 40% at midterm follow-up.4 Although leaving the glenoid component retroverted may be considered, surgeons should develop awareness of the possibility of peg penetration of the anterior glenoid neck. Additionally, retroversion in excess of 5°may increase the risk of recurrent posterior subluxation, resulting in early glenoid loosening.5-7 Results of aTSA under significant glenoid deficiency are inferior to those of aTSA patients without glenoid deficiency.8 Such findings have been extremely inferior in patients with significant glenoid wear, prompting numerous surgeons to abandon aTSA in this population in favor of reverse TSA (RTSA) due to improved bony fixation.
In 2010, augmented anatomic glenoids were first introduced as a wedge (Exactech) and as a step shortly thereafter (DePuy Synthes; Figures 1A-1C). More recently, hemi-wedges have been introduced (Wright Medical Group). Augments have gained popularity due to improved range of motion vs reverse shoulder arthroplasty (RSA). However, debates remain regarding the use of posteriorly augmented components in the setting of posterior glenoid bone loss.8 Augments serve as another viable option for handling glenoid bone deficiency in aTSA.
Glenoid bone loss in RTSA presents similar options to aTSA. However, screw fixation of the glenoid component offers several distinct advantages. Baseplate fixation can readily be used with bone grafting and with a highly anticipated success rate. With multiple screw options, 100% support of the baseplate is not mandatory. Although bony increase offset RSAs (BIO-RSAs) have shown success, augmentation with allograft or autograft increases operative time and relies on osseous integration for long-term implant success.9 Metal augmented baseplates were first introduced in 2011 (Exactech) as a means of managing glenoid bone loss without structural grafting. Although initial results have been encouraging, additional studies are needed to assess the longevity of these implants (Figures 1A-1C).
aTSA AUGMENTS
aTSA augments were introduced as a means of correcting acquired glenoid bone deficiency, restoring native glenoid version, correcting humeral subluxation, and preserving the native subchondral bone. Compared with glenoid bone grafting, augmented glenoid components decrease operative time, allow for a technically easier operation, and require no bone healing for clinical success. Early and midterm results are encouraging, showing similar findings comparable to those of aTSA in non-glenoid deficient shoulders.10-12
Continue to: INDICATIONS
INDICATIONS
Indications and limitations for augmented aTSA glenoids remain incompletely defined. The most common indication for an augmented aTSA is osteoarthritis with a B2 glenoid. We recommend augments in the occurrence of any indication of significant eccentric glenoid wear. With the expertise of surgeons, deformities of up to 20° to 25° of deformity can be readily handled with good predictability. More severe deformities can be managed with augmented aTSA components, but early failure rates may be high. The most severe acquired deformities remain best managed with RTSA. Currently, we prefer RTSA when glenoid bone loss exceeds 25°. With the widespread availability of computed tomography (CT) scans with 3-dimensional (3-D) reconstruction, glenoid bone defects are increasingly recognized. When correcting deformity, surgeons should strive to limit residual retroversion to a maximum of 5°.13 Preoperative planning software and computer-assisted surgery (ExactechGPS) may allow surgeons to better define the limits of augmented glenoid fixation prior to the date of surgery. We routinely utilize computer-guided glenoid preparation to control glenoid version to within 5° of neutral position.
The differences between B3 and a true type C glenoid must be recognized. Although B3 glenoids may still be a candidate for an augmented anatomic glenoid component, type C glenoids are not. Developmental abnormalities of type C glenoid occur simultaneously with humeral deformities, including medialized posterior rotator cuff musculature. Correction of the joint line to neutral version may not replicate the non-diseased state of a dysplastic type shoulder. Davis and colleagues14 have proposed treating these patients by leaving both the humerus and glenoid in their native version without correction.
TECHNIQUE
The implant that we have the most experience with is an 8° full-wedge augmented glenoid component. Such an implant is typically utilized for B2 glenoids. We recommend that a high-quality CT scan be performed for preoperative planning. As a general rule, the starting point often lies close to the ridge of B2 glenoid and more anterior than the apparent glenoid center, which is viewed intraoperatively due to asymmetric posterior wear. Full-wedge component is utilized to ream the ridge separating the neo and paleoglenoids to create a flat surface. This condition is best achieved by drilling a pilot hole at the planned glenoid central peg position to prevent the reamer from sliding anteriorly during reaming. Glenoid preparation begins with the smallest reamer until the ridge has been flattened, and the reamer makes full contact with the glenoid. The reamer diameter is then increased based on glenoid size. Slightly downsizing the glenoid implant will require less reaming to achieve full backside support. Once the glenoid is properly reamed, the central and peripheral peg holes are drilled using the appropriate guides. Holes are then dried, and all-polyethylene or composite glenoid component (either partially or completely cemented) is installed using favored cementing techniques. The advantage of composite glenoid component is that the central cage allows for bone ingrowth and may potentially improve long-term implant survival. Press fit of the central cage requires no waiting time for glenoid cement hardening before proceeding to the humerus. When placing an augmented component, adequate glenoid exposure is imperative to allow in-line placement and appropriate seating of the component without impingement on adjacent retractors.
When using the step-augmented glenoid, the paleoglenoid is prepared in a similar fashion to a standard aTSA. Once the paleoglenoid has been reamed to a neutral position, a protector plate is placed onto the paleoglenoid. and a step-cut saw is used to prepare the posterior stepped bone cut. Peripheral pegs are then drilled, and the component is installed in routine fashion. When using hemi-wedge augments, the paleoglenoid is again prepared in a similar fashion as a standard glenoid component over a cannulated guidewire. The neoglenoid is subsequently prepared using a specialized angled reamer with a positive stop to prevent over-reaming. These glenoid implants improve rotational force neutralization given the absence of flat back against the glenoid. All 3 designs preserve bone when compared with eccentric reaming alone,15 with the half-augmented wedge preserving the most bone.
Table 1. Results of Various Augmented Glenoid Components in Anatomic Total Shoulder
Arthroplasty
| Augment | American Shoulder and Elbow Surgeons Score | Constant Score | Active Forward Flexion | Active External Rotation | ||||||||||||||||
8° cage (N = 21) |
|
|
|
|
| |||||||||||||||
All-polyethylene 8° (N = 45) |
|
|
|
|
| |||||||||||||||
All-polyethylene 16° (N = 7) |
|
|
|
|
|
RESULTS
In our institution, we first used all-polyethylene posteriorly augmented glenoid components in 2010. Between 2010 and 2015, 45 patients received an 8° all-polyethylene posterior augment, and 7 patients received a 16° augment. In 2015, we transitioned to the composite caged posterior augment. All patients in our database who received an augmented glenoid component experienced improvement in active forward elevation, external rotation, American Shoulder and Elbow Surgeons (ASES), and Constant scores (Table 1). Minimum follow-up was 1 year for patients receiving both an 8° cage (mean, 1.48 years) and an 8° all-polyethylene augment (mean, 3.18 years). Figures 2A-2C show a patient with significant posterior glenoid wear and humeral head subluxation treated with an 8° wedge composite posterior augment glenoid 3 years postoperative.
Continue to: COMPLICATIONS
COMPLICATIONS
Two complications developed in the group undergoing composite cage augment. One patient experienced glenoid loosening after a motor vehicle accident. Another patient sustained significant intraoperative tuberosity avulsion during implantation of the humeral component, requiring a change of implant and tuberosity fixation. Although no complications were noted in the 8° all-polyethylene group, 3 patients in the 16° augment group sustained complications. One of these patients suffered a cardiac event that was unrelated to the implant. Two complications in this group were both related to loosening of the glenoid component, requiring subsequent revision.
DISCUSSION
The first report on augmented aTSA was published in 2008, and it involved a 5° augmented, anatomic glenoid.12 One study was based on a small series of augments; the poor results led the reporting surgeons to subsequently abandon the implant.12 This early design produced a correction on the articular side of the implant rather than the pathologic bony side. By performing such correction, the component pegs remained anteriorly oriented, placing the component at risk of perforation through the anterior glenoid neck. All current augment designs feature pegs that are oriented down the glenoid vault, with corrections occurring on the bony surface. This condition requires 2 different axes for reaming the glenoid and drilling the pegs. This approach allows the pegs to be directed down the glenoid neck, and is a far superior solution to neutralizing shear forces when compared with the implants used in the 1990s.
Early to midterm results of modern aTSA augments have been extremely encouraging with low revision rates. The main concern of recurrent posterior subluxation has been rarely reported. The concerns over glenoid loosening due to high shear forces, similarly, have not been described to date. However, surgeons should remain cautious, as longer-term follow-up remains unavailable.
The main advantage of aTSA augments is their capacity to preserve bone compared with eccentric reaming and better long-term stability. Each of the augment designs requires varying amounts of bone removal. Through biomechanics and using finite element analysis, the 3 augment types act differently, with no design demonstrating remarkable biomechanical superiority.6 Favorito and colleagues16 performed a retrospective review of 22 patients who underwent aTSA using an all-polyethylene, posteriorly augmented, and stepped glenoid component for posterior bone loss. At an average follow-up of 36 months, all patients experienced improvements in active forward elevation, external rotation, visual analog scale, Short Form-36 Physical Component Summary, and Western Ontario Osteoarthritis of the Shoulder scores. The authors noted that 2 patients (9%) experienced complications: 1 with an anterior dislocation and the other with recurrent posterior instability requiring revision. Sandow and Schutz17 reported the preliminary results of 10 patients who underwent aTSA using trabecular metal augment with a minimum of 2-year follow-up. All patients received either a 15° or 30° posterior, metal-backed augment for severe glenoid bone loss (Walch grade B2 or C). At a minimum of 2-year follow-up, all patients received correction to within 10° of neutral glenoid version, without any complications nor implant failures.
Regardless of augment design, all current components restore the native glenoid version, improving the length and subsequent tension of rotator cuff musculature. Similarly, re-centering the humeral head decreases the forces on the glenoid and allows for optimal function with decreasing loss of vital subchondral bone.
Continue to: RTSA AUGMENTS
RTSA AUGMENTS
Similar to anatomic augments, metal augments were introduced for use with RTSA in 2011. Unlike anatomic augments, those for RTSA were manufactured with metal. Given the difference in bony wear patterns in patients requiring RTSA, augments were available in a number of configurations. With CTA, wear is most commonly superior. Leaving a superiorly inclined baseplate must be avoided due to risks of notching, loosening, and early failure. However, correcting this tilt will require significant reaming of the inferior glenoid. A superior augment is ideally suited for this bone-loss pattern. If the glenoid is retroverted significantly, difficulty can also arise during glenoid preparation and baseplate placement. Posterior augments may ease this aspect of the procedure. Posterior augments feature the additional benefits of tensioning any remaining posterior rotator cuff, minimizing posterior inferior impingement, and technically easing the operation.18 As we improve our awareness of glenoid orientation using computer navigation, a posterior-superior augmented implant is commonly needed to simultaneously optimize the baseplate position and to minimize reaming (Figure 3). The posterior-superior augmented baseplate has become the most commonly used baseplate augment of choice in 90% of our RTSA cases that require an augment.
INDICATIONS
Augmented RTSA baseplates are indicated when adequate backside contact cannot be achieved with eccentric reaming, thus compromising potential fixation. In our practice, we preferably use augments at <50% contact with the backside of the baseplate. Excessive superior inclination is observed in a CTA setting, commonly indicating the use of superior augments. Similarly, severe primary osteoarthritis may contain elements of posterior bone loss, leading to increased retroversion, which is where we use posterior augments. When patients exhibit combined deformities, or when the surgeon wishes to tension the posterior rotator cuff, a posterior-superior augmented glenoid baseplate is used. For extremely severe defects, we have combined bone grafting and augments. In patients with a highly deficient glenoid but good quality of the remaining bone stock, an augment allows for better contact with less reaming although it is not fully supported when compared with a non-augmented baseplate. Bone grafts can function similarly, but the autograft humeral head is not constantly present in revision situations and requires increased operative time to allow for precision carpentry. Additionally, the success of BIO-RSA requires healing of bone graft on the native glenoid to support the baseplate.19 Jones and colleagues9 compared metal augmented RTSA with BIO-RSA and presented equivalent results.
To minimize reaming and to obtain appropriately inferior inclination, we have discovered preoperative templating and intraoperative, computer-guided glenoid preparation to be extremely valuable (ExactechGPS). These tools allow appropriate assessment of augments and for minimal bone removal when preparing the glenoid.
TECHNIQUE
When using an augment, a fine-cut CT scan is highly recommended to aid in surgery planning. We also find 3-D reconstructions to be helpful. Preoperative planning software also allows surgeons to maximize fixation of implant within the glenoid vault. The starting point for reaming is planned based on CT. Some surgeons using augments perform minimal or no reaming at all, electing to remove the remaining cartilage with a Cobb elevator. Different reaming and drilling axes are used when using augments. In cases of severe glenoid deformity and unavailability of computer assistance, a guide wire with inferior inclination can be installed based on CT scan. Penetration of this wire down the glenoid neck can be palpated and compared with the preoperative plan. We generally prefer at least 24 mm of bone containment for the central cage. Once the surgeon is satisfied with the placement of the wire, the appropriate augment guide is placed, followed by a second guide wire. This second wire acts as the reaming axis. The first wire is removed, and the glenoid is reamed with a cannulated reamer. Once reaming is completed, the original wire is replaced in the same hole and trajectory, and the reaming wire is removed. The first wire is then drilled with a cannulated drill for the central cage. The augmented baseplate is then impacted into place, and screw fixation is performed. Again, intraoperative computer guidance allows for precision screw placement with maximal bone attachment.
Table 2. Results of Reverse Total Shoulder Arthroplasty Augmented Baseplates
| Augment | American Shoulder and Elbow Surgeons Score | Constant Score | Active Forward Flexion | Active External Rotation | ||||||||||||||||
Superior (N = 22) |
|
|
|
|
| |||||||||||||||
Posterior (N = 50) |
|
|
|
|
| |||||||||||||||
Posterosuperior (N = 67) |
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RESULTS
Based on our experience, glenoid augments for RTSA have performed well at short- and mid-term follow-up. From October 2011 to July 2016, 139 patients undergoing RTSA received a posterior, superior, or posterior-superior augmented glenoid baseplate. All groups demonstrated improvements in functional outcome measures, including Constant, ASES, Shoulder Pain and Disability Index, and Simple Shoulder Test scores compared with baseline values (Table 2). The posterior-superior augment group experienced the most significant improvement in active forward flexion and external rotation, whereas the posterior augment group experienced the most significant improvement in ASES and Constant scores. Figures 4A-4C displays the radiographs of a patient with significant glenoid wear treated with a posterior-superior augment RTSA.
Continue to: COMPLICATIONS
COMPLICATIONS
In the superior augment group, 3 patients (13%) sustained 5 complications. One patient sustained 3 separate episodes of instability, eventually requiring revision of prosthesis. In the posterior augment group, 4 patients (8%) sustained complications. Two of the 4 patients presented postoperative humeral fractures related to traumatic events, whereas another patient sustained an intraoperative tuberosity fracture. The last complication in this group involved a postoperative draining wound that was treated with oral antibiotics.
Nine complications developed in the posterior-superior augment group (13%); these complications included aseptic baseplate loosening (5), glenoid fracture (1), humeral fracture (1), acromial stress fracture (1), and cerebrovascular accident (1).
DISCUSSION
As the use of augments in RTSA is relatively new, significantly scarce data exist regarding their outcomes and longevity. A few studies have focused on the short-term outcomes of these augments. Jones and colleagues9 performed a retrospective review of 80 patients who underwent RTSA and required either a structural bone graft or an augmented glenoid baseplate.9 They observed that although all patients showed improvements in pain, range of motion, and functional scores, the structural bone graft group incurred a 14.6% complication rate compared with none observed in the augment group. Additionally, Jones and colleagues9 noted that the augmented baseplate group exhibited a significantly lower rate of scapular notching compared with the bone-graft group (10% vs 18.5%) at similar follow-up intervals. A separate study by Wright and colleagues18 compared posterior vs superior augmented baseplates in RTSA. The posterior augment group demonstrated lower rates of scapular notching (6.3% vs 14.3%) and showed more significant improvements in Constant, ASES, and active forward elevation measures, compared with the superior augment group.
As more manufacturers develop augments for RTSA, and as ExactechGPS uses become more widespread, the use of RTSA baseplate augments will continually grow. Custom implants using massive metal augments are now also being introduced. Although currently too expensive for most cases, as technology drives the cost down, every patient may receive customized augmented implants in the future.
The advantages of augmented baseplate designs include minimized reaming and notching, improved tension of the remaining rotator cuff, and decreased operating room time. The disadvantages include increased cost and lack of mid- or long-term clinical data. The concerns with baseplate loosening with augments in RTSA are much less than those with augments for aTSA due to the outstanding baseplate fixation that can be achieved in RTSA.
Continue to: CONLCLUSION
CONCLUSION
Augments offer an excellent tool for surgeons performing both aTSA and RTSA with glenoid bone loss. Use of augments will become more common as more manufacturers develop them. Although clinical results fall short in full midterm, they have been positive for both augmented RTSA and aTSA. Concerns arise when performing augmented aTSA, as an upper limit of correction has not been defined with regard to component failure. Currently, no data support the maximum amount of correction that can be achieved. In our current practice, we face difficulty in correcting more than 25° of version in young active patients with aTSA augment. Beyond this point, we perform a RTSA with an augment. In older patients or low-demand patients, we only correct minor deformities (<20°) with an aTSA augment, opting instead for an augmented RTSA due to the lower midterm failure rates observed with this implant.
1. Sirveaux F, Favard L, Oudet D, Huquet D, Walch G, Molé D. Grammont inverted total shoulder arthroplasty in the treatment of glenohumeral osteoarthritis with massive rupture of the cuff. J Bone Joint Surg Br. 2004;86(3):388-395. doi:10.1302/0301-620X.86B3.
2. Churchill RS, Spencer Jr EE, Fehringer EV. Quantification of B2 glenoid morphology in total shoulder arthroplasty. J Shoulder Elbow Surg. 2015;24(8):1212-1217. doi:10.1016/j.jse.2015.01.007.
3. Bercik MJ, Kruse K, Yalizis M, Gauci MO, Chaoui J, Walch G. A modification to the Walch classification of the glenoid in primary glenohumeral osteoarthritis using three-dimensional imaging. J Shoulder Elbow Surg. 2016;25(10):1601-1606. doi:10.1016/j.jse.2016.03.010.
4. Klika BJ, Wooten CW, Sperling JW, et al. Structural bone grafting for glenoid deficiency in primary total shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(7):1066-1072. doi:10.1016/j.jse.2013.09.017.
5. Franklin JL, Barrett WP, Jackins SE, Matsen FA 3rd. Glenoid loosening in total shoulder arthroplasty. Association with rotator cuff deficiency. J Arthroplasty. 1988;3(1):39-46.
6. Hermida JC, Flores-Hernandez C, Hoenecke HR, D’Lima DD. Augmented wedge-shaped glenoid component for the correction of glenoid retroversion: a finite element analysis. J Shoulder Elbow Surg. 2014;23(3):347-354. doi:10.1016/j.jse.2013.06.008.
7. Ho JC, Sabesan VJ, Iannotti JP. Glenoid component retroversion is associated with osteolysis. J Bone Joint Surg Am. 2013;95(12):e82. doi:10.2106/JBJS.L.00336.
8. Denard PJ, Walch G. Current concepts in the surgical management of primary glenohumeral arthritis with a biconcave glenoid. J Shoulder Elbow Surg. 2013;22(11):1589-1598. doi:10.1016/j.jse.2013.06.017.
9. Jones RB, Wright TW, Roche CP. Bone grafting the glenoid versus use of augmented glenoid baseplates with reverse shoulder arthroplasty. Bull Hosp Jt Dis (2013). 2015;73(suppl 1):S129-S135.
10. Hsu JE, Ricchetti ET, Huffman GR, Iannotti JP, Glaser DL. Addressing glenoid bone deficiency and asymmetric posterior erosion in shoulder arthroplasty. J Shoulder Elbow Surg. 2013;22(9):1298-1308. doi:10.1016/j.jse.2013.04.014.
11. Cil A, Sperling JW, Cofield RH. Nonstandard glenoid components for bone deficiencies in shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(7):e149-e157. doi:10.1016/j.jse.2013.09.023.
12. Rice RS, Sperling JW, Miletti J, Schleck C, Cofield RH. Augmented glenoid component for bone deficiency in shoulder arthroplasty. Clin Orthop Relat Res. 2008;466(3):579-583. doi:10.1007/s11999-007-0104-4.
13. Sabesan V, Callanan M, Sharma V, Iannotti JP. Correction of acquired glenoid bone loss in osteoarthritis with a standard versus an augmented glenoid component. J Shoulder Elbow Surg. 2014;23(7):964-973. doi:10.1016/j.jse.2013.09.019.
14. Davis DE, Acevedo D, Williams A, Williams G. Total shoulder arthroplasty using an inlay mini-glenoid component for glenoid deficiency: a 2-year follow-up of 9 shoulders in 7 patients. J Shoulder Elbow Surg. 2016;25(8):1354-1361. doi:10.1016/j.jse.2015.12.010.
15. Kersten AD, Flores-Hernandez C, Hoenecke HR, D'Lima DD. Posterior augmented glenoid designs preserve more bone in biconcave glenoids. J Shoulder Elbow Surg. 2015;24(7):1135-1141. doi:10.1016/j.jse.2014.12.007.
16. Favorito PJ, Freed RJ, Passanise AM, Brown MJ. Total shoulder arthroplasty for glenohumeral arthritis associated with posterior glenoid bone loss: results of an all-polyethylene, posteriorly augmented glenoid component. J Shoulder Elbow Surg. 2016;25(10):1681-1689. doi:10.1016/j.jse.2016.02.020.
17. Sandow M, Schutz C. Total shoulder arthroplasty using trabecular metal augments to address glenoid retroversion: the preliminary result of 10 patients with minimum 2-year follow-up. J Shoulder Elbow Surg. 2016;25(4):598-607. doi:10.1016/j.jse.2016.01.001.
18. Wright TW, Roche CP, Wright L, Flurin PH, Crosby LA, Zuckerman JD. Reverse shoulder arthroplasty augments for glenoid wear: A comparison of posterior augments to superior augments. Bull Hosp Jt Dis. 2015;73(suppl 1):S124-S128.
19. Boileau P, Morin-Salvo N, Gauci MO, et al. Angled BIO-RSA (bony-increased offset-reverse shoulder arthroplasty): a solution for the management glenoid bone loss and erosion. J Shoulder Elbow Surg. 2017;26(12):2133-2142. doi:10.1016/j.jse.2017.05.024.
ABSTRACT
Glenoid bone deficiency in the setting of shoulder replacement surgery is far more common than originally reported. The frequency and severity of the glenoid defects are noted to be more common and severe with the advent of computer-assisted surgery. The results of an anatomic total shoulder arthroplasty (aTSA) with glenoid deficiency have been reported to be inferior to aTSA patients without a glenoid deficiency. Options for treating the glenoid deficiency include eccentric reaming, bone grafting, and the use of augmented glenoid components. The purpose of this article is to present the indications, technique, and results of augmented glenoids for both aTSA and reverse TSA (RTSA).
Augments for both aTSA and RTSA are viable options. They preserve subchondral bone at the same time as optimizing the joint line without the need for bone grafts. Complications, revisions and results are as good as compared to shoulder arthroplasties without glenoid wear.
Continue to: Glenoid bone deficiency...
Glenoid bone deficiency in arthritic or cuff-deficient shoulder has been reported in up to 50% of shoulder defect cases.1,2 The type and severity of glenoid deformities vary depending on the underlying pathology and time of manifestation. Osteoarthritis with bone loss typically results in posterior or posterior inferior glenoid wear and is commonly classified as Walch types B1 or B2 (biconcave). In cases of severe erosion, B3 classification has been proposed; in this classification, bone loss becomes extremely severe, progressing to resemble a type C glenoid. Unlike primary osteoarthritis, inflammatory arthropathy more commonly causes central loss of glenoid bone (Walch A2). With the rotator cuff insufficiency, superior migration of the humeral head occurs. As these conditions progress, cuff tear arthropathy (CTA) changes result in superior or posterior-superior bone loss.1 Anterior bone loss (type D) will be rarely encountered due to recurrent anterior instability.3
Classically, with anatomic total shoulder arthroplasty (aTSA), the surgeon considers several options for managing glenoid deficiencies. The most commonly employed technique involves eccentrically reaming the glenoid and correcting the deformity. This procedure is relatively easy but features significant drawbacks, such as sacrificing the subchondral bone, medializing the glenohumeral joint line, and secondarily shrinking the glenoid surface area. Other options include structural bone grafting behind the glenoid component. Most anatomic prosthetic glenoids prove to be unsuitable for fixation of structural bone graft. Therefore, the graft is first internally fixed, followed by placement of the glenoid component. Cement, which is commonly used for glenoid fixation, may potentially inhibit bone-graft healing. Reports using this technique documented high radiographic failure rate of up to 40% at midterm follow-up.4 Although leaving the glenoid component retroverted may be considered, surgeons should develop awareness of the possibility of peg penetration of the anterior glenoid neck. Additionally, retroversion in excess of 5°may increase the risk of recurrent posterior subluxation, resulting in early glenoid loosening.5-7 Results of aTSA under significant glenoid deficiency are inferior to those of aTSA patients without glenoid deficiency.8 Such findings have been extremely inferior in patients with significant glenoid wear, prompting numerous surgeons to abandon aTSA in this population in favor of reverse TSA (RTSA) due to improved bony fixation.
In 2010, augmented anatomic glenoids were first introduced as a wedge (Exactech) and as a step shortly thereafter (DePuy Synthes; Figures 1A-1C). More recently, hemi-wedges have been introduced (Wright Medical Group). Augments have gained popularity due to improved range of motion vs reverse shoulder arthroplasty (RSA). However, debates remain regarding the use of posteriorly augmented components in the setting of posterior glenoid bone loss.8 Augments serve as another viable option for handling glenoid bone deficiency in aTSA.
Glenoid bone loss in RTSA presents similar options to aTSA. However, screw fixation of the glenoid component offers several distinct advantages. Baseplate fixation can readily be used with bone grafting and with a highly anticipated success rate. With multiple screw options, 100% support of the baseplate is not mandatory. Although bony increase offset RSAs (BIO-RSAs) have shown success, augmentation with allograft or autograft increases operative time and relies on osseous integration for long-term implant success.9 Metal augmented baseplates were first introduced in 2011 (Exactech) as a means of managing glenoid bone loss without structural grafting. Although initial results have been encouraging, additional studies are needed to assess the longevity of these implants (Figures 1A-1C).
aTSA AUGMENTS
aTSA augments were introduced as a means of correcting acquired glenoid bone deficiency, restoring native glenoid version, correcting humeral subluxation, and preserving the native subchondral bone. Compared with glenoid bone grafting, augmented glenoid components decrease operative time, allow for a technically easier operation, and require no bone healing for clinical success. Early and midterm results are encouraging, showing similar findings comparable to those of aTSA in non-glenoid deficient shoulders.10-12
Continue to: INDICATIONS
INDICATIONS
Indications and limitations for augmented aTSA glenoids remain incompletely defined. The most common indication for an augmented aTSA is osteoarthritis with a B2 glenoid. We recommend augments in the occurrence of any indication of significant eccentric glenoid wear. With the expertise of surgeons, deformities of up to 20° to 25° of deformity can be readily handled with good predictability. More severe deformities can be managed with augmented aTSA components, but early failure rates may be high. The most severe acquired deformities remain best managed with RTSA. Currently, we prefer RTSA when glenoid bone loss exceeds 25°. With the widespread availability of computed tomography (CT) scans with 3-dimensional (3-D) reconstruction, glenoid bone defects are increasingly recognized. When correcting deformity, surgeons should strive to limit residual retroversion to a maximum of 5°.13 Preoperative planning software and computer-assisted surgery (ExactechGPS) may allow surgeons to better define the limits of augmented glenoid fixation prior to the date of surgery. We routinely utilize computer-guided glenoid preparation to control glenoid version to within 5° of neutral position.
The differences between B3 and a true type C glenoid must be recognized. Although B3 glenoids may still be a candidate for an augmented anatomic glenoid component, type C glenoids are not. Developmental abnormalities of type C glenoid occur simultaneously with humeral deformities, including medialized posterior rotator cuff musculature. Correction of the joint line to neutral version may not replicate the non-diseased state of a dysplastic type shoulder. Davis and colleagues14 have proposed treating these patients by leaving both the humerus and glenoid in their native version without correction.
TECHNIQUE
The implant that we have the most experience with is an 8° full-wedge augmented glenoid component. Such an implant is typically utilized for B2 glenoids. We recommend that a high-quality CT scan be performed for preoperative planning. As a general rule, the starting point often lies close to the ridge of B2 glenoid and more anterior than the apparent glenoid center, which is viewed intraoperatively due to asymmetric posterior wear. Full-wedge component is utilized to ream the ridge separating the neo and paleoglenoids to create a flat surface. This condition is best achieved by drilling a pilot hole at the planned glenoid central peg position to prevent the reamer from sliding anteriorly during reaming. Glenoid preparation begins with the smallest reamer until the ridge has been flattened, and the reamer makes full contact with the glenoid. The reamer diameter is then increased based on glenoid size. Slightly downsizing the glenoid implant will require less reaming to achieve full backside support. Once the glenoid is properly reamed, the central and peripheral peg holes are drilled using the appropriate guides. Holes are then dried, and all-polyethylene or composite glenoid component (either partially or completely cemented) is installed using favored cementing techniques. The advantage of composite glenoid component is that the central cage allows for bone ingrowth and may potentially improve long-term implant survival. Press fit of the central cage requires no waiting time for glenoid cement hardening before proceeding to the humerus. When placing an augmented component, adequate glenoid exposure is imperative to allow in-line placement and appropriate seating of the component without impingement on adjacent retractors.
When using the step-augmented glenoid, the paleoglenoid is prepared in a similar fashion to a standard aTSA. Once the paleoglenoid has been reamed to a neutral position, a protector plate is placed onto the paleoglenoid. and a step-cut saw is used to prepare the posterior stepped bone cut. Peripheral pegs are then drilled, and the component is installed in routine fashion. When using hemi-wedge augments, the paleoglenoid is again prepared in a similar fashion as a standard glenoid component over a cannulated guidewire. The neoglenoid is subsequently prepared using a specialized angled reamer with a positive stop to prevent over-reaming. These glenoid implants improve rotational force neutralization given the absence of flat back against the glenoid. All 3 designs preserve bone when compared with eccentric reaming alone,15 with the half-augmented wedge preserving the most bone.
Table 1. Results of Various Augmented Glenoid Components in Anatomic Total Shoulder
Arthroplasty
| Augment | American Shoulder and Elbow Surgeons Score | Constant Score | Active Forward Flexion | Active External Rotation | ||||||||||||||||
8° cage (N = 21) |
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All-polyethylene 8° (N = 45) |
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All-polyethylene 16° (N = 7) |
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RESULTS
In our institution, we first used all-polyethylene posteriorly augmented glenoid components in 2010. Between 2010 and 2015, 45 patients received an 8° all-polyethylene posterior augment, and 7 patients received a 16° augment. In 2015, we transitioned to the composite caged posterior augment. All patients in our database who received an augmented glenoid component experienced improvement in active forward elevation, external rotation, American Shoulder and Elbow Surgeons (ASES), and Constant scores (Table 1). Minimum follow-up was 1 year for patients receiving both an 8° cage (mean, 1.48 years) and an 8° all-polyethylene augment (mean, 3.18 years). Figures 2A-2C show a patient with significant posterior glenoid wear and humeral head subluxation treated with an 8° wedge composite posterior augment glenoid 3 years postoperative.
Continue to: COMPLICATIONS
COMPLICATIONS
Two complications developed in the group undergoing composite cage augment. One patient experienced glenoid loosening after a motor vehicle accident. Another patient sustained significant intraoperative tuberosity avulsion during implantation of the humeral component, requiring a change of implant and tuberosity fixation. Although no complications were noted in the 8° all-polyethylene group, 3 patients in the 16° augment group sustained complications. One of these patients suffered a cardiac event that was unrelated to the implant. Two complications in this group were both related to loosening of the glenoid component, requiring subsequent revision.
DISCUSSION
The first report on augmented aTSA was published in 2008, and it involved a 5° augmented, anatomic glenoid.12 One study was based on a small series of augments; the poor results led the reporting surgeons to subsequently abandon the implant.12 This early design produced a correction on the articular side of the implant rather than the pathologic bony side. By performing such correction, the component pegs remained anteriorly oriented, placing the component at risk of perforation through the anterior glenoid neck. All current augment designs feature pegs that are oriented down the glenoid vault, with corrections occurring on the bony surface. This condition requires 2 different axes for reaming the glenoid and drilling the pegs. This approach allows the pegs to be directed down the glenoid neck, and is a far superior solution to neutralizing shear forces when compared with the implants used in the 1990s.
Early to midterm results of modern aTSA augments have been extremely encouraging with low revision rates. The main concern of recurrent posterior subluxation has been rarely reported. The concerns over glenoid loosening due to high shear forces, similarly, have not been described to date. However, surgeons should remain cautious, as longer-term follow-up remains unavailable.
The main advantage of aTSA augments is their capacity to preserve bone compared with eccentric reaming and better long-term stability. Each of the augment designs requires varying amounts of bone removal. Through biomechanics and using finite element analysis, the 3 augment types act differently, with no design demonstrating remarkable biomechanical superiority.6 Favorito and colleagues16 performed a retrospective review of 22 patients who underwent aTSA using an all-polyethylene, posteriorly augmented, and stepped glenoid component for posterior bone loss. At an average follow-up of 36 months, all patients experienced improvements in active forward elevation, external rotation, visual analog scale, Short Form-36 Physical Component Summary, and Western Ontario Osteoarthritis of the Shoulder scores. The authors noted that 2 patients (9%) experienced complications: 1 with an anterior dislocation and the other with recurrent posterior instability requiring revision. Sandow and Schutz17 reported the preliminary results of 10 patients who underwent aTSA using trabecular metal augment with a minimum of 2-year follow-up. All patients received either a 15° or 30° posterior, metal-backed augment for severe glenoid bone loss (Walch grade B2 or C). At a minimum of 2-year follow-up, all patients received correction to within 10° of neutral glenoid version, without any complications nor implant failures.
Regardless of augment design, all current components restore the native glenoid version, improving the length and subsequent tension of rotator cuff musculature. Similarly, re-centering the humeral head decreases the forces on the glenoid and allows for optimal function with decreasing loss of vital subchondral bone.
Continue to: RTSA AUGMENTS
RTSA AUGMENTS
Similar to anatomic augments, metal augments were introduced for use with RTSA in 2011. Unlike anatomic augments, those for RTSA were manufactured with metal. Given the difference in bony wear patterns in patients requiring RTSA, augments were available in a number of configurations. With CTA, wear is most commonly superior. Leaving a superiorly inclined baseplate must be avoided due to risks of notching, loosening, and early failure. However, correcting this tilt will require significant reaming of the inferior glenoid. A superior augment is ideally suited for this bone-loss pattern. If the glenoid is retroverted significantly, difficulty can also arise during glenoid preparation and baseplate placement. Posterior augments may ease this aspect of the procedure. Posterior augments feature the additional benefits of tensioning any remaining posterior rotator cuff, minimizing posterior inferior impingement, and technically easing the operation.18 As we improve our awareness of glenoid orientation using computer navigation, a posterior-superior augmented implant is commonly needed to simultaneously optimize the baseplate position and to minimize reaming (Figure 3). The posterior-superior augmented baseplate has become the most commonly used baseplate augment of choice in 90% of our RTSA cases that require an augment.
INDICATIONS
Augmented RTSA baseplates are indicated when adequate backside contact cannot be achieved with eccentric reaming, thus compromising potential fixation. In our practice, we preferably use augments at <50% contact with the backside of the baseplate. Excessive superior inclination is observed in a CTA setting, commonly indicating the use of superior augments. Similarly, severe primary osteoarthritis may contain elements of posterior bone loss, leading to increased retroversion, which is where we use posterior augments. When patients exhibit combined deformities, or when the surgeon wishes to tension the posterior rotator cuff, a posterior-superior augmented glenoid baseplate is used. For extremely severe defects, we have combined bone grafting and augments. In patients with a highly deficient glenoid but good quality of the remaining bone stock, an augment allows for better contact with less reaming although it is not fully supported when compared with a non-augmented baseplate. Bone grafts can function similarly, but the autograft humeral head is not constantly present in revision situations and requires increased operative time to allow for precision carpentry. Additionally, the success of BIO-RSA requires healing of bone graft on the native glenoid to support the baseplate.19 Jones and colleagues9 compared metal augmented RTSA with BIO-RSA and presented equivalent results.
To minimize reaming and to obtain appropriately inferior inclination, we have discovered preoperative templating and intraoperative, computer-guided glenoid preparation to be extremely valuable (ExactechGPS). These tools allow appropriate assessment of augments and for minimal bone removal when preparing the glenoid.
TECHNIQUE
When using an augment, a fine-cut CT scan is highly recommended to aid in surgery planning. We also find 3-D reconstructions to be helpful. Preoperative planning software also allows surgeons to maximize fixation of implant within the glenoid vault. The starting point for reaming is planned based on CT. Some surgeons using augments perform minimal or no reaming at all, electing to remove the remaining cartilage with a Cobb elevator. Different reaming and drilling axes are used when using augments. In cases of severe glenoid deformity and unavailability of computer assistance, a guide wire with inferior inclination can be installed based on CT scan. Penetration of this wire down the glenoid neck can be palpated and compared with the preoperative plan. We generally prefer at least 24 mm of bone containment for the central cage. Once the surgeon is satisfied with the placement of the wire, the appropriate augment guide is placed, followed by a second guide wire. This second wire acts as the reaming axis. The first wire is removed, and the glenoid is reamed with a cannulated reamer. Once reaming is completed, the original wire is replaced in the same hole and trajectory, and the reaming wire is removed. The first wire is then drilled with a cannulated drill for the central cage. The augmented baseplate is then impacted into place, and screw fixation is performed. Again, intraoperative computer guidance allows for precision screw placement with maximal bone attachment.
Table 2. Results of Reverse Total Shoulder Arthroplasty Augmented Baseplates
| Augment | American Shoulder and Elbow Surgeons Score | Constant Score | Active Forward Flexion | Active External Rotation | ||||||||||||||||
Superior (N = 22) |
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Posterior (N = 50) |
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Posterosuperior (N = 67) |
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RESULTS
Based on our experience, glenoid augments for RTSA have performed well at short- and mid-term follow-up. From October 2011 to July 2016, 139 patients undergoing RTSA received a posterior, superior, or posterior-superior augmented glenoid baseplate. All groups demonstrated improvements in functional outcome measures, including Constant, ASES, Shoulder Pain and Disability Index, and Simple Shoulder Test scores compared with baseline values (Table 2). The posterior-superior augment group experienced the most significant improvement in active forward flexion and external rotation, whereas the posterior augment group experienced the most significant improvement in ASES and Constant scores. Figures 4A-4C displays the radiographs of a patient with significant glenoid wear treated with a posterior-superior augment RTSA.
Continue to: COMPLICATIONS
COMPLICATIONS
In the superior augment group, 3 patients (13%) sustained 5 complications. One patient sustained 3 separate episodes of instability, eventually requiring revision of prosthesis. In the posterior augment group, 4 patients (8%) sustained complications. Two of the 4 patients presented postoperative humeral fractures related to traumatic events, whereas another patient sustained an intraoperative tuberosity fracture. The last complication in this group involved a postoperative draining wound that was treated with oral antibiotics.
Nine complications developed in the posterior-superior augment group (13%); these complications included aseptic baseplate loosening (5), glenoid fracture (1), humeral fracture (1), acromial stress fracture (1), and cerebrovascular accident (1).
DISCUSSION
As the use of augments in RTSA is relatively new, significantly scarce data exist regarding their outcomes and longevity. A few studies have focused on the short-term outcomes of these augments. Jones and colleagues9 performed a retrospective review of 80 patients who underwent RTSA and required either a structural bone graft or an augmented glenoid baseplate.9 They observed that although all patients showed improvements in pain, range of motion, and functional scores, the structural bone graft group incurred a 14.6% complication rate compared with none observed in the augment group. Additionally, Jones and colleagues9 noted that the augmented baseplate group exhibited a significantly lower rate of scapular notching compared with the bone-graft group (10% vs 18.5%) at similar follow-up intervals. A separate study by Wright and colleagues18 compared posterior vs superior augmented baseplates in RTSA. The posterior augment group demonstrated lower rates of scapular notching (6.3% vs 14.3%) and showed more significant improvements in Constant, ASES, and active forward elevation measures, compared with the superior augment group.
As more manufacturers develop augments for RTSA, and as ExactechGPS uses become more widespread, the use of RTSA baseplate augments will continually grow. Custom implants using massive metal augments are now also being introduced. Although currently too expensive for most cases, as technology drives the cost down, every patient may receive customized augmented implants in the future.
The advantages of augmented baseplate designs include minimized reaming and notching, improved tension of the remaining rotator cuff, and decreased operating room time. The disadvantages include increased cost and lack of mid- or long-term clinical data. The concerns with baseplate loosening with augments in RTSA are much less than those with augments for aTSA due to the outstanding baseplate fixation that can be achieved in RTSA.
Continue to: CONLCLUSION
CONCLUSION
Augments offer an excellent tool for surgeons performing both aTSA and RTSA with glenoid bone loss. Use of augments will become more common as more manufacturers develop them. Although clinical results fall short in full midterm, they have been positive for both augmented RTSA and aTSA. Concerns arise when performing augmented aTSA, as an upper limit of correction has not been defined with regard to component failure. Currently, no data support the maximum amount of correction that can be achieved. In our current practice, we face difficulty in correcting more than 25° of version in young active patients with aTSA augment. Beyond this point, we perform a RTSA with an augment. In older patients or low-demand patients, we only correct minor deformities (<20°) with an aTSA augment, opting instead for an augmented RTSA due to the lower midterm failure rates observed with this implant.
ABSTRACT
Glenoid bone deficiency in the setting of shoulder replacement surgery is far more common than originally reported. The frequency and severity of the glenoid defects are noted to be more common and severe with the advent of computer-assisted surgery. The results of an anatomic total shoulder arthroplasty (aTSA) with glenoid deficiency have been reported to be inferior to aTSA patients without a glenoid deficiency. Options for treating the glenoid deficiency include eccentric reaming, bone grafting, and the use of augmented glenoid components. The purpose of this article is to present the indications, technique, and results of augmented glenoids for both aTSA and reverse TSA (RTSA).
Augments for both aTSA and RTSA are viable options. They preserve subchondral bone at the same time as optimizing the joint line without the need for bone grafts. Complications, revisions and results are as good as compared to shoulder arthroplasties without glenoid wear.
Continue to: Glenoid bone deficiency...
Glenoid bone deficiency in arthritic or cuff-deficient shoulder has been reported in up to 50% of shoulder defect cases.1,2 The type and severity of glenoid deformities vary depending on the underlying pathology and time of manifestation. Osteoarthritis with bone loss typically results in posterior or posterior inferior glenoid wear and is commonly classified as Walch types B1 or B2 (biconcave). In cases of severe erosion, B3 classification has been proposed; in this classification, bone loss becomes extremely severe, progressing to resemble a type C glenoid. Unlike primary osteoarthritis, inflammatory arthropathy more commonly causes central loss of glenoid bone (Walch A2). With the rotator cuff insufficiency, superior migration of the humeral head occurs. As these conditions progress, cuff tear arthropathy (CTA) changes result in superior or posterior-superior bone loss.1 Anterior bone loss (type D) will be rarely encountered due to recurrent anterior instability.3
Classically, with anatomic total shoulder arthroplasty (aTSA), the surgeon considers several options for managing glenoid deficiencies. The most commonly employed technique involves eccentrically reaming the glenoid and correcting the deformity. This procedure is relatively easy but features significant drawbacks, such as sacrificing the subchondral bone, medializing the glenohumeral joint line, and secondarily shrinking the glenoid surface area. Other options include structural bone grafting behind the glenoid component. Most anatomic prosthetic glenoids prove to be unsuitable for fixation of structural bone graft. Therefore, the graft is first internally fixed, followed by placement of the glenoid component. Cement, which is commonly used for glenoid fixation, may potentially inhibit bone-graft healing. Reports using this technique documented high radiographic failure rate of up to 40% at midterm follow-up.4 Although leaving the glenoid component retroverted may be considered, surgeons should develop awareness of the possibility of peg penetration of the anterior glenoid neck. Additionally, retroversion in excess of 5°may increase the risk of recurrent posterior subluxation, resulting in early glenoid loosening.5-7 Results of aTSA under significant glenoid deficiency are inferior to those of aTSA patients without glenoid deficiency.8 Such findings have been extremely inferior in patients with significant glenoid wear, prompting numerous surgeons to abandon aTSA in this population in favor of reverse TSA (RTSA) due to improved bony fixation.
In 2010, augmented anatomic glenoids were first introduced as a wedge (Exactech) and as a step shortly thereafter (DePuy Synthes; Figures 1A-1C). More recently, hemi-wedges have been introduced (Wright Medical Group). Augments have gained popularity due to improved range of motion vs reverse shoulder arthroplasty (RSA). However, debates remain regarding the use of posteriorly augmented components in the setting of posterior glenoid bone loss.8 Augments serve as another viable option for handling glenoid bone deficiency in aTSA.
Glenoid bone loss in RTSA presents similar options to aTSA. However, screw fixation of the glenoid component offers several distinct advantages. Baseplate fixation can readily be used with bone grafting and with a highly anticipated success rate. With multiple screw options, 100% support of the baseplate is not mandatory. Although bony increase offset RSAs (BIO-RSAs) have shown success, augmentation with allograft or autograft increases operative time and relies on osseous integration for long-term implant success.9 Metal augmented baseplates were first introduced in 2011 (Exactech) as a means of managing glenoid bone loss without structural grafting. Although initial results have been encouraging, additional studies are needed to assess the longevity of these implants (Figures 1A-1C).
aTSA AUGMENTS
aTSA augments were introduced as a means of correcting acquired glenoid bone deficiency, restoring native glenoid version, correcting humeral subluxation, and preserving the native subchondral bone. Compared with glenoid bone grafting, augmented glenoid components decrease operative time, allow for a technically easier operation, and require no bone healing for clinical success. Early and midterm results are encouraging, showing similar findings comparable to those of aTSA in non-glenoid deficient shoulders.10-12
Continue to: INDICATIONS
INDICATIONS
Indications and limitations for augmented aTSA glenoids remain incompletely defined. The most common indication for an augmented aTSA is osteoarthritis with a B2 glenoid. We recommend augments in the occurrence of any indication of significant eccentric glenoid wear. With the expertise of surgeons, deformities of up to 20° to 25° of deformity can be readily handled with good predictability. More severe deformities can be managed with augmented aTSA components, but early failure rates may be high. The most severe acquired deformities remain best managed with RTSA. Currently, we prefer RTSA when glenoid bone loss exceeds 25°. With the widespread availability of computed tomography (CT) scans with 3-dimensional (3-D) reconstruction, glenoid bone defects are increasingly recognized. When correcting deformity, surgeons should strive to limit residual retroversion to a maximum of 5°.13 Preoperative planning software and computer-assisted surgery (ExactechGPS) may allow surgeons to better define the limits of augmented glenoid fixation prior to the date of surgery. We routinely utilize computer-guided glenoid preparation to control glenoid version to within 5° of neutral position.
The differences between B3 and a true type C glenoid must be recognized. Although B3 glenoids may still be a candidate for an augmented anatomic glenoid component, type C glenoids are not. Developmental abnormalities of type C glenoid occur simultaneously with humeral deformities, including medialized posterior rotator cuff musculature. Correction of the joint line to neutral version may not replicate the non-diseased state of a dysplastic type shoulder. Davis and colleagues14 have proposed treating these patients by leaving both the humerus and glenoid in their native version without correction.
TECHNIQUE
The implant that we have the most experience with is an 8° full-wedge augmented glenoid component. Such an implant is typically utilized for B2 glenoids. We recommend that a high-quality CT scan be performed for preoperative planning. As a general rule, the starting point often lies close to the ridge of B2 glenoid and more anterior than the apparent glenoid center, which is viewed intraoperatively due to asymmetric posterior wear. Full-wedge component is utilized to ream the ridge separating the neo and paleoglenoids to create a flat surface. This condition is best achieved by drilling a pilot hole at the planned glenoid central peg position to prevent the reamer from sliding anteriorly during reaming. Glenoid preparation begins with the smallest reamer until the ridge has been flattened, and the reamer makes full contact with the glenoid. The reamer diameter is then increased based on glenoid size. Slightly downsizing the glenoid implant will require less reaming to achieve full backside support. Once the glenoid is properly reamed, the central and peripheral peg holes are drilled using the appropriate guides. Holes are then dried, and all-polyethylene or composite glenoid component (either partially or completely cemented) is installed using favored cementing techniques. The advantage of composite glenoid component is that the central cage allows for bone ingrowth and may potentially improve long-term implant survival. Press fit of the central cage requires no waiting time for glenoid cement hardening before proceeding to the humerus. When placing an augmented component, adequate glenoid exposure is imperative to allow in-line placement and appropriate seating of the component without impingement on adjacent retractors.
When using the step-augmented glenoid, the paleoglenoid is prepared in a similar fashion to a standard aTSA. Once the paleoglenoid has been reamed to a neutral position, a protector plate is placed onto the paleoglenoid. and a step-cut saw is used to prepare the posterior stepped bone cut. Peripheral pegs are then drilled, and the component is installed in routine fashion. When using hemi-wedge augments, the paleoglenoid is again prepared in a similar fashion as a standard glenoid component over a cannulated guidewire. The neoglenoid is subsequently prepared using a specialized angled reamer with a positive stop to prevent over-reaming. These glenoid implants improve rotational force neutralization given the absence of flat back against the glenoid. All 3 designs preserve bone when compared with eccentric reaming alone,15 with the half-augmented wedge preserving the most bone.
Table 1. Results of Various Augmented Glenoid Components in Anatomic Total Shoulder
Arthroplasty
| Augment | American Shoulder and Elbow Surgeons Score | Constant Score | Active Forward Flexion | Active External Rotation | ||||||||||||||||
8° cage (N = 21) |
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All-polyethylene 8° (N = 45) |
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All-polyethylene 16° (N = 7) |
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RESULTS
In our institution, we first used all-polyethylene posteriorly augmented glenoid components in 2010. Between 2010 and 2015, 45 patients received an 8° all-polyethylene posterior augment, and 7 patients received a 16° augment. In 2015, we transitioned to the composite caged posterior augment. All patients in our database who received an augmented glenoid component experienced improvement in active forward elevation, external rotation, American Shoulder and Elbow Surgeons (ASES), and Constant scores (Table 1). Minimum follow-up was 1 year for patients receiving both an 8° cage (mean, 1.48 years) and an 8° all-polyethylene augment (mean, 3.18 years). Figures 2A-2C show a patient with significant posterior glenoid wear and humeral head subluxation treated with an 8° wedge composite posterior augment glenoid 3 years postoperative.
Continue to: COMPLICATIONS
COMPLICATIONS
Two complications developed in the group undergoing composite cage augment. One patient experienced glenoid loosening after a motor vehicle accident. Another patient sustained significant intraoperative tuberosity avulsion during implantation of the humeral component, requiring a change of implant and tuberosity fixation. Although no complications were noted in the 8° all-polyethylene group, 3 patients in the 16° augment group sustained complications. One of these patients suffered a cardiac event that was unrelated to the implant. Two complications in this group were both related to loosening of the glenoid component, requiring subsequent revision.
DISCUSSION
The first report on augmented aTSA was published in 2008, and it involved a 5° augmented, anatomic glenoid.12 One study was based on a small series of augments; the poor results led the reporting surgeons to subsequently abandon the implant.12 This early design produced a correction on the articular side of the implant rather than the pathologic bony side. By performing such correction, the component pegs remained anteriorly oriented, placing the component at risk of perforation through the anterior glenoid neck. All current augment designs feature pegs that are oriented down the glenoid vault, with corrections occurring on the bony surface. This condition requires 2 different axes for reaming the glenoid and drilling the pegs. This approach allows the pegs to be directed down the glenoid neck, and is a far superior solution to neutralizing shear forces when compared with the implants used in the 1990s.
Early to midterm results of modern aTSA augments have been extremely encouraging with low revision rates. The main concern of recurrent posterior subluxation has been rarely reported. The concerns over glenoid loosening due to high shear forces, similarly, have not been described to date. However, surgeons should remain cautious, as longer-term follow-up remains unavailable.
The main advantage of aTSA augments is their capacity to preserve bone compared with eccentric reaming and better long-term stability. Each of the augment designs requires varying amounts of bone removal. Through biomechanics and using finite element analysis, the 3 augment types act differently, with no design demonstrating remarkable biomechanical superiority.6 Favorito and colleagues16 performed a retrospective review of 22 patients who underwent aTSA using an all-polyethylene, posteriorly augmented, and stepped glenoid component for posterior bone loss. At an average follow-up of 36 months, all patients experienced improvements in active forward elevation, external rotation, visual analog scale, Short Form-36 Physical Component Summary, and Western Ontario Osteoarthritis of the Shoulder scores. The authors noted that 2 patients (9%) experienced complications: 1 with an anterior dislocation and the other with recurrent posterior instability requiring revision. Sandow and Schutz17 reported the preliminary results of 10 patients who underwent aTSA using trabecular metal augment with a minimum of 2-year follow-up. All patients received either a 15° or 30° posterior, metal-backed augment for severe glenoid bone loss (Walch grade B2 or C). At a minimum of 2-year follow-up, all patients received correction to within 10° of neutral glenoid version, without any complications nor implant failures.
Regardless of augment design, all current components restore the native glenoid version, improving the length and subsequent tension of rotator cuff musculature. Similarly, re-centering the humeral head decreases the forces on the glenoid and allows for optimal function with decreasing loss of vital subchondral bone.
Continue to: RTSA AUGMENTS
RTSA AUGMENTS
Similar to anatomic augments, metal augments were introduced for use with RTSA in 2011. Unlike anatomic augments, those for RTSA were manufactured with metal. Given the difference in bony wear patterns in patients requiring RTSA, augments were available in a number of configurations. With CTA, wear is most commonly superior. Leaving a superiorly inclined baseplate must be avoided due to risks of notching, loosening, and early failure. However, correcting this tilt will require significant reaming of the inferior glenoid. A superior augment is ideally suited for this bone-loss pattern. If the glenoid is retroverted significantly, difficulty can also arise during glenoid preparation and baseplate placement. Posterior augments may ease this aspect of the procedure. Posterior augments feature the additional benefits of tensioning any remaining posterior rotator cuff, minimizing posterior inferior impingement, and technically easing the operation.18 As we improve our awareness of glenoid orientation using computer navigation, a posterior-superior augmented implant is commonly needed to simultaneously optimize the baseplate position and to minimize reaming (Figure 3). The posterior-superior augmented baseplate has become the most commonly used baseplate augment of choice in 90% of our RTSA cases that require an augment.
INDICATIONS
Augmented RTSA baseplates are indicated when adequate backside contact cannot be achieved with eccentric reaming, thus compromising potential fixation. In our practice, we preferably use augments at <50% contact with the backside of the baseplate. Excessive superior inclination is observed in a CTA setting, commonly indicating the use of superior augments. Similarly, severe primary osteoarthritis may contain elements of posterior bone loss, leading to increased retroversion, which is where we use posterior augments. When patients exhibit combined deformities, or when the surgeon wishes to tension the posterior rotator cuff, a posterior-superior augmented glenoid baseplate is used. For extremely severe defects, we have combined bone grafting and augments. In patients with a highly deficient glenoid but good quality of the remaining bone stock, an augment allows for better contact with less reaming although it is not fully supported when compared with a non-augmented baseplate. Bone grafts can function similarly, but the autograft humeral head is not constantly present in revision situations and requires increased operative time to allow for precision carpentry. Additionally, the success of BIO-RSA requires healing of bone graft on the native glenoid to support the baseplate.19 Jones and colleagues9 compared metal augmented RTSA with BIO-RSA and presented equivalent results.
To minimize reaming and to obtain appropriately inferior inclination, we have discovered preoperative templating and intraoperative, computer-guided glenoid preparation to be extremely valuable (ExactechGPS). These tools allow appropriate assessment of augments and for minimal bone removal when preparing the glenoid.
TECHNIQUE
When using an augment, a fine-cut CT scan is highly recommended to aid in surgery planning. We also find 3-D reconstructions to be helpful. Preoperative planning software also allows surgeons to maximize fixation of implant within the glenoid vault. The starting point for reaming is planned based on CT. Some surgeons using augments perform minimal or no reaming at all, electing to remove the remaining cartilage with a Cobb elevator. Different reaming and drilling axes are used when using augments. In cases of severe glenoid deformity and unavailability of computer assistance, a guide wire with inferior inclination can be installed based on CT scan. Penetration of this wire down the glenoid neck can be palpated and compared with the preoperative plan. We generally prefer at least 24 mm of bone containment for the central cage. Once the surgeon is satisfied with the placement of the wire, the appropriate augment guide is placed, followed by a second guide wire. This second wire acts as the reaming axis. The first wire is removed, and the glenoid is reamed with a cannulated reamer. Once reaming is completed, the original wire is replaced in the same hole and trajectory, and the reaming wire is removed. The first wire is then drilled with a cannulated drill for the central cage. The augmented baseplate is then impacted into place, and screw fixation is performed. Again, intraoperative computer guidance allows for precision screw placement with maximal bone attachment.
Table 2. Results of Reverse Total Shoulder Arthroplasty Augmented Baseplates
| Augment | American Shoulder and Elbow Surgeons Score | Constant Score | Active Forward Flexion | Active External Rotation | ||||||||||||||||
Superior (N = 22) |
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Posterior (N = 50) |
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Posterosuperior (N = 67) |
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RESULTS
Based on our experience, glenoid augments for RTSA have performed well at short- and mid-term follow-up. From October 2011 to July 2016, 139 patients undergoing RTSA received a posterior, superior, or posterior-superior augmented glenoid baseplate. All groups demonstrated improvements in functional outcome measures, including Constant, ASES, Shoulder Pain and Disability Index, and Simple Shoulder Test scores compared with baseline values (Table 2). The posterior-superior augment group experienced the most significant improvement in active forward flexion and external rotation, whereas the posterior augment group experienced the most significant improvement in ASES and Constant scores. Figures 4A-4C displays the radiographs of a patient with significant glenoid wear treated with a posterior-superior augment RTSA.
Continue to: COMPLICATIONS
COMPLICATIONS
In the superior augment group, 3 patients (13%) sustained 5 complications. One patient sustained 3 separate episodes of instability, eventually requiring revision of prosthesis. In the posterior augment group, 4 patients (8%) sustained complications. Two of the 4 patients presented postoperative humeral fractures related to traumatic events, whereas another patient sustained an intraoperative tuberosity fracture. The last complication in this group involved a postoperative draining wound that was treated with oral antibiotics.
Nine complications developed in the posterior-superior augment group (13%); these complications included aseptic baseplate loosening (5), glenoid fracture (1), humeral fracture (1), acromial stress fracture (1), and cerebrovascular accident (1).
DISCUSSION
As the use of augments in RTSA is relatively new, significantly scarce data exist regarding their outcomes and longevity. A few studies have focused on the short-term outcomes of these augments. Jones and colleagues9 performed a retrospective review of 80 patients who underwent RTSA and required either a structural bone graft or an augmented glenoid baseplate.9 They observed that although all patients showed improvements in pain, range of motion, and functional scores, the structural bone graft group incurred a 14.6% complication rate compared with none observed in the augment group. Additionally, Jones and colleagues9 noted that the augmented baseplate group exhibited a significantly lower rate of scapular notching compared with the bone-graft group (10% vs 18.5%) at similar follow-up intervals. A separate study by Wright and colleagues18 compared posterior vs superior augmented baseplates in RTSA. The posterior augment group demonstrated lower rates of scapular notching (6.3% vs 14.3%) and showed more significant improvements in Constant, ASES, and active forward elevation measures, compared with the superior augment group.
As more manufacturers develop augments for RTSA, and as ExactechGPS uses become more widespread, the use of RTSA baseplate augments will continually grow. Custom implants using massive metal augments are now also being introduced. Although currently too expensive for most cases, as technology drives the cost down, every patient may receive customized augmented implants in the future.
The advantages of augmented baseplate designs include minimized reaming and notching, improved tension of the remaining rotator cuff, and decreased operating room time. The disadvantages include increased cost and lack of mid- or long-term clinical data. The concerns with baseplate loosening with augments in RTSA are much less than those with augments for aTSA due to the outstanding baseplate fixation that can be achieved in RTSA.
Continue to: CONLCLUSION
CONCLUSION
Augments offer an excellent tool for surgeons performing both aTSA and RTSA with glenoid bone loss. Use of augments will become more common as more manufacturers develop them. Although clinical results fall short in full midterm, they have been positive for both augmented RTSA and aTSA. Concerns arise when performing augmented aTSA, as an upper limit of correction has not been defined with regard to component failure. Currently, no data support the maximum amount of correction that can be achieved. In our current practice, we face difficulty in correcting more than 25° of version in young active patients with aTSA augment. Beyond this point, we perform a RTSA with an augment. In older patients or low-demand patients, we only correct minor deformities (<20°) with an aTSA augment, opting instead for an augmented RTSA due to the lower midterm failure rates observed with this implant.
1. Sirveaux F, Favard L, Oudet D, Huquet D, Walch G, Molé D. Grammont inverted total shoulder arthroplasty in the treatment of glenohumeral osteoarthritis with massive rupture of the cuff. J Bone Joint Surg Br. 2004;86(3):388-395. doi:10.1302/0301-620X.86B3.
2. Churchill RS, Spencer Jr EE, Fehringer EV. Quantification of B2 glenoid morphology in total shoulder arthroplasty. J Shoulder Elbow Surg. 2015;24(8):1212-1217. doi:10.1016/j.jse.2015.01.007.
3. Bercik MJ, Kruse K, Yalizis M, Gauci MO, Chaoui J, Walch G. A modification to the Walch classification of the glenoid in primary glenohumeral osteoarthritis using three-dimensional imaging. J Shoulder Elbow Surg. 2016;25(10):1601-1606. doi:10.1016/j.jse.2016.03.010.
4. Klika BJ, Wooten CW, Sperling JW, et al. Structural bone grafting for glenoid deficiency in primary total shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(7):1066-1072. doi:10.1016/j.jse.2013.09.017.
5. Franklin JL, Barrett WP, Jackins SE, Matsen FA 3rd. Glenoid loosening in total shoulder arthroplasty. Association with rotator cuff deficiency. J Arthroplasty. 1988;3(1):39-46.
6. Hermida JC, Flores-Hernandez C, Hoenecke HR, D’Lima DD. Augmented wedge-shaped glenoid component for the correction of glenoid retroversion: a finite element analysis. J Shoulder Elbow Surg. 2014;23(3):347-354. doi:10.1016/j.jse.2013.06.008.
7. Ho JC, Sabesan VJ, Iannotti JP. Glenoid component retroversion is associated with osteolysis. J Bone Joint Surg Am. 2013;95(12):e82. doi:10.2106/JBJS.L.00336.
8. Denard PJ, Walch G. Current concepts in the surgical management of primary glenohumeral arthritis with a biconcave glenoid. J Shoulder Elbow Surg. 2013;22(11):1589-1598. doi:10.1016/j.jse.2013.06.017.
9. Jones RB, Wright TW, Roche CP. Bone grafting the glenoid versus use of augmented glenoid baseplates with reverse shoulder arthroplasty. Bull Hosp Jt Dis (2013). 2015;73(suppl 1):S129-S135.
10. Hsu JE, Ricchetti ET, Huffman GR, Iannotti JP, Glaser DL. Addressing glenoid bone deficiency and asymmetric posterior erosion in shoulder arthroplasty. J Shoulder Elbow Surg. 2013;22(9):1298-1308. doi:10.1016/j.jse.2013.04.014.
11. Cil A, Sperling JW, Cofield RH. Nonstandard glenoid components for bone deficiencies in shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(7):e149-e157. doi:10.1016/j.jse.2013.09.023.
12. Rice RS, Sperling JW, Miletti J, Schleck C, Cofield RH. Augmented glenoid component for bone deficiency in shoulder arthroplasty. Clin Orthop Relat Res. 2008;466(3):579-583. doi:10.1007/s11999-007-0104-4.
13. Sabesan V, Callanan M, Sharma V, Iannotti JP. Correction of acquired glenoid bone loss in osteoarthritis with a standard versus an augmented glenoid component. J Shoulder Elbow Surg. 2014;23(7):964-973. doi:10.1016/j.jse.2013.09.019.
14. Davis DE, Acevedo D, Williams A, Williams G. Total shoulder arthroplasty using an inlay mini-glenoid component for glenoid deficiency: a 2-year follow-up of 9 shoulders in 7 patients. J Shoulder Elbow Surg. 2016;25(8):1354-1361. doi:10.1016/j.jse.2015.12.010.
15. Kersten AD, Flores-Hernandez C, Hoenecke HR, D'Lima DD. Posterior augmented glenoid designs preserve more bone in biconcave glenoids. J Shoulder Elbow Surg. 2015;24(7):1135-1141. doi:10.1016/j.jse.2014.12.007.
16. Favorito PJ, Freed RJ, Passanise AM, Brown MJ. Total shoulder arthroplasty for glenohumeral arthritis associated with posterior glenoid bone loss: results of an all-polyethylene, posteriorly augmented glenoid component. J Shoulder Elbow Surg. 2016;25(10):1681-1689. doi:10.1016/j.jse.2016.02.020.
17. Sandow M, Schutz C. Total shoulder arthroplasty using trabecular metal augments to address glenoid retroversion: the preliminary result of 10 patients with minimum 2-year follow-up. J Shoulder Elbow Surg. 2016;25(4):598-607. doi:10.1016/j.jse.2016.01.001.
18. Wright TW, Roche CP, Wright L, Flurin PH, Crosby LA, Zuckerman JD. Reverse shoulder arthroplasty augments for glenoid wear: A comparison of posterior augments to superior augments. Bull Hosp Jt Dis. 2015;73(suppl 1):S124-S128.
19. Boileau P, Morin-Salvo N, Gauci MO, et al. Angled BIO-RSA (bony-increased offset-reverse shoulder arthroplasty): a solution for the management glenoid bone loss and erosion. J Shoulder Elbow Surg. 2017;26(12):2133-2142. doi:10.1016/j.jse.2017.05.024.
1. Sirveaux F, Favard L, Oudet D, Huquet D, Walch G, Molé D. Grammont inverted total shoulder arthroplasty in the treatment of glenohumeral osteoarthritis with massive rupture of the cuff. J Bone Joint Surg Br. 2004;86(3):388-395. doi:10.1302/0301-620X.86B3.
2. Churchill RS, Spencer Jr EE, Fehringer EV. Quantification of B2 glenoid morphology in total shoulder arthroplasty. J Shoulder Elbow Surg. 2015;24(8):1212-1217. doi:10.1016/j.jse.2015.01.007.
3. Bercik MJ, Kruse K, Yalizis M, Gauci MO, Chaoui J, Walch G. A modification to the Walch classification of the glenoid in primary glenohumeral osteoarthritis using three-dimensional imaging. J Shoulder Elbow Surg. 2016;25(10):1601-1606. doi:10.1016/j.jse.2016.03.010.
4. Klika BJ, Wooten CW, Sperling JW, et al. Structural bone grafting for glenoid deficiency in primary total shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(7):1066-1072. doi:10.1016/j.jse.2013.09.017.
5. Franklin JL, Barrett WP, Jackins SE, Matsen FA 3rd. Glenoid loosening in total shoulder arthroplasty. Association with rotator cuff deficiency. J Arthroplasty. 1988;3(1):39-46.
6. Hermida JC, Flores-Hernandez C, Hoenecke HR, D’Lima DD. Augmented wedge-shaped glenoid component for the correction of glenoid retroversion: a finite element analysis. J Shoulder Elbow Surg. 2014;23(3):347-354. doi:10.1016/j.jse.2013.06.008.
7. Ho JC, Sabesan VJ, Iannotti JP. Glenoid component retroversion is associated with osteolysis. J Bone Joint Surg Am. 2013;95(12):e82. doi:10.2106/JBJS.L.00336.
8. Denard PJ, Walch G. Current concepts in the surgical management of primary glenohumeral arthritis with a biconcave glenoid. J Shoulder Elbow Surg. 2013;22(11):1589-1598. doi:10.1016/j.jse.2013.06.017.
9. Jones RB, Wright TW, Roche CP. Bone grafting the glenoid versus use of augmented glenoid baseplates with reverse shoulder arthroplasty. Bull Hosp Jt Dis (2013). 2015;73(suppl 1):S129-S135.
10. Hsu JE, Ricchetti ET, Huffman GR, Iannotti JP, Glaser DL. Addressing glenoid bone deficiency and asymmetric posterior erosion in shoulder arthroplasty. J Shoulder Elbow Surg. 2013;22(9):1298-1308. doi:10.1016/j.jse.2013.04.014.
11. Cil A, Sperling JW, Cofield RH. Nonstandard glenoid components for bone deficiencies in shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(7):e149-e157. doi:10.1016/j.jse.2013.09.023.
12. Rice RS, Sperling JW, Miletti J, Schleck C, Cofield RH. Augmented glenoid component for bone deficiency in shoulder arthroplasty. Clin Orthop Relat Res. 2008;466(3):579-583. doi:10.1007/s11999-007-0104-4.
13. Sabesan V, Callanan M, Sharma V, Iannotti JP. Correction of acquired glenoid bone loss in osteoarthritis with a standard versus an augmented glenoid component. J Shoulder Elbow Surg. 2014;23(7):964-973. doi:10.1016/j.jse.2013.09.019.
14. Davis DE, Acevedo D, Williams A, Williams G. Total shoulder arthroplasty using an inlay mini-glenoid component for glenoid deficiency: a 2-year follow-up of 9 shoulders in 7 patients. J Shoulder Elbow Surg. 2016;25(8):1354-1361. doi:10.1016/j.jse.2015.12.010.
15. Kersten AD, Flores-Hernandez C, Hoenecke HR, D'Lima DD. Posterior augmented glenoid designs preserve more bone in biconcave glenoids. J Shoulder Elbow Surg. 2015;24(7):1135-1141. doi:10.1016/j.jse.2014.12.007.
16. Favorito PJ, Freed RJ, Passanise AM, Brown MJ. Total shoulder arthroplasty for glenohumeral arthritis associated with posterior glenoid bone loss: results of an all-polyethylene, posteriorly augmented glenoid component. J Shoulder Elbow Surg. 2016;25(10):1681-1689. doi:10.1016/j.jse.2016.02.020.
17. Sandow M, Schutz C. Total shoulder arthroplasty using trabecular metal augments to address glenoid retroversion: the preliminary result of 10 patients with minimum 2-year follow-up. J Shoulder Elbow Surg. 2016;25(4):598-607. doi:10.1016/j.jse.2016.01.001.
18. Wright TW, Roche CP, Wright L, Flurin PH, Crosby LA, Zuckerman JD. Reverse shoulder arthroplasty augments for glenoid wear: A comparison of posterior augments to superior augments. Bull Hosp Jt Dis. 2015;73(suppl 1):S124-S128.
19. Boileau P, Morin-Salvo N, Gauci MO, et al. Angled BIO-RSA (bony-increased offset-reverse shoulder arthroplasty): a solution for the management glenoid bone loss and erosion. J Shoulder Elbow Surg. 2017;26(12):2133-2142. doi:10.1016/j.jse.2017.05.024.
TAKE-HOME POINTS
- Glenoid defects are very common.
- Options for treating glenoid defects include eccentric reaming, bone grafting, and augmented glenoids.
- As computer-assisted surgery use becomes more widespread the use of augments in both TSA and RTSA will become very common.
- Subchondral bone is precious and cannot be replaced once reamed away. Eccentric glenoids introduce a mechanism to minimize reaming and preserve this precious bone.
- On short-term to midterm follow-up augments perform at least as well if not better than non-augmented glenoid components with complication rate and revisions likewise similar.
Patient-Specific Guides/Instrumentation in Shoulder Arthroplasty
ABSTRACT
Optimal outcomes following total shoulder arthroplasty TSA and reverse shoulder arthroplasty RSA are dependent on proper implant position. Multiple cadaver studies have demonstrated improved accuracy of implant positioning with use of patient-specific guides/instrumentation compared to traditional methods. At this time, there are 3 commercially available single use patient-specific instrumentation systems and 1 commercially available reusable patient-specific instrumentation system. Currently though, there are no studies comparing the clinical outcomes of patient-specific guides to those of traditional methods of glenoid placement, and limited research has been done comparing the accuracy of each system’s 3-dimensional planning software. Future work is necessary to elucidate the ideal indications for the use of patient-specific guides and instrumentation, but it is likely, particularly in the setting of advanced glenoid deformity, that these systems will improve a surgeon's ability to put the implant in the best position possible.
Continue to: Optimal functional recovery...
Optimal functional recovery and implant longevity following both total shoulder arthroplasty (TSA) and reverse shoulder arthroplasty (RSA) depend, in large part, on proper placement of the glenoid component. Glenoid component malpositioning has an adverse effect on shoulder stability, range of motion (ROM), impingement, and glenoid implant longevity.
Traditionally, glenoid component positioning has been done manually by the surgeons based on their review of preoperative films and knowledge of glenoid anatomy. Anatomic studies have demonstrated high individual variability in the version of the native glenoid, thus making ideal placement of the initial glenoid guide pin difficult using standard guide pin guides.1
The following 2 methods have been described for improving the accuracy of glenoid guide pin insertion and subsequent glenoid implant placement: (1) computerized navigation and (2) patient-specific guides/instrumentation. Although navigated shoulder systems have demonstrated improved accuracy in glenoid placement compared with traditional methods, navigated systems require often large and expensive systems for implementation. The majority of them also require placement of guide pins or arrays on scapular bony landmarks, likely leading to an increase in operative time and possible iatrogenic complications, including fracture and pin site infections.
This review focuses on the use of patient-specific guides/instrumentation in shoulder arthroplasty. This includes the topic of proper glenoid and glenosphere placement as well as patient-specific guides/instrumentation and their accuracy.
GLENOID PLACEMENT
Glenohumeral osteoarthritis is the most common indication for TSA2 and commonly results in glenoid deformity. Using computed tomography (CT) scans of 45 arthritic shoulders and 19 normal shoulders, Mullaji and colleagues3 reported that the anteroposterior dimensions of the glenoid were increased by an average of 5 mm to 8 mm in osteoarthritic shoulders and by an average of 6 mm in rheumatoid arthritic shoulders compared to those in normal shoulders. A retrospective review of serial CT scans performed preoperatively on 113 osteoarthritic shoulders by Walch and colleagues4 demonstrated an average retroversion of 16°, and it has been the basis for the commonly used Walch classification of glenoid wear in osteoarthritis. Increased glenoid wear and increased glenoid retroversion make the proper restoration of glenoid version, inclination, and offset during shoulder arthroplasty more difficult and lead to increased glenoid component malpositioning.
Continue to: The ideal placement of the glenoid...
The ideal placement of the glenoid to maximize function, ROM, and implant longevity is in a mechanically neutral alignment with no superoinferior inclination1 and neutral version with respect to the transverse axis of the scapula.5
Improper glenoid positioning has an adverse effect on the functional results of shoulder arthroplasty. Yian and colleagues6 evaluated 47 cemented, pegged glenoids using standard radiography and CT scans at a mean follow-up of 40 months. They observed a significant correlation between increased glenoid component retroversion and lower Constant scores. Hasan and colleagues7 evaluated 139 consecutive patients who were dissatisfied with the result of their primary arthroplasty and found that 28% of them had at least 1 substantially malpositioned component identified either on radiography or during a revision surgery. They also found a significant correlation between stiffness, instability, and component malposition in their cohort.
Glenoid longevity is also dependent on proper component positioning, with the worst outcomes coming if the glenoid is malaligned with either superior or inferior inclination. Hasan and colleagues7 found that of their 74 patients with failed TSAs, 44 patients (59%) demonstrated mechanical loosening of their glenoid components either radiographically or during revision surgery, and 10 of their 44 patients with loose glenoids (23%) also had a malpositioned component. Using finite element analysis, Hopkins and colleagues8 analyzed the stresses through the cement mantle in glenoid prostheses that were centrally aligned, superiorly inclined, inferiorly inclined, anteverted, and retroverted. They found that malalignment of the glenoid increases the stresses through the cement mantle, leading to increased likelihood of mantle failure compared to that of centrally aligned glenoids, especially if there is malalignment with superior or inferior inclination or retroversion.
The accuracy of traditional methods of glenoid placement using an initial guide pin is limited and decreases with increasing amounts of glenoid deformity and retroversion. Iannotti and colleagues 9 investigated 13 patients undergoing TSA with an average preoperative retroversion of 13° and evaluated them using a 3-dimensional (3-D) surgical simulator. They found that the postoperative glenoid version was within 5° of ideal version in only 7 of their 13 patients (54%) and within 10° of ideal version in only 10 of their 13 patients (77%). In their study, the ideal version was considered to be the version as close to perpendicular to the plane of the scapula as possible with complete contact of the back side of the component on glenoid bone and maintenance of the center peg of the component within bone. In addition, they found that of their 7 patients with preoperative retroversion >10°, only 1 patient (14%) had a postoperative glenoid with <10° of retroversion with regard to the plane of the scapula and that all 6 of their patients with preoperative glenoid retroversion of <10° had a postoperative glenoid version of <10°.
Preoperative CT scans are much more accurate at determining glenoid version and thus how much glenoid correction is required to reestablish neutral version than plain radiography. Nyffeler and colleagues10 compared CT scans with axillary views for comparing glenoid version in 25 patients with no shoulder prosthesis present and 25 patients with a TSA in place. They found that glenoid retroversion was overestimated on plain radiographs in 86% of their patients with an average difference between CT and plain radiography of 6.4° and a maximum difference of 21°. They also found poor interobserver reliability in the plain radiography group and good interobserver reliability in the CT group, with coefficients of correlation of 0.77 for the plain radiography group and 0.93 for the CT group. Thus, they concluded that glenoid version cannot be accurately measured by plain radiography and that CT should be used. Hoenecke and colleagues11 subsequently evaluated 33 patients scheduled for TSA and found that CT version measurements made on 2-dimensional (2-D) CT slices compared with 3-D-reconstructed models of the same CT slices differed by an average of 5.1° because the axial CT slices were most often made perpendicular to the axis of the patient’s torso and not perpendicular to the body of the scapula. Accurate version assessment is critically important in planning for the degree of correction required to restore neutral glenoid version, and differences of 6.4° between CT assessment and plain radiography, and 5.1° between 2-D and 3-D CT scan assessments may lead to inadequate version correction intraoperatively and inferior postoperative results.
Continue to: GLENOSPHERE PLACEMENT
GLENOSPHERE PLACEMENT
The most common indication for reverse TSA is rotator cuff arthropathy characterized by rotator cuff dysfunction and end-stage glenohumeral arthritis.12 These patients require accurate and reproducible glenoid placement to optimize their postoperative range of motion and stability and minimize scapular notching.
Ideal glenosphere placement is the location and orientation that maximizes impingement-free ROM and stability while avoiding notching. Individual patient anatomy determines ideal placement; however, several guidelines for placement include inferior translation on the glenoid with neutral to inferior inclination. Gutiérrez and colleagues13 developed a computer model to assess the hierarchy of surgical factors affecting the ROM after a reverse TSA. They found that lateralizing the center of rotation gave the largest increase in impingement-free abduction, followed closely by inferior translation of the glenosphere on the glenoid.
Avoiding scapular notching is also a very important factor in ideal glenosphere placement. Scapular notching can be described as impingement of the humeral cup against the scapular neck during arm adduction and/or humeral rotation. Gutiérrez and colleagues13 also found that decreasing the neck shaft angle to create a more varus proximal humerus was the most important factor in increasing the impingement-free adduction. Roche and colleagues14 reviewed the radiographs of 151 patients who underwent primary reverse TSA at a mean follow-up of 28.3 months postoperatively; they found that 13.2% of their patients had a notch and that, on average, their patients who had no scapular notch had significantly more inferior glenosphere overhang than those who had a scapular notch. Poon and colleagues15 found that a glenosphere overhang of >3.5 mm prevented notching in their randomized control trial comparing concentrically and eccentrically placed glenospheres. Multiple other studies have demonstrated similar results and recommended inferior glenoid translation and inferior glenoid inclination to avoid scapular notching.16,17 Lévigne and colleagues18 retrospectively reviewed 337 reverse TSAs and observed a correlation between scapular notching and radiolucencies around the glenosphere component, with 14% of patients with scapular notching displaying radiolucencies vs 4% of patients without scapula notching displaying radiolucencies.
Several studies have also focused on the ideal amount of inferior glenoid inclination to maximize impingement-free ROM. Li and colleagues17 performed a computer simulation study on the Comprehensive Reverse Shoulder System (Zimmer Biomet) to determine impingement-free internal and external ROM with varying amounts of glenosphere offset, translation, and inclination. They found that progressive glenosphere inferior inclination up to 30° improved impingement-free rotational ROM at all degrees of scaption. Gutiérrez and colleagues19 used computer modeling to compare concentrically placed glenospheres in neutral inclination with eccentrically placed glenospheres in varying degrees of inclination. They found that the lowest forces across the baseplate occurred in the lateralized and inferiorly inclined glenospheres, and the highest forces occurred in the lateralized and superiorly inclined glenospheres. Together, these studies show that inferior glenoid inclination increases impingement-free ROM and, combined with lateralization, may result in improved glenosphere longevity due to significantly decreased forces at the RSA glenoid baseplate when compared to that at superiorly inclined glenoids.
The ideal amount of mediolateral glenosphere offset has not been well defined. Grammont design systems place the center of rotation of the glenosphere medial to the glenoid baseplate together with valgus humeral component neck shaft angles of around 155°. These design elements are believed to decrease shear stresses through the glenoid baseplate to the glenoid interface and improve shoulder stability, but they are also associated with reduced impingement-free ROM and increased rates of scapular notching.13 This effect is accentuated in patients with preexisting glenoid bone loss and/or congenitally short scapular necks that further medialize the glenosphere. Medialization of the glenosphere may also shorten the remaining rotator cuff muscles and result in decreased implant stability and external rotation strength. Several implant systems have options to vary the amount of lateral offset. The correct amount of lateral offset for each patient requires the understanding that improving patients’ impingement-free ROM by increasing the amount of lateral offset comes at the price of increasing the shear forces experienced by the interface between the glenoid baseplate and the glenoid. As glenoid fixation technology improves increased lateralization of glenospheres without increased rates of glenoid baseplate, loosening should improve the ROM after reverse TSA.
Continue to: Regardless of the intraoperative goals...
Regardless of the intraoperative goals for placement and orientation of the glenosphere components, it is vitally important to accurately and consistently meet those goals for achieving optimal patient outcomes. Verborgt and colleagues20 implanted 7 glenospheres in cadaveric specimens without any glenohumeral arthritis using standard techniques to evaluate the accuracy of glenosphere version and inclination. Their goal was to place components in neutral version and with 10° of inferior inclination. Their average glenoid version postoperatively was 8.7° of anteversion, and their average inclination was 0.9° of superior inclination. Throckmorton and colleagues21 randomized 35 cadaveric shoulders to receive either an anatomic or a reverse total shoulder prosthesis from high-, mid-, and low-volume surgeons. They found that components placed using traditional guides averaged 6° of deviation in version and 5° of deviation in inclination from their target values, with no significant differences between surgeons of different volumes.
PATIENT-SPECIFIC GUIDES/INSTRUMENTATION
Patient-specific guides/instrumentation and intraoperative navigation are the 2 techniques that have been used to improve the accuracy of glenoid and glenosphere placement. Both techniques require the use of high-resolution CT scans and computer software to determine the proper position for glenoid or glenosphere placement based on the patient’s individual anatomy. Patient-specific guides and instrumentation use the data acquired from a CT scan to generate a preoperative plan for the location and orientation of the glenoid baseplate. Once the surgeon approves the preoperative plan, a patient-specific guide is created using the patient’s glenoid as a reference for the location and orientation of the central guide pin. The location of the central guide pin on the glenoid determines the center of the glenoid baseplate, and the guide pin’s orientation determines the version and inclination of the glenoid or the glenosphere. Once the guide pin is placed in the glenoid, the remainder of the glenoid implantation uses the guide pin as a reference, and, in that way, patient-specific guides control the orientation of the glenoid at the time of surgery.
Intraoperative navigation uses an optical tracking system to determine the location and orientation of the central guide pin. Navigation systems require intraoperative calibration of the optical tracking system before they can track the location of implantation relative to bony landmarks on the patient’s scapula. Their advantage over patient-specific instrumentation (PSI) is that they do not require the manufacture of a custom guide; however, they may add significantly increased cost and surgical time due to the need for calibration prior to use and the cost of the navigation system along with any disposable components associated with it. Kircher and colleagues22 performed a prospective randomized clinical study of navigation-aided TSA compared with conventional TSA and found that operating time was significantly increased for the navigated group with an average operating room time of 169.5 minutes compared to 138 minutes for the conventional group. They also found that navigation had to be abandoned in 37.5% of their navigated patients due to technical errors during glenoid referencing.
COMMERCIAL PATIENT-SPECIFIC INSTRUMENTATION SYSTEMS
The 2 types of PSI that are currently available are single-use PSI and reusable PSI. The single-use PSI involves the fabrication of unique guides based on surgeon-approved preoperative plans generated by computer-software-processed preoperative CT scans. The guides are fabricated to rest on the glenoid articular surface and direct the guide pin to the correct location and in the correct direction to place the glenoid baseplate in the desired position with the desired version and inclination. Most of these systems also provide a 3-D model of the patient’s glenoid so that surgeons can visualize glenoid deformities and the correct guide placement on the glenoid. Single-use PSI systems are available from DJO Global, Wright Medical Group, and Zimmer Biomet. The second category of PSI is reusable and is available from Arthrex. The guide pin for this system is adjusted to fit individual patient anatomy and guide the guide pin into the glenoid in a location and orientation preplanned on the CT-scan-based computer software or using a 3-D model of the patient’s glenoid (Table).
Table. Details of Available Patient-Specific Instrumentation Systems
| System | Manufacturer | Single-Use/Reusable | Guides |
| MatchPoint System | DJO Global | Single-use | Central guide pin |
| Blueprint 3D Planning + PSI | Wright Medical Group | Single-use | Central guide pin |
| Zimmer Patient Specific Instruments Shoulder | Zimmer Biomet | Single-use | Central guide pin, reaming guide, roll guide, screw drill guide |
| Virtual Implant Positioning System | Arthrex | Reusable | Central guide pin |
The DJO Global patient-specific guide is termed as the MatchPoint System. This system creates 3-D renderings of the scapula and allows the surgeon to manipulate the glenoid baseplate on the scapula. The surgeon chooses the glenoid baseplate, location, version, and inclination on the computerized 3-D model. The system then fabricates a guide pin matching the computerized template that references the patient’s glenoid surface with a hook to orient it against the coracoid. A 3-D model of the glenoid is also provided along with the customized guide pin.
Continue to: Blueprint 3D Planning + PSI...
Blueprint 3D Planning + PSI (Wright Medical Group) allows custom placement of the glenoid version, inclination, and position on computerized 3-D models of the patient’s scapula. This PSI references the glenoid with 4 feet that captures the edge of the patient’s glenoid at specific locations and is unique because it allows the surgeon to control where on the glenoid edge to 4 feet contact as long as 1 foot is placed on the posterior edge of the glenoid and the remaining 3 feet are placed on the anterior edge of the glenoid. A 3-D model of the glenoid is also provided with this guide.
The Zimmer Biomet patient-specific guide is termed as the Zimmer Patient Specific Instruments Shoulder. Its computer software allows custom placement of the glenoid as well, but it also includes computerized customization of the reaming depth, screw angles, and screw lengths to optimize fixation. Their system includes a central guide pin to set the glenoid baseplate’s location and orientation, a reaming guide to control reaming depth and direction, a roll guide to control the glenoid baseplate’s rotation, and a drill guide to control the screw direction. They also provide a 3-D model of the glenoid.
The Arthrex Virtual Implant Positioning (VIP) System is similar to other systems in that its 3-D planning software is based on CT images uploaded by the surgeon. The unique aspect of this system is that the guide pin is adjusted by the surgeon for each individual patient based on instructions generated by the planning software; however, after use, the instruments are resterilized and reused on subsequent patients (Figures 1A, 1B). In this manner, their instruments are reusable and allow custom adjustment for each patient with the ability to set the pin location and glenoid version in a patient-specific manner. This has the potential benefit of keeping costs down. For more complex deformity cases, the Arthrex VIP System can also 3-D-print a sterile model of the glenoid to help surgeons appreciate the deformity better (Figure 2).
DATA ON PATIENT-SPECIFIC INSTRUMENTS
Several studies have measured the accuracy of patient-specific guides and have compared the accuracy of patient-specific guides to that of traditional methods. Levy and colleagues23 investigated the accuracy of single-use patient-specific guides compared to that of preoperative plans. They used patient-specific guides on 14 cadaveric shoulders based on plans developed by virtual preoperative 3-D planning system using CT images. Once the guide pin was drilled using the patient-specific guide, they obtained a second CT scan to compare the accuracy of the patient-specific guide to the surgical plan generated preoperatively. They found that the translational accuracy of the starting point for the guide pin averaged 1.2 mm ± 0.7 mm, the accuracy of the inferior inclination was 1.2° ± 1.2°, and the accuracy of the glenoid version was 2.6° ± 1.7°. They concluded that patient-specific guides were highly accurate in reproducing the starting point, inclination, and version set on preoperative guides.
Walch and colleagues24 subsequently performed a similar study using 15 cadaveric scapulae without any other shoulder soft tissue or bone attached. They also used CT-scan-based 3-D planning software to plan their glenoid placement with a subsequently fabricated single-use patient-specific guide used to place a guide pin. They obtained a second CT scan after guide pin implantation and compared the preoperative plan with the subsequent guide pin. They found a mean entry point position error of 1.05 mm ± 0.31 mm, a mean inclination error of 1.42° ± 1.37°, and a mean version error of 1.64° ± 1.01°.
Continue to: Throckmorton and colleagues...
Throckmorton and colleagues21 used 70 cadaveric shoulders with radiographically confirmed arthritis and randomized them to undergo either anatomic or reverse TSA using either a patient-specific guide or standard instrumentation. Postoperative CT scans were used to evaluate the glenoid inclination, version, and starting point. They found that glenoid components implanted using patient-specific guides were more accurate than those placed using traditional instrumentation. The average deviation from intended inclination was 3° for patient-specific guides and 7° for traditional instrumentation, the average deviation from intended version was 5° for patient-specific guides and 8° for traditional instrumentation, and the average deviation in intended starting point was 2 mm for patient-specific guides and 3 mm for traditional instrumentation. They also analyzed significantly malpositioned components as defined by a variation in version or inclination of >10° or >4 mm in starting point. They found that 6 of their 35 glenoids using patient-specific guides were significantly malpositioned compared to 23 of 35 glenoids using traditional instrumentation. They concluded that patient-specific guides were more accurate and reduced the number of significantly malpositioned implants when compared with traditional instrumentation.
Early and colleagues25 analyzed the effect of severe glenoid bone defects on the accuracy of patient-specific guides compared with traditional guides. Using 10 cadaveric shoulders, they created anterior, central, or posterior glenoid defects using a reamer and chisel to erode the bone past the coracoid base. Subsequent CT scans were performed on the specimens, and patient-specific guides were fabricated and used for reverse TSA in 5 of the 10 specimens. A reverse TSA was performed using traditional instrumentation in the remaining 5 specimens. They found that the average deviation in inclination and version from preoperative plan was more accurate in the patient-specific guide cohort than that in the traditional instrument cohort, with an average deviation in inclination and version of 1.2° ± 1.2° and 1.8° ± 1.2° respectively for the cohort using patient-specific instruments vs 2.8° ± 1.8° and 3.5° ± 3° for the cohort using traditional instruments. They also found that their total bone screw lengths were longer in the patient-specific guide group than those in the traditional group, with screws averaging 52% of preoperatively planned length in the traditional instrument cohort vs 89% of preoperatively planned length in the patient-specific instrument cohort.
Gauci and colleagues26 measured the accuracy of patient-specific guides in vivo in 17 patients receiving TSA. Preoperative CT scans were used to fabricate patient-specific guides, and postoperative CT scans were used to measure version, inclination, and error of entry in comparison with the templated goals used to create patient-specific guides. They found a mean error in version and inclination of 3.4° and 1.8°, respectively, and a mean error in entry of 0.9 mm of translation on the glenoid. Dallalana and colleagues27 performed a very similar study on 20 patients and found a mean deviation in glenoid version of 1.8° ± 1.9°, a mean deviation in glenoid inclination of 1.3° ± 1.0°, a mean translation in anterior-posterior plane of 0.5 mm ± 0.3 mm, and a mean translation in the superior-inferior plane of 0.8 mm ± 0.5 mm.
Hendel and colleagues28 performed a randomized prospective clinical trial comparing patient-specific guides with traditional methods for glenoid insertion. They randomized 31 patients to receive a glenoid implant using either a patient-specific guide or traditional methods and compared glenoid retroversion and inclination with their preoperative plan. They found an average version deviation of 6.9° in the traditional method cohort and 4.3° in the patient-specific guide cohort. Their average deviation in inclination was 11.6° in the traditional method cohort and 2.9° in the patient-specific guide cohort. For patients with preoperative retroversion >16°, the average deviation was 10° in the standard surgical cohort and 1.2° in the patient-specific instrument cohort. Their data suggest that increasing preoperative retroversion leads to an increased version variation from preoperative plan.
Iannotti and colleagues29 randomly assigned 46 patients to preoperatively undergo either CT scan with 3-D templating of glenoid component without patient-specific guide fabrication or CT scan with 3-D templating and patient-specific guide fabrication prior to receiving a TSA. They recorded the postoperative inclination and version for each patient and compared them to those of a nonrandomized control group of 17 patients who underwent TSA using standard instrumentation. They found no difference between the cohorts with or without patient-specific guide use with regard to implant location, inclination, or version; however, they did find a difference between the combined 3-D templating cohort compared with their standard instrumentation cohort. They concluded that 3-D templating significantly improved the surgeons’ ability to correctly position the glenoid component with or without the fabrication and the use of a patient-specific guide.
Continue to: Denard and colleagues...
Denard and colleagues30 compared the preoperative glenoid version and inclination measurements obtained using the Blueprint 3D Planning + PSI software and the VIP System 3D planning software. They analyzed the preoperative CT scans of 63 consecutive patients undergoing either TSA or reverse TSA using both the Blueprint and the VIP System 3D planning software and compared the resulting native glenoid version and inclination measured by the software. They found a statistically significant difference (P = 0.04) in the version measurements provided by the different planning software; however, the differences found in inclination did not reach statistical significance (P = 0.463). In 19 of the 63 patients (30%), the version measurements between the systems were >5°, and in 29 of the 63 patients (46%), the inclination measurements between the systems were 5° or greater. In addition, 12 of the 63 patients (19%) had both version and inclination measurement differences of >5° between the systems. In total, they found that 35 of the 63 patients had at least 1 measurement that varied by >5° between the systems, and that in 15 patients (24%), 1 measurement varied by >10°. Their data demonstrate considerable variability in the preoperative measurements provided by different 3-D planning software systems, and that further study of each commercially available 3-D planning software system is needed to evaluate their accuracy.
CONCLUSION
Optimal outcomes following TSA and reverse TSA are dependent on proper implant position. Multiple studies have demonstrated improved accuracy in implant positioning with the use of patient-specific guides compared to that with traditional methods. Currently, there are no studies comparing the clinical outcomes of patient-specific guides to those of traditional methods of glenoid placement, and limited research had been done comparing the accuracy of each system’s 3-D planning software with each other and with standardized measurements of glenoid version and inclination. Further research is required to determine the accuracy of each commercially available 3-D planning software system as well as the clinical benefit of patient-specific guides in shoulder arthroplasty.
1. Churchill RS, Brems JJ, Kotschi H. Glenoid size, inclination, and version: an anatomic study. J Shoulder Elbow Surg. 2001;10(4):327-332. doi:10.1067/mse.2001.115269.
2. Norris TR, Iannotti JP. Functional outcome after shoulder arthroplasty for primary osteoarthritis: a multicenter study. J Shoulder Elbow Surg. 2002;11(2):130-135. doi:10.1067/mse.2002.121146.
3. Mullaji AB, Beddow FH, Lamb GH. CT measurement of glenoid erosion in arthritis. J Bone Joint Surg Br. 1994;76(3):384-388.
4. Walch G, Badet R, Boulahia A, Khoury A. Morphologic study of the glenoid in primary glenohumeral osteoarthritis. J Arthroplasty. 1999;14(6):756-760.
5. RJ Friedman, KB Hawthorne, BM Genez. The use of computerized tomography in the measurement of glenoid version. J Bone Joint Surg. 1992;74(7):1032-1037. doi:10.2106/00004623-199274070-00009.
6. Yian EH, Werner CM, Nyffeler RW, et al. Radiographic and computed tomography analysis of cemented pegged polyethylene glenoid components in total shoulder replacement. J Bone Joint Surg. 2005;87(9):1928-1936. doi:10.2106/00004623-200509000-00004.
7. Hasan SS, Leith JM, Campbell B, Kapil R, Smith KL, Matsen FA. Characteristics of unsatisfactory shoulder arthroplasties. J Shoulder Elbow Surg. 2002;11(5):431-441.
8. Hopkins AR, Hansen UN, Amis AA, Emery R. The effects of glenoid component alignment variations on cement mantle stresses in total shoulder arthroplasty. J Shoulder Elbow Surg. 2004;13(6):668-675. doi:10.1016/S1058274604001399.
9. Iannotti JP, Greeson C, Downing D, Sabesan V, Bryan JA. Effect of glenoid deformity on glenoid component placement in primary shoulder arthroplasty. J Shoulder Elbow Surg. 2012;21(1):48-55. doi:10.1016/j.jse.2011.02.011.
10. Nyffeler RW, Jost B, Pfirrmann CWA, Gerber C. Measurement of glenoid version: conventional radiographs versus computed tomography scans. J Shoulder Elbow Surg. 2003;12(5):493-496. doi:10.1016/S1058274603001812.
11. Hoenecke HR, Hermida JC, Flores-Hernandez C, D'Lima DD. Accuracy of CT-based measurements of glenoid version for total shoulder arthroplasty. J Shoulder Elbow Surg. 2010;19(2):166-171. doi:10.1016/j.jse.2009.08.009.
12. Wall B, Nové-Josserand L, O'Connor DP, Edwards TB, Walch G. Reverse total shoulder arthroplasty: a review of results according to etiology. J Bone Joint Surg Am. 2007;89(7):1476-1485. doi:10.2106/JBJS.F.00666.
13. Gutiérrez S, Comiskey 4, Charles A, Luo Z, Pupello DR, Frankle MA. Range of impingement-free abduction and adduction deficit after reverse shoulder arthroplasty. hierarchy of surgical and implant-design-related factors. J Bone Joint Surg Am. 2008;90(12):2606-2615. doi:10.2106/JBJS.H.00012.
14. Roche CP, Marczuk Y, Wright TW, et al. Scapular notching and osteophyte formation after reverse shoulder replacement: Radiological analysis of implant position in male and female patients. Bone Joint J. 2013;95-B(4):530-535. doi:10.1302/0301-620X.95B4.30442.
15. Poon PC, Chou J, Young SW, Astley T. A comparison of concentric and eccentric glenospheres in reverse shoulder arthroplasty: a randomized controlled trial. J Bone Joint Surg Am. 2014;96(16):e138. doi:10.2106/JBJS.M.00941.
16. Nyffeler RW, Werner CML, Gerber C. Biomechanical relevance of glenoid component positioning in the reverse delta III total shoulder prosthesis. J Shoulder Elbow Surg. 2005;14(5):524-528. doi:10.1016/j.jse.2004.09.010.
17. Li X, Knutson Z, Choi D, et al. Effects of glenosphere positioning on impingement-free internal and external rotation after reverse total shoulder arthroplasty. J Shoulder Elbow Surg. 2013;22(6):807-813. doi:10.1016/j.jse.2012.07.013.
18. Lévigne C, Boileau P, Favard L, et al. Scapular notching in reverse shoulder arthroplasty. J Shoulder Elbow Surg. 2008;17(6):925-935. doi:10.1016/j.jse.2008.02.010.
19. Gutiérrez S, Walker M, Willis M, Pupello DR, Frankle MA. Effects of tilt and glenosphere eccentricity on baseplate/bone interface forces in a computational model, validated by a mechanical model, of reverse shoulder arthroplasty. J Shoulder Elbow Surg. 2011;20(5):732-739. doi:10.1016/j.jse.2010.10.035.
20. Verborgt O, De Smedt T, Vanhees M, Clockaerts S, Parizel PM, Van Glabbeek F. Accuracy of placement of the glenoid component in reversed shoulder arthroplasty with and without navigation. J Shoulder Elbow Surg. 2011;20(1):21-26. doi:10.1016/j.jse.2010.07.014.
21. Throckmorton TW, Gulotta LV, Bonnarens FO, et al. Patient-specific targeting guides compared with traditional instrumentation for glenoid component placement in shoulder arthroplasty: A multi-surgeon study in 70 arthritic cadaver specimens. J Shoulder Elbow Surg. 2015;24(6):965-971. doi:10.1016/j.jse.2014.10.013.
22. Kircher J, Wiedemann M, Magosch P, Lichtenberg S, Habermeyer P. Improved accuracy of glenoid positioning in total shoulder arthroplasty with intraoperative navigation: a prospective-randomized clinical study. J Shoulder Elbow Surg. 2009;18(4):515-520. doi:10.1016/j.jse.2009.03.014.
23. Levy JC, Everding NG, Frankle MA, Keppler LJ. Accuracy of patient-specific guided glenoid baseplate positioning for reverse shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(10):1563-1567. doi:10.1016/j.jse.2014.01.051.
24. Walch G, Vezeridis PS, Boileau P, Deransart P, Chaoui J. Three-dimensional planning and use of patient-specific guides improve glenoid component position: an in vitro study. J Shoulder Elbow Surg. 2015;24(2):302-309. doi:10.1016/j.jse.2014.05.029.
25. Eraly K, Stoffelen D, Vander Sloten J, Jonkers I, Debeer P. A patient-specific guide for optimizing custom-made glenoid implantation in cases of severe glenoid defects: an in vitro study. J Shoulder Elbow Surg. 2016;25(5):837-845. doi:10.1016/j.jse.2015.09.034.
26. Gauci MO, Boileau P, Baba M, Chaoui J, Walch G. Patient-specific glenoid guides provide accuracy and reproducibility in total shoulder arthroplasty. Bone Joint J. 2016;98-B(8):1080-1085. doi:10.1302/0301-620X.98B8.37257.
27. Dallalana RJ, McMahon RA, East B, Geraghty L. Accuracy of patient-specific instrumentation in anatomic and reverse total shoulder arthroplasty. Int J Shoulder Surg. 2016;10(2):59-66. doi:10.4103/09736042.180717.
28. Hendel MD, Bryan JA, Barsoum WK, et al. Comparison of patient-specific instruments with standard surgical instruments in determining glenoid component position: a randomized prospective clinical trial. J Bone Joint Surg. 2012;94(23):2167-2175. doi:10.2106/JBJS.K.01209.
29. Iannotti JP, Weiner S, Rodriguez E, et al. Three-dimensional imaging and templating improve glenoid implant positioning. J Bone Joint Surg. 2015;97(8):651-658. doi:10.2106/JBJS.N.00493.
30. Denard PJ, Provencher MT, Lädermann A, Romeo AA, Dines JS. Version and inclination obtained with 3D planning in total shoulder arthroplasty: do different programs produce the same results? SECEC-ESSSE Congress, Berlin 2017. 2017.
ABSTRACT
Optimal outcomes following total shoulder arthroplasty TSA and reverse shoulder arthroplasty RSA are dependent on proper implant position. Multiple cadaver studies have demonstrated improved accuracy of implant positioning with use of patient-specific guides/instrumentation compared to traditional methods. At this time, there are 3 commercially available single use patient-specific instrumentation systems and 1 commercially available reusable patient-specific instrumentation system. Currently though, there are no studies comparing the clinical outcomes of patient-specific guides to those of traditional methods of glenoid placement, and limited research has been done comparing the accuracy of each system’s 3-dimensional planning software. Future work is necessary to elucidate the ideal indications for the use of patient-specific guides and instrumentation, but it is likely, particularly in the setting of advanced glenoid deformity, that these systems will improve a surgeon's ability to put the implant in the best position possible.
Continue to: Optimal functional recovery...
Optimal functional recovery and implant longevity following both total shoulder arthroplasty (TSA) and reverse shoulder arthroplasty (RSA) depend, in large part, on proper placement of the glenoid component. Glenoid component malpositioning has an adverse effect on shoulder stability, range of motion (ROM), impingement, and glenoid implant longevity.
Traditionally, glenoid component positioning has been done manually by the surgeons based on their review of preoperative films and knowledge of glenoid anatomy. Anatomic studies have demonstrated high individual variability in the version of the native glenoid, thus making ideal placement of the initial glenoid guide pin difficult using standard guide pin guides.1
The following 2 methods have been described for improving the accuracy of glenoid guide pin insertion and subsequent glenoid implant placement: (1) computerized navigation and (2) patient-specific guides/instrumentation. Although navigated shoulder systems have demonstrated improved accuracy in glenoid placement compared with traditional methods, navigated systems require often large and expensive systems for implementation. The majority of them also require placement of guide pins or arrays on scapular bony landmarks, likely leading to an increase in operative time and possible iatrogenic complications, including fracture and pin site infections.
This review focuses on the use of patient-specific guides/instrumentation in shoulder arthroplasty. This includes the topic of proper glenoid and glenosphere placement as well as patient-specific guides/instrumentation and their accuracy.
GLENOID PLACEMENT
Glenohumeral osteoarthritis is the most common indication for TSA2 and commonly results in glenoid deformity. Using computed tomography (CT) scans of 45 arthritic shoulders and 19 normal shoulders, Mullaji and colleagues3 reported that the anteroposterior dimensions of the glenoid were increased by an average of 5 mm to 8 mm in osteoarthritic shoulders and by an average of 6 mm in rheumatoid arthritic shoulders compared to those in normal shoulders. A retrospective review of serial CT scans performed preoperatively on 113 osteoarthritic shoulders by Walch and colleagues4 demonstrated an average retroversion of 16°, and it has been the basis for the commonly used Walch classification of glenoid wear in osteoarthritis. Increased glenoid wear and increased glenoid retroversion make the proper restoration of glenoid version, inclination, and offset during shoulder arthroplasty more difficult and lead to increased glenoid component malpositioning.
Continue to: The ideal placement of the glenoid...
The ideal placement of the glenoid to maximize function, ROM, and implant longevity is in a mechanically neutral alignment with no superoinferior inclination1 and neutral version with respect to the transverse axis of the scapula.5
Improper glenoid positioning has an adverse effect on the functional results of shoulder arthroplasty. Yian and colleagues6 evaluated 47 cemented, pegged glenoids using standard radiography and CT scans at a mean follow-up of 40 months. They observed a significant correlation between increased glenoid component retroversion and lower Constant scores. Hasan and colleagues7 evaluated 139 consecutive patients who were dissatisfied with the result of their primary arthroplasty and found that 28% of them had at least 1 substantially malpositioned component identified either on radiography or during a revision surgery. They also found a significant correlation between stiffness, instability, and component malposition in their cohort.
Glenoid longevity is also dependent on proper component positioning, with the worst outcomes coming if the glenoid is malaligned with either superior or inferior inclination. Hasan and colleagues7 found that of their 74 patients with failed TSAs, 44 patients (59%) demonstrated mechanical loosening of their glenoid components either radiographically or during revision surgery, and 10 of their 44 patients with loose glenoids (23%) also had a malpositioned component. Using finite element analysis, Hopkins and colleagues8 analyzed the stresses through the cement mantle in glenoid prostheses that were centrally aligned, superiorly inclined, inferiorly inclined, anteverted, and retroverted. They found that malalignment of the glenoid increases the stresses through the cement mantle, leading to increased likelihood of mantle failure compared to that of centrally aligned glenoids, especially if there is malalignment with superior or inferior inclination or retroversion.
The accuracy of traditional methods of glenoid placement using an initial guide pin is limited and decreases with increasing amounts of glenoid deformity and retroversion. Iannotti and colleagues 9 investigated 13 patients undergoing TSA with an average preoperative retroversion of 13° and evaluated them using a 3-dimensional (3-D) surgical simulator. They found that the postoperative glenoid version was within 5° of ideal version in only 7 of their 13 patients (54%) and within 10° of ideal version in only 10 of their 13 patients (77%). In their study, the ideal version was considered to be the version as close to perpendicular to the plane of the scapula as possible with complete contact of the back side of the component on glenoid bone and maintenance of the center peg of the component within bone. In addition, they found that of their 7 patients with preoperative retroversion >10°, only 1 patient (14%) had a postoperative glenoid with <10° of retroversion with regard to the plane of the scapula and that all 6 of their patients with preoperative glenoid retroversion of <10° had a postoperative glenoid version of <10°.
Preoperative CT scans are much more accurate at determining glenoid version and thus how much glenoid correction is required to reestablish neutral version than plain radiography. Nyffeler and colleagues10 compared CT scans with axillary views for comparing glenoid version in 25 patients with no shoulder prosthesis present and 25 patients with a TSA in place. They found that glenoid retroversion was overestimated on plain radiographs in 86% of their patients with an average difference between CT and plain radiography of 6.4° and a maximum difference of 21°. They also found poor interobserver reliability in the plain radiography group and good interobserver reliability in the CT group, with coefficients of correlation of 0.77 for the plain radiography group and 0.93 for the CT group. Thus, they concluded that glenoid version cannot be accurately measured by plain radiography and that CT should be used. Hoenecke and colleagues11 subsequently evaluated 33 patients scheduled for TSA and found that CT version measurements made on 2-dimensional (2-D) CT slices compared with 3-D-reconstructed models of the same CT slices differed by an average of 5.1° because the axial CT slices were most often made perpendicular to the axis of the patient’s torso and not perpendicular to the body of the scapula. Accurate version assessment is critically important in planning for the degree of correction required to restore neutral glenoid version, and differences of 6.4° between CT assessment and plain radiography, and 5.1° between 2-D and 3-D CT scan assessments may lead to inadequate version correction intraoperatively and inferior postoperative results.
Continue to: GLENOSPHERE PLACEMENT
GLENOSPHERE PLACEMENT
The most common indication for reverse TSA is rotator cuff arthropathy characterized by rotator cuff dysfunction and end-stage glenohumeral arthritis.12 These patients require accurate and reproducible glenoid placement to optimize their postoperative range of motion and stability and minimize scapular notching.
Ideal glenosphere placement is the location and orientation that maximizes impingement-free ROM and stability while avoiding notching. Individual patient anatomy determines ideal placement; however, several guidelines for placement include inferior translation on the glenoid with neutral to inferior inclination. Gutiérrez and colleagues13 developed a computer model to assess the hierarchy of surgical factors affecting the ROM after a reverse TSA. They found that lateralizing the center of rotation gave the largest increase in impingement-free abduction, followed closely by inferior translation of the glenosphere on the glenoid.
Avoiding scapular notching is also a very important factor in ideal glenosphere placement. Scapular notching can be described as impingement of the humeral cup against the scapular neck during arm adduction and/or humeral rotation. Gutiérrez and colleagues13 also found that decreasing the neck shaft angle to create a more varus proximal humerus was the most important factor in increasing the impingement-free adduction. Roche and colleagues14 reviewed the radiographs of 151 patients who underwent primary reverse TSA at a mean follow-up of 28.3 months postoperatively; they found that 13.2% of their patients had a notch and that, on average, their patients who had no scapular notch had significantly more inferior glenosphere overhang than those who had a scapular notch. Poon and colleagues15 found that a glenosphere overhang of >3.5 mm prevented notching in their randomized control trial comparing concentrically and eccentrically placed glenospheres. Multiple other studies have demonstrated similar results and recommended inferior glenoid translation and inferior glenoid inclination to avoid scapular notching.16,17 Lévigne and colleagues18 retrospectively reviewed 337 reverse TSAs and observed a correlation between scapular notching and radiolucencies around the glenosphere component, with 14% of patients with scapular notching displaying radiolucencies vs 4% of patients without scapula notching displaying radiolucencies.
Several studies have also focused on the ideal amount of inferior glenoid inclination to maximize impingement-free ROM. Li and colleagues17 performed a computer simulation study on the Comprehensive Reverse Shoulder System (Zimmer Biomet) to determine impingement-free internal and external ROM with varying amounts of glenosphere offset, translation, and inclination. They found that progressive glenosphere inferior inclination up to 30° improved impingement-free rotational ROM at all degrees of scaption. Gutiérrez and colleagues19 used computer modeling to compare concentrically placed glenospheres in neutral inclination with eccentrically placed glenospheres in varying degrees of inclination. They found that the lowest forces across the baseplate occurred in the lateralized and inferiorly inclined glenospheres, and the highest forces occurred in the lateralized and superiorly inclined glenospheres. Together, these studies show that inferior glenoid inclination increases impingement-free ROM and, combined with lateralization, may result in improved glenosphere longevity due to significantly decreased forces at the RSA glenoid baseplate when compared to that at superiorly inclined glenoids.
The ideal amount of mediolateral glenosphere offset has not been well defined. Grammont design systems place the center of rotation of the glenosphere medial to the glenoid baseplate together with valgus humeral component neck shaft angles of around 155°. These design elements are believed to decrease shear stresses through the glenoid baseplate to the glenoid interface and improve shoulder stability, but they are also associated with reduced impingement-free ROM and increased rates of scapular notching.13 This effect is accentuated in patients with preexisting glenoid bone loss and/or congenitally short scapular necks that further medialize the glenosphere. Medialization of the glenosphere may also shorten the remaining rotator cuff muscles and result in decreased implant stability and external rotation strength. Several implant systems have options to vary the amount of lateral offset. The correct amount of lateral offset for each patient requires the understanding that improving patients’ impingement-free ROM by increasing the amount of lateral offset comes at the price of increasing the shear forces experienced by the interface between the glenoid baseplate and the glenoid. As glenoid fixation technology improves increased lateralization of glenospheres without increased rates of glenoid baseplate, loosening should improve the ROM after reverse TSA.
Continue to: Regardless of the intraoperative goals...
Regardless of the intraoperative goals for placement and orientation of the glenosphere components, it is vitally important to accurately and consistently meet those goals for achieving optimal patient outcomes. Verborgt and colleagues20 implanted 7 glenospheres in cadaveric specimens without any glenohumeral arthritis using standard techniques to evaluate the accuracy of glenosphere version and inclination. Their goal was to place components in neutral version and with 10° of inferior inclination. Their average glenoid version postoperatively was 8.7° of anteversion, and their average inclination was 0.9° of superior inclination. Throckmorton and colleagues21 randomized 35 cadaveric shoulders to receive either an anatomic or a reverse total shoulder prosthesis from high-, mid-, and low-volume surgeons. They found that components placed using traditional guides averaged 6° of deviation in version and 5° of deviation in inclination from their target values, with no significant differences between surgeons of different volumes.
PATIENT-SPECIFIC GUIDES/INSTRUMENTATION
Patient-specific guides/instrumentation and intraoperative navigation are the 2 techniques that have been used to improve the accuracy of glenoid and glenosphere placement. Both techniques require the use of high-resolution CT scans and computer software to determine the proper position for glenoid or glenosphere placement based on the patient’s individual anatomy. Patient-specific guides and instrumentation use the data acquired from a CT scan to generate a preoperative plan for the location and orientation of the glenoid baseplate. Once the surgeon approves the preoperative plan, a patient-specific guide is created using the patient’s glenoid as a reference for the location and orientation of the central guide pin. The location of the central guide pin on the glenoid determines the center of the glenoid baseplate, and the guide pin’s orientation determines the version and inclination of the glenoid or the glenosphere. Once the guide pin is placed in the glenoid, the remainder of the glenoid implantation uses the guide pin as a reference, and, in that way, patient-specific guides control the orientation of the glenoid at the time of surgery.
Intraoperative navigation uses an optical tracking system to determine the location and orientation of the central guide pin. Navigation systems require intraoperative calibration of the optical tracking system before they can track the location of implantation relative to bony landmarks on the patient’s scapula. Their advantage over patient-specific instrumentation (PSI) is that they do not require the manufacture of a custom guide; however, they may add significantly increased cost and surgical time due to the need for calibration prior to use and the cost of the navigation system along with any disposable components associated with it. Kircher and colleagues22 performed a prospective randomized clinical study of navigation-aided TSA compared with conventional TSA and found that operating time was significantly increased for the navigated group with an average operating room time of 169.5 minutes compared to 138 minutes for the conventional group. They also found that navigation had to be abandoned in 37.5% of their navigated patients due to technical errors during glenoid referencing.
COMMERCIAL PATIENT-SPECIFIC INSTRUMENTATION SYSTEMS
The 2 types of PSI that are currently available are single-use PSI and reusable PSI. The single-use PSI involves the fabrication of unique guides based on surgeon-approved preoperative plans generated by computer-software-processed preoperative CT scans. The guides are fabricated to rest on the glenoid articular surface and direct the guide pin to the correct location and in the correct direction to place the glenoid baseplate in the desired position with the desired version and inclination. Most of these systems also provide a 3-D model of the patient’s glenoid so that surgeons can visualize glenoid deformities and the correct guide placement on the glenoid. Single-use PSI systems are available from DJO Global, Wright Medical Group, and Zimmer Biomet. The second category of PSI is reusable and is available from Arthrex. The guide pin for this system is adjusted to fit individual patient anatomy and guide the guide pin into the glenoid in a location and orientation preplanned on the CT-scan-based computer software or using a 3-D model of the patient’s glenoid (Table).
Table. Details of Available Patient-Specific Instrumentation Systems
| System | Manufacturer | Single-Use/Reusable | Guides |
| MatchPoint System | DJO Global | Single-use | Central guide pin |
| Blueprint 3D Planning + PSI | Wright Medical Group | Single-use | Central guide pin |
| Zimmer Patient Specific Instruments Shoulder | Zimmer Biomet | Single-use | Central guide pin, reaming guide, roll guide, screw drill guide |
| Virtual Implant Positioning System | Arthrex | Reusable | Central guide pin |
The DJO Global patient-specific guide is termed as the MatchPoint System. This system creates 3-D renderings of the scapula and allows the surgeon to manipulate the glenoid baseplate on the scapula. The surgeon chooses the glenoid baseplate, location, version, and inclination on the computerized 3-D model. The system then fabricates a guide pin matching the computerized template that references the patient’s glenoid surface with a hook to orient it against the coracoid. A 3-D model of the glenoid is also provided along with the customized guide pin.
Continue to: Blueprint 3D Planning + PSI...
Blueprint 3D Planning + PSI (Wright Medical Group) allows custom placement of the glenoid version, inclination, and position on computerized 3-D models of the patient’s scapula. This PSI references the glenoid with 4 feet that captures the edge of the patient’s glenoid at specific locations and is unique because it allows the surgeon to control where on the glenoid edge to 4 feet contact as long as 1 foot is placed on the posterior edge of the glenoid and the remaining 3 feet are placed on the anterior edge of the glenoid. A 3-D model of the glenoid is also provided with this guide.
The Zimmer Biomet patient-specific guide is termed as the Zimmer Patient Specific Instruments Shoulder. Its computer software allows custom placement of the glenoid as well, but it also includes computerized customization of the reaming depth, screw angles, and screw lengths to optimize fixation. Their system includes a central guide pin to set the glenoid baseplate’s location and orientation, a reaming guide to control reaming depth and direction, a roll guide to control the glenoid baseplate’s rotation, and a drill guide to control the screw direction. They also provide a 3-D model of the glenoid.
The Arthrex Virtual Implant Positioning (VIP) System is similar to other systems in that its 3-D planning software is based on CT images uploaded by the surgeon. The unique aspect of this system is that the guide pin is adjusted by the surgeon for each individual patient based on instructions generated by the planning software; however, after use, the instruments are resterilized and reused on subsequent patients (Figures 1A, 1B). In this manner, their instruments are reusable and allow custom adjustment for each patient with the ability to set the pin location and glenoid version in a patient-specific manner. This has the potential benefit of keeping costs down. For more complex deformity cases, the Arthrex VIP System can also 3-D-print a sterile model of the glenoid to help surgeons appreciate the deformity better (Figure 2).
DATA ON PATIENT-SPECIFIC INSTRUMENTS
Several studies have measured the accuracy of patient-specific guides and have compared the accuracy of patient-specific guides to that of traditional methods. Levy and colleagues23 investigated the accuracy of single-use patient-specific guides compared to that of preoperative plans. They used patient-specific guides on 14 cadaveric shoulders based on plans developed by virtual preoperative 3-D planning system using CT images. Once the guide pin was drilled using the patient-specific guide, they obtained a second CT scan to compare the accuracy of the patient-specific guide to the surgical plan generated preoperatively. They found that the translational accuracy of the starting point for the guide pin averaged 1.2 mm ± 0.7 mm, the accuracy of the inferior inclination was 1.2° ± 1.2°, and the accuracy of the glenoid version was 2.6° ± 1.7°. They concluded that patient-specific guides were highly accurate in reproducing the starting point, inclination, and version set on preoperative guides.
Walch and colleagues24 subsequently performed a similar study using 15 cadaveric scapulae without any other shoulder soft tissue or bone attached. They also used CT-scan-based 3-D planning software to plan their glenoid placement with a subsequently fabricated single-use patient-specific guide used to place a guide pin. They obtained a second CT scan after guide pin implantation and compared the preoperative plan with the subsequent guide pin. They found a mean entry point position error of 1.05 mm ± 0.31 mm, a mean inclination error of 1.42° ± 1.37°, and a mean version error of 1.64° ± 1.01°.
Continue to: Throckmorton and colleagues...
Throckmorton and colleagues21 used 70 cadaveric shoulders with radiographically confirmed arthritis and randomized them to undergo either anatomic or reverse TSA using either a patient-specific guide or standard instrumentation. Postoperative CT scans were used to evaluate the glenoid inclination, version, and starting point. They found that glenoid components implanted using patient-specific guides were more accurate than those placed using traditional instrumentation. The average deviation from intended inclination was 3° for patient-specific guides and 7° for traditional instrumentation, the average deviation from intended version was 5° for patient-specific guides and 8° for traditional instrumentation, and the average deviation in intended starting point was 2 mm for patient-specific guides and 3 mm for traditional instrumentation. They also analyzed significantly malpositioned components as defined by a variation in version or inclination of >10° or >4 mm in starting point. They found that 6 of their 35 glenoids using patient-specific guides were significantly malpositioned compared to 23 of 35 glenoids using traditional instrumentation. They concluded that patient-specific guides were more accurate and reduced the number of significantly malpositioned implants when compared with traditional instrumentation.
Early and colleagues25 analyzed the effect of severe glenoid bone defects on the accuracy of patient-specific guides compared with traditional guides. Using 10 cadaveric shoulders, they created anterior, central, or posterior glenoid defects using a reamer and chisel to erode the bone past the coracoid base. Subsequent CT scans were performed on the specimens, and patient-specific guides were fabricated and used for reverse TSA in 5 of the 10 specimens. A reverse TSA was performed using traditional instrumentation in the remaining 5 specimens. They found that the average deviation in inclination and version from preoperative plan was more accurate in the patient-specific guide cohort than that in the traditional instrument cohort, with an average deviation in inclination and version of 1.2° ± 1.2° and 1.8° ± 1.2° respectively for the cohort using patient-specific instruments vs 2.8° ± 1.8° and 3.5° ± 3° for the cohort using traditional instruments. They also found that their total bone screw lengths were longer in the patient-specific guide group than those in the traditional group, with screws averaging 52% of preoperatively planned length in the traditional instrument cohort vs 89% of preoperatively planned length in the patient-specific instrument cohort.
Gauci and colleagues26 measured the accuracy of patient-specific guides in vivo in 17 patients receiving TSA. Preoperative CT scans were used to fabricate patient-specific guides, and postoperative CT scans were used to measure version, inclination, and error of entry in comparison with the templated goals used to create patient-specific guides. They found a mean error in version and inclination of 3.4° and 1.8°, respectively, and a mean error in entry of 0.9 mm of translation on the glenoid. Dallalana and colleagues27 performed a very similar study on 20 patients and found a mean deviation in glenoid version of 1.8° ± 1.9°, a mean deviation in glenoid inclination of 1.3° ± 1.0°, a mean translation in anterior-posterior plane of 0.5 mm ± 0.3 mm, and a mean translation in the superior-inferior plane of 0.8 mm ± 0.5 mm.
Hendel and colleagues28 performed a randomized prospective clinical trial comparing patient-specific guides with traditional methods for glenoid insertion. They randomized 31 patients to receive a glenoid implant using either a patient-specific guide or traditional methods and compared glenoid retroversion and inclination with their preoperative plan. They found an average version deviation of 6.9° in the traditional method cohort and 4.3° in the patient-specific guide cohort. Their average deviation in inclination was 11.6° in the traditional method cohort and 2.9° in the patient-specific guide cohort. For patients with preoperative retroversion >16°, the average deviation was 10° in the standard surgical cohort and 1.2° in the patient-specific instrument cohort. Their data suggest that increasing preoperative retroversion leads to an increased version variation from preoperative plan.
Iannotti and colleagues29 randomly assigned 46 patients to preoperatively undergo either CT scan with 3-D templating of glenoid component without patient-specific guide fabrication or CT scan with 3-D templating and patient-specific guide fabrication prior to receiving a TSA. They recorded the postoperative inclination and version for each patient and compared them to those of a nonrandomized control group of 17 patients who underwent TSA using standard instrumentation. They found no difference between the cohorts with or without patient-specific guide use with regard to implant location, inclination, or version; however, they did find a difference between the combined 3-D templating cohort compared with their standard instrumentation cohort. They concluded that 3-D templating significantly improved the surgeons’ ability to correctly position the glenoid component with or without the fabrication and the use of a patient-specific guide.
Continue to: Denard and colleagues...
Denard and colleagues30 compared the preoperative glenoid version and inclination measurements obtained using the Blueprint 3D Planning + PSI software and the VIP System 3D planning software. They analyzed the preoperative CT scans of 63 consecutive patients undergoing either TSA or reverse TSA using both the Blueprint and the VIP System 3D planning software and compared the resulting native glenoid version and inclination measured by the software. They found a statistically significant difference (P = 0.04) in the version measurements provided by the different planning software; however, the differences found in inclination did not reach statistical significance (P = 0.463). In 19 of the 63 patients (30%), the version measurements between the systems were >5°, and in 29 of the 63 patients (46%), the inclination measurements between the systems were 5° or greater. In addition, 12 of the 63 patients (19%) had both version and inclination measurement differences of >5° between the systems. In total, they found that 35 of the 63 patients had at least 1 measurement that varied by >5° between the systems, and that in 15 patients (24%), 1 measurement varied by >10°. Their data demonstrate considerable variability in the preoperative measurements provided by different 3-D planning software systems, and that further study of each commercially available 3-D planning software system is needed to evaluate their accuracy.
CONCLUSION
Optimal outcomes following TSA and reverse TSA are dependent on proper implant position. Multiple studies have demonstrated improved accuracy in implant positioning with the use of patient-specific guides compared to that with traditional methods. Currently, there are no studies comparing the clinical outcomes of patient-specific guides to those of traditional methods of glenoid placement, and limited research had been done comparing the accuracy of each system’s 3-D planning software with each other and with standardized measurements of glenoid version and inclination. Further research is required to determine the accuracy of each commercially available 3-D planning software system as well as the clinical benefit of patient-specific guides in shoulder arthroplasty.
ABSTRACT
Optimal outcomes following total shoulder arthroplasty TSA and reverse shoulder arthroplasty RSA are dependent on proper implant position. Multiple cadaver studies have demonstrated improved accuracy of implant positioning with use of patient-specific guides/instrumentation compared to traditional methods. At this time, there are 3 commercially available single use patient-specific instrumentation systems and 1 commercially available reusable patient-specific instrumentation system. Currently though, there are no studies comparing the clinical outcomes of patient-specific guides to those of traditional methods of glenoid placement, and limited research has been done comparing the accuracy of each system’s 3-dimensional planning software. Future work is necessary to elucidate the ideal indications for the use of patient-specific guides and instrumentation, but it is likely, particularly in the setting of advanced glenoid deformity, that these systems will improve a surgeon's ability to put the implant in the best position possible.
Continue to: Optimal functional recovery...
Optimal functional recovery and implant longevity following both total shoulder arthroplasty (TSA) and reverse shoulder arthroplasty (RSA) depend, in large part, on proper placement of the glenoid component. Glenoid component malpositioning has an adverse effect on shoulder stability, range of motion (ROM), impingement, and glenoid implant longevity.
Traditionally, glenoid component positioning has been done manually by the surgeons based on their review of preoperative films and knowledge of glenoid anatomy. Anatomic studies have demonstrated high individual variability in the version of the native glenoid, thus making ideal placement of the initial glenoid guide pin difficult using standard guide pin guides.1
The following 2 methods have been described for improving the accuracy of glenoid guide pin insertion and subsequent glenoid implant placement: (1) computerized navigation and (2) patient-specific guides/instrumentation. Although navigated shoulder systems have demonstrated improved accuracy in glenoid placement compared with traditional methods, navigated systems require often large and expensive systems for implementation. The majority of them also require placement of guide pins or arrays on scapular bony landmarks, likely leading to an increase in operative time and possible iatrogenic complications, including fracture and pin site infections.
This review focuses on the use of patient-specific guides/instrumentation in shoulder arthroplasty. This includes the topic of proper glenoid and glenosphere placement as well as patient-specific guides/instrumentation and their accuracy.
GLENOID PLACEMENT
Glenohumeral osteoarthritis is the most common indication for TSA2 and commonly results in glenoid deformity. Using computed tomography (CT) scans of 45 arthritic shoulders and 19 normal shoulders, Mullaji and colleagues3 reported that the anteroposterior dimensions of the glenoid were increased by an average of 5 mm to 8 mm in osteoarthritic shoulders and by an average of 6 mm in rheumatoid arthritic shoulders compared to those in normal shoulders. A retrospective review of serial CT scans performed preoperatively on 113 osteoarthritic shoulders by Walch and colleagues4 demonstrated an average retroversion of 16°, and it has been the basis for the commonly used Walch classification of glenoid wear in osteoarthritis. Increased glenoid wear and increased glenoid retroversion make the proper restoration of glenoid version, inclination, and offset during shoulder arthroplasty more difficult and lead to increased glenoid component malpositioning.
Continue to: The ideal placement of the glenoid...
The ideal placement of the glenoid to maximize function, ROM, and implant longevity is in a mechanically neutral alignment with no superoinferior inclination1 and neutral version with respect to the transverse axis of the scapula.5
Improper glenoid positioning has an adverse effect on the functional results of shoulder arthroplasty. Yian and colleagues6 evaluated 47 cemented, pegged glenoids using standard radiography and CT scans at a mean follow-up of 40 months. They observed a significant correlation between increased glenoid component retroversion and lower Constant scores. Hasan and colleagues7 evaluated 139 consecutive patients who were dissatisfied with the result of their primary arthroplasty and found that 28% of them had at least 1 substantially malpositioned component identified either on radiography or during a revision surgery. They also found a significant correlation between stiffness, instability, and component malposition in their cohort.
Glenoid longevity is also dependent on proper component positioning, with the worst outcomes coming if the glenoid is malaligned with either superior or inferior inclination. Hasan and colleagues7 found that of their 74 patients with failed TSAs, 44 patients (59%) demonstrated mechanical loosening of their glenoid components either radiographically or during revision surgery, and 10 of their 44 patients with loose glenoids (23%) also had a malpositioned component. Using finite element analysis, Hopkins and colleagues8 analyzed the stresses through the cement mantle in glenoid prostheses that were centrally aligned, superiorly inclined, inferiorly inclined, anteverted, and retroverted. They found that malalignment of the glenoid increases the stresses through the cement mantle, leading to increased likelihood of mantle failure compared to that of centrally aligned glenoids, especially if there is malalignment with superior or inferior inclination or retroversion.
The accuracy of traditional methods of glenoid placement using an initial guide pin is limited and decreases with increasing amounts of glenoid deformity and retroversion. Iannotti and colleagues 9 investigated 13 patients undergoing TSA with an average preoperative retroversion of 13° and evaluated them using a 3-dimensional (3-D) surgical simulator. They found that the postoperative glenoid version was within 5° of ideal version in only 7 of their 13 patients (54%) and within 10° of ideal version in only 10 of their 13 patients (77%). In their study, the ideal version was considered to be the version as close to perpendicular to the plane of the scapula as possible with complete contact of the back side of the component on glenoid bone and maintenance of the center peg of the component within bone. In addition, they found that of their 7 patients with preoperative retroversion >10°, only 1 patient (14%) had a postoperative glenoid with <10° of retroversion with regard to the plane of the scapula and that all 6 of their patients with preoperative glenoid retroversion of <10° had a postoperative glenoid version of <10°.
Preoperative CT scans are much more accurate at determining glenoid version and thus how much glenoid correction is required to reestablish neutral version than plain radiography. Nyffeler and colleagues10 compared CT scans with axillary views for comparing glenoid version in 25 patients with no shoulder prosthesis present and 25 patients with a TSA in place. They found that glenoid retroversion was overestimated on plain radiographs in 86% of their patients with an average difference between CT and plain radiography of 6.4° and a maximum difference of 21°. They also found poor interobserver reliability in the plain radiography group and good interobserver reliability in the CT group, with coefficients of correlation of 0.77 for the plain radiography group and 0.93 for the CT group. Thus, they concluded that glenoid version cannot be accurately measured by plain radiography and that CT should be used. Hoenecke and colleagues11 subsequently evaluated 33 patients scheduled for TSA and found that CT version measurements made on 2-dimensional (2-D) CT slices compared with 3-D-reconstructed models of the same CT slices differed by an average of 5.1° because the axial CT slices were most often made perpendicular to the axis of the patient’s torso and not perpendicular to the body of the scapula. Accurate version assessment is critically important in planning for the degree of correction required to restore neutral glenoid version, and differences of 6.4° between CT assessment and plain radiography, and 5.1° between 2-D and 3-D CT scan assessments may lead to inadequate version correction intraoperatively and inferior postoperative results.
Continue to: GLENOSPHERE PLACEMENT
GLENOSPHERE PLACEMENT
The most common indication for reverse TSA is rotator cuff arthropathy characterized by rotator cuff dysfunction and end-stage glenohumeral arthritis.12 These patients require accurate and reproducible glenoid placement to optimize their postoperative range of motion and stability and minimize scapular notching.
Ideal glenosphere placement is the location and orientation that maximizes impingement-free ROM and stability while avoiding notching. Individual patient anatomy determines ideal placement; however, several guidelines for placement include inferior translation on the glenoid with neutral to inferior inclination. Gutiérrez and colleagues13 developed a computer model to assess the hierarchy of surgical factors affecting the ROM after a reverse TSA. They found that lateralizing the center of rotation gave the largest increase in impingement-free abduction, followed closely by inferior translation of the glenosphere on the glenoid.
Avoiding scapular notching is also a very important factor in ideal glenosphere placement. Scapular notching can be described as impingement of the humeral cup against the scapular neck during arm adduction and/or humeral rotation. Gutiérrez and colleagues13 also found that decreasing the neck shaft angle to create a more varus proximal humerus was the most important factor in increasing the impingement-free adduction. Roche and colleagues14 reviewed the radiographs of 151 patients who underwent primary reverse TSA at a mean follow-up of 28.3 months postoperatively; they found that 13.2% of their patients had a notch and that, on average, their patients who had no scapular notch had significantly more inferior glenosphere overhang than those who had a scapular notch. Poon and colleagues15 found that a glenosphere overhang of >3.5 mm prevented notching in their randomized control trial comparing concentrically and eccentrically placed glenospheres. Multiple other studies have demonstrated similar results and recommended inferior glenoid translation and inferior glenoid inclination to avoid scapular notching.16,17 Lévigne and colleagues18 retrospectively reviewed 337 reverse TSAs and observed a correlation between scapular notching and radiolucencies around the glenosphere component, with 14% of patients with scapular notching displaying radiolucencies vs 4% of patients without scapula notching displaying radiolucencies.
Several studies have also focused on the ideal amount of inferior glenoid inclination to maximize impingement-free ROM. Li and colleagues17 performed a computer simulation study on the Comprehensive Reverse Shoulder System (Zimmer Biomet) to determine impingement-free internal and external ROM with varying amounts of glenosphere offset, translation, and inclination. They found that progressive glenosphere inferior inclination up to 30° improved impingement-free rotational ROM at all degrees of scaption. Gutiérrez and colleagues19 used computer modeling to compare concentrically placed glenospheres in neutral inclination with eccentrically placed glenospheres in varying degrees of inclination. They found that the lowest forces across the baseplate occurred in the lateralized and inferiorly inclined glenospheres, and the highest forces occurred in the lateralized and superiorly inclined glenospheres. Together, these studies show that inferior glenoid inclination increases impingement-free ROM and, combined with lateralization, may result in improved glenosphere longevity due to significantly decreased forces at the RSA glenoid baseplate when compared to that at superiorly inclined glenoids.
The ideal amount of mediolateral glenosphere offset has not been well defined. Grammont design systems place the center of rotation of the glenosphere medial to the glenoid baseplate together with valgus humeral component neck shaft angles of around 155°. These design elements are believed to decrease shear stresses through the glenoid baseplate to the glenoid interface and improve shoulder stability, but they are also associated with reduced impingement-free ROM and increased rates of scapular notching.13 This effect is accentuated in patients with preexisting glenoid bone loss and/or congenitally short scapular necks that further medialize the glenosphere. Medialization of the glenosphere may also shorten the remaining rotator cuff muscles and result in decreased implant stability and external rotation strength. Several implant systems have options to vary the amount of lateral offset. The correct amount of lateral offset for each patient requires the understanding that improving patients’ impingement-free ROM by increasing the amount of lateral offset comes at the price of increasing the shear forces experienced by the interface between the glenoid baseplate and the glenoid. As glenoid fixation technology improves increased lateralization of glenospheres without increased rates of glenoid baseplate, loosening should improve the ROM after reverse TSA.
Continue to: Regardless of the intraoperative goals...
Regardless of the intraoperative goals for placement and orientation of the glenosphere components, it is vitally important to accurately and consistently meet those goals for achieving optimal patient outcomes. Verborgt and colleagues20 implanted 7 glenospheres in cadaveric specimens without any glenohumeral arthritis using standard techniques to evaluate the accuracy of glenosphere version and inclination. Their goal was to place components in neutral version and with 10° of inferior inclination. Their average glenoid version postoperatively was 8.7° of anteversion, and their average inclination was 0.9° of superior inclination. Throckmorton and colleagues21 randomized 35 cadaveric shoulders to receive either an anatomic or a reverse total shoulder prosthesis from high-, mid-, and low-volume surgeons. They found that components placed using traditional guides averaged 6° of deviation in version and 5° of deviation in inclination from their target values, with no significant differences between surgeons of different volumes.
PATIENT-SPECIFIC GUIDES/INSTRUMENTATION
Patient-specific guides/instrumentation and intraoperative navigation are the 2 techniques that have been used to improve the accuracy of glenoid and glenosphere placement. Both techniques require the use of high-resolution CT scans and computer software to determine the proper position for glenoid or glenosphere placement based on the patient’s individual anatomy. Patient-specific guides and instrumentation use the data acquired from a CT scan to generate a preoperative plan for the location and orientation of the glenoid baseplate. Once the surgeon approves the preoperative plan, a patient-specific guide is created using the patient’s glenoid as a reference for the location and orientation of the central guide pin. The location of the central guide pin on the glenoid determines the center of the glenoid baseplate, and the guide pin’s orientation determines the version and inclination of the glenoid or the glenosphere. Once the guide pin is placed in the glenoid, the remainder of the glenoid implantation uses the guide pin as a reference, and, in that way, patient-specific guides control the orientation of the glenoid at the time of surgery.
Intraoperative navigation uses an optical tracking system to determine the location and orientation of the central guide pin. Navigation systems require intraoperative calibration of the optical tracking system before they can track the location of implantation relative to bony landmarks on the patient’s scapula. Their advantage over patient-specific instrumentation (PSI) is that they do not require the manufacture of a custom guide; however, they may add significantly increased cost and surgical time due to the need for calibration prior to use and the cost of the navigation system along with any disposable components associated with it. Kircher and colleagues22 performed a prospective randomized clinical study of navigation-aided TSA compared with conventional TSA and found that operating time was significantly increased for the navigated group with an average operating room time of 169.5 minutes compared to 138 minutes for the conventional group. They also found that navigation had to be abandoned in 37.5% of their navigated patients due to technical errors during glenoid referencing.
COMMERCIAL PATIENT-SPECIFIC INSTRUMENTATION SYSTEMS
The 2 types of PSI that are currently available are single-use PSI and reusable PSI. The single-use PSI involves the fabrication of unique guides based on surgeon-approved preoperative plans generated by computer-software-processed preoperative CT scans. The guides are fabricated to rest on the glenoid articular surface and direct the guide pin to the correct location and in the correct direction to place the glenoid baseplate in the desired position with the desired version and inclination. Most of these systems also provide a 3-D model of the patient’s glenoid so that surgeons can visualize glenoid deformities and the correct guide placement on the glenoid. Single-use PSI systems are available from DJO Global, Wright Medical Group, and Zimmer Biomet. The second category of PSI is reusable and is available from Arthrex. The guide pin for this system is adjusted to fit individual patient anatomy and guide the guide pin into the glenoid in a location and orientation preplanned on the CT-scan-based computer software or using a 3-D model of the patient’s glenoid (Table).
Table. Details of Available Patient-Specific Instrumentation Systems
| System | Manufacturer | Single-Use/Reusable | Guides |
| MatchPoint System | DJO Global | Single-use | Central guide pin |
| Blueprint 3D Planning + PSI | Wright Medical Group | Single-use | Central guide pin |
| Zimmer Patient Specific Instruments Shoulder | Zimmer Biomet | Single-use | Central guide pin, reaming guide, roll guide, screw drill guide |
| Virtual Implant Positioning System | Arthrex | Reusable | Central guide pin |
The DJO Global patient-specific guide is termed as the MatchPoint System. This system creates 3-D renderings of the scapula and allows the surgeon to manipulate the glenoid baseplate on the scapula. The surgeon chooses the glenoid baseplate, location, version, and inclination on the computerized 3-D model. The system then fabricates a guide pin matching the computerized template that references the patient’s glenoid surface with a hook to orient it against the coracoid. A 3-D model of the glenoid is also provided along with the customized guide pin.
Continue to: Blueprint 3D Planning + PSI...
Blueprint 3D Planning + PSI (Wright Medical Group) allows custom placement of the glenoid version, inclination, and position on computerized 3-D models of the patient’s scapula. This PSI references the glenoid with 4 feet that captures the edge of the patient’s glenoid at specific locations and is unique because it allows the surgeon to control where on the glenoid edge to 4 feet contact as long as 1 foot is placed on the posterior edge of the glenoid and the remaining 3 feet are placed on the anterior edge of the glenoid. A 3-D model of the glenoid is also provided with this guide.
The Zimmer Biomet patient-specific guide is termed as the Zimmer Patient Specific Instruments Shoulder. Its computer software allows custom placement of the glenoid as well, but it also includes computerized customization of the reaming depth, screw angles, and screw lengths to optimize fixation. Their system includes a central guide pin to set the glenoid baseplate’s location and orientation, a reaming guide to control reaming depth and direction, a roll guide to control the glenoid baseplate’s rotation, and a drill guide to control the screw direction. They also provide a 3-D model of the glenoid.
The Arthrex Virtual Implant Positioning (VIP) System is similar to other systems in that its 3-D planning software is based on CT images uploaded by the surgeon. The unique aspect of this system is that the guide pin is adjusted by the surgeon for each individual patient based on instructions generated by the planning software; however, after use, the instruments are resterilized and reused on subsequent patients (Figures 1A, 1B). In this manner, their instruments are reusable and allow custom adjustment for each patient with the ability to set the pin location and glenoid version in a patient-specific manner. This has the potential benefit of keeping costs down. For more complex deformity cases, the Arthrex VIP System can also 3-D-print a sterile model of the glenoid to help surgeons appreciate the deformity better (Figure 2).
DATA ON PATIENT-SPECIFIC INSTRUMENTS
Several studies have measured the accuracy of patient-specific guides and have compared the accuracy of patient-specific guides to that of traditional methods. Levy and colleagues23 investigated the accuracy of single-use patient-specific guides compared to that of preoperative plans. They used patient-specific guides on 14 cadaveric shoulders based on plans developed by virtual preoperative 3-D planning system using CT images. Once the guide pin was drilled using the patient-specific guide, they obtained a second CT scan to compare the accuracy of the patient-specific guide to the surgical plan generated preoperatively. They found that the translational accuracy of the starting point for the guide pin averaged 1.2 mm ± 0.7 mm, the accuracy of the inferior inclination was 1.2° ± 1.2°, and the accuracy of the glenoid version was 2.6° ± 1.7°. They concluded that patient-specific guides were highly accurate in reproducing the starting point, inclination, and version set on preoperative guides.
Walch and colleagues24 subsequently performed a similar study using 15 cadaveric scapulae without any other shoulder soft tissue or bone attached. They also used CT-scan-based 3-D planning software to plan their glenoid placement with a subsequently fabricated single-use patient-specific guide used to place a guide pin. They obtained a second CT scan after guide pin implantation and compared the preoperative plan with the subsequent guide pin. They found a mean entry point position error of 1.05 mm ± 0.31 mm, a mean inclination error of 1.42° ± 1.37°, and a mean version error of 1.64° ± 1.01°.
Continue to: Throckmorton and colleagues...
Throckmorton and colleagues21 used 70 cadaveric shoulders with radiographically confirmed arthritis and randomized them to undergo either anatomic or reverse TSA using either a patient-specific guide or standard instrumentation. Postoperative CT scans were used to evaluate the glenoid inclination, version, and starting point. They found that glenoid components implanted using patient-specific guides were more accurate than those placed using traditional instrumentation. The average deviation from intended inclination was 3° for patient-specific guides and 7° for traditional instrumentation, the average deviation from intended version was 5° for patient-specific guides and 8° for traditional instrumentation, and the average deviation in intended starting point was 2 mm for patient-specific guides and 3 mm for traditional instrumentation. They also analyzed significantly malpositioned components as defined by a variation in version or inclination of >10° or >4 mm in starting point. They found that 6 of their 35 glenoids using patient-specific guides were significantly malpositioned compared to 23 of 35 glenoids using traditional instrumentation. They concluded that patient-specific guides were more accurate and reduced the number of significantly malpositioned implants when compared with traditional instrumentation.
Early and colleagues25 analyzed the effect of severe glenoid bone defects on the accuracy of patient-specific guides compared with traditional guides. Using 10 cadaveric shoulders, they created anterior, central, or posterior glenoid defects using a reamer and chisel to erode the bone past the coracoid base. Subsequent CT scans were performed on the specimens, and patient-specific guides were fabricated and used for reverse TSA in 5 of the 10 specimens. A reverse TSA was performed using traditional instrumentation in the remaining 5 specimens. They found that the average deviation in inclination and version from preoperative plan was more accurate in the patient-specific guide cohort than that in the traditional instrument cohort, with an average deviation in inclination and version of 1.2° ± 1.2° and 1.8° ± 1.2° respectively for the cohort using patient-specific instruments vs 2.8° ± 1.8° and 3.5° ± 3° for the cohort using traditional instruments. They also found that their total bone screw lengths were longer in the patient-specific guide group than those in the traditional group, with screws averaging 52% of preoperatively planned length in the traditional instrument cohort vs 89% of preoperatively planned length in the patient-specific instrument cohort.
Gauci and colleagues26 measured the accuracy of patient-specific guides in vivo in 17 patients receiving TSA. Preoperative CT scans were used to fabricate patient-specific guides, and postoperative CT scans were used to measure version, inclination, and error of entry in comparison with the templated goals used to create patient-specific guides. They found a mean error in version and inclination of 3.4° and 1.8°, respectively, and a mean error in entry of 0.9 mm of translation on the glenoid. Dallalana and colleagues27 performed a very similar study on 20 patients and found a mean deviation in glenoid version of 1.8° ± 1.9°, a mean deviation in glenoid inclination of 1.3° ± 1.0°, a mean translation in anterior-posterior plane of 0.5 mm ± 0.3 mm, and a mean translation in the superior-inferior plane of 0.8 mm ± 0.5 mm.
Hendel and colleagues28 performed a randomized prospective clinical trial comparing patient-specific guides with traditional methods for glenoid insertion. They randomized 31 patients to receive a glenoid implant using either a patient-specific guide or traditional methods and compared glenoid retroversion and inclination with their preoperative plan. They found an average version deviation of 6.9° in the traditional method cohort and 4.3° in the patient-specific guide cohort. Their average deviation in inclination was 11.6° in the traditional method cohort and 2.9° in the patient-specific guide cohort. For patients with preoperative retroversion >16°, the average deviation was 10° in the standard surgical cohort and 1.2° in the patient-specific instrument cohort. Their data suggest that increasing preoperative retroversion leads to an increased version variation from preoperative plan.
Iannotti and colleagues29 randomly assigned 46 patients to preoperatively undergo either CT scan with 3-D templating of glenoid component without patient-specific guide fabrication or CT scan with 3-D templating and patient-specific guide fabrication prior to receiving a TSA. They recorded the postoperative inclination and version for each patient and compared them to those of a nonrandomized control group of 17 patients who underwent TSA using standard instrumentation. They found no difference between the cohorts with or without patient-specific guide use with regard to implant location, inclination, or version; however, they did find a difference between the combined 3-D templating cohort compared with their standard instrumentation cohort. They concluded that 3-D templating significantly improved the surgeons’ ability to correctly position the glenoid component with or without the fabrication and the use of a patient-specific guide.
Continue to: Denard and colleagues...
Denard and colleagues30 compared the preoperative glenoid version and inclination measurements obtained using the Blueprint 3D Planning + PSI software and the VIP System 3D planning software. They analyzed the preoperative CT scans of 63 consecutive patients undergoing either TSA or reverse TSA using both the Blueprint and the VIP System 3D planning software and compared the resulting native glenoid version and inclination measured by the software. They found a statistically significant difference (P = 0.04) in the version measurements provided by the different planning software; however, the differences found in inclination did not reach statistical significance (P = 0.463). In 19 of the 63 patients (30%), the version measurements between the systems were >5°, and in 29 of the 63 patients (46%), the inclination measurements between the systems were 5° or greater. In addition, 12 of the 63 patients (19%) had both version and inclination measurement differences of >5° between the systems. In total, they found that 35 of the 63 patients had at least 1 measurement that varied by >5° between the systems, and that in 15 patients (24%), 1 measurement varied by >10°. Their data demonstrate considerable variability in the preoperative measurements provided by different 3-D planning software systems, and that further study of each commercially available 3-D planning software system is needed to evaluate their accuracy.
CONCLUSION
Optimal outcomes following TSA and reverse TSA are dependent on proper implant position. Multiple studies have demonstrated improved accuracy in implant positioning with the use of patient-specific guides compared to that with traditional methods. Currently, there are no studies comparing the clinical outcomes of patient-specific guides to those of traditional methods of glenoid placement, and limited research had been done comparing the accuracy of each system’s 3-D planning software with each other and with standardized measurements of glenoid version and inclination. Further research is required to determine the accuracy of each commercially available 3-D planning software system as well as the clinical benefit of patient-specific guides in shoulder arthroplasty.
1. Churchill RS, Brems JJ, Kotschi H. Glenoid size, inclination, and version: an anatomic study. J Shoulder Elbow Surg. 2001;10(4):327-332. doi:10.1067/mse.2001.115269.
2. Norris TR, Iannotti JP. Functional outcome after shoulder arthroplasty for primary osteoarthritis: a multicenter study. J Shoulder Elbow Surg. 2002;11(2):130-135. doi:10.1067/mse.2002.121146.
3. Mullaji AB, Beddow FH, Lamb GH. CT measurement of glenoid erosion in arthritis. J Bone Joint Surg Br. 1994;76(3):384-388.
4. Walch G, Badet R, Boulahia A, Khoury A. Morphologic study of the glenoid in primary glenohumeral osteoarthritis. J Arthroplasty. 1999;14(6):756-760.
5. RJ Friedman, KB Hawthorne, BM Genez. The use of computerized tomography in the measurement of glenoid version. J Bone Joint Surg. 1992;74(7):1032-1037. doi:10.2106/00004623-199274070-00009.
6. Yian EH, Werner CM, Nyffeler RW, et al. Radiographic and computed tomography analysis of cemented pegged polyethylene glenoid components in total shoulder replacement. J Bone Joint Surg. 2005;87(9):1928-1936. doi:10.2106/00004623-200509000-00004.
7. Hasan SS, Leith JM, Campbell B, Kapil R, Smith KL, Matsen FA. Characteristics of unsatisfactory shoulder arthroplasties. J Shoulder Elbow Surg. 2002;11(5):431-441.
8. Hopkins AR, Hansen UN, Amis AA, Emery R. The effects of glenoid component alignment variations on cement mantle stresses in total shoulder arthroplasty. J Shoulder Elbow Surg. 2004;13(6):668-675. doi:10.1016/S1058274604001399.
9. Iannotti JP, Greeson C, Downing D, Sabesan V, Bryan JA. Effect of glenoid deformity on glenoid component placement in primary shoulder arthroplasty. J Shoulder Elbow Surg. 2012;21(1):48-55. doi:10.1016/j.jse.2011.02.011.
10. Nyffeler RW, Jost B, Pfirrmann CWA, Gerber C. Measurement of glenoid version: conventional radiographs versus computed tomography scans. J Shoulder Elbow Surg. 2003;12(5):493-496. doi:10.1016/S1058274603001812.
11. Hoenecke HR, Hermida JC, Flores-Hernandez C, D'Lima DD. Accuracy of CT-based measurements of glenoid version for total shoulder arthroplasty. J Shoulder Elbow Surg. 2010;19(2):166-171. doi:10.1016/j.jse.2009.08.009.
12. Wall B, Nové-Josserand L, O'Connor DP, Edwards TB, Walch G. Reverse total shoulder arthroplasty: a review of results according to etiology. J Bone Joint Surg Am. 2007;89(7):1476-1485. doi:10.2106/JBJS.F.00666.
13. Gutiérrez S, Comiskey 4, Charles A, Luo Z, Pupello DR, Frankle MA. Range of impingement-free abduction and adduction deficit after reverse shoulder arthroplasty. hierarchy of surgical and implant-design-related factors. J Bone Joint Surg Am. 2008;90(12):2606-2615. doi:10.2106/JBJS.H.00012.
14. Roche CP, Marczuk Y, Wright TW, et al. Scapular notching and osteophyte formation after reverse shoulder replacement: Radiological analysis of implant position in male and female patients. Bone Joint J. 2013;95-B(4):530-535. doi:10.1302/0301-620X.95B4.30442.
15. Poon PC, Chou J, Young SW, Astley T. A comparison of concentric and eccentric glenospheres in reverse shoulder arthroplasty: a randomized controlled trial. J Bone Joint Surg Am. 2014;96(16):e138. doi:10.2106/JBJS.M.00941.
16. Nyffeler RW, Werner CML, Gerber C. Biomechanical relevance of glenoid component positioning in the reverse delta III total shoulder prosthesis. J Shoulder Elbow Surg. 2005;14(5):524-528. doi:10.1016/j.jse.2004.09.010.
17. Li X, Knutson Z, Choi D, et al. Effects of glenosphere positioning on impingement-free internal and external rotation after reverse total shoulder arthroplasty. J Shoulder Elbow Surg. 2013;22(6):807-813. doi:10.1016/j.jse.2012.07.013.
18. Lévigne C, Boileau P, Favard L, et al. Scapular notching in reverse shoulder arthroplasty. J Shoulder Elbow Surg. 2008;17(6):925-935. doi:10.1016/j.jse.2008.02.010.
19. Gutiérrez S, Walker M, Willis M, Pupello DR, Frankle MA. Effects of tilt and glenosphere eccentricity on baseplate/bone interface forces in a computational model, validated by a mechanical model, of reverse shoulder arthroplasty. J Shoulder Elbow Surg. 2011;20(5):732-739. doi:10.1016/j.jse.2010.10.035.
20. Verborgt O, De Smedt T, Vanhees M, Clockaerts S, Parizel PM, Van Glabbeek F. Accuracy of placement of the glenoid component in reversed shoulder arthroplasty with and without navigation. J Shoulder Elbow Surg. 2011;20(1):21-26. doi:10.1016/j.jse.2010.07.014.
21. Throckmorton TW, Gulotta LV, Bonnarens FO, et al. Patient-specific targeting guides compared with traditional instrumentation for glenoid component placement in shoulder arthroplasty: A multi-surgeon study in 70 arthritic cadaver specimens. J Shoulder Elbow Surg. 2015;24(6):965-971. doi:10.1016/j.jse.2014.10.013.
22. Kircher J, Wiedemann M, Magosch P, Lichtenberg S, Habermeyer P. Improved accuracy of glenoid positioning in total shoulder arthroplasty with intraoperative navigation: a prospective-randomized clinical study. J Shoulder Elbow Surg. 2009;18(4):515-520. doi:10.1016/j.jse.2009.03.014.
23. Levy JC, Everding NG, Frankle MA, Keppler LJ. Accuracy of patient-specific guided glenoid baseplate positioning for reverse shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(10):1563-1567. doi:10.1016/j.jse.2014.01.051.
24. Walch G, Vezeridis PS, Boileau P, Deransart P, Chaoui J. Three-dimensional planning and use of patient-specific guides improve glenoid component position: an in vitro study. J Shoulder Elbow Surg. 2015;24(2):302-309. doi:10.1016/j.jse.2014.05.029.
25. Eraly K, Stoffelen D, Vander Sloten J, Jonkers I, Debeer P. A patient-specific guide for optimizing custom-made glenoid implantation in cases of severe glenoid defects: an in vitro study. J Shoulder Elbow Surg. 2016;25(5):837-845. doi:10.1016/j.jse.2015.09.034.
26. Gauci MO, Boileau P, Baba M, Chaoui J, Walch G. Patient-specific glenoid guides provide accuracy and reproducibility in total shoulder arthroplasty. Bone Joint J. 2016;98-B(8):1080-1085. doi:10.1302/0301-620X.98B8.37257.
27. Dallalana RJ, McMahon RA, East B, Geraghty L. Accuracy of patient-specific instrumentation in anatomic and reverse total shoulder arthroplasty. Int J Shoulder Surg. 2016;10(2):59-66. doi:10.4103/09736042.180717.
28. Hendel MD, Bryan JA, Barsoum WK, et al. Comparison of patient-specific instruments with standard surgical instruments in determining glenoid component position: a randomized prospective clinical trial. J Bone Joint Surg. 2012;94(23):2167-2175. doi:10.2106/JBJS.K.01209.
29. Iannotti JP, Weiner S, Rodriguez E, et al. Three-dimensional imaging and templating improve glenoid implant positioning. J Bone Joint Surg. 2015;97(8):651-658. doi:10.2106/JBJS.N.00493.
30. Denard PJ, Provencher MT, Lädermann A, Romeo AA, Dines JS. Version and inclination obtained with 3D planning in total shoulder arthroplasty: do different programs produce the same results? SECEC-ESSSE Congress, Berlin 2017. 2017.
1. Churchill RS, Brems JJ, Kotschi H. Glenoid size, inclination, and version: an anatomic study. J Shoulder Elbow Surg. 2001;10(4):327-332. doi:10.1067/mse.2001.115269.
2. Norris TR, Iannotti JP. Functional outcome after shoulder arthroplasty for primary osteoarthritis: a multicenter study. J Shoulder Elbow Surg. 2002;11(2):130-135. doi:10.1067/mse.2002.121146.
3. Mullaji AB, Beddow FH, Lamb GH. CT measurement of glenoid erosion in arthritis. J Bone Joint Surg Br. 1994;76(3):384-388.
4. Walch G, Badet R, Boulahia A, Khoury A. Morphologic study of the glenoid in primary glenohumeral osteoarthritis. J Arthroplasty. 1999;14(6):756-760.
5. RJ Friedman, KB Hawthorne, BM Genez. The use of computerized tomography in the measurement of glenoid version. J Bone Joint Surg. 1992;74(7):1032-1037. doi:10.2106/00004623-199274070-00009.
6. Yian EH, Werner CM, Nyffeler RW, et al. Radiographic and computed tomography analysis of cemented pegged polyethylene glenoid components in total shoulder replacement. J Bone Joint Surg. 2005;87(9):1928-1936. doi:10.2106/00004623-200509000-00004.
7. Hasan SS, Leith JM, Campbell B, Kapil R, Smith KL, Matsen FA. Characteristics of unsatisfactory shoulder arthroplasties. J Shoulder Elbow Surg. 2002;11(5):431-441.
8. Hopkins AR, Hansen UN, Amis AA, Emery R. The effects of glenoid component alignment variations on cement mantle stresses in total shoulder arthroplasty. J Shoulder Elbow Surg. 2004;13(6):668-675. doi:10.1016/S1058274604001399.
9. Iannotti JP, Greeson C, Downing D, Sabesan V, Bryan JA. Effect of glenoid deformity on glenoid component placement in primary shoulder arthroplasty. J Shoulder Elbow Surg. 2012;21(1):48-55. doi:10.1016/j.jse.2011.02.011.
10. Nyffeler RW, Jost B, Pfirrmann CWA, Gerber C. Measurement of glenoid version: conventional radiographs versus computed tomography scans. J Shoulder Elbow Surg. 2003;12(5):493-496. doi:10.1016/S1058274603001812.
11. Hoenecke HR, Hermida JC, Flores-Hernandez C, D'Lima DD. Accuracy of CT-based measurements of glenoid version for total shoulder arthroplasty. J Shoulder Elbow Surg. 2010;19(2):166-171. doi:10.1016/j.jse.2009.08.009.
12. Wall B, Nové-Josserand L, O'Connor DP, Edwards TB, Walch G. Reverse total shoulder arthroplasty: a review of results according to etiology. J Bone Joint Surg Am. 2007;89(7):1476-1485. doi:10.2106/JBJS.F.00666.
13. Gutiérrez S, Comiskey 4, Charles A, Luo Z, Pupello DR, Frankle MA. Range of impingement-free abduction and adduction deficit after reverse shoulder arthroplasty. hierarchy of surgical and implant-design-related factors. J Bone Joint Surg Am. 2008;90(12):2606-2615. doi:10.2106/JBJS.H.00012.
14. Roche CP, Marczuk Y, Wright TW, et al. Scapular notching and osteophyte formation after reverse shoulder replacement: Radiological analysis of implant position in male and female patients. Bone Joint J. 2013;95-B(4):530-535. doi:10.1302/0301-620X.95B4.30442.
15. Poon PC, Chou J, Young SW, Astley T. A comparison of concentric and eccentric glenospheres in reverse shoulder arthroplasty: a randomized controlled trial. J Bone Joint Surg Am. 2014;96(16):e138. doi:10.2106/JBJS.M.00941.
16. Nyffeler RW, Werner CML, Gerber C. Biomechanical relevance of glenoid component positioning in the reverse delta III total shoulder prosthesis. J Shoulder Elbow Surg. 2005;14(5):524-528. doi:10.1016/j.jse.2004.09.010.
17. Li X, Knutson Z, Choi D, et al. Effects of glenosphere positioning on impingement-free internal and external rotation after reverse total shoulder arthroplasty. J Shoulder Elbow Surg. 2013;22(6):807-813. doi:10.1016/j.jse.2012.07.013.
18. Lévigne C, Boileau P, Favard L, et al. Scapular notching in reverse shoulder arthroplasty. J Shoulder Elbow Surg. 2008;17(6):925-935. doi:10.1016/j.jse.2008.02.010.
19. Gutiérrez S, Walker M, Willis M, Pupello DR, Frankle MA. Effects of tilt and glenosphere eccentricity on baseplate/bone interface forces in a computational model, validated by a mechanical model, of reverse shoulder arthroplasty. J Shoulder Elbow Surg. 2011;20(5):732-739. doi:10.1016/j.jse.2010.10.035.
20. Verborgt O, De Smedt T, Vanhees M, Clockaerts S, Parizel PM, Van Glabbeek F. Accuracy of placement of the glenoid component in reversed shoulder arthroplasty with and without navigation. J Shoulder Elbow Surg. 2011;20(1):21-26. doi:10.1016/j.jse.2010.07.014.
21. Throckmorton TW, Gulotta LV, Bonnarens FO, et al. Patient-specific targeting guides compared with traditional instrumentation for glenoid component placement in shoulder arthroplasty: A multi-surgeon study in 70 arthritic cadaver specimens. J Shoulder Elbow Surg. 2015;24(6):965-971. doi:10.1016/j.jse.2014.10.013.
22. Kircher J, Wiedemann M, Magosch P, Lichtenberg S, Habermeyer P. Improved accuracy of glenoid positioning in total shoulder arthroplasty with intraoperative navigation: a prospective-randomized clinical study. J Shoulder Elbow Surg. 2009;18(4):515-520. doi:10.1016/j.jse.2009.03.014.
23. Levy JC, Everding NG, Frankle MA, Keppler LJ. Accuracy of patient-specific guided glenoid baseplate positioning for reverse shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(10):1563-1567. doi:10.1016/j.jse.2014.01.051.
24. Walch G, Vezeridis PS, Boileau P, Deransart P, Chaoui J. Three-dimensional planning and use of patient-specific guides improve glenoid component position: an in vitro study. J Shoulder Elbow Surg. 2015;24(2):302-309. doi:10.1016/j.jse.2014.05.029.
25. Eraly K, Stoffelen D, Vander Sloten J, Jonkers I, Debeer P. A patient-specific guide for optimizing custom-made glenoid implantation in cases of severe glenoid defects: an in vitro study. J Shoulder Elbow Surg. 2016;25(5):837-845. doi:10.1016/j.jse.2015.09.034.
26. Gauci MO, Boileau P, Baba M, Chaoui J, Walch G. Patient-specific glenoid guides provide accuracy and reproducibility in total shoulder arthroplasty. Bone Joint J. 2016;98-B(8):1080-1085. doi:10.1302/0301-620X.98B8.37257.
27. Dallalana RJ, McMahon RA, East B, Geraghty L. Accuracy of patient-specific instrumentation in anatomic and reverse total shoulder arthroplasty. Int J Shoulder Surg. 2016;10(2):59-66. doi:10.4103/09736042.180717.
28. Hendel MD, Bryan JA, Barsoum WK, et al. Comparison of patient-specific instruments with standard surgical instruments in determining glenoid component position: a randomized prospective clinical trial. J Bone Joint Surg. 2012;94(23):2167-2175. doi:10.2106/JBJS.K.01209.
29. Iannotti JP, Weiner S, Rodriguez E, et al. Three-dimensional imaging and templating improve glenoid implant positioning. J Bone Joint Surg. 2015;97(8):651-658. doi:10.2106/JBJS.N.00493.
30. Denard PJ, Provencher MT, Lädermann A, Romeo AA, Dines JS. Version and inclination obtained with 3D planning in total shoulder arthroplasty: do different programs produce the same results? SECEC-ESSSE Congress, Berlin 2017. 2017.
TAKE-HOME POINTS
- Optimal outcomes following TSA and RSA are dependent on proper implant position.
- Patient-specific guides/instrumentation result in improved accuracy of implant positioning compared to traditional methods.
- Currently, there are no clinical studies demonstrating superiority of patient-specific guide/instrumentation use on patient outcomes.
- At this time there are 3 commercially available single use patient-specific instrumentation systems (DJO Global, Wright Medical Group, and Zimmer Biomet) and 1 commercially available reusable patient-specific instrumentation system (Arthrex).
- Limited research is available comparing the accuracy of different commercially available 3-D planning systems.
Humeral Bone Loss in Revision Shoulder Arthroplasty
ABSTRACT
Revision shoulder arthroplasty is becoming more prevalent as the rate of primary shoulder arthroplasty in the US continues to increase. The management of proximal humeral bone loss in the revision setting presents a difficult problem without a clear solution. Different preoperative diagnoses often lead to distinctly different patterns of bone loss. Successful management of these cases requires a clear understanding of the normal anatomy of the proximal humerus, as well as structural limitations imposed by significant bone loss and the effect this loss has on component fixation. Our preferred technique differs depending on the pattern of bone loss encountered. The use of allograft-prosthetic composites, the cement-within-cement technique, and combinations of these strategies comprise the mainstay of our treatment algorithm. This article focuses on indications, surgical techniques, and some of the published outcomes using these strategies in the management of proximal humeral bone loss.
Continue to: The demand for shoulder arthroplasty...
The demand for shoulder arthroplasty (SA) has increased significantly over the past decade, with a 200% increase witnessed from 2011 to 2015.1 SA performed in patients younger than 55 years is expected to increase 333% between 2011 to 2030.2 With increasing rates of SA being performed in younger patient populations, rates of revision SA also can be expected to climb. Revision to reverse shoulder arthroplasty (RSA) has arisen as a viable option in these patients, and multiple studies demonstrate excellent outcomes that can be obtained with RSA.3-11
Despite significant improvements obtained in revision SA since the mainstream acceptance of RSA, bone loss remains a problematic issue. Loss of humeral bone stock, in particular, can be a challenging problem to solve with multiple clinical implications. Biomechanical studies have demonstrated that if bone loss is left unaddressed, increased bending and torsional forces on the prosthesis result, which ultimately contribute to increased micromotion and eventual component failure.12 In addition, existing challenges are associated with the lack of attachment sites for both multiple muscles and tendons. Also, there is a loss of the normal lateralized pull of the deltoid, which results in a decreased amount of force generated by this muscle.13,14 Ultimately, the increased loss of bone can lead to a devastating situation where there is not enough bone to provide adequate fixation while maintaining the appropriate humeral length necessary to achieve stability of the articulation, which will inevitably lead to instability.4,15 Therefore, techniques are needed to address proximal humeral bone loss while maintaining as much native humeral bone as possible.
PROXIMAL HUMERUS: ANATOMICAL CONSIDERATIONS
The anatomy of the proximal humerus has been studied in great detail and reported in a number of different studies.16-23 The average humeral head thickness (24 mm in men and 19 mm in women) and offset relative to the humeral shaft (2.1 mm posterior and 6.6 mm medial) act to tension the rotator cuff musculature appropriately and contribute to a wrapping effect that allows the deltoid to function more effectively.13,14 Knowledge regarding the rotator cuff footprint has advanced over the past 10 years, specifically with regard to the supraspinatus and infraspinatus.24 The current belief is that the supraspinatus has a triangular insertion onto the most anterior aspect of the greater tuberosity, with a maximum medial-to-lateral length of 6.9 mm and a maximum anterior-to-posterior width of 12.6 mm. The infraspinatus insertion has a trapezoidal insertion, with a maximum medial-to-lateral length of 10.2 mm and anterior-to-posterior width of 32.7 mm. The subscapularis, by far the largest of all the rotator cuff muscles, has a complex geometry with regard to its insertion on the lesser tuberosity, with 4 different insertion points and an overall lateral footprint measuring 37.6 mm and a medial footprint measuring 40.7 mm.25 Finally, the teres minor, with the smallest volume of all the rotator cuff muscles, inserts immediately inferior to the infraspinatus along the inferior facet of the greater tuberosity.26
Aside from the rotator cuff, there are various other muscles and tendons that insert about the proximal humerus and are essential for normal function. The deltoid, which inserts at a point approximately 6 cm from the greater tuberosity along the length of the humerus, with an insertion length between 5 cm to 7 cm,13,27 is the primary mover of the shoulder and essential for proper function after RSA.28,29 The pectoralis major tendon, which begins inserting at a point approximately 5.6 cm from the humeral head and spans a distance of 7.7 cm along the length of the humerus,30-32 is important not only for function but as an anatomical landmark in reconstruction. Lastly, the latissimus dorsi and teres major, which share a role in extension, adduction, and internal rotation of the glenohumeral joint, insert along the floor and medial lip of the intertubercular groove of the humerus, respectively.33,34 In addition to their role in tendon transfer procedures because of treating irreparable posterosuperior cuff and subscapularis tears,35,36 it has been suggested that these tendons may play some role in glenohumeral joint stability.37
In addition to the loss of muscular attachments, the absence of proximal humeral bone stock, in and of itself, can have deleterious effects on fixation of the humeral component. RSA is a semiconstrained device, which results in increased transmission of forces to the interface between the humeral implant and its surrounding structures, including cement (when present) and the bone itself. When there is the absence of significant amounts of bone, the remaining bone must now account for an even higher proportion of these forces. A previous biomechanical study showed that cemented humeral stems demonstrated significantly increased micromotion in the presence of proximal humeral bone loss, particularly when a modular humeral component was used.12
Continue to: TYPES OF BONE LOSS
TYPES OF BONE LOSS
There are a variety of different etiologies of proximal humeral bone loss that result in distinctly different clinical presentations. These can be fairly mild, as is the case of isolated resorption of the greater tuberosity in a non-united proximal humerus fracture (Figure 1). Alternatively, they can be severe, as seen in a grossly loose cemented long-stemmed component that is freely mobile, creating a windshield-wiper effect throughout the length of the humerus (Figure 2). This can be somewhat deceiving, however, as the amount of bone loss, as well as the pathophysiologic process that led to the bone loss, are important factors to determine ideal reconstructive methods. In the case of a failed open reduction internal fixation, where the tuberosity has failed to unite or has been resected, there is much less of a biologic response in comparison with implant loosening associated with osteolysis. This latter condition will be associated with a much more destructive inflammatory response resulting in poor tissue quality and often dramatic thinning of the cortex. If one simply measured the distance from the most proximal remaining bone stock to the area where the greater tuberosity should be, a loose stem with subsidence and ballooning of the cortices may appear to have a similar amount of bone loss as a failed hemiarthroplasty for fracture with a well-fixed stem. However, intraoperatively, one will find that the bone that appeared to be present radiographically in the case of the loose stem is of such poor quality that it cannot reasonably provide any beneficial fixation. In light of this, different treatment modalities are recommended for different types of bone loss, and the revision surgeon must be able to anticipate this and possess a full armamentarium of options to treat these challenging cases successfully.
INDICATIONS
Our technique to manage proximal humeral bone loss is dependent on both the quantity of bone loss, which can be measured radiographically, as well as the anticipated inflammatory response described above. As both the destructive process and the amount of bone loss increase, the importance of more advanced reconstructive procedures that will sustain implant security and soft-tissue management becomes apparent. In the least destructive cases with <5 cm of bone loss, successful revision can typically be accomplished with stem removal and placement of a new monoblock humeral stem. In cases where more advanced destructive pathology is present, and bone loss is >5 cm, an allograft-prosthetic composite (APC) is typically used. In both scenarios, if the stem being revised is cemented and the cement mantle remains intact, and of reasonable length, consideration is given to the cement-within-cement technique. Finally, in the most destructive cases where bone loss exceeds 10 cm and a large biological response is anticipated (eg, periprosthetic fractures with humeral loosening), the use of a longer diaphyseal-incorporating APC is often necessary. This prosthetic composite can be combined with a cement-within-cement technique as well.
It is important to comment on the implications of using modular stems in this setting. With advanced bone loss, a situation is often encountered where the newly implanted stem geometry and working length may be insufficient to acquire adequate rotational stability. In this setting, if a modular junction is positioned close to the stem and cement/bone interface, it will be exposed to very high stress concentrations which can lead to component fracture38 as well as taper corrosion, also referred to as trunnionosis. This latter phenomenon, which has been well studied in the total hip arthroplasty literature with the use of modular components,39 is especially relevant given the high torsional loads imparted at the modular junction. Ultimately, high torsional loads lead to micromotion and electrochemical ion release via degradation of the passivation layer, initiating the process of mechanically assisted crevice corrosion.40 For these reasons, when a modular stem must be used in the presence of mild to moderate bone loss, using a proximal humeral allograft to protect the junction or to provide additional fixation may be implemented with a lower threshold than when using a monoblock stem.
SURGICAL TECHNIQUE: ALLOGRAFT-PROSTHETIC COMPOSITES
A standard deltopectoral approach is used, taking care to preserve all viable muscular attachments to the proximal humerus. After removal of the prosthetic humeral head, the decision to proceed with removal of the stem at this juncture is based on several factors. If the remaining proximal humeral bone is so compromised that it might not be able to withstand the forces exerted upon it during retraction for glenoid exposure, the component is left in place. Additionally, if there is consideration that the glenoid-sided bone loss may be so severe that a glenoid baseplate cannot be implanted, and the stem remains well fixed, it is retained so that it can be converted to a hemiarthroplasty.
If neither of the above issues is present, the humeral stem is removed. If a well-fixed press-fit stem is in place, it is typically removed using a combination of burrs and osteotomes to disrupt the bone-implant interface, and the stem is then carefully removed using an impactor and mallet. If a cemented stem is present, the stem is removed in a similar manner, and the cement mantle is left in place if stable, in anticipation of a cement-within-cement technique. If the mantle is disrupted, standard cement removal instruments are used to remove all cement from the canal meticulously.
Continue to: Management of the glenoid...
Management of the glenoid can have significant implications with regard to the humerus. Most notably, the size of the glenosphere has direct implications on the fixation of the humeral component. Use of larger diameter glenospheres result in increased contact area between the glenosphere and humerosocket, adding constraint to the articulation and further increasing the stresses at the implant-bone interface. As such, the use of larger glenospheres to prevent instability must be balanced with the resulting implications on humeral component fixation, especially in cases of severe bone loss.
After implanting the appropriate glenosphere, attention is then turned back to the humerus. Trial implants are sequentially used to obtain adequate humeral length and stability. Once this is accomplished, the amount of humeral bone loss is quantified by measuring the distance from the superior aspect of the medial humeral tray to the medial humeral shaft. If this number is >5 cm (Figure 3), the decision is made to proceed with an APC. The allograft humeral head is cut, cancellous bone is removed, and a step-cut is performed, with the medial portion of the allograft measuring the same length as that of bone loss and the lateral plate extending an additional several centimeters distally (Figure 4). Additional soft tissue is removed from the allograft, leaving the subscapularis stump intact for later repair with the patient’s native tissue. The allograft is secured to the patient’s proximal humerus using multiple cerclage wires, and the humeral stem is cemented into place. The final construct is shown in Figure 5.
ADDITIONAL CONSIDERATIONS: CASES OF ADVANCED BONE LOSS
In cases of advanced humeral bone loss, as is often seen when revising loose humeral stems, larger allografts that span a significant length of the diaphysis are often required. This type of bone loss has implications with regard to how the deltoid insertion is managed. Interestingly, even in situations when the vast majority of the remaining diaphysis consists of ectatic egg-shell bone, the deltoid tuberosity remains of fairly substantial quality due to the continued pull of the muscular insertion on this area. This fragment is isolated, carefully mobilized, and subsequently repaired back on top of the allograft using cables.
POSTOPERATIVE CARE
Patients are kept in a shoulder immobilizer for 6 weeks after surgery to facilitate allograft incorporation and subscapularis tendon healing. During this time, pendulum exercises are initiated. Active assisted range of motion (ROM) exercises begin after 6 weeks, consisting of supine forward elevation. A sling is given to be used in public. Light strengthening exercises begin at 3 months postoperatively.
DISCUSSION
In cases of mild to moderate proximal humeral bone loss, RSA using a long-stem humeral component without allograft augmentation is a viable option. Budge and colleagues38 demonstrated excellent results in a population of 15 patients with an average of 38 mm of proximal humeral bone loss without use of allografts. Interestingly, they noted 1 case of component fracture in a modular prosthesis and therefore concluded that monoblock humeral stems should be used in the absence of allograft augmentation.
Continue to: In more advanced cases of bone loss...
In more advanced cases of bone loss, our data shows that use of APCs can result in equally satisfactory results. In a series of 25 patients with an average bone loss of 54 mm, patients were able to achieve statistically significant improvements in pain, ROM, and function with high rates of allograft incorporation.9 Overall, a low rate of complications was noted, including 1 infection. This finding is consistent with an additional study looking specifically at factors associated with infection in revision SA, which found that the use of allografts was not associated with increased risk of infection.41
As stated previously, the size of allograft needed for the APC construct is related to the distinct pathology encountered. In our experience, we have noted that well-fixed stems can be treated with short metaphyseal APCs in 85% of cases. On the other hand, loose stems require long allografts measuring >10 cm in 90% of cases. As such, these cases typically require mobilization of the deltoid insertion as described above, and therefore it is important that the surgeon is prepared for this aspect of the procedure preoperatively.
Finally, the cement-within-cement technique, originally popularized for use in revision total hip arthroplasty, has demonstrated reliable results when utilized in revision SA.42 To date, there are no recommendations regarding the minimal length of existing cement mantle that is needed to perform this technique. In situations in which the length of the cement mantle is questionable, our preference is to combine the cement-within-cement technique with an APC when possible.
1. Day JS, Lau E, Ong KL, Williams GR, Ramsey ML, Kurtz SM. Prevalence and projections of total shoulder and elbow arthroplasty in the United States to 2015. J Shoulder Elbow Surg. 2010;19(8):1115-1120. doi:10.1016/j.jse.2010.02.009.
2. Padegimas EM, Maltenfort M, Lazarus MD, Ramsey ML, Williams GR, Namdari S. Future patient demand for shoulder arthroplasty by younger patients: national projections. Clin Orthop Relat Res. 2015;473(6):1860-1867. doi:10.1007/s11999-015-4231-z.
3. Walker M, Willis MP, Brooks JP, Pupello D, Mulieri PJ, Frankle MA. The use of the reverse shoulder arthroplasty for treatment of failed total shoulder arthroplasty. J Shoulder Elbow Surg. 2012;21(4):514-522. doi:10.1016/j.jse.2011.03.006.
4. Levy JC, Virani N, Pupello D, et al. Use of the reverse shoulder prosthesis for the treatment of failed hemiarthroplasty in patients with glenohumeral arthritis and rotator cuff deficiency. J Bone Joint Surg Br. 2007;89(2):189-195. doi:10.1302/0301-620X.89B2.
5. Melis B, Bonnevialle N, Neyton L, et al. Glenoid loosening and failure in anatomical total shoulder arthroplasty: is revision with a reverse shoulder arthroplasty a reliable option? J Shoulder Elbow Surg. 2012;21(3):342-349. doi:10.1016/j.jse.2011.05.021.
6. Deutsch A, Abboud JA, Kelly J, et al. Clinical results of revision shoulder arthroplasty for glenoid component loosening. J Shoulder Elbow Surg. 2007;16(6):706-716. doi:10.1016/j.jse.2007.01.007.
7. Kelly JD, Zhao JX, Hobgood ER, Norris TR. Clinical results of revision shoulder arthroplasty using the reverse prosthesis. J Shoulder Elbow Surg. 2012;21(11):1516-1525. doi:10.1016/j.jse.2011.11.021.
8. Black EM, Roberts SM, Siegel E, Yannopoulos P, Higgins LD, Warner JJP. Reverse shoulder arthroplasty as salvage for failed prior arthroplasty in patients 65 years of age or younger. J Shoulder Elbow Surg. 2014;23(7):1036-1042. doi:10.1016/j.jse.2014.02.019.
9. Composite P, Chacon BA, Virani N, et al. Revision arthroplasty with use of a reverse shoulder. J Bone Joint Surg. 2009;1:119-127. doi:10.2106/JBJS.H.00094.
10. Klein SM, Dunning P, Mulieri P, Pupello D, Downes K, Frankle MA. Effects of acquired glenoid bone defects on surgical technique and clinical outcomes in reverse shoulder arthroplasty. J Bone Joint Surg Am. 2010;92(5):1144-1154. doi:10.2106/JBJS.I.00778.
11. Patel DN, Young B, Onyekwelu I, Zuckerman JD, Kwon YW. Reverse total shoulder arthroplasty for failed shoulder arthroplasty. J Shoulder Elbow Surg. 2012;21(11):1478-1483. doi:10.1016/j.jse.2011.11.004.
12. Cuff D, Levy JC, Gutiérrez S, Frankle MA. Torsional stability of modular and non-modular reverse shoulder humeral components in a proximal humeral bone loss model. J Shoulder Elbow Surg. 2011;20(4):646-651. doi:10.1016/j.jse.2010.10.026.
13. Morgan SJ, Furry K, Parekh A, Agudelo JF, Smith WR. The deltoid muscle: an anatomic description of the deltoid insertion to the proximal humerus. J Orthop Trauma. 2006;20(1):19-21. doi:10.1097/01.bot.0000187063.43267.18.
14. Gagey O, Hue E. Mechanics of the deltoid muscle. A new approach. Clin Orthop Relat Res. 2000;375:250-257. doi:10.1097/00003086-200006000-00030.
15. De Wilde L, Plasschaert F. Prosthetic treatment and functional recovery of the shoulder after tumor resection 10 years ago: a case report. J Shoulder Elbow Surg. 2005;14(6):645-649. doi:10.1016/j.jse.2004.11.001.
16. Wataru S, Kazuomi S, Yoshikazu N, Hiroaki I, Takaharu Y, Hideki Y. Three-dimensional morphological analysis of humeral heads: a study in cadavers. Acta Orthop. 2005;76(3):392-396. doi:10.1080/00016470510030878.
17. Tillett E, Smith M, Fulcher M, Shanklin J. Anatomic determination of humeral head retroversion: the relationship of the central axis of the humeral head to the bicipital groove. J Shoulder Elbow Surg. 1993;2(5):255-256. doi:10.1016/S1058-2746(09)80085-2.
18. Doyle AJ, Burks RT. Comparison of humeral head retroversion with the humeral axis/biceps groove relationship: a study in live subjects and cadavers. J Shoulder Elbow Surg. 1998;7(5):453-457. doi:10.1016/S1058-2746(98)90193-8.
19. Johnson JW, Thostenson JD, Suva LJ, Hasan SA. Relationship of bicipital groove rotation with humeral head retroversion: a three-dimensional computed tomographic analysis. J Bone Joint Surg Am. 2013;95(8):719-724. doi:10.2106/JBJS.J.00085.
20. Hromádka R, Kuběna AA, Pokorný D, Popelka S, Jahoda D, Sosna A. Lesser tuberosity is more reliable than bicipital groove when determining orientation of humeral head in primary shoulder arthroplasty. Surg Radiol Anat. 2010;32(1):31-37. doi:10.1007/s00276-009-0543-6.
21. Hertel R, Knothe U, Ballmer FT. Geometry of the proximal humerus and implications for prosthetic design. J Shoulder Elbow Surg. 2002;11(4):331-338. doi:10.1067/mse.2002.124429.
22. Pearl ML. Proximal humeral anatomy in shoulder arthroplasty: Implications for prosthetic design and surgical technique. J Shoulder Elbow Surg. 2005;14(suppl 1):99-104. doi:10.1016/j.jse.2004.09.025.
23. Robertson DD, Yuan J, Bigliani LU, Flatow EL, Yamaguchi K. Three-dimensional analysis of the proximal part of the humerus: relevance to arthroplasty. J Bone Joint Surg Am. 2000;82-A(11):1594-1602.
24. Mochizuki T, Sugaya H, Uomizu M, et al. Humeral insertion of the supraspinatus and infraspinatus. J Bone Joint Surg Am. 2008;90(5):962-969. doi:10.2106/JBJS.G.00427.
25. Arai R, Sugaya H, Mochizuki T, Nimura A, Moriishi J, Akita K. Subscapularis tendon tear: an anatomic and clinical investigation. Arthroscopy. 2008;24(9):997-1004. doi:10.1016/j.arthro.2008.04.076.
26. Nimura A, Kato A, Yamaguchi K, et al. The superior capsule of the shoulder joint complements the insertion of the rotator cuff. J Shoulder Elbow Surg. 2012;21(7):867-872. doi:10.1016/j.jse.2011.04.034.
27. Rispoli DM, Athwal GS, Sperling JW, Cofield RH. The anatomy of the deltoid insertion. J Shoulder Elbow Surg. 2009;18(3):386-390. doi:10.1016/j.jse.2008.10.012.
28. Schwartz DG, Kang SH, Lynch TS, et al. The anterior deltoid’s importance in reverse shoulder arthroplasty: a cadaveric biomechanical study. J Shoulder Elbow Surg. 2013;22(3):357-364. doi:10.1016/j.jse.2012.02.002.
29. Walker M, Brooks J, Willis M, Frankle M. How reverse shoulder arthroplasty works. Clinical Orthop Relat Res. 2011;469(9):2440-2451. doi:10.1007/s11999-011-1892-0.
30. Torrens C, Corrales M, Melendo E, Solano A, Rodríguez-Baeza A, Cáceres E. The pectoralis major tendon as a reference for restoring humeral length and retroversion with hemiarthroplasty for fracture. J Shoulder Elbow Surg. 2008;17(6):947-950. doi:10.1016/j.jse.2008.05.041.
31. Ponce BA, Thompson KJ, Rosenzweig SD, et al. Re-evaluation of pectoralis major height as an anatomic reference for humeral height in fracture hemiarthroplasty. J Shoulder Elbow Surg. 2013;22(11):1567-1572. doi:10.1016/j.jse.2013.01.039.
32. LaFrance R, Madsen W, Yaseen Z, Giordano B, Maloney M, Voloshin I. Relevant anatomic landmarks and measurements for biceps tenodesis. Am J Sports Med. 2013;41(6):1395-1399. doi:10.1177/0363546513482297.
33. Beck PA, Hoffer MM. Latissimus dorsi and teres major tendons: separate or conjoint tendons? J Pediatr Orthop. 1989;9(3):308-309.
34. Bhatt CR, Prajapati B, Patil DS, Patel VD, Singh BGP, Mehta CD. Variation in the insertion of the latissimus dorsi & its clinical importance. J Orthop. 2013;10(1):25-28. doi:10.1016/j.jor.2013.01.002.
35. Gerber C, Maquieira G, Espinosa N. Latissimus dorsi transfer for the treatment of irreparable rotator cuff tears. J Bone Joint Surg. 2006;88(1):113-120. doi:10.2106/JBJS.E.00282.
36. Elhassan B, Christensen TJ, Wagner ER. Feasibility of latissimus and teres major transfer to reconstruct irreparable subscapularis tendon tear: an anatomic study. J Shoulder Elbow Surg. 2014;23(4):492-499. doi:10.1016/j.jse.2013.07.046.
37. Pouliart N, Gagey O. Significance of the latissimus dorsi for shoulder instability. II. Its influence on dislocation behavior in a sequential cutting protocol of the glenohumeral capsule. Clin Anat. 2005;18(7):500-509. doi:10.1002/ca.20181.
38. Budge MD, Moravek JE, Zimel MN, Nolan EM, Wiater JM. Reverse total shoulder arthroplasty for the management of failed shoulder arthroplasty with proximal humeral bone loss: is allograft augmentation necessary? J Shoulder Elbow Surg. 2013;22(6):739-744. doi:10.1016/j.jse.2012.08.008.
39. Weiser MC, Lavernia CJ. Trunnionosis in total hip arthroplasty. J Bone Joint Surg Am. 2017;99(17):27-29. doi:10.2106/JBJS.17.00345.
40. Cohen J. Current concepts review. Corrosion of metal orthopaedic implants. J Bone Joint Surg Am. 1998;80(10):1554.
41. Meijer ST, Paulino Pereira NR, Nota SPFT, Ferrone ML, Schwab JH, Lozano Calderón SA. Factors associated with infection after reconstructive shoulder surgery for proximal humerus tumors. J Shoulder Elbow Surg. 2017;26(6):931-938. doi:10.1016/j.jse.2016.10.014.
42. Wagner ER, Houdek MT, Hernandez NM, Cofield RH, Sánchez-Sotelo J, Sperling JW. Cement-within-cement technique in revision reverse shoulder arthroplasty. J Shoulder Elbow Surg. 2017;26(8):1448-1453. doi:10.1016/j.jse.2017.01.013.
ABSTRACT
Revision shoulder arthroplasty is becoming more prevalent as the rate of primary shoulder arthroplasty in the US continues to increase. The management of proximal humeral bone loss in the revision setting presents a difficult problem without a clear solution. Different preoperative diagnoses often lead to distinctly different patterns of bone loss. Successful management of these cases requires a clear understanding of the normal anatomy of the proximal humerus, as well as structural limitations imposed by significant bone loss and the effect this loss has on component fixation. Our preferred technique differs depending on the pattern of bone loss encountered. The use of allograft-prosthetic composites, the cement-within-cement technique, and combinations of these strategies comprise the mainstay of our treatment algorithm. This article focuses on indications, surgical techniques, and some of the published outcomes using these strategies in the management of proximal humeral bone loss.
Continue to: The demand for shoulder arthroplasty...
The demand for shoulder arthroplasty (SA) has increased significantly over the past decade, with a 200% increase witnessed from 2011 to 2015.1 SA performed in patients younger than 55 years is expected to increase 333% between 2011 to 2030.2 With increasing rates of SA being performed in younger patient populations, rates of revision SA also can be expected to climb. Revision to reverse shoulder arthroplasty (RSA) has arisen as a viable option in these patients, and multiple studies demonstrate excellent outcomes that can be obtained with RSA.3-11
Despite significant improvements obtained in revision SA since the mainstream acceptance of RSA, bone loss remains a problematic issue. Loss of humeral bone stock, in particular, can be a challenging problem to solve with multiple clinical implications. Biomechanical studies have demonstrated that if bone loss is left unaddressed, increased bending and torsional forces on the prosthesis result, which ultimately contribute to increased micromotion and eventual component failure.12 In addition, existing challenges are associated with the lack of attachment sites for both multiple muscles and tendons. Also, there is a loss of the normal lateralized pull of the deltoid, which results in a decreased amount of force generated by this muscle.13,14 Ultimately, the increased loss of bone can lead to a devastating situation where there is not enough bone to provide adequate fixation while maintaining the appropriate humeral length necessary to achieve stability of the articulation, which will inevitably lead to instability.4,15 Therefore, techniques are needed to address proximal humeral bone loss while maintaining as much native humeral bone as possible.
PROXIMAL HUMERUS: ANATOMICAL CONSIDERATIONS
The anatomy of the proximal humerus has been studied in great detail and reported in a number of different studies.16-23 The average humeral head thickness (24 mm in men and 19 mm in women) and offset relative to the humeral shaft (2.1 mm posterior and 6.6 mm medial) act to tension the rotator cuff musculature appropriately and contribute to a wrapping effect that allows the deltoid to function more effectively.13,14 Knowledge regarding the rotator cuff footprint has advanced over the past 10 years, specifically with regard to the supraspinatus and infraspinatus.24 The current belief is that the supraspinatus has a triangular insertion onto the most anterior aspect of the greater tuberosity, with a maximum medial-to-lateral length of 6.9 mm and a maximum anterior-to-posterior width of 12.6 mm. The infraspinatus insertion has a trapezoidal insertion, with a maximum medial-to-lateral length of 10.2 mm and anterior-to-posterior width of 32.7 mm. The subscapularis, by far the largest of all the rotator cuff muscles, has a complex geometry with regard to its insertion on the lesser tuberosity, with 4 different insertion points and an overall lateral footprint measuring 37.6 mm and a medial footprint measuring 40.7 mm.25 Finally, the teres minor, with the smallest volume of all the rotator cuff muscles, inserts immediately inferior to the infraspinatus along the inferior facet of the greater tuberosity.26
Aside from the rotator cuff, there are various other muscles and tendons that insert about the proximal humerus and are essential for normal function. The deltoid, which inserts at a point approximately 6 cm from the greater tuberosity along the length of the humerus, with an insertion length between 5 cm to 7 cm,13,27 is the primary mover of the shoulder and essential for proper function after RSA.28,29 The pectoralis major tendon, which begins inserting at a point approximately 5.6 cm from the humeral head and spans a distance of 7.7 cm along the length of the humerus,30-32 is important not only for function but as an anatomical landmark in reconstruction. Lastly, the latissimus dorsi and teres major, which share a role in extension, adduction, and internal rotation of the glenohumeral joint, insert along the floor and medial lip of the intertubercular groove of the humerus, respectively.33,34 In addition to their role in tendon transfer procedures because of treating irreparable posterosuperior cuff and subscapularis tears,35,36 it has been suggested that these tendons may play some role in glenohumeral joint stability.37
In addition to the loss of muscular attachments, the absence of proximal humeral bone stock, in and of itself, can have deleterious effects on fixation of the humeral component. RSA is a semiconstrained device, which results in increased transmission of forces to the interface between the humeral implant and its surrounding structures, including cement (when present) and the bone itself. When there is the absence of significant amounts of bone, the remaining bone must now account for an even higher proportion of these forces. A previous biomechanical study showed that cemented humeral stems demonstrated significantly increased micromotion in the presence of proximal humeral bone loss, particularly when a modular humeral component was used.12
Continue to: TYPES OF BONE LOSS
TYPES OF BONE LOSS
There are a variety of different etiologies of proximal humeral bone loss that result in distinctly different clinical presentations. These can be fairly mild, as is the case of isolated resorption of the greater tuberosity in a non-united proximal humerus fracture (Figure 1). Alternatively, they can be severe, as seen in a grossly loose cemented long-stemmed component that is freely mobile, creating a windshield-wiper effect throughout the length of the humerus (Figure 2). This can be somewhat deceiving, however, as the amount of bone loss, as well as the pathophysiologic process that led to the bone loss, are important factors to determine ideal reconstructive methods. In the case of a failed open reduction internal fixation, where the tuberosity has failed to unite or has been resected, there is much less of a biologic response in comparison with implant loosening associated with osteolysis. This latter condition will be associated with a much more destructive inflammatory response resulting in poor tissue quality and often dramatic thinning of the cortex. If one simply measured the distance from the most proximal remaining bone stock to the area where the greater tuberosity should be, a loose stem with subsidence and ballooning of the cortices may appear to have a similar amount of bone loss as a failed hemiarthroplasty for fracture with a well-fixed stem. However, intraoperatively, one will find that the bone that appeared to be present radiographically in the case of the loose stem is of such poor quality that it cannot reasonably provide any beneficial fixation. In light of this, different treatment modalities are recommended for different types of bone loss, and the revision surgeon must be able to anticipate this and possess a full armamentarium of options to treat these challenging cases successfully.
INDICATIONS
Our technique to manage proximal humeral bone loss is dependent on both the quantity of bone loss, which can be measured radiographically, as well as the anticipated inflammatory response described above. As both the destructive process and the amount of bone loss increase, the importance of more advanced reconstructive procedures that will sustain implant security and soft-tissue management becomes apparent. In the least destructive cases with <5 cm of bone loss, successful revision can typically be accomplished with stem removal and placement of a new monoblock humeral stem. In cases where more advanced destructive pathology is present, and bone loss is >5 cm, an allograft-prosthetic composite (APC) is typically used. In both scenarios, if the stem being revised is cemented and the cement mantle remains intact, and of reasonable length, consideration is given to the cement-within-cement technique. Finally, in the most destructive cases where bone loss exceeds 10 cm and a large biological response is anticipated (eg, periprosthetic fractures with humeral loosening), the use of a longer diaphyseal-incorporating APC is often necessary. This prosthetic composite can be combined with a cement-within-cement technique as well.
It is important to comment on the implications of using modular stems in this setting. With advanced bone loss, a situation is often encountered where the newly implanted stem geometry and working length may be insufficient to acquire adequate rotational stability. In this setting, if a modular junction is positioned close to the stem and cement/bone interface, it will be exposed to very high stress concentrations which can lead to component fracture38 as well as taper corrosion, also referred to as trunnionosis. This latter phenomenon, which has been well studied in the total hip arthroplasty literature with the use of modular components,39 is especially relevant given the high torsional loads imparted at the modular junction. Ultimately, high torsional loads lead to micromotion and electrochemical ion release via degradation of the passivation layer, initiating the process of mechanically assisted crevice corrosion.40 For these reasons, when a modular stem must be used in the presence of mild to moderate bone loss, using a proximal humeral allograft to protect the junction or to provide additional fixation may be implemented with a lower threshold than when using a monoblock stem.
SURGICAL TECHNIQUE: ALLOGRAFT-PROSTHETIC COMPOSITES
A standard deltopectoral approach is used, taking care to preserve all viable muscular attachments to the proximal humerus. After removal of the prosthetic humeral head, the decision to proceed with removal of the stem at this juncture is based on several factors. If the remaining proximal humeral bone is so compromised that it might not be able to withstand the forces exerted upon it during retraction for glenoid exposure, the component is left in place. Additionally, if there is consideration that the glenoid-sided bone loss may be so severe that a glenoid baseplate cannot be implanted, and the stem remains well fixed, it is retained so that it can be converted to a hemiarthroplasty.
If neither of the above issues is present, the humeral stem is removed. If a well-fixed press-fit stem is in place, it is typically removed using a combination of burrs and osteotomes to disrupt the bone-implant interface, and the stem is then carefully removed using an impactor and mallet. If a cemented stem is present, the stem is removed in a similar manner, and the cement mantle is left in place if stable, in anticipation of a cement-within-cement technique. If the mantle is disrupted, standard cement removal instruments are used to remove all cement from the canal meticulously.
Continue to: Management of the glenoid...
Management of the glenoid can have significant implications with regard to the humerus. Most notably, the size of the glenosphere has direct implications on the fixation of the humeral component. Use of larger diameter glenospheres result in increased contact area between the glenosphere and humerosocket, adding constraint to the articulation and further increasing the stresses at the implant-bone interface. As such, the use of larger glenospheres to prevent instability must be balanced with the resulting implications on humeral component fixation, especially in cases of severe bone loss.
After implanting the appropriate glenosphere, attention is then turned back to the humerus. Trial implants are sequentially used to obtain adequate humeral length and stability. Once this is accomplished, the amount of humeral bone loss is quantified by measuring the distance from the superior aspect of the medial humeral tray to the medial humeral shaft. If this number is >5 cm (Figure 3), the decision is made to proceed with an APC. The allograft humeral head is cut, cancellous bone is removed, and a step-cut is performed, with the medial portion of the allograft measuring the same length as that of bone loss and the lateral plate extending an additional several centimeters distally (Figure 4). Additional soft tissue is removed from the allograft, leaving the subscapularis stump intact for later repair with the patient’s native tissue. The allograft is secured to the patient’s proximal humerus using multiple cerclage wires, and the humeral stem is cemented into place. The final construct is shown in Figure 5.
ADDITIONAL CONSIDERATIONS: CASES OF ADVANCED BONE LOSS
In cases of advanced humeral bone loss, as is often seen when revising loose humeral stems, larger allografts that span a significant length of the diaphysis are often required. This type of bone loss has implications with regard to how the deltoid insertion is managed. Interestingly, even in situations when the vast majority of the remaining diaphysis consists of ectatic egg-shell bone, the deltoid tuberosity remains of fairly substantial quality due to the continued pull of the muscular insertion on this area. This fragment is isolated, carefully mobilized, and subsequently repaired back on top of the allograft using cables.
POSTOPERATIVE CARE
Patients are kept in a shoulder immobilizer for 6 weeks after surgery to facilitate allograft incorporation and subscapularis tendon healing. During this time, pendulum exercises are initiated. Active assisted range of motion (ROM) exercises begin after 6 weeks, consisting of supine forward elevation. A sling is given to be used in public. Light strengthening exercises begin at 3 months postoperatively.
DISCUSSION
In cases of mild to moderate proximal humeral bone loss, RSA using a long-stem humeral component without allograft augmentation is a viable option. Budge and colleagues38 demonstrated excellent results in a population of 15 patients with an average of 38 mm of proximal humeral bone loss without use of allografts. Interestingly, they noted 1 case of component fracture in a modular prosthesis and therefore concluded that monoblock humeral stems should be used in the absence of allograft augmentation.
Continue to: In more advanced cases of bone loss...
In more advanced cases of bone loss, our data shows that use of APCs can result in equally satisfactory results. In a series of 25 patients with an average bone loss of 54 mm, patients were able to achieve statistically significant improvements in pain, ROM, and function with high rates of allograft incorporation.9 Overall, a low rate of complications was noted, including 1 infection. This finding is consistent with an additional study looking specifically at factors associated with infection in revision SA, which found that the use of allografts was not associated with increased risk of infection.41
As stated previously, the size of allograft needed for the APC construct is related to the distinct pathology encountered. In our experience, we have noted that well-fixed stems can be treated with short metaphyseal APCs in 85% of cases. On the other hand, loose stems require long allografts measuring >10 cm in 90% of cases. As such, these cases typically require mobilization of the deltoid insertion as described above, and therefore it is important that the surgeon is prepared for this aspect of the procedure preoperatively.
Finally, the cement-within-cement technique, originally popularized for use in revision total hip arthroplasty, has demonstrated reliable results when utilized in revision SA.42 To date, there are no recommendations regarding the minimal length of existing cement mantle that is needed to perform this technique. In situations in which the length of the cement mantle is questionable, our preference is to combine the cement-within-cement technique with an APC when possible.
ABSTRACT
Revision shoulder arthroplasty is becoming more prevalent as the rate of primary shoulder arthroplasty in the US continues to increase. The management of proximal humeral bone loss in the revision setting presents a difficult problem without a clear solution. Different preoperative diagnoses often lead to distinctly different patterns of bone loss. Successful management of these cases requires a clear understanding of the normal anatomy of the proximal humerus, as well as structural limitations imposed by significant bone loss and the effect this loss has on component fixation. Our preferred technique differs depending on the pattern of bone loss encountered. The use of allograft-prosthetic composites, the cement-within-cement technique, and combinations of these strategies comprise the mainstay of our treatment algorithm. This article focuses on indications, surgical techniques, and some of the published outcomes using these strategies in the management of proximal humeral bone loss.
Continue to: The demand for shoulder arthroplasty...
The demand for shoulder arthroplasty (SA) has increased significantly over the past decade, with a 200% increase witnessed from 2011 to 2015.1 SA performed in patients younger than 55 years is expected to increase 333% between 2011 to 2030.2 With increasing rates of SA being performed in younger patient populations, rates of revision SA also can be expected to climb. Revision to reverse shoulder arthroplasty (RSA) has arisen as a viable option in these patients, and multiple studies demonstrate excellent outcomes that can be obtained with RSA.3-11
Despite significant improvements obtained in revision SA since the mainstream acceptance of RSA, bone loss remains a problematic issue. Loss of humeral bone stock, in particular, can be a challenging problem to solve with multiple clinical implications. Biomechanical studies have demonstrated that if bone loss is left unaddressed, increased bending and torsional forces on the prosthesis result, which ultimately contribute to increased micromotion and eventual component failure.12 In addition, existing challenges are associated with the lack of attachment sites for both multiple muscles and tendons. Also, there is a loss of the normal lateralized pull of the deltoid, which results in a decreased amount of force generated by this muscle.13,14 Ultimately, the increased loss of bone can lead to a devastating situation where there is not enough bone to provide adequate fixation while maintaining the appropriate humeral length necessary to achieve stability of the articulation, which will inevitably lead to instability.4,15 Therefore, techniques are needed to address proximal humeral bone loss while maintaining as much native humeral bone as possible.
PROXIMAL HUMERUS: ANATOMICAL CONSIDERATIONS
The anatomy of the proximal humerus has been studied in great detail and reported in a number of different studies.16-23 The average humeral head thickness (24 mm in men and 19 mm in women) and offset relative to the humeral shaft (2.1 mm posterior and 6.6 mm medial) act to tension the rotator cuff musculature appropriately and contribute to a wrapping effect that allows the deltoid to function more effectively.13,14 Knowledge regarding the rotator cuff footprint has advanced over the past 10 years, specifically with regard to the supraspinatus and infraspinatus.24 The current belief is that the supraspinatus has a triangular insertion onto the most anterior aspect of the greater tuberosity, with a maximum medial-to-lateral length of 6.9 mm and a maximum anterior-to-posterior width of 12.6 mm. The infraspinatus insertion has a trapezoidal insertion, with a maximum medial-to-lateral length of 10.2 mm and anterior-to-posterior width of 32.7 mm. The subscapularis, by far the largest of all the rotator cuff muscles, has a complex geometry with regard to its insertion on the lesser tuberosity, with 4 different insertion points and an overall lateral footprint measuring 37.6 mm and a medial footprint measuring 40.7 mm.25 Finally, the teres minor, with the smallest volume of all the rotator cuff muscles, inserts immediately inferior to the infraspinatus along the inferior facet of the greater tuberosity.26
Aside from the rotator cuff, there are various other muscles and tendons that insert about the proximal humerus and are essential for normal function. The deltoid, which inserts at a point approximately 6 cm from the greater tuberosity along the length of the humerus, with an insertion length between 5 cm to 7 cm,13,27 is the primary mover of the shoulder and essential for proper function after RSA.28,29 The pectoralis major tendon, which begins inserting at a point approximately 5.6 cm from the humeral head and spans a distance of 7.7 cm along the length of the humerus,30-32 is important not only for function but as an anatomical landmark in reconstruction. Lastly, the latissimus dorsi and teres major, which share a role in extension, adduction, and internal rotation of the glenohumeral joint, insert along the floor and medial lip of the intertubercular groove of the humerus, respectively.33,34 In addition to their role in tendon transfer procedures because of treating irreparable posterosuperior cuff and subscapularis tears,35,36 it has been suggested that these tendons may play some role in glenohumeral joint stability.37
In addition to the loss of muscular attachments, the absence of proximal humeral bone stock, in and of itself, can have deleterious effects on fixation of the humeral component. RSA is a semiconstrained device, which results in increased transmission of forces to the interface between the humeral implant and its surrounding structures, including cement (when present) and the bone itself. When there is the absence of significant amounts of bone, the remaining bone must now account for an even higher proportion of these forces. A previous biomechanical study showed that cemented humeral stems demonstrated significantly increased micromotion in the presence of proximal humeral bone loss, particularly when a modular humeral component was used.12
Continue to: TYPES OF BONE LOSS
TYPES OF BONE LOSS
There are a variety of different etiologies of proximal humeral bone loss that result in distinctly different clinical presentations. These can be fairly mild, as is the case of isolated resorption of the greater tuberosity in a non-united proximal humerus fracture (Figure 1). Alternatively, they can be severe, as seen in a grossly loose cemented long-stemmed component that is freely mobile, creating a windshield-wiper effect throughout the length of the humerus (Figure 2). This can be somewhat deceiving, however, as the amount of bone loss, as well as the pathophysiologic process that led to the bone loss, are important factors to determine ideal reconstructive methods. In the case of a failed open reduction internal fixation, where the tuberosity has failed to unite or has been resected, there is much less of a biologic response in comparison with implant loosening associated with osteolysis. This latter condition will be associated with a much more destructive inflammatory response resulting in poor tissue quality and often dramatic thinning of the cortex. If one simply measured the distance from the most proximal remaining bone stock to the area where the greater tuberosity should be, a loose stem with subsidence and ballooning of the cortices may appear to have a similar amount of bone loss as a failed hemiarthroplasty for fracture with a well-fixed stem. However, intraoperatively, one will find that the bone that appeared to be present radiographically in the case of the loose stem is of such poor quality that it cannot reasonably provide any beneficial fixation. In light of this, different treatment modalities are recommended for different types of bone loss, and the revision surgeon must be able to anticipate this and possess a full armamentarium of options to treat these challenging cases successfully.
INDICATIONS
Our technique to manage proximal humeral bone loss is dependent on both the quantity of bone loss, which can be measured radiographically, as well as the anticipated inflammatory response described above. As both the destructive process and the amount of bone loss increase, the importance of more advanced reconstructive procedures that will sustain implant security and soft-tissue management becomes apparent. In the least destructive cases with <5 cm of bone loss, successful revision can typically be accomplished with stem removal and placement of a new monoblock humeral stem. In cases where more advanced destructive pathology is present, and bone loss is >5 cm, an allograft-prosthetic composite (APC) is typically used. In both scenarios, if the stem being revised is cemented and the cement mantle remains intact, and of reasonable length, consideration is given to the cement-within-cement technique. Finally, in the most destructive cases where bone loss exceeds 10 cm and a large biological response is anticipated (eg, periprosthetic fractures with humeral loosening), the use of a longer diaphyseal-incorporating APC is often necessary. This prosthetic composite can be combined with a cement-within-cement technique as well.
It is important to comment on the implications of using modular stems in this setting. With advanced bone loss, a situation is often encountered where the newly implanted stem geometry and working length may be insufficient to acquire adequate rotational stability. In this setting, if a modular junction is positioned close to the stem and cement/bone interface, it will be exposed to very high stress concentrations which can lead to component fracture38 as well as taper corrosion, also referred to as trunnionosis. This latter phenomenon, which has been well studied in the total hip arthroplasty literature with the use of modular components,39 is especially relevant given the high torsional loads imparted at the modular junction. Ultimately, high torsional loads lead to micromotion and electrochemical ion release via degradation of the passivation layer, initiating the process of mechanically assisted crevice corrosion.40 For these reasons, when a modular stem must be used in the presence of mild to moderate bone loss, using a proximal humeral allograft to protect the junction or to provide additional fixation may be implemented with a lower threshold than when using a monoblock stem.
SURGICAL TECHNIQUE: ALLOGRAFT-PROSTHETIC COMPOSITES
A standard deltopectoral approach is used, taking care to preserve all viable muscular attachments to the proximal humerus. After removal of the prosthetic humeral head, the decision to proceed with removal of the stem at this juncture is based on several factors. If the remaining proximal humeral bone is so compromised that it might not be able to withstand the forces exerted upon it during retraction for glenoid exposure, the component is left in place. Additionally, if there is consideration that the glenoid-sided bone loss may be so severe that a glenoid baseplate cannot be implanted, and the stem remains well fixed, it is retained so that it can be converted to a hemiarthroplasty.
If neither of the above issues is present, the humeral stem is removed. If a well-fixed press-fit stem is in place, it is typically removed using a combination of burrs and osteotomes to disrupt the bone-implant interface, and the stem is then carefully removed using an impactor and mallet. If a cemented stem is present, the stem is removed in a similar manner, and the cement mantle is left in place if stable, in anticipation of a cement-within-cement technique. If the mantle is disrupted, standard cement removal instruments are used to remove all cement from the canal meticulously.
Continue to: Management of the glenoid...
Management of the glenoid can have significant implications with regard to the humerus. Most notably, the size of the glenosphere has direct implications on the fixation of the humeral component. Use of larger diameter glenospheres result in increased contact area between the glenosphere and humerosocket, adding constraint to the articulation and further increasing the stresses at the implant-bone interface. As such, the use of larger glenospheres to prevent instability must be balanced with the resulting implications on humeral component fixation, especially in cases of severe bone loss.
After implanting the appropriate glenosphere, attention is then turned back to the humerus. Trial implants are sequentially used to obtain adequate humeral length and stability. Once this is accomplished, the amount of humeral bone loss is quantified by measuring the distance from the superior aspect of the medial humeral tray to the medial humeral shaft. If this number is >5 cm (Figure 3), the decision is made to proceed with an APC. The allograft humeral head is cut, cancellous bone is removed, and a step-cut is performed, with the medial portion of the allograft measuring the same length as that of bone loss and the lateral plate extending an additional several centimeters distally (Figure 4). Additional soft tissue is removed from the allograft, leaving the subscapularis stump intact for later repair with the patient’s native tissue. The allograft is secured to the patient’s proximal humerus using multiple cerclage wires, and the humeral stem is cemented into place. The final construct is shown in Figure 5.
ADDITIONAL CONSIDERATIONS: CASES OF ADVANCED BONE LOSS
In cases of advanced humeral bone loss, as is often seen when revising loose humeral stems, larger allografts that span a significant length of the diaphysis are often required. This type of bone loss has implications with regard to how the deltoid insertion is managed. Interestingly, even in situations when the vast majority of the remaining diaphysis consists of ectatic egg-shell bone, the deltoid tuberosity remains of fairly substantial quality due to the continued pull of the muscular insertion on this area. This fragment is isolated, carefully mobilized, and subsequently repaired back on top of the allograft using cables.
POSTOPERATIVE CARE
Patients are kept in a shoulder immobilizer for 6 weeks after surgery to facilitate allograft incorporation and subscapularis tendon healing. During this time, pendulum exercises are initiated. Active assisted range of motion (ROM) exercises begin after 6 weeks, consisting of supine forward elevation. A sling is given to be used in public. Light strengthening exercises begin at 3 months postoperatively.
DISCUSSION
In cases of mild to moderate proximal humeral bone loss, RSA using a long-stem humeral component without allograft augmentation is a viable option. Budge and colleagues38 demonstrated excellent results in a population of 15 patients with an average of 38 mm of proximal humeral bone loss without use of allografts. Interestingly, they noted 1 case of component fracture in a modular prosthesis and therefore concluded that monoblock humeral stems should be used in the absence of allograft augmentation.
Continue to: In more advanced cases of bone loss...
In more advanced cases of bone loss, our data shows that use of APCs can result in equally satisfactory results. In a series of 25 patients with an average bone loss of 54 mm, patients were able to achieve statistically significant improvements in pain, ROM, and function with high rates of allograft incorporation.9 Overall, a low rate of complications was noted, including 1 infection. This finding is consistent with an additional study looking specifically at factors associated with infection in revision SA, which found that the use of allografts was not associated with increased risk of infection.41
As stated previously, the size of allograft needed for the APC construct is related to the distinct pathology encountered. In our experience, we have noted that well-fixed stems can be treated with short metaphyseal APCs in 85% of cases. On the other hand, loose stems require long allografts measuring >10 cm in 90% of cases. As such, these cases typically require mobilization of the deltoid insertion as described above, and therefore it is important that the surgeon is prepared for this aspect of the procedure preoperatively.
Finally, the cement-within-cement technique, originally popularized for use in revision total hip arthroplasty, has demonstrated reliable results when utilized in revision SA.42 To date, there are no recommendations regarding the minimal length of existing cement mantle that is needed to perform this technique. In situations in which the length of the cement mantle is questionable, our preference is to combine the cement-within-cement technique with an APC when possible.
1. Day JS, Lau E, Ong KL, Williams GR, Ramsey ML, Kurtz SM. Prevalence and projections of total shoulder and elbow arthroplasty in the United States to 2015. J Shoulder Elbow Surg. 2010;19(8):1115-1120. doi:10.1016/j.jse.2010.02.009.
2. Padegimas EM, Maltenfort M, Lazarus MD, Ramsey ML, Williams GR, Namdari S. Future patient demand for shoulder arthroplasty by younger patients: national projections. Clin Orthop Relat Res. 2015;473(6):1860-1867. doi:10.1007/s11999-015-4231-z.
3. Walker M, Willis MP, Brooks JP, Pupello D, Mulieri PJ, Frankle MA. The use of the reverse shoulder arthroplasty for treatment of failed total shoulder arthroplasty. J Shoulder Elbow Surg. 2012;21(4):514-522. doi:10.1016/j.jse.2011.03.006.
4. Levy JC, Virani N, Pupello D, et al. Use of the reverse shoulder prosthesis for the treatment of failed hemiarthroplasty in patients with glenohumeral arthritis and rotator cuff deficiency. J Bone Joint Surg Br. 2007;89(2):189-195. doi:10.1302/0301-620X.89B2.
5. Melis B, Bonnevialle N, Neyton L, et al. Glenoid loosening and failure in anatomical total shoulder arthroplasty: is revision with a reverse shoulder arthroplasty a reliable option? J Shoulder Elbow Surg. 2012;21(3):342-349. doi:10.1016/j.jse.2011.05.021.
6. Deutsch A, Abboud JA, Kelly J, et al. Clinical results of revision shoulder arthroplasty for glenoid component loosening. J Shoulder Elbow Surg. 2007;16(6):706-716. doi:10.1016/j.jse.2007.01.007.
7. Kelly JD, Zhao JX, Hobgood ER, Norris TR. Clinical results of revision shoulder arthroplasty using the reverse prosthesis. J Shoulder Elbow Surg. 2012;21(11):1516-1525. doi:10.1016/j.jse.2011.11.021.
8. Black EM, Roberts SM, Siegel E, Yannopoulos P, Higgins LD, Warner JJP. Reverse shoulder arthroplasty as salvage for failed prior arthroplasty in patients 65 years of age or younger. J Shoulder Elbow Surg. 2014;23(7):1036-1042. doi:10.1016/j.jse.2014.02.019.
9. Composite P, Chacon BA, Virani N, et al. Revision arthroplasty with use of a reverse shoulder. J Bone Joint Surg. 2009;1:119-127. doi:10.2106/JBJS.H.00094.
10. Klein SM, Dunning P, Mulieri P, Pupello D, Downes K, Frankle MA. Effects of acquired glenoid bone defects on surgical technique and clinical outcomes in reverse shoulder arthroplasty. J Bone Joint Surg Am. 2010;92(5):1144-1154. doi:10.2106/JBJS.I.00778.
11. Patel DN, Young B, Onyekwelu I, Zuckerman JD, Kwon YW. Reverse total shoulder arthroplasty for failed shoulder arthroplasty. J Shoulder Elbow Surg. 2012;21(11):1478-1483. doi:10.1016/j.jse.2011.11.004.
12. Cuff D, Levy JC, Gutiérrez S, Frankle MA. Torsional stability of modular and non-modular reverse shoulder humeral components in a proximal humeral bone loss model. J Shoulder Elbow Surg. 2011;20(4):646-651. doi:10.1016/j.jse.2010.10.026.
13. Morgan SJ, Furry K, Parekh A, Agudelo JF, Smith WR. The deltoid muscle: an anatomic description of the deltoid insertion to the proximal humerus. J Orthop Trauma. 2006;20(1):19-21. doi:10.1097/01.bot.0000187063.43267.18.
14. Gagey O, Hue E. Mechanics of the deltoid muscle. A new approach. Clin Orthop Relat Res. 2000;375:250-257. doi:10.1097/00003086-200006000-00030.
15. De Wilde L, Plasschaert F. Prosthetic treatment and functional recovery of the shoulder after tumor resection 10 years ago: a case report. J Shoulder Elbow Surg. 2005;14(6):645-649. doi:10.1016/j.jse.2004.11.001.
16. Wataru S, Kazuomi S, Yoshikazu N, Hiroaki I, Takaharu Y, Hideki Y. Three-dimensional morphological analysis of humeral heads: a study in cadavers. Acta Orthop. 2005;76(3):392-396. doi:10.1080/00016470510030878.
17. Tillett E, Smith M, Fulcher M, Shanklin J. Anatomic determination of humeral head retroversion: the relationship of the central axis of the humeral head to the bicipital groove. J Shoulder Elbow Surg. 1993;2(5):255-256. doi:10.1016/S1058-2746(09)80085-2.
18. Doyle AJ, Burks RT. Comparison of humeral head retroversion with the humeral axis/biceps groove relationship: a study in live subjects and cadavers. J Shoulder Elbow Surg. 1998;7(5):453-457. doi:10.1016/S1058-2746(98)90193-8.
19. Johnson JW, Thostenson JD, Suva LJ, Hasan SA. Relationship of bicipital groove rotation with humeral head retroversion: a three-dimensional computed tomographic analysis. J Bone Joint Surg Am. 2013;95(8):719-724. doi:10.2106/JBJS.J.00085.
20. Hromádka R, Kuběna AA, Pokorný D, Popelka S, Jahoda D, Sosna A. Lesser tuberosity is more reliable than bicipital groove when determining orientation of humeral head in primary shoulder arthroplasty. Surg Radiol Anat. 2010;32(1):31-37. doi:10.1007/s00276-009-0543-6.
21. Hertel R, Knothe U, Ballmer FT. Geometry of the proximal humerus and implications for prosthetic design. J Shoulder Elbow Surg. 2002;11(4):331-338. doi:10.1067/mse.2002.124429.
22. Pearl ML. Proximal humeral anatomy in shoulder arthroplasty: Implications for prosthetic design and surgical technique. J Shoulder Elbow Surg. 2005;14(suppl 1):99-104. doi:10.1016/j.jse.2004.09.025.
23. Robertson DD, Yuan J, Bigliani LU, Flatow EL, Yamaguchi K. Three-dimensional analysis of the proximal part of the humerus: relevance to arthroplasty. J Bone Joint Surg Am. 2000;82-A(11):1594-1602.
24. Mochizuki T, Sugaya H, Uomizu M, et al. Humeral insertion of the supraspinatus and infraspinatus. J Bone Joint Surg Am. 2008;90(5):962-969. doi:10.2106/JBJS.G.00427.
25. Arai R, Sugaya H, Mochizuki T, Nimura A, Moriishi J, Akita K. Subscapularis tendon tear: an anatomic and clinical investigation. Arthroscopy. 2008;24(9):997-1004. doi:10.1016/j.arthro.2008.04.076.
26. Nimura A, Kato A, Yamaguchi K, et al. The superior capsule of the shoulder joint complements the insertion of the rotator cuff. J Shoulder Elbow Surg. 2012;21(7):867-872. doi:10.1016/j.jse.2011.04.034.
27. Rispoli DM, Athwal GS, Sperling JW, Cofield RH. The anatomy of the deltoid insertion. J Shoulder Elbow Surg. 2009;18(3):386-390. doi:10.1016/j.jse.2008.10.012.
28. Schwartz DG, Kang SH, Lynch TS, et al. The anterior deltoid’s importance in reverse shoulder arthroplasty: a cadaveric biomechanical study. J Shoulder Elbow Surg. 2013;22(3):357-364. doi:10.1016/j.jse.2012.02.002.
29. Walker M, Brooks J, Willis M, Frankle M. How reverse shoulder arthroplasty works. Clinical Orthop Relat Res. 2011;469(9):2440-2451. doi:10.1007/s11999-011-1892-0.
30. Torrens C, Corrales M, Melendo E, Solano A, Rodríguez-Baeza A, Cáceres E. The pectoralis major tendon as a reference for restoring humeral length and retroversion with hemiarthroplasty for fracture. J Shoulder Elbow Surg. 2008;17(6):947-950. doi:10.1016/j.jse.2008.05.041.
31. Ponce BA, Thompson KJ, Rosenzweig SD, et al. Re-evaluation of pectoralis major height as an anatomic reference for humeral height in fracture hemiarthroplasty. J Shoulder Elbow Surg. 2013;22(11):1567-1572. doi:10.1016/j.jse.2013.01.039.
32. LaFrance R, Madsen W, Yaseen Z, Giordano B, Maloney M, Voloshin I. Relevant anatomic landmarks and measurements for biceps tenodesis. Am J Sports Med. 2013;41(6):1395-1399. doi:10.1177/0363546513482297.
33. Beck PA, Hoffer MM. Latissimus dorsi and teres major tendons: separate or conjoint tendons? J Pediatr Orthop. 1989;9(3):308-309.
34. Bhatt CR, Prajapati B, Patil DS, Patel VD, Singh BGP, Mehta CD. Variation in the insertion of the latissimus dorsi & its clinical importance. J Orthop. 2013;10(1):25-28. doi:10.1016/j.jor.2013.01.002.
35. Gerber C, Maquieira G, Espinosa N. Latissimus dorsi transfer for the treatment of irreparable rotator cuff tears. J Bone Joint Surg. 2006;88(1):113-120. doi:10.2106/JBJS.E.00282.
36. Elhassan B, Christensen TJ, Wagner ER. Feasibility of latissimus and teres major transfer to reconstruct irreparable subscapularis tendon tear: an anatomic study. J Shoulder Elbow Surg. 2014;23(4):492-499. doi:10.1016/j.jse.2013.07.046.
37. Pouliart N, Gagey O. Significance of the latissimus dorsi for shoulder instability. II. Its influence on dislocation behavior in a sequential cutting protocol of the glenohumeral capsule. Clin Anat. 2005;18(7):500-509. doi:10.1002/ca.20181.
38. Budge MD, Moravek JE, Zimel MN, Nolan EM, Wiater JM. Reverse total shoulder arthroplasty for the management of failed shoulder arthroplasty with proximal humeral bone loss: is allograft augmentation necessary? J Shoulder Elbow Surg. 2013;22(6):739-744. doi:10.1016/j.jse.2012.08.008.
39. Weiser MC, Lavernia CJ. Trunnionosis in total hip arthroplasty. J Bone Joint Surg Am. 2017;99(17):27-29. doi:10.2106/JBJS.17.00345.
40. Cohen J. Current concepts review. Corrosion of metal orthopaedic implants. J Bone Joint Surg Am. 1998;80(10):1554.
41. Meijer ST, Paulino Pereira NR, Nota SPFT, Ferrone ML, Schwab JH, Lozano Calderón SA. Factors associated with infection after reconstructive shoulder surgery for proximal humerus tumors. J Shoulder Elbow Surg. 2017;26(6):931-938. doi:10.1016/j.jse.2016.10.014.
42. Wagner ER, Houdek MT, Hernandez NM, Cofield RH, Sánchez-Sotelo J, Sperling JW. Cement-within-cement technique in revision reverse shoulder arthroplasty. J Shoulder Elbow Surg. 2017;26(8):1448-1453. doi:10.1016/j.jse.2017.01.013.
1. Day JS, Lau E, Ong KL, Williams GR, Ramsey ML, Kurtz SM. Prevalence and projections of total shoulder and elbow arthroplasty in the United States to 2015. J Shoulder Elbow Surg. 2010;19(8):1115-1120. doi:10.1016/j.jse.2010.02.009.
2. Padegimas EM, Maltenfort M, Lazarus MD, Ramsey ML, Williams GR, Namdari S. Future patient demand for shoulder arthroplasty by younger patients: national projections. Clin Orthop Relat Res. 2015;473(6):1860-1867. doi:10.1007/s11999-015-4231-z.
3. Walker M, Willis MP, Brooks JP, Pupello D, Mulieri PJ, Frankle MA. The use of the reverse shoulder arthroplasty for treatment of failed total shoulder arthroplasty. J Shoulder Elbow Surg. 2012;21(4):514-522. doi:10.1016/j.jse.2011.03.006.
4. Levy JC, Virani N, Pupello D, et al. Use of the reverse shoulder prosthesis for the treatment of failed hemiarthroplasty in patients with glenohumeral arthritis and rotator cuff deficiency. J Bone Joint Surg Br. 2007;89(2):189-195. doi:10.1302/0301-620X.89B2.
5. Melis B, Bonnevialle N, Neyton L, et al. Glenoid loosening and failure in anatomical total shoulder arthroplasty: is revision with a reverse shoulder arthroplasty a reliable option? J Shoulder Elbow Surg. 2012;21(3):342-349. doi:10.1016/j.jse.2011.05.021.
6. Deutsch A, Abboud JA, Kelly J, et al. Clinical results of revision shoulder arthroplasty for glenoid component loosening. J Shoulder Elbow Surg. 2007;16(6):706-716. doi:10.1016/j.jse.2007.01.007.
7. Kelly JD, Zhao JX, Hobgood ER, Norris TR. Clinical results of revision shoulder arthroplasty using the reverse prosthesis. J Shoulder Elbow Surg. 2012;21(11):1516-1525. doi:10.1016/j.jse.2011.11.021.
8. Black EM, Roberts SM, Siegel E, Yannopoulos P, Higgins LD, Warner JJP. Reverse shoulder arthroplasty as salvage for failed prior arthroplasty in patients 65 years of age or younger. J Shoulder Elbow Surg. 2014;23(7):1036-1042. doi:10.1016/j.jse.2014.02.019.
9. Composite P, Chacon BA, Virani N, et al. Revision arthroplasty with use of a reverse shoulder. J Bone Joint Surg. 2009;1:119-127. doi:10.2106/JBJS.H.00094.
10. Klein SM, Dunning P, Mulieri P, Pupello D, Downes K, Frankle MA. Effects of acquired glenoid bone defects on surgical technique and clinical outcomes in reverse shoulder arthroplasty. J Bone Joint Surg Am. 2010;92(5):1144-1154. doi:10.2106/JBJS.I.00778.
11. Patel DN, Young B, Onyekwelu I, Zuckerman JD, Kwon YW. Reverse total shoulder arthroplasty for failed shoulder arthroplasty. J Shoulder Elbow Surg. 2012;21(11):1478-1483. doi:10.1016/j.jse.2011.11.004.
12. Cuff D, Levy JC, Gutiérrez S, Frankle MA. Torsional stability of modular and non-modular reverse shoulder humeral components in a proximal humeral bone loss model. J Shoulder Elbow Surg. 2011;20(4):646-651. doi:10.1016/j.jse.2010.10.026.
13. Morgan SJ, Furry K, Parekh A, Agudelo JF, Smith WR. The deltoid muscle: an anatomic description of the deltoid insertion to the proximal humerus. J Orthop Trauma. 2006;20(1):19-21. doi:10.1097/01.bot.0000187063.43267.18.
14. Gagey O, Hue E. Mechanics of the deltoid muscle. A new approach. Clin Orthop Relat Res. 2000;375:250-257. doi:10.1097/00003086-200006000-00030.
15. De Wilde L, Plasschaert F. Prosthetic treatment and functional recovery of the shoulder after tumor resection 10 years ago: a case report. J Shoulder Elbow Surg. 2005;14(6):645-649. doi:10.1016/j.jse.2004.11.001.
16. Wataru S, Kazuomi S, Yoshikazu N, Hiroaki I, Takaharu Y, Hideki Y. Three-dimensional morphological analysis of humeral heads: a study in cadavers. Acta Orthop. 2005;76(3):392-396. doi:10.1080/00016470510030878.
17. Tillett E, Smith M, Fulcher M, Shanklin J. Anatomic determination of humeral head retroversion: the relationship of the central axis of the humeral head to the bicipital groove. J Shoulder Elbow Surg. 1993;2(5):255-256. doi:10.1016/S1058-2746(09)80085-2.
18. Doyle AJ, Burks RT. Comparison of humeral head retroversion with the humeral axis/biceps groove relationship: a study in live subjects and cadavers. J Shoulder Elbow Surg. 1998;7(5):453-457. doi:10.1016/S1058-2746(98)90193-8.
19. Johnson JW, Thostenson JD, Suva LJ, Hasan SA. Relationship of bicipital groove rotation with humeral head retroversion: a three-dimensional computed tomographic analysis. J Bone Joint Surg Am. 2013;95(8):719-724. doi:10.2106/JBJS.J.00085.
20. Hromádka R, Kuběna AA, Pokorný D, Popelka S, Jahoda D, Sosna A. Lesser tuberosity is more reliable than bicipital groove when determining orientation of humeral head in primary shoulder arthroplasty. Surg Radiol Anat. 2010;32(1):31-37. doi:10.1007/s00276-009-0543-6.
21. Hertel R, Knothe U, Ballmer FT. Geometry of the proximal humerus and implications for prosthetic design. J Shoulder Elbow Surg. 2002;11(4):331-338. doi:10.1067/mse.2002.124429.
22. Pearl ML. Proximal humeral anatomy in shoulder arthroplasty: Implications for prosthetic design and surgical technique. J Shoulder Elbow Surg. 2005;14(suppl 1):99-104. doi:10.1016/j.jse.2004.09.025.
23. Robertson DD, Yuan J, Bigliani LU, Flatow EL, Yamaguchi K. Three-dimensional analysis of the proximal part of the humerus: relevance to arthroplasty. J Bone Joint Surg Am. 2000;82-A(11):1594-1602.
24. Mochizuki T, Sugaya H, Uomizu M, et al. Humeral insertion of the supraspinatus and infraspinatus. J Bone Joint Surg Am. 2008;90(5):962-969. doi:10.2106/JBJS.G.00427.
25. Arai R, Sugaya H, Mochizuki T, Nimura A, Moriishi J, Akita K. Subscapularis tendon tear: an anatomic and clinical investigation. Arthroscopy. 2008;24(9):997-1004. doi:10.1016/j.arthro.2008.04.076.
26. Nimura A, Kato A, Yamaguchi K, et al. The superior capsule of the shoulder joint complements the insertion of the rotator cuff. J Shoulder Elbow Surg. 2012;21(7):867-872. doi:10.1016/j.jse.2011.04.034.
27. Rispoli DM, Athwal GS, Sperling JW, Cofield RH. The anatomy of the deltoid insertion. J Shoulder Elbow Surg. 2009;18(3):386-390. doi:10.1016/j.jse.2008.10.012.
28. Schwartz DG, Kang SH, Lynch TS, et al. The anterior deltoid’s importance in reverse shoulder arthroplasty: a cadaveric biomechanical study. J Shoulder Elbow Surg. 2013;22(3):357-364. doi:10.1016/j.jse.2012.02.002.
29. Walker M, Brooks J, Willis M, Frankle M. How reverse shoulder arthroplasty works. Clinical Orthop Relat Res. 2011;469(9):2440-2451. doi:10.1007/s11999-011-1892-0.
30. Torrens C, Corrales M, Melendo E, Solano A, Rodríguez-Baeza A, Cáceres E. The pectoralis major tendon as a reference for restoring humeral length and retroversion with hemiarthroplasty for fracture. J Shoulder Elbow Surg. 2008;17(6):947-950. doi:10.1016/j.jse.2008.05.041.
31. Ponce BA, Thompson KJ, Rosenzweig SD, et al. Re-evaluation of pectoralis major height as an anatomic reference for humeral height in fracture hemiarthroplasty. J Shoulder Elbow Surg. 2013;22(11):1567-1572. doi:10.1016/j.jse.2013.01.039.
32. LaFrance R, Madsen W, Yaseen Z, Giordano B, Maloney M, Voloshin I. Relevant anatomic landmarks and measurements for biceps tenodesis. Am J Sports Med. 2013;41(6):1395-1399. doi:10.1177/0363546513482297.
33. Beck PA, Hoffer MM. Latissimus dorsi and teres major tendons: separate or conjoint tendons? J Pediatr Orthop. 1989;9(3):308-309.
34. Bhatt CR, Prajapati B, Patil DS, Patel VD, Singh BGP, Mehta CD. Variation in the insertion of the latissimus dorsi & its clinical importance. J Orthop. 2013;10(1):25-28. doi:10.1016/j.jor.2013.01.002.
35. Gerber C, Maquieira G, Espinosa N. Latissimus dorsi transfer for the treatment of irreparable rotator cuff tears. J Bone Joint Surg. 2006;88(1):113-120. doi:10.2106/JBJS.E.00282.
36. Elhassan B, Christensen TJ, Wagner ER. Feasibility of latissimus and teres major transfer to reconstruct irreparable subscapularis tendon tear: an anatomic study. J Shoulder Elbow Surg. 2014;23(4):492-499. doi:10.1016/j.jse.2013.07.046.
37. Pouliart N, Gagey O. Significance of the latissimus dorsi for shoulder instability. II. Its influence on dislocation behavior in a sequential cutting protocol of the glenohumeral capsule. Clin Anat. 2005;18(7):500-509. doi:10.1002/ca.20181.
38. Budge MD, Moravek JE, Zimel MN, Nolan EM, Wiater JM. Reverse total shoulder arthroplasty for the management of failed shoulder arthroplasty with proximal humeral bone loss: is allograft augmentation necessary? J Shoulder Elbow Surg. 2013;22(6):739-744. doi:10.1016/j.jse.2012.08.008.
39. Weiser MC, Lavernia CJ. Trunnionosis in total hip arthroplasty. J Bone Joint Surg Am. 2017;99(17):27-29. doi:10.2106/JBJS.17.00345.
40. Cohen J. Current concepts review. Corrosion of metal orthopaedic implants. J Bone Joint Surg Am. 1998;80(10):1554.
41. Meijer ST, Paulino Pereira NR, Nota SPFT, Ferrone ML, Schwab JH, Lozano Calderón SA. Factors associated with infection after reconstructive shoulder surgery for proximal humerus tumors. J Shoulder Elbow Surg. 2017;26(6):931-938. doi:10.1016/j.jse.2016.10.014.
42. Wagner ER, Houdek MT, Hernandez NM, Cofield RH, Sánchez-Sotelo J, Sperling JW. Cement-within-cement technique in revision reverse shoulder arthroplasty. J Shoulder Elbow Surg. 2017;26(8):1448-1453. doi:10.1016/j.jse.2017.01.013.
TAKE-HOME POINTS
- Different preoperative diagnoses lead to distinct patterns of bone loss in revision shoulder arthroplasty.
- A variety of techniques should be utilized to address the specific pathologies encountered.
- Advanced proximal humeral bone loss results in limited substrate available for humeral component fixation.
- Monoblock humeral stems can be used without allografts in cases with mild humeral bone loss.
- The revision of loose humeral stems dictates the use of large diaphyseal allografts in the majority of cases.
Treating Humeral Bone Loss in Shoulder Arthroplasty: Modular Humeral Components or Allografts
ABSTRACT
Reconstructing proximal humeral bone loss in the setting of shoulder arthroplasty can be a daunting task. Proposed techniques include long-stemmed humeral components, allograft-prosthesis composites (APCs), and modular endoprosthetic reconstruction. While unsupported long-stemmed components are at high risk for component loosening, APC reconstruction techniques have been reported with success. However, graft resorption and eventual failure are significant concerns. Modular endoprosthetic systems allow bone deficiencies to be reconstructed with metal, which may allow for a more durable reconstruction.
Continue to: Shoulder arthroplasty is an established procedure...
Shoulder arthroplasty is an established procedure with good results for restoring motion and decreasing pain for a variety of indications, including arthritis, fracture, posttraumatic sequelae, and tumor resection.1-4 As the population ages, the incidence of these shoulder disorders increases, with the incidence of total shoulder arthroplasty (TSA) and reverse total shoulder arthroplasty (RTSA) increasing at faster rates than that of hemiarthroplasty.5,6 These expanding indications will, in turn, result in more revisions that would present challenges for surgeons.1,7,8
The glenoid component is much more commonly revised than the humeral component; however, the humeral component may also require revision or removal to allow exposure of the glenoid component.9 Revision of the humeral stem might be required in cases of infection, periprosthetic fracture, dislocation, or aseptic loosening.10 The survival rate of humeral stems is generally >90% at 10 years and >80% at 20-year follow-up.7 Despite these good survival rates, a revision setting the humeral component requires exchange in about half of all cases.11
Humeral bone loss or deficiency is one of the challenges encountered in both primary and revision TSA. The amount of proximal bone loss can be determined by measuring the distance from the top of the prosthesis laterally to the intact lateral cortex.12 Methods for treating bone loss may involve monoblock revision stems to bypass the deficiency, allografts to rebuild the bone stock, or modular components or endoprostheses to restore the length and stability of the extremity.
Proximal humeral bone loss may make component positioning difficult and may create problems with fixation of the humeral stem. Proper sizing and placement of components are important for improving postoperative function, decreasing component wear and instability, and restoring humeral height and offset. Determining the appropriate center of rotation is important for the function and avoidance of impingement on the acromion, as well as for the restoration of the lever arm of the deltoid without overtensioning. The selection of components with the correct size and the accurate intraoperative placement are important to restore humeral height and offset.13,14 Components must be positioned <4 mm from the height of the greater tuberosity and <8 mm of offset to avoid compromising motion.15 De Wilde and Walch16 described about 3 patients who underwent revision reverse shoulder arthroplasty after failure of the humeral implant because of inadequate proximal humeral bone stock. They concluded that treatment of the bone loss was critical to achieve a successful outcome.
LONG-STEMMED HUMERAL COMPONENTS WITHOUT GRAFTING
There is some evidence indicating that humeral bone loss can be managed without allograft or augmentation. Owens and colleagues17 evaluated the use of intermediate- or long-stemmed humeral components for primary shoulder arthroplasty in 17 patients with severe proximal humeral bone loss and in 18 patients with large humeral canals. The stems were fully cemented, cemented distally only with proximal allografting, and uncemented. Indications for fully cemented stems were loss of proximal bone that could be filled with a proximal cement mantle to ensure a secure fit. Distal cement fixation was applied when there was significant proximal bone loss and was often supplemented with cancellous or structural allograft and/or cancellous autograft. Intraoperative complications included cortical perforation or cement extrusion in 16% of patients. Excellent or satisfactory results were obtained in 21 (60%) of the 35 shoulders, 14 (78%) of the 18 shoulders with large humeral canals, and 7 (41%) of the 17 shoulders with bone loss. All the 17 components implanted in patients with proximal humeral bone loss were stable with no gross loosening at an average 6-year follow-up.
Continue to: Budge and colleagues...
Budge and colleagues12 prospectively enrolled 15 patients with substantial proximal humeral bone loss (38.4 mm) who had conversion to RTSA without allografting after a failed TSA. All patients showed improvements in terms of the American Shoulder and Elbow Surgeons (ASES) score, subjective shoulder value, Constant score, and Visual Analog Scale (VAS) pain score, as well as an improved active range of motion (ROM) and good radiographic outcomes at 2-year follow-up. Although the complication rate was high (7 of 15), most of the complications were minor, with only 2 requiring operative intervention. The only component fracture occurred in a patient with a modular prosthesis that was unsupported by bone proximally. Budge and colleagues12 suggested that concerns about prosthetic fracture can be alleviated using a nonmodular monoblock design. No prosthesis-related complications occurred in their series, leading them to recommend monoblock humeral stems in patients with severe proximal humeral bone loss.
Stephens and colleagues18 reported revision to RTSA in 32 patients with hemiarthroplasties, half of whom had proximal humeral bone loss (average 36.3 mm). Of these 16 patients, 10 were treated with monoblock stems and 6 with modular components, with cement fixation of all implants. At an average 4-year follow-up, patients with proximal bone loss had improved motion and outcomes, and decreased pain compared to their preoperative condition; however, they had lower functional and pain ratings, as well as less ROM compared to those of patients with intact proximal bone stock. Complications occurred in 5 (31%) of those with bone loss and in 1 (0.6%) of those without bone loss. Three of the 16 patients with bone loss had humeral stem loosening, with 2 of the 3 having subsidence. Only 1 patient required return to the operating room for the treatment of a periprosthetic fracture sustained in a fall. Of the 16 patients with bone loss, 14 patients demonstrated scapular notching, which was severe in 5 of them. Because patients with altered humeral length and/or standard length stems had worse outcomes, the authors recommended longer stems to improve fixation and advocated the use of a long-stemmed monoblock prosthesis over an allograft-prosthesis composite (APC).18
However, Werner and colleagues19 reported high rates of loosening and distal migration with the use of long-stemmed humeral implants in 50 patients with revision RTSA. They noted periprosthetic lucency on radiographs in 48% of patients, with more than half of them requiring revision. In 6 patients with subsidence of the humeral shaft, revision was done using custom, modular implants, with the anatomic curve being further stabilized using distal screw and cable fixation to provide rotational stability.
Using a biomechanical model, Cuff and colleagues20 compared 3 RTSA humeral designs, 2 modular designs, and 1 monoblock design in 12 intact models and in 12 models simulating 5 cm of proximal humeral bone loss. They observed that proximal humeral bone loss led to increased humeral component micromotion and rotational instability. The bone loss group had 5 failures compared to 2 in the control group. All failures occurred in those with modular components, whereas those with monoblock implants had no failures.
ALLOGRAFT-PROSTHESIS COMPOSITE
Composite treatment with a humeral stem and a metaphyseal allograft was described by Kassab and colleagues21 in 2005 and Levy and colleagues22 in 2007 (Figures 1A-1C) in patients with tumor resections21 or failed hemiarthroplasties.22 Allograft was used when there was insufficient metaphyseal bone to support the implant, and a graft was fashioned and fixed with cerclage wire before the component was cemented in place. In the 29 patients reported by Levy and colleagues,22 subjective and objective measurements trended toward better results in those with an APC than in those with RTSA alone, but this difference did not reach statistical significance. Several authors have identified a lack of proximal humeral bone support as 1 of the 4 possible causes of failure, and suggested that the allograft provides structural support, serves as an attachment for subscapularis repair, and maximizes deltoid function by increasing lateral offset and setting the moment arm of the deltoid.21-23
Continue to: In a prospective study of RTSA...
In a prospective study of RTSA using structural allografts for failed hemiarthroplasty in 25 patients with an average bone loss of 5 cm, 19 patients (76%) reported good or excellent results, 5 reported satisfactory results, and 1 patient reported an unsatisfactory result.1 Patients had significantly improved forward flexion, abduction, and external rotation and improved outcome scores (ASES and SST). Graft incorporation was good, with 88% and 79% incorporation in the metaphysis and diaphysis, respectively. This technique used a fresh-frozen proximal humeral allograft to fashion a custom proximal block with a lateral step-cut, which was fixed around the stem with cables. A long stem and cement were used. If there was no cement mantle remaining or if the medial portion of the graft was longer than 120 mm, the cement mantle was completely excised. The allograft stump of the subscapularis was used to repair the subscapularis tendon either end-to-end or pants-over-vest. The authors noted that the subscapularis repair provided increased stability; the only dislocation not caused by trauma did not have an identifiable tendon to repair. In this manner, APC reconstruction provided structural and rotational support to the humeral stem as well as bone stock for future revision.1,20
One significant concern with APC reconstruction is the potential for graft resorption, which can lead to humeral stem loosening, loss of contour of the tuberosity, or weakening to the point of fracture.24,25 This may be worsened by stress shielding of the allograft by distal stem cement fixation.26 Other concerns include the cost of the allograft, increased risk of de novo infection, donor-to-host infection, increased operative time and complexity, and failure of allograft incorporation.
The use of a proximal femoral allograft has been described when there is a lack of a proximal humeral allograft.1,27 Kelly and colleagues27 described good results in 2 patients in whom proximal femoral allograft was used along with bone morphogenetic protein, cemented long-stemmed revision implants, and locking plate augmentation.
ENDOPROSTHETIC RECONSTRUCTION
Various forms of prosthetic augmentation have been described to compensate for proximal humeral bone loss, with the majority of reports involving the use of endoprosthetic replacement for tumor procedures.28-31 Use of endoprostheses has also been described for revision procedures in patients with rheumatoid arthritis with massive bone loss, demonstrating modest improvements compared to severe preoperative functional limitations.32
Tumor patients, as well as revision arthroplasty patients, may present difficulties with prosthetic fixation due to massive bone loss. Chao and colleagues29 reported about the long-term outcomes after the use of implants with a porous ongrowth surface and extracortical bridging bone graft in multiple anatomic locations, including the proximal humerus, the proximal and distal femur, and the femoral diaphysis. In 3 patients with proximal humeral reconstruction, the measured ongrowth was only 30%. Given the small number of patients with a proximal humerus, no statistical significance was observed in the prosthesis location and the amount of bony ongrowth, but it was far less than that in the lower extremity.
Continue to: Endoprosthetic reconstruction...
Endoprosthetic reconstruction of the proximal humerus is commonly used for tumor resection that resulted in bone loss. Cannon and colleagues28 reported a 97.6% survival rate at a mean follow-up of 30 months in 83 patients with modular and custom reconstruction with a unipolar head. The ROM was limited, but the prosthesis provided adequate stability to allow elbow and hand function. Proximal migration of the prosthetic head was noticed with increasing frequency as the length of follow-up increased.
Use of an endoprosthesis with compressive osteointegration (Zimmer Biomet) has been described in lower extremities and more recently with follow-up on several cases, including 2 proximal humeral replacements for oncology patients to treat severe bone loss. One case was for a primary sarcoma resection, and the other was for the revision of aseptic loosening of a previous endoprosthesis. Follow-up periods for these 2 patients were 54 and 141 months, respectively. Both these patients had complications, but both retained the endoprosthesis. The authors concluded that this is a salvage operation with high risk.30 In another study, Guven and colleagues31 reported about reverse endoprosthetic reconstruction for tumor resection with bone loss. The ROM was improved, with a mean active forward elevation of 96° (range, 30°-160°), an abduction of 88° (range, 30-160°), and an external rotation of 13° (range, 0°-20°).
Modular endoprostheses have been evaluated as a method for improving bone fixation and restoring soft-tissue tension, while avoiding the complications associated with traditional endoprostheses or allografts (Figures 2A-2D). These systems allow precise adjustments of length using different trial lengths intraoperatively to obtain proper stability and deltoid tension. Of the 12 patients in a 2 center study, 11 had cementless components inserted using a press-fit technique (unpublished data, J. Feldman). At a minimum 2-year follow-up, the patients had an average improvement in forward elevation from 78° to 97°. Excluding 2 patients with loss of the deltoid tuberosity, the forward elevation averaged 109°. There were significant improvements in internal rotation (from 18° to 38°), as well as in the scores of Quick Disabilities of the Arm, Shoulder and Hand (DASH), forward elevation strength, ASES, and VAS pain. However, the overall complication rate was 41%. Therefore, despite these promising early results, longer-term studies are needed.
CONCLUSION
Proximal humeral bone loss remains a significant challenge for the shoulder arthroplasty surgeon. In the setting of a primary or a revision arthroplasty, the bone stock must be thoroughly evaluated during preoperative planning, and a surgical plan for addressing the deficits should be developed. Because proximal humeral bone loss may contribute to prosthetic failure, every effort should be made to reconstitute the bone stock.16 If the bone loss is less extensive, impaction grafting may be considered. Options to address massive proximal humeral bone loss include APCs and endoprosthetic reconstruction. The use of an allograft allows subscapularis repair, which may help stabilize the shoulder and restore the natural lever arm, as well as the tension of the deltoid.1,21-23 In addition, it helps avoid rotational instability and micromotion and provides bone stock for future revisions. However, concern persists regarding allograft resorption over time. More recently, modular endoprosthetic reconstruction systems have been developed to address bone deficiency with metal augmentation. Early clinical results demonstrate a high complication rate in this complex cohort of patients, not unlike those in the series of APCs, but clinical outcomes were improved compared to those in historical series. Nevertheless, longer-term clinical studies are necessary to determine the role of these modular endoprosthetic implant systems.
1. Chacon A, Virani N, Shannon R, Levy JC, Pupello D, Frankle M. Revision arthroplasty with use of a reverse shoulder prosthesis-allograft composite. J Bone Joint Surg Am. 2009;91(1):119-127. doi:10.2106/JBJS.H.00094.
2. Hattrup SJ, Waldrop R, Sanchez-Sotelo J. Reverse total shoulder arthroplasty for posttraumatic sequelae. J Orthop Trauma. 2016;30(2):e41-e47. doi:10.1097/BOT.0000000000000416.
3. Sewell MD, Kang SN, Al-Hadithy N, et al. Management of peri-prosthetic fracture of the humerus with severe bone loss and loosening of the humeral component after total shoulder replacement. J Bone Joint Surg Br. 2012;94(10):1382-1389. doi:10.1302/0301-620X.94B10.29248.
4. Trompeter AJ, Gupta RR. The management of complex periprosthetic humeral fractures: a case series of strut allograft augmentation, and a review of the literature. Strategies Trauma Limb Reconstr. 2013;8(1):43-51. doi:10.1007/s11751-013-0155-x.
5. Khatib O, Onyekwelu I, Yu S, Zuckerman JD. Shoulder arthroplasty in New York State, 1991 to 2010: changing patterns of utilization. J Shoulder Elbow Surg. 2015;24(10):e286-e291. doi:10.1016/j.jse.2015.05.038.
6. Kim SH, Wise BL, Zhang Y, Szabo RM. Increasing incidence of shoulder arthroplasty in the United States. J Bone Joint Surg Am. 2011;93(24):2249-2254. doi:10.2106/JBJS.J.01994.
7. Cil A, Veillette CJ, Sanchez-Sotelo J, Sperling JW, Schleck CD, Cofield RH. Survivorship of the humeral component in shoulder arthroplasty. J Shoulder Elbow Surg. 2010;19(1):143-150. doi:10.1016/j.jse.2009.04.011.
8. Wright TW. Revision of humeral components in shoulder arthroplasty. Bull Hosp Jt Dis. 2013;71(2 suppl):S77-S81.
9. Duquin TR, Sperling JW. Revision shoulder arthroplasty—how to manage the humerus. Oper Tech Orthop. 2011;21(1):44-51. doi:10.1053/j.oto.2010.09.008.
10. Cil A, Veillette CJ, Sanchez-Sotelo J, Sperling JW, Schleck C, Cofield RH. Revision of the humeral component for aseptic loosening in arthroplasty of the shoulder. J Bone Joint Surg Br. 2009;91(1):75-81. doi:10.1302/0301-620X.91B1.21094.
11. Cofield RH. Revision of hemiarthroplasty to total shoulder arthroplasty. In: Zuckerman JD, ed. Advanced Reconstruction: Shoulder. 1st edition. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2007;613-622.
12. Budge MD, Moravek JE, Zimel MN, Nolan EM, Wiater JM. Reverse total shoulder arthroplasty for the management of failed shoulder arthroplasty with proximal humeral bone loss: is allograft augmentation necessary? J Shoulder Elbow Surg. 2013;22(6):739-744. doi:10.1016/j.jse.2012.08.008.
13. Boileau P, Walch G. The three-dimensional geometry of the proximal humerus. Implications for surgical technique and prosthetic design. J Bone Joint Surg Br. 1997;79(5):857-865.
14. Throckmorton TW. Reconstructive procedures of the shoulder and elbow. In: Azar FM, Beaty JH, Canale ST, eds. Campbell’s Operative Orthopaedics. 13th edition. Philadelphia, PA: Elsevier; 2017;570-622.
15. Williams GR Jr, Wong KL, Pepe MD, et al. The effect of articular malposition after total shoulder arthroplasty on glenohumeral translations, range of motion, and subacromial impingement. J Shoulder Elbow Surg. 2001;10(5):399-409. doi:10.1067/mse.2001.116871.
16. De Wilde L, Walch G. Humeral prosthetic failure of reversed total shoulder arthroplasty: a report of three cases. J Shoulder Elbow Surg. 2006;15(2):260-264. doi:10.1016/j.jse.2005.07.014.
17. Owens CJ, Sperling JW, Cofield RH. Utility and complications of long-stem humeral components in revision shoulder arthroplasty. J Shoulder Elbow Surg. 2013;22(7):e7-e12. doi:10.1016/j.jse.2012.10.034.
18. Stephens SP, Paisley KC, Giveans MR, Wirth MA. The effect of proximal humeral bone loss on revision reverse total shoulder arthroplasty. J Shoulder Elbow Surg. 2015;24(10):1519-1526. doi:10.1016/j.jse.2015.02.020.
19. Werner BS, Abdelkawi AF, Boehm D, et al. Long-term analysis of revision reverse shoulder arthroplasty using cemented long stems. J Shoulder Elbow Surg. 2017;26(2):273-278. doi:10.1016/j.jse.2016.05.015.
20. Cuff D, Levy JC, Gutiérrez S, Frankle MA. Torsional stability of modular and non-modular reverse shoulder humeral components in a proximal humeral bone loss model. J Shoulder Elbow Surg. 2011;20(4):646-651. doi:10.1016/j.jse.2010.10.026.
21. Kassab M, Dumaine V, Babinet A, Ouaknine M, Tomeno B, Anract P. Twenty nine shoulder reconstructions after resection of the proximal humerus for neoplasm with mean 7-year follow-up. Rev Chir Orthop Reparatrice Appar Mot. 2005;91(1):15-23.
22. Levy J, Frankle M, Mighell M, Pupello D. The use of the reverse shoulder prosthesis for the treatment of failed hemiarthroplasty for proximal humeral fracture. J Bone Joint Surg. 2007;98(2):292-300. doi:10.2106/JBJS.E.01310.
23. Gagey O, Pourjamasb B, Court C. Revision arthroplasty of the shoulder for painful glenoid loosening: a series of 14 cases with acromial prostheses reviewed at four year follow up. Rev Chir Reparatrice Appar Mot. 2001;87(3):221-228.
24. Abdeen A, Hoang BH, Althanasina EA, Morris CD, Boland PJ, Healey JH. Allograft-prosthesis composite reconstruction of the proximal part of the humerus: functional outcome and survivorship. J Bone Joint Surg Am. 2009;91(10):2406-2415. doi:10.2106/JBJS.H.00815.
25. Getty PJ, Peabody TD. Complications and functional outcomes of reconstruction with an osteoarticular allograft after intra-articular resection of the proximal aspect of the humerus. J Bone Joint Surg Am. 1999;81(8):1138-1146.
26. Chen CF, Chen WM, Cheng YC, Chiang CC, Huang CK, Chen TH. Extracorporeally irradiated autograft-prosthetic composite arthroplasty using AML® extensively porous-coated stem for proximal femur reconstruction: a clinical analysis of 14 patients. J Surg Oncol. 2009;100(5):418-422. doi:10.1002/jso.21351.
27. Kelly JD 2nd, Purchase RJ, Kam G, Norris TR. Alloprosthetic composite reconstruction using the reverse shoulder arthroplasty. Tech Shoulder Elbow Surg. 2009;10(1):5-10.
28. Cannon CP, Paraliticci GU, Lin PP, Lewis VO, Yasko AW. Functional outcome following endoprosthetic reconstruction of the proximal humerus. J Shoulder Elbow Surg. 2009;18(5):705-710. doi:10.1016/j.jse.2008.10.011.
29. Chao EY, Fuchs B, Rowland CM, Ilstrup DM, Pritchard DJ, Sim FH. Long-term results of segmental prosthesis fixation by extracortical bone-bridging and ingrowth. J Bone Joint Surg Am. 2004;86-A(5):948-955.
30. Goulding KA, Schwartz A, Hattrup SJ, et al. Use of compressive osseointegration endoprostheses for massive bone loss from tumor and failed arthroplasty: a viable option in the upper extremity. Clin Orthop Relat Res. 2017;475(6):1702-1711. doi:10.1007/s11999-017-5258-0.
31. Guven MF, Aslan L, Botanlioglu H, Kaynak G, Kesmezacar H, Babacan M. Functional outcome of reverse shoulder tumor prosthesis in the treatment of proximal humeral tumors. J Shoulder Elbow Surg. 2016;25(1):e1-e6. doi:10.1016/j.jse.2015.06.012.
32. Wang ML, Ballard BL, Kulidjian AA, Abrams RA. Upper extremity reconstruction with a humeral tumor endoprosthesis: a novel salvage procedure after multiple revisions of total shoulder and elbow replacement. J Shoulder Elbow Surg. 2011;20(1):e1-e8. doi:10.1016/j.jse.2010.07.018.
ABSTRACT
Reconstructing proximal humeral bone loss in the setting of shoulder arthroplasty can be a daunting task. Proposed techniques include long-stemmed humeral components, allograft-prosthesis composites (APCs), and modular endoprosthetic reconstruction. While unsupported long-stemmed components are at high risk for component loosening, APC reconstruction techniques have been reported with success. However, graft resorption and eventual failure are significant concerns. Modular endoprosthetic systems allow bone deficiencies to be reconstructed with metal, which may allow for a more durable reconstruction.
Continue to: Shoulder arthroplasty is an established procedure...
Shoulder arthroplasty is an established procedure with good results for restoring motion and decreasing pain for a variety of indications, including arthritis, fracture, posttraumatic sequelae, and tumor resection.1-4 As the population ages, the incidence of these shoulder disorders increases, with the incidence of total shoulder arthroplasty (TSA) and reverse total shoulder arthroplasty (RTSA) increasing at faster rates than that of hemiarthroplasty.5,6 These expanding indications will, in turn, result in more revisions that would present challenges for surgeons.1,7,8
The glenoid component is much more commonly revised than the humeral component; however, the humeral component may also require revision or removal to allow exposure of the glenoid component.9 Revision of the humeral stem might be required in cases of infection, periprosthetic fracture, dislocation, or aseptic loosening.10 The survival rate of humeral stems is generally >90% at 10 years and >80% at 20-year follow-up.7 Despite these good survival rates, a revision setting the humeral component requires exchange in about half of all cases.11
Humeral bone loss or deficiency is one of the challenges encountered in both primary and revision TSA. The amount of proximal bone loss can be determined by measuring the distance from the top of the prosthesis laterally to the intact lateral cortex.12 Methods for treating bone loss may involve monoblock revision stems to bypass the deficiency, allografts to rebuild the bone stock, or modular components or endoprostheses to restore the length and stability of the extremity.
Proximal humeral bone loss may make component positioning difficult and may create problems with fixation of the humeral stem. Proper sizing and placement of components are important for improving postoperative function, decreasing component wear and instability, and restoring humeral height and offset. Determining the appropriate center of rotation is important for the function and avoidance of impingement on the acromion, as well as for the restoration of the lever arm of the deltoid without overtensioning. The selection of components with the correct size and the accurate intraoperative placement are important to restore humeral height and offset.13,14 Components must be positioned <4 mm from the height of the greater tuberosity and <8 mm of offset to avoid compromising motion.15 De Wilde and Walch16 described about 3 patients who underwent revision reverse shoulder arthroplasty after failure of the humeral implant because of inadequate proximal humeral bone stock. They concluded that treatment of the bone loss was critical to achieve a successful outcome.
LONG-STEMMED HUMERAL COMPONENTS WITHOUT GRAFTING
There is some evidence indicating that humeral bone loss can be managed without allograft or augmentation. Owens and colleagues17 evaluated the use of intermediate- or long-stemmed humeral components for primary shoulder arthroplasty in 17 patients with severe proximal humeral bone loss and in 18 patients with large humeral canals. The stems were fully cemented, cemented distally only with proximal allografting, and uncemented. Indications for fully cemented stems were loss of proximal bone that could be filled with a proximal cement mantle to ensure a secure fit. Distal cement fixation was applied when there was significant proximal bone loss and was often supplemented with cancellous or structural allograft and/or cancellous autograft. Intraoperative complications included cortical perforation or cement extrusion in 16% of patients. Excellent or satisfactory results were obtained in 21 (60%) of the 35 shoulders, 14 (78%) of the 18 shoulders with large humeral canals, and 7 (41%) of the 17 shoulders with bone loss. All the 17 components implanted in patients with proximal humeral bone loss were stable with no gross loosening at an average 6-year follow-up.
Continue to: Budge and colleagues...
Budge and colleagues12 prospectively enrolled 15 patients with substantial proximal humeral bone loss (38.4 mm) who had conversion to RTSA without allografting after a failed TSA. All patients showed improvements in terms of the American Shoulder and Elbow Surgeons (ASES) score, subjective shoulder value, Constant score, and Visual Analog Scale (VAS) pain score, as well as an improved active range of motion (ROM) and good radiographic outcomes at 2-year follow-up. Although the complication rate was high (7 of 15), most of the complications were minor, with only 2 requiring operative intervention. The only component fracture occurred in a patient with a modular prosthesis that was unsupported by bone proximally. Budge and colleagues12 suggested that concerns about prosthetic fracture can be alleviated using a nonmodular monoblock design. No prosthesis-related complications occurred in their series, leading them to recommend monoblock humeral stems in patients with severe proximal humeral bone loss.
Stephens and colleagues18 reported revision to RTSA in 32 patients with hemiarthroplasties, half of whom had proximal humeral bone loss (average 36.3 mm). Of these 16 patients, 10 were treated with monoblock stems and 6 with modular components, with cement fixation of all implants. At an average 4-year follow-up, patients with proximal bone loss had improved motion and outcomes, and decreased pain compared to their preoperative condition; however, they had lower functional and pain ratings, as well as less ROM compared to those of patients with intact proximal bone stock. Complications occurred in 5 (31%) of those with bone loss and in 1 (0.6%) of those without bone loss. Three of the 16 patients with bone loss had humeral stem loosening, with 2 of the 3 having subsidence. Only 1 patient required return to the operating room for the treatment of a periprosthetic fracture sustained in a fall. Of the 16 patients with bone loss, 14 patients demonstrated scapular notching, which was severe in 5 of them. Because patients with altered humeral length and/or standard length stems had worse outcomes, the authors recommended longer stems to improve fixation and advocated the use of a long-stemmed monoblock prosthesis over an allograft-prosthesis composite (APC).18
However, Werner and colleagues19 reported high rates of loosening and distal migration with the use of long-stemmed humeral implants in 50 patients with revision RTSA. They noted periprosthetic lucency on radiographs in 48% of patients, with more than half of them requiring revision. In 6 patients with subsidence of the humeral shaft, revision was done using custom, modular implants, with the anatomic curve being further stabilized using distal screw and cable fixation to provide rotational stability.
Using a biomechanical model, Cuff and colleagues20 compared 3 RTSA humeral designs, 2 modular designs, and 1 monoblock design in 12 intact models and in 12 models simulating 5 cm of proximal humeral bone loss. They observed that proximal humeral bone loss led to increased humeral component micromotion and rotational instability. The bone loss group had 5 failures compared to 2 in the control group. All failures occurred in those with modular components, whereas those with monoblock implants had no failures.
ALLOGRAFT-PROSTHESIS COMPOSITE
Composite treatment with a humeral stem and a metaphyseal allograft was described by Kassab and colleagues21 in 2005 and Levy and colleagues22 in 2007 (Figures 1A-1C) in patients with tumor resections21 or failed hemiarthroplasties.22 Allograft was used when there was insufficient metaphyseal bone to support the implant, and a graft was fashioned and fixed with cerclage wire before the component was cemented in place. In the 29 patients reported by Levy and colleagues,22 subjective and objective measurements trended toward better results in those with an APC than in those with RTSA alone, but this difference did not reach statistical significance. Several authors have identified a lack of proximal humeral bone support as 1 of the 4 possible causes of failure, and suggested that the allograft provides structural support, serves as an attachment for subscapularis repair, and maximizes deltoid function by increasing lateral offset and setting the moment arm of the deltoid.21-23
Continue to: In a prospective study of RTSA...
In a prospective study of RTSA using structural allografts for failed hemiarthroplasty in 25 patients with an average bone loss of 5 cm, 19 patients (76%) reported good or excellent results, 5 reported satisfactory results, and 1 patient reported an unsatisfactory result.1 Patients had significantly improved forward flexion, abduction, and external rotation and improved outcome scores (ASES and SST). Graft incorporation was good, with 88% and 79% incorporation in the metaphysis and diaphysis, respectively. This technique used a fresh-frozen proximal humeral allograft to fashion a custom proximal block with a lateral step-cut, which was fixed around the stem with cables. A long stem and cement were used. If there was no cement mantle remaining or if the medial portion of the graft was longer than 120 mm, the cement mantle was completely excised. The allograft stump of the subscapularis was used to repair the subscapularis tendon either end-to-end or pants-over-vest. The authors noted that the subscapularis repair provided increased stability; the only dislocation not caused by trauma did not have an identifiable tendon to repair. In this manner, APC reconstruction provided structural and rotational support to the humeral stem as well as bone stock for future revision.1,20
One significant concern with APC reconstruction is the potential for graft resorption, which can lead to humeral stem loosening, loss of contour of the tuberosity, or weakening to the point of fracture.24,25 This may be worsened by stress shielding of the allograft by distal stem cement fixation.26 Other concerns include the cost of the allograft, increased risk of de novo infection, donor-to-host infection, increased operative time and complexity, and failure of allograft incorporation.
The use of a proximal femoral allograft has been described when there is a lack of a proximal humeral allograft.1,27 Kelly and colleagues27 described good results in 2 patients in whom proximal femoral allograft was used along with bone morphogenetic protein, cemented long-stemmed revision implants, and locking plate augmentation.
ENDOPROSTHETIC RECONSTRUCTION
Various forms of prosthetic augmentation have been described to compensate for proximal humeral bone loss, with the majority of reports involving the use of endoprosthetic replacement for tumor procedures.28-31 Use of endoprostheses has also been described for revision procedures in patients with rheumatoid arthritis with massive bone loss, demonstrating modest improvements compared to severe preoperative functional limitations.32
Tumor patients, as well as revision arthroplasty patients, may present difficulties with prosthetic fixation due to massive bone loss. Chao and colleagues29 reported about the long-term outcomes after the use of implants with a porous ongrowth surface and extracortical bridging bone graft in multiple anatomic locations, including the proximal humerus, the proximal and distal femur, and the femoral diaphysis. In 3 patients with proximal humeral reconstruction, the measured ongrowth was only 30%. Given the small number of patients with a proximal humerus, no statistical significance was observed in the prosthesis location and the amount of bony ongrowth, but it was far less than that in the lower extremity.
Continue to: Endoprosthetic reconstruction...
Endoprosthetic reconstruction of the proximal humerus is commonly used for tumor resection that resulted in bone loss. Cannon and colleagues28 reported a 97.6% survival rate at a mean follow-up of 30 months in 83 patients with modular and custom reconstruction with a unipolar head. The ROM was limited, but the prosthesis provided adequate stability to allow elbow and hand function. Proximal migration of the prosthetic head was noticed with increasing frequency as the length of follow-up increased.
Use of an endoprosthesis with compressive osteointegration (Zimmer Biomet) has been described in lower extremities and more recently with follow-up on several cases, including 2 proximal humeral replacements for oncology patients to treat severe bone loss. One case was for a primary sarcoma resection, and the other was for the revision of aseptic loosening of a previous endoprosthesis. Follow-up periods for these 2 patients were 54 and 141 months, respectively. Both these patients had complications, but both retained the endoprosthesis. The authors concluded that this is a salvage operation with high risk.30 In another study, Guven and colleagues31 reported about reverse endoprosthetic reconstruction for tumor resection with bone loss. The ROM was improved, with a mean active forward elevation of 96° (range, 30°-160°), an abduction of 88° (range, 30-160°), and an external rotation of 13° (range, 0°-20°).
Modular endoprostheses have been evaluated as a method for improving bone fixation and restoring soft-tissue tension, while avoiding the complications associated with traditional endoprostheses or allografts (Figures 2A-2D). These systems allow precise adjustments of length using different trial lengths intraoperatively to obtain proper stability and deltoid tension. Of the 12 patients in a 2 center study, 11 had cementless components inserted using a press-fit technique (unpublished data, J. Feldman). At a minimum 2-year follow-up, the patients had an average improvement in forward elevation from 78° to 97°. Excluding 2 patients with loss of the deltoid tuberosity, the forward elevation averaged 109°. There were significant improvements in internal rotation (from 18° to 38°), as well as in the scores of Quick Disabilities of the Arm, Shoulder and Hand (DASH), forward elevation strength, ASES, and VAS pain. However, the overall complication rate was 41%. Therefore, despite these promising early results, longer-term studies are needed.
CONCLUSION
Proximal humeral bone loss remains a significant challenge for the shoulder arthroplasty surgeon. In the setting of a primary or a revision arthroplasty, the bone stock must be thoroughly evaluated during preoperative planning, and a surgical plan for addressing the deficits should be developed. Because proximal humeral bone loss may contribute to prosthetic failure, every effort should be made to reconstitute the bone stock.16 If the bone loss is less extensive, impaction grafting may be considered. Options to address massive proximal humeral bone loss include APCs and endoprosthetic reconstruction. The use of an allograft allows subscapularis repair, which may help stabilize the shoulder and restore the natural lever arm, as well as the tension of the deltoid.1,21-23 In addition, it helps avoid rotational instability and micromotion and provides bone stock for future revisions. However, concern persists regarding allograft resorption over time. More recently, modular endoprosthetic reconstruction systems have been developed to address bone deficiency with metal augmentation. Early clinical results demonstrate a high complication rate in this complex cohort of patients, not unlike those in the series of APCs, but clinical outcomes were improved compared to those in historical series. Nevertheless, longer-term clinical studies are necessary to determine the role of these modular endoprosthetic implant systems.
ABSTRACT
Reconstructing proximal humeral bone loss in the setting of shoulder arthroplasty can be a daunting task. Proposed techniques include long-stemmed humeral components, allograft-prosthesis composites (APCs), and modular endoprosthetic reconstruction. While unsupported long-stemmed components are at high risk for component loosening, APC reconstruction techniques have been reported with success. However, graft resorption and eventual failure are significant concerns. Modular endoprosthetic systems allow bone deficiencies to be reconstructed with metal, which may allow for a more durable reconstruction.
Continue to: Shoulder arthroplasty is an established procedure...
Shoulder arthroplasty is an established procedure with good results for restoring motion and decreasing pain for a variety of indications, including arthritis, fracture, posttraumatic sequelae, and tumor resection.1-4 As the population ages, the incidence of these shoulder disorders increases, with the incidence of total shoulder arthroplasty (TSA) and reverse total shoulder arthroplasty (RTSA) increasing at faster rates than that of hemiarthroplasty.5,6 These expanding indications will, in turn, result in more revisions that would present challenges for surgeons.1,7,8
The glenoid component is much more commonly revised than the humeral component; however, the humeral component may also require revision or removal to allow exposure of the glenoid component.9 Revision of the humeral stem might be required in cases of infection, periprosthetic fracture, dislocation, or aseptic loosening.10 The survival rate of humeral stems is generally >90% at 10 years and >80% at 20-year follow-up.7 Despite these good survival rates, a revision setting the humeral component requires exchange in about half of all cases.11
Humeral bone loss or deficiency is one of the challenges encountered in both primary and revision TSA. The amount of proximal bone loss can be determined by measuring the distance from the top of the prosthesis laterally to the intact lateral cortex.12 Methods for treating bone loss may involve monoblock revision stems to bypass the deficiency, allografts to rebuild the bone stock, or modular components or endoprostheses to restore the length and stability of the extremity.
Proximal humeral bone loss may make component positioning difficult and may create problems with fixation of the humeral stem. Proper sizing and placement of components are important for improving postoperative function, decreasing component wear and instability, and restoring humeral height and offset. Determining the appropriate center of rotation is important for the function and avoidance of impingement on the acromion, as well as for the restoration of the lever arm of the deltoid without overtensioning. The selection of components with the correct size and the accurate intraoperative placement are important to restore humeral height and offset.13,14 Components must be positioned <4 mm from the height of the greater tuberosity and <8 mm of offset to avoid compromising motion.15 De Wilde and Walch16 described about 3 patients who underwent revision reverse shoulder arthroplasty after failure of the humeral implant because of inadequate proximal humeral bone stock. They concluded that treatment of the bone loss was critical to achieve a successful outcome.
LONG-STEMMED HUMERAL COMPONENTS WITHOUT GRAFTING
There is some evidence indicating that humeral bone loss can be managed without allograft or augmentation. Owens and colleagues17 evaluated the use of intermediate- or long-stemmed humeral components for primary shoulder arthroplasty in 17 patients with severe proximal humeral bone loss and in 18 patients with large humeral canals. The stems were fully cemented, cemented distally only with proximal allografting, and uncemented. Indications for fully cemented stems were loss of proximal bone that could be filled with a proximal cement mantle to ensure a secure fit. Distal cement fixation was applied when there was significant proximal bone loss and was often supplemented with cancellous or structural allograft and/or cancellous autograft. Intraoperative complications included cortical perforation or cement extrusion in 16% of patients. Excellent or satisfactory results were obtained in 21 (60%) of the 35 shoulders, 14 (78%) of the 18 shoulders with large humeral canals, and 7 (41%) of the 17 shoulders with bone loss. All the 17 components implanted in patients with proximal humeral bone loss were stable with no gross loosening at an average 6-year follow-up.
Continue to: Budge and colleagues...
Budge and colleagues12 prospectively enrolled 15 patients with substantial proximal humeral bone loss (38.4 mm) who had conversion to RTSA without allografting after a failed TSA. All patients showed improvements in terms of the American Shoulder and Elbow Surgeons (ASES) score, subjective shoulder value, Constant score, and Visual Analog Scale (VAS) pain score, as well as an improved active range of motion (ROM) and good radiographic outcomes at 2-year follow-up. Although the complication rate was high (7 of 15), most of the complications were minor, with only 2 requiring operative intervention. The only component fracture occurred in a patient with a modular prosthesis that was unsupported by bone proximally. Budge and colleagues12 suggested that concerns about prosthetic fracture can be alleviated using a nonmodular monoblock design. No prosthesis-related complications occurred in their series, leading them to recommend monoblock humeral stems in patients with severe proximal humeral bone loss.
Stephens and colleagues18 reported revision to RTSA in 32 patients with hemiarthroplasties, half of whom had proximal humeral bone loss (average 36.3 mm). Of these 16 patients, 10 were treated with monoblock stems and 6 with modular components, with cement fixation of all implants. At an average 4-year follow-up, patients with proximal bone loss had improved motion and outcomes, and decreased pain compared to their preoperative condition; however, they had lower functional and pain ratings, as well as less ROM compared to those of patients with intact proximal bone stock. Complications occurred in 5 (31%) of those with bone loss and in 1 (0.6%) of those without bone loss. Three of the 16 patients with bone loss had humeral stem loosening, with 2 of the 3 having subsidence. Only 1 patient required return to the operating room for the treatment of a periprosthetic fracture sustained in a fall. Of the 16 patients with bone loss, 14 patients demonstrated scapular notching, which was severe in 5 of them. Because patients with altered humeral length and/or standard length stems had worse outcomes, the authors recommended longer stems to improve fixation and advocated the use of a long-stemmed monoblock prosthesis over an allograft-prosthesis composite (APC).18
However, Werner and colleagues19 reported high rates of loosening and distal migration with the use of long-stemmed humeral implants in 50 patients with revision RTSA. They noted periprosthetic lucency on radiographs in 48% of patients, with more than half of them requiring revision. In 6 patients with subsidence of the humeral shaft, revision was done using custom, modular implants, with the anatomic curve being further stabilized using distal screw and cable fixation to provide rotational stability.
Using a biomechanical model, Cuff and colleagues20 compared 3 RTSA humeral designs, 2 modular designs, and 1 monoblock design in 12 intact models and in 12 models simulating 5 cm of proximal humeral bone loss. They observed that proximal humeral bone loss led to increased humeral component micromotion and rotational instability. The bone loss group had 5 failures compared to 2 in the control group. All failures occurred in those with modular components, whereas those with monoblock implants had no failures.
ALLOGRAFT-PROSTHESIS COMPOSITE
Composite treatment with a humeral stem and a metaphyseal allograft was described by Kassab and colleagues21 in 2005 and Levy and colleagues22 in 2007 (Figures 1A-1C) in patients with tumor resections21 or failed hemiarthroplasties.22 Allograft was used when there was insufficient metaphyseal bone to support the implant, and a graft was fashioned and fixed with cerclage wire before the component was cemented in place. In the 29 patients reported by Levy and colleagues,22 subjective and objective measurements trended toward better results in those with an APC than in those with RTSA alone, but this difference did not reach statistical significance. Several authors have identified a lack of proximal humeral bone support as 1 of the 4 possible causes of failure, and suggested that the allograft provides structural support, serves as an attachment for subscapularis repair, and maximizes deltoid function by increasing lateral offset and setting the moment arm of the deltoid.21-23
Continue to: In a prospective study of RTSA...
In a prospective study of RTSA using structural allografts for failed hemiarthroplasty in 25 patients with an average bone loss of 5 cm, 19 patients (76%) reported good or excellent results, 5 reported satisfactory results, and 1 patient reported an unsatisfactory result.1 Patients had significantly improved forward flexion, abduction, and external rotation and improved outcome scores (ASES and SST). Graft incorporation was good, with 88% and 79% incorporation in the metaphysis and diaphysis, respectively. This technique used a fresh-frozen proximal humeral allograft to fashion a custom proximal block with a lateral step-cut, which was fixed around the stem with cables. A long stem and cement were used. If there was no cement mantle remaining or if the medial portion of the graft was longer than 120 mm, the cement mantle was completely excised. The allograft stump of the subscapularis was used to repair the subscapularis tendon either end-to-end or pants-over-vest. The authors noted that the subscapularis repair provided increased stability; the only dislocation not caused by trauma did not have an identifiable tendon to repair. In this manner, APC reconstruction provided structural and rotational support to the humeral stem as well as bone stock for future revision.1,20
One significant concern with APC reconstruction is the potential for graft resorption, which can lead to humeral stem loosening, loss of contour of the tuberosity, or weakening to the point of fracture.24,25 This may be worsened by stress shielding of the allograft by distal stem cement fixation.26 Other concerns include the cost of the allograft, increased risk of de novo infection, donor-to-host infection, increased operative time and complexity, and failure of allograft incorporation.
The use of a proximal femoral allograft has been described when there is a lack of a proximal humeral allograft.1,27 Kelly and colleagues27 described good results in 2 patients in whom proximal femoral allograft was used along with bone morphogenetic protein, cemented long-stemmed revision implants, and locking plate augmentation.
ENDOPROSTHETIC RECONSTRUCTION
Various forms of prosthetic augmentation have been described to compensate for proximal humeral bone loss, with the majority of reports involving the use of endoprosthetic replacement for tumor procedures.28-31 Use of endoprostheses has also been described for revision procedures in patients with rheumatoid arthritis with massive bone loss, demonstrating modest improvements compared to severe preoperative functional limitations.32
Tumor patients, as well as revision arthroplasty patients, may present difficulties with prosthetic fixation due to massive bone loss. Chao and colleagues29 reported about the long-term outcomes after the use of implants with a porous ongrowth surface and extracortical bridging bone graft in multiple anatomic locations, including the proximal humerus, the proximal and distal femur, and the femoral diaphysis. In 3 patients with proximal humeral reconstruction, the measured ongrowth was only 30%. Given the small number of patients with a proximal humerus, no statistical significance was observed in the prosthesis location and the amount of bony ongrowth, but it was far less than that in the lower extremity.
Continue to: Endoprosthetic reconstruction...
Endoprosthetic reconstruction of the proximal humerus is commonly used for tumor resection that resulted in bone loss. Cannon and colleagues28 reported a 97.6% survival rate at a mean follow-up of 30 months in 83 patients with modular and custom reconstruction with a unipolar head. The ROM was limited, but the prosthesis provided adequate stability to allow elbow and hand function. Proximal migration of the prosthetic head was noticed with increasing frequency as the length of follow-up increased.
Use of an endoprosthesis with compressive osteointegration (Zimmer Biomet) has been described in lower extremities and more recently with follow-up on several cases, including 2 proximal humeral replacements for oncology patients to treat severe bone loss. One case was for a primary sarcoma resection, and the other was for the revision of aseptic loosening of a previous endoprosthesis. Follow-up periods for these 2 patients were 54 and 141 months, respectively. Both these patients had complications, but both retained the endoprosthesis. The authors concluded that this is a salvage operation with high risk.30 In another study, Guven and colleagues31 reported about reverse endoprosthetic reconstruction for tumor resection with bone loss. The ROM was improved, with a mean active forward elevation of 96° (range, 30°-160°), an abduction of 88° (range, 30-160°), and an external rotation of 13° (range, 0°-20°).
Modular endoprostheses have been evaluated as a method for improving bone fixation and restoring soft-tissue tension, while avoiding the complications associated with traditional endoprostheses or allografts (Figures 2A-2D). These systems allow precise adjustments of length using different trial lengths intraoperatively to obtain proper stability and deltoid tension. Of the 12 patients in a 2 center study, 11 had cementless components inserted using a press-fit technique (unpublished data, J. Feldman). At a minimum 2-year follow-up, the patients had an average improvement in forward elevation from 78° to 97°. Excluding 2 patients with loss of the deltoid tuberosity, the forward elevation averaged 109°. There were significant improvements in internal rotation (from 18° to 38°), as well as in the scores of Quick Disabilities of the Arm, Shoulder and Hand (DASH), forward elevation strength, ASES, and VAS pain. However, the overall complication rate was 41%. Therefore, despite these promising early results, longer-term studies are needed.
CONCLUSION
Proximal humeral bone loss remains a significant challenge for the shoulder arthroplasty surgeon. In the setting of a primary or a revision arthroplasty, the bone stock must be thoroughly evaluated during preoperative planning, and a surgical plan for addressing the deficits should be developed. Because proximal humeral bone loss may contribute to prosthetic failure, every effort should be made to reconstitute the bone stock.16 If the bone loss is less extensive, impaction grafting may be considered. Options to address massive proximal humeral bone loss include APCs and endoprosthetic reconstruction. The use of an allograft allows subscapularis repair, which may help stabilize the shoulder and restore the natural lever arm, as well as the tension of the deltoid.1,21-23 In addition, it helps avoid rotational instability and micromotion and provides bone stock for future revisions. However, concern persists regarding allograft resorption over time. More recently, modular endoprosthetic reconstruction systems have been developed to address bone deficiency with metal augmentation. Early clinical results demonstrate a high complication rate in this complex cohort of patients, not unlike those in the series of APCs, but clinical outcomes were improved compared to those in historical series. Nevertheless, longer-term clinical studies are necessary to determine the role of these modular endoprosthetic implant systems.
1. Chacon A, Virani N, Shannon R, Levy JC, Pupello D, Frankle M. Revision arthroplasty with use of a reverse shoulder prosthesis-allograft composite. J Bone Joint Surg Am. 2009;91(1):119-127. doi:10.2106/JBJS.H.00094.
2. Hattrup SJ, Waldrop R, Sanchez-Sotelo J. Reverse total shoulder arthroplasty for posttraumatic sequelae. J Orthop Trauma. 2016;30(2):e41-e47. doi:10.1097/BOT.0000000000000416.
3. Sewell MD, Kang SN, Al-Hadithy N, et al. Management of peri-prosthetic fracture of the humerus with severe bone loss and loosening of the humeral component after total shoulder replacement. J Bone Joint Surg Br. 2012;94(10):1382-1389. doi:10.1302/0301-620X.94B10.29248.
4. Trompeter AJ, Gupta RR. The management of complex periprosthetic humeral fractures: a case series of strut allograft augmentation, and a review of the literature. Strategies Trauma Limb Reconstr. 2013;8(1):43-51. doi:10.1007/s11751-013-0155-x.
5. Khatib O, Onyekwelu I, Yu S, Zuckerman JD. Shoulder arthroplasty in New York State, 1991 to 2010: changing patterns of utilization. J Shoulder Elbow Surg. 2015;24(10):e286-e291. doi:10.1016/j.jse.2015.05.038.
6. Kim SH, Wise BL, Zhang Y, Szabo RM. Increasing incidence of shoulder arthroplasty in the United States. J Bone Joint Surg Am. 2011;93(24):2249-2254. doi:10.2106/JBJS.J.01994.
7. Cil A, Veillette CJ, Sanchez-Sotelo J, Sperling JW, Schleck CD, Cofield RH. Survivorship of the humeral component in shoulder arthroplasty. J Shoulder Elbow Surg. 2010;19(1):143-150. doi:10.1016/j.jse.2009.04.011.
8. Wright TW. Revision of humeral components in shoulder arthroplasty. Bull Hosp Jt Dis. 2013;71(2 suppl):S77-S81.
9. Duquin TR, Sperling JW. Revision shoulder arthroplasty—how to manage the humerus. Oper Tech Orthop. 2011;21(1):44-51. doi:10.1053/j.oto.2010.09.008.
10. Cil A, Veillette CJ, Sanchez-Sotelo J, Sperling JW, Schleck C, Cofield RH. Revision of the humeral component for aseptic loosening in arthroplasty of the shoulder. J Bone Joint Surg Br. 2009;91(1):75-81. doi:10.1302/0301-620X.91B1.21094.
11. Cofield RH. Revision of hemiarthroplasty to total shoulder arthroplasty. In: Zuckerman JD, ed. Advanced Reconstruction: Shoulder. 1st edition. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2007;613-622.
12. Budge MD, Moravek JE, Zimel MN, Nolan EM, Wiater JM. Reverse total shoulder arthroplasty for the management of failed shoulder arthroplasty with proximal humeral bone loss: is allograft augmentation necessary? J Shoulder Elbow Surg. 2013;22(6):739-744. doi:10.1016/j.jse.2012.08.008.
13. Boileau P, Walch G. The three-dimensional geometry of the proximal humerus. Implications for surgical technique and prosthetic design. J Bone Joint Surg Br. 1997;79(5):857-865.
14. Throckmorton TW. Reconstructive procedures of the shoulder and elbow. In: Azar FM, Beaty JH, Canale ST, eds. Campbell’s Operative Orthopaedics. 13th edition. Philadelphia, PA: Elsevier; 2017;570-622.
15. Williams GR Jr, Wong KL, Pepe MD, et al. The effect of articular malposition after total shoulder arthroplasty on glenohumeral translations, range of motion, and subacromial impingement. J Shoulder Elbow Surg. 2001;10(5):399-409. doi:10.1067/mse.2001.116871.
16. De Wilde L, Walch G. Humeral prosthetic failure of reversed total shoulder arthroplasty: a report of three cases. J Shoulder Elbow Surg. 2006;15(2):260-264. doi:10.1016/j.jse.2005.07.014.
17. Owens CJ, Sperling JW, Cofield RH. Utility and complications of long-stem humeral components in revision shoulder arthroplasty. J Shoulder Elbow Surg. 2013;22(7):e7-e12. doi:10.1016/j.jse.2012.10.034.
18. Stephens SP, Paisley KC, Giveans MR, Wirth MA. The effect of proximal humeral bone loss on revision reverse total shoulder arthroplasty. J Shoulder Elbow Surg. 2015;24(10):1519-1526. doi:10.1016/j.jse.2015.02.020.
19. Werner BS, Abdelkawi AF, Boehm D, et al. Long-term analysis of revision reverse shoulder arthroplasty using cemented long stems. J Shoulder Elbow Surg. 2017;26(2):273-278. doi:10.1016/j.jse.2016.05.015.
20. Cuff D, Levy JC, Gutiérrez S, Frankle MA. Torsional stability of modular and non-modular reverse shoulder humeral components in a proximal humeral bone loss model. J Shoulder Elbow Surg. 2011;20(4):646-651. doi:10.1016/j.jse.2010.10.026.
21. Kassab M, Dumaine V, Babinet A, Ouaknine M, Tomeno B, Anract P. Twenty nine shoulder reconstructions after resection of the proximal humerus for neoplasm with mean 7-year follow-up. Rev Chir Orthop Reparatrice Appar Mot. 2005;91(1):15-23.
22. Levy J, Frankle M, Mighell M, Pupello D. The use of the reverse shoulder prosthesis for the treatment of failed hemiarthroplasty for proximal humeral fracture. J Bone Joint Surg. 2007;98(2):292-300. doi:10.2106/JBJS.E.01310.
23. Gagey O, Pourjamasb B, Court C. Revision arthroplasty of the shoulder for painful glenoid loosening: a series of 14 cases with acromial prostheses reviewed at four year follow up. Rev Chir Reparatrice Appar Mot. 2001;87(3):221-228.
24. Abdeen A, Hoang BH, Althanasina EA, Morris CD, Boland PJ, Healey JH. Allograft-prosthesis composite reconstruction of the proximal part of the humerus: functional outcome and survivorship. J Bone Joint Surg Am. 2009;91(10):2406-2415. doi:10.2106/JBJS.H.00815.
25. Getty PJ, Peabody TD. Complications and functional outcomes of reconstruction with an osteoarticular allograft after intra-articular resection of the proximal aspect of the humerus. J Bone Joint Surg Am. 1999;81(8):1138-1146.
26. Chen CF, Chen WM, Cheng YC, Chiang CC, Huang CK, Chen TH. Extracorporeally irradiated autograft-prosthetic composite arthroplasty using AML® extensively porous-coated stem for proximal femur reconstruction: a clinical analysis of 14 patients. J Surg Oncol. 2009;100(5):418-422. doi:10.1002/jso.21351.
27. Kelly JD 2nd, Purchase RJ, Kam G, Norris TR. Alloprosthetic composite reconstruction using the reverse shoulder arthroplasty. Tech Shoulder Elbow Surg. 2009;10(1):5-10.
28. Cannon CP, Paraliticci GU, Lin PP, Lewis VO, Yasko AW. Functional outcome following endoprosthetic reconstruction of the proximal humerus. J Shoulder Elbow Surg. 2009;18(5):705-710. doi:10.1016/j.jse.2008.10.011.
29. Chao EY, Fuchs B, Rowland CM, Ilstrup DM, Pritchard DJ, Sim FH. Long-term results of segmental prosthesis fixation by extracortical bone-bridging and ingrowth. J Bone Joint Surg Am. 2004;86-A(5):948-955.
30. Goulding KA, Schwartz A, Hattrup SJ, et al. Use of compressive osseointegration endoprostheses for massive bone loss from tumor and failed arthroplasty: a viable option in the upper extremity. Clin Orthop Relat Res. 2017;475(6):1702-1711. doi:10.1007/s11999-017-5258-0.
31. Guven MF, Aslan L, Botanlioglu H, Kaynak G, Kesmezacar H, Babacan M. Functional outcome of reverse shoulder tumor prosthesis in the treatment of proximal humeral tumors. J Shoulder Elbow Surg. 2016;25(1):e1-e6. doi:10.1016/j.jse.2015.06.012.
32. Wang ML, Ballard BL, Kulidjian AA, Abrams RA. Upper extremity reconstruction with a humeral tumor endoprosthesis: a novel salvage procedure after multiple revisions of total shoulder and elbow replacement. J Shoulder Elbow Surg. 2011;20(1):e1-e8. doi:10.1016/j.jse.2010.07.018.
1. Chacon A, Virani N, Shannon R, Levy JC, Pupello D, Frankle M. Revision arthroplasty with use of a reverse shoulder prosthesis-allograft composite. J Bone Joint Surg Am. 2009;91(1):119-127. doi:10.2106/JBJS.H.00094.
2. Hattrup SJ, Waldrop R, Sanchez-Sotelo J. Reverse total shoulder arthroplasty for posttraumatic sequelae. J Orthop Trauma. 2016;30(2):e41-e47. doi:10.1097/BOT.0000000000000416.
3. Sewell MD, Kang SN, Al-Hadithy N, et al. Management of peri-prosthetic fracture of the humerus with severe bone loss and loosening of the humeral component after total shoulder replacement. J Bone Joint Surg Br. 2012;94(10):1382-1389. doi:10.1302/0301-620X.94B10.29248.
4. Trompeter AJ, Gupta RR. The management of complex periprosthetic humeral fractures: a case series of strut allograft augmentation, and a review of the literature. Strategies Trauma Limb Reconstr. 2013;8(1):43-51. doi:10.1007/s11751-013-0155-x.
5. Khatib O, Onyekwelu I, Yu S, Zuckerman JD. Shoulder arthroplasty in New York State, 1991 to 2010: changing patterns of utilization. J Shoulder Elbow Surg. 2015;24(10):e286-e291. doi:10.1016/j.jse.2015.05.038.
6. Kim SH, Wise BL, Zhang Y, Szabo RM. Increasing incidence of shoulder arthroplasty in the United States. J Bone Joint Surg Am. 2011;93(24):2249-2254. doi:10.2106/JBJS.J.01994.
7. Cil A, Veillette CJ, Sanchez-Sotelo J, Sperling JW, Schleck CD, Cofield RH. Survivorship of the humeral component in shoulder arthroplasty. J Shoulder Elbow Surg. 2010;19(1):143-150. doi:10.1016/j.jse.2009.04.011.
8. Wright TW. Revision of humeral components in shoulder arthroplasty. Bull Hosp Jt Dis. 2013;71(2 suppl):S77-S81.
9. Duquin TR, Sperling JW. Revision shoulder arthroplasty—how to manage the humerus. Oper Tech Orthop. 2011;21(1):44-51. doi:10.1053/j.oto.2010.09.008.
10. Cil A, Veillette CJ, Sanchez-Sotelo J, Sperling JW, Schleck C, Cofield RH. Revision of the humeral component for aseptic loosening in arthroplasty of the shoulder. J Bone Joint Surg Br. 2009;91(1):75-81. doi:10.1302/0301-620X.91B1.21094.
11. Cofield RH. Revision of hemiarthroplasty to total shoulder arthroplasty. In: Zuckerman JD, ed. Advanced Reconstruction: Shoulder. 1st edition. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2007;613-622.
12. Budge MD, Moravek JE, Zimel MN, Nolan EM, Wiater JM. Reverse total shoulder arthroplasty for the management of failed shoulder arthroplasty with proximal humeral bone loss: is allograft augmentation necessary? J Shoulder Elbow Surg. 2013;22(6):739-744. doi:10.1016/j.jse.2012.08.008.
13. Boileau P, Walch G. The three-dimensional geometry of the proximal humerus. Implications for surgical technique and prosthetic design. J Bone Joint Surg Br. 1997;79(5):857-865.
14. Throckmorton TW. Reconstructive procedures of the shoulder and elbow. In: Azar FM, Beaty JH, Canale ST, eds. Campbell’s Operative Orthopaedics. 13th edition. Philadelphia, PA: Elsevier; 2017;570-622.
15. Williams GR Jr, Wong KL, Pepe MD, et al. The effect of articular malposition after total shoulder arthroplasty on glenohumeral translations, range of motion, and subacromial impingement. J Shoulder Elbow Surg. 2001;10(5):399-409. doi:10.1067/mse.2001.116871.
16. De Wilde L, Walch G. Humeral prosthetic failure of reversed total shoulder arthroplasty: a report of three cases. J Shoulder Elbow Surg. 2006;15(2):260-264. doi:10.1016/j.jse.2005.07.014.
17. Owens CJ, Sperling JW, Cofield RH. Utility and complications of long-stem humeral components in revision shoulder arthroplasty. J Shoulder Elbow Surg. 2013;22(7):e7-e12. doi:10.1016/j.jse.2012.10.034.
18. Stephens SP, Paisley KC, Giveans MR, Wirth MA. The effect of proximal humeral bone loss on revision reverse total shoulder arthroplasty. J Shoulder Elbow Surg. 2015;24(10):1519-1526. doi:10.1016/j.jse.2015.02.020.
19. Werner BS, Abdelkawi AF, Boehm D, et al. Long-term analysis of revision reverse shoulder arthroplasty using cemented long stems. J Shoulder Elbow Surg. 2017;26(2):273-278. doi:10.1016/j.jse.2016.05.015.
20. Cuff D, Levy JC, Gutiérrez S, Frankle MA. Torsional stability of modular and non-modular reverse shoulder humeral components in a proximal humeral bone loss model. J Shoulder Elbow Surg. 2011;20(4):646-651. doi:10.1016/j.jse.2010.10.026.
21. Kassab M, Dumaine V, Babinet A, Ouaknine M, Tomeno B, Anract P. Twenty nine shoulder reconstructions after resection of the proximal humerus for neoplasm with mean 7-year follow-up. Rev Chir Orthop Reparatrice Appar Mot. 2005;91(1):15-23.
22. Levy J, Frankle M, Mighell M, Pupello D. The use of the reverse shoulder prosthesis for the treatment of failed hemiarthroplasty for proximal humeral fracture. J Bone Joint Surg. 2007;98(2):292-300. doi:10.2106/JBJS.E.01310.
23. Gagey O, Pourjamasb B, Court C. Revision arthroplasty of the shoulder for painful glenoid loosening: a series of 14 cases with acromial prostheses reviewed at four year follow up. Rev Chir Reparatrice Appar Mot. 2001;87(3):221-228.
24. Abdeen A, Hoang BH, Althanasina EA, Morris CD, Boland PJ, Healey JH. Allograft-prosthesis composite reconstruction of the proximal part of the humerus: functional outcome and survivorship. J Bone Joint Surg Am. 2009;91(10):2406-2415. doi:10.2106/JBJS.H.00815.
25. Getty PJ, Peabody TD. Complications and functional outcomes of reconstruction with an osteoarticular allograft after intra-articular resection of the proximal aspect of the humerus. J Bone Joint Surg Am. 1999;81(8):1138-1146.
26. Chen CF, Chen WM, Cheng YC, Chiang CC, Huang CK, Chen TH. Extracorporeally irradiated autograft-prosthetic composite arthroplasty using AML® extensively porous-coated stem for proximal femur reconstruction: a clinical analysis of 14 patients. J Surg Oncol. 2009;100(5):418-422. doi:10.1002/jso.21351.
27. Kelly JD 2nd, Purchase RJ, Kam G, Norris TR. Alloprosthetic composite reconstruction using the reverse shoulder arthroplasty. Tech Shoulder Elbow Surg. 2009;10(1):5-10.
28. Cannon CP, Paraliticci GU, Lin PP, Lewis VO, Yasko AW. Functional outcome following endoprosthetic reconstruction of the proximal humerus. J Shoulder Elbow Surg. 2009;18(5):705-710. doi:10.1016/j.jse.2008.10.011.
29. Chao EY, Fuchs B, Rowland CM, Ilstrup DM, Pritchard DJ, Sim FH. Long-term results of segmental prosthesis fixation by extracortical bone-bridging and ingrowth. J Bone Joint Surg Am. 2004;86-A(5):948-955.
30. Goulding KA, Schwartz A, Hattrup SJ, et al. Use of compressive osseointegration endoprostheses for massive bone loss from tumor and failed arthroplasty: a viable option in the upper extremity. Clin Orthop Relat Res. 2017;475(6):1702-1711. doi:10.1007/s11999-017-5258-0.
31. Guven MF, Aslan L, Botanlioglu H, Kaynak G, Kesmezacar H, Babacan M. Functional outcome of reverse shoulder tumor prosthesis in the treatment of proximal humeral tumors. J Shoulder Elbow Surg. 2016;25(1):e1-e6. doi:10.1016/j.jse.2015.06.012.
32. Wang ML, Ballard BL, Kulidjian AA, Abrams RA. Upper extremity reconstruction with a humeral tumor endoprosthesis: a novel salvage procedure after multiple revisions of total shoulder and elbow replacement. J Shoulder Elbow Surg. 2011;20(1):e1-e8. doi:10.1016/j.jse.2010.07.018.
TAKE-HOME POINTS
- Proximal humeral bone loss presents a significant challenge for the shoulder arthroplasty surgeon.
- Unsupported long-stemmed humeral components in this setting are prone to early loosening.
- APCs can rebuild proximal humeral bone stock, but have concerns with graft resorption and long-term failure.
- Modular endoprosthetic reconstruction of proximal humeral bone loss potentially allows those deficiencies to be addressed in a more durable fashion.
- Longer-term and larger studies are needed to determine the optimal reconstruction technique for proximal humeral bone loss.
Use of a Novel Magnesium-Based Resorbable Bone Cement for Augmenting Anchor and Tendon Fixation
ABSTRACT
The aim of this study was to assess the efficacy and safety of a novel magnesium-based resorbable bone cement (OsteoCrete, Bone Solutions Incorporated) for anchor and tendon fixation.
Cadaveric humeral testing involved straight pull-to-failure of rotator cuff suture anchors; OsteoCrete was injected through one anchor, and a second anchor served as the uninjected control. Testing was conducted 15 minutes post-injection. A canine preclinical model was used to evaluate the safety of the following parameters: Rotator cuff repair: A double-row technique was used to repair transected infraspinatus tendons; OsteoCrete was injected through both anchors in one limb, and the contralateral limb served as the uninjected control. Biceps tenodesis: The transected biceps tendon was implanted into a proximal humeral socket with a transcortical button; OsteoCrete was injected into the socket of one limb, and a screw was used for final fixation in the contralateral control limb. Nondestructive biomechanical testing and histologic assessment were performed after 12 weeks.
OsteoCrete-augmented anchors showed significantly higher load-to-failure compared to that with uninjected controls. In cadaveric humeri with reduced bone quality, OsteoCrete increased the mean load-to-failure by 99%. Within the preclinical model, there were no complications or statistically significant biomechanical/histologic differences between the techniques.
OsteoCrete has the potential for safely providing improved suture anchor and tissue fixation in patients with poor bone or tissue quality.
Continue to: Calcium phosphate bone void fillers...
Calcium phosphate bone void fillers have been commonly used in orthopedic surgery for several applications, including, but not limited to, a variety of fracture fixation or augmentation procedures.1-8 Continuing research on calcium phosphates has evidenced that the addition of magnesium phosphate to the formulation results in improved reactivity of the bone void filler. An in vitro study demonstrated enhanced attachment and proliferation of MG63 osteoblast-like cells on calcium magnesium phosphate cement (CMPC), in comparison with calcium phosphate cement (CPC), along with increased cellular alkaline phosphatase activity.9 The authors further explored the proliferation rates of MG63 cells by comparing CMPC with CPC and magnesium phosphate cement (MPC), and observed significantly increased proliferation of cells on CMPC. They also compared CMPC and CPC using a rabbit bone void model and observed substantial CMPC resorption with new bone formation at the 3-month time point and further reported that the majority of the defect had filled with new bone at 6 months, whereas CPC resulted in <10% new bone formation after 6 months.10 The authors continued to study the differences between CPC, MPC, and CMPC and identified increased proliferation of bone marrow stromal cells (bMSCs), when the cells were associated with CMPC and MPC, and when compared to that with CPC. The osteogenic differentiation of bMSCs was highest in the CMPC and CPC groups, when compared to that in the MPC group, with no significant difference between the CMPC and CPC groups. The authors also compared these 3 different formulations using a rabbit maxillary sinus floor elevation model, in which CMPC resulted in increased new bone formation and mineralization compared to that with CPC and MPC, which was further enhanced with the addition of bMSCs.11
These studies highlight the importance of having both a magnesium phosphate and a calcium phosphate component for a resorbable cement intended for use as a bone void filler. The rationale behind this strategy is related to the release of magnesium ions from the magnesium phosphate component. Magnesium has been shown to increase the proliferation of bMSCs, improve the attachment and growth of osteoblasts, stimulate the proteins involved in bone regeneration, enhance new bone formation, and boost bone mineralization.12,13
OsteoCrete (Bone Solutions Incorporation) is a novel CMPC composed of magnesium oxide, monopotassium phosphate, monosodium phosphate, hydroxyapatite, and sucrose. OsteoCrete has been demonstrated to significantly increase peak torque-to-failure of stainless-steel cortical bone screw fixation, when compared with screw fixation without augmentation and screw fixation with calcium phosphate augmentation using an in vivo equine model. In the same study, the authors showed that OsteoCrete resulted in an interface toughness that was significantly increased compared to that with no treatment, CPC augmentation, and polymethylmethacrylate (PMMA) augmentation. At 6 months after implantation, woven bone had replaced 69% of the OsteoCrete at the screw interface, compared to 44% of that with CPC.14 An equine study examined the effects of OsteoCrete on bone stability and healing using a metatarsal osteotomy model; the study reported significantly improved radiographic callus formation and a greater amount of new bone formation within the fracture gap when compared to that with CPC augmentation or no augmentation. OsteoCrete also secured the fragment significantly better than the CPC and control groups based on a decreased fracture gap over time.15 Another study using a preclinical anterior cruciate ligament (ACL) reconstruction model reported that OsteoCrete resulted in significantly better new bone formation in the tibial tunnel, a smaller amount of fibrous tissue, more cartilage formation at the tendon-bone interface, and a higher ultimate load-to-failure compared to that with standard ACL reconstruction in the contralateral limb after 6 weeks.16 OsteoCrete and PMMA were evaluated in terms of biomechanical fixation of a stemless humeral prosthesis, with data showing that both groups have higher failure loads, failure displacements, and failure cycles when compared to those with the control, nonaugmented group.17 Another preclinical model evaluated cranial bone flap augmentation with 2 resorbable cements and highlighted faster cement resorption and replacement with bone, along with superior stability within the OsteoCrete group compared to that with CPC.18 In a preclinical bone void study conducted for obtaining US Food and Drug Administration 510(k) clearance, OsteoCrete resulted in 83% greater resorption than that with CPC after 12 weeks and 35% greater resorption at 26 weeks, with 84% of OsteoCrete being resorbed and replaced with woven or lamellar mineralized bone of normal morphology at the 26-week time point (unpublished data provided by Bone Solutions Incorporated [BSI]).
These data indicate that CMPCs such as OsteoCrete appear to have potential benefits for augmenting the healing of bone implants and bone soft tissue. Therefore, the objective of this study was to assess the safety and efficacy of OsteoCrete in applications for the augmentation of anchor and tendon fixation in rotator cuff repair and biceps tenodesis procedures, respectively. Improving healing for these 2 commonly performed procedures would be of great benefit in improving the functional outcomes and mitigating the complications and morbidity.
MATERIALS AND METHODS
IN VITRO STUDY METHODS
Cadaveric humeri (N = 12, six matched pairs) of females (age, 70-75 years) were warmed to 37°C prior to testing. Two 4.75-mm vented anchors (SwiveLock, Arthrex) with FiberTape were implanted into a lateral row position (anterior and posterior anchor positioning) of a double-row rotator cuff repair within the greater tuberosity. One anchor was injected with 1 ml of OsteoCrete–after preparation according to the manufacturer’s instructions–through the cannulation channel after placement, and the other anchor served as the uninjected control for each humerus. For the six matched pairs, the OsteoCrete group and the control group were rotated with respect to anterior vs posterior location within the lateral row position. After 15 minutes of the injection, straight pull-to-failure (12 in/min) was performed. Data were compared between the groups for significant (P < .05) differences using t-tests and Pearson correlation.
Continue to: IN VIVO STUDY METHODS
IN VIVO STUDY METHODS
With Institutional Animal Care and Use Committee approval, adult (age, 2-4 years) purpose-bred dogs (N = 8) underwent aseptic surgery of both forelimbs for rotator cuff (infraspinatus) tendon repair (Figure 1) and biceps tenodesis (Figure 2). For the rotator cuff repair, two 4.75-mm vented anchors (1 medial and 1 lateral) with FiberTape were used in a modified double-row technique to repair the acutely transected infraspinatus tendon. In one limb, 1 ml of OsteoCrete was injected through both anchors; the other limb served as the uninjected control. For the biceps tenodesis procedure, the long head of the biceps tendon was transected at its origin and whip-stitched. The tendon was transposed and inserted into a 7-mm diameter socket drilled into the proximal humerus using a tension-slide technique with a transcortical button for fixation. In one limb, 1 ml of OsteoCrete was injected into the socket prior to final tensioning and tying. In the contralateral limb, a 7-mm interference screw (Bio-Tenodesis™ Screw, Arthrex) was inserted into the socket after tensioning and tying. The dogs were allowed to perform out-of-kennel monitored exercise daily for a period of 12 weeks after surgery and were then sacrificed.
The infraspinatus and biceps bone-tendon-muscle units were excised en bloc. Custom-designed jigs were used for biomechanical testing of the bone-tendon-muscle units along the anatomical vector of muscle contraction. Optical markers were mounted at standardized anatomical locations. Elongation of the repair site was defined as the change in distance between markers and was measured to 0.01-mm resolution using an optical tracking system (Optotrak Certus, NDI), synchronized with measurement of the applied tension load. The bone-tendon-muscle units were loaded in tension to 3-mm elongation at a displacement controlled rate of 0.01 mm/s. Load at 1-mm, 2-mm, and 3-mm displacement of the tendon-bone junction was extracted from the load vs the displacement curve of each sample. Stiffness was calculated as the slope of the linear portion of the load vs the displacement curve.19,20
For histologic assessments, sections of each treatment site were obtained using a microsaw and alternated between decalcified and non-decalcified processing. For decalcified bone processing, formalin-fixed tissues were placed in 10% ethylenediaminetetraacetic acid with phosphate-buffered saline for 39 days and then processed routinely for the assessment of sections stained with hematoxylin and eosin (H&E), toluidine blue, and picrosirius red. For non-decalcified bone processing, the tissues were dehydrated through a series of graded ethyl alcohol solutions, embedded in PMMA, sectioned, and stained with toluidine blue and Goldner’s trichrome. Two pathologists who were blinded to the clinical application and the differences between techniques assessed the histologic sections and scored each section using the modified Bonar score that assesses cell morphology, collagen arrangement, cellularity, vascularity, and extracellular matrix using a 15-point scale, where a higher score indicates more pathology.21
Categorical data were compared for detecting statistically significant differences using the rank sum test. Continuous data were compared for identifying statistically significant differences using the t-test or one-way ANOVA. Significance was set at P < .05.
RESULTS
IN VITRO RESULTS
OsteoCrete-augmented anchors (mean = 225 N; range, 158-287 N) had significantly (P < .001) higher pull-out load-to-failure compared to that in the uninjected controls (mean = 161 N; range, 68-202 N), which translated to a 50% mean increase (range, 3%-134%) in load-to-failure (Table 1). For humeri with reduced bone quality (control anchors that failed at <160 N, 4 humeri), the mean increase in load-to-failure for OsteoCrete-augmented anchors was 99% (range, 58%-135%), with the difference between mean values being again significantly different (OsteoCrete mean = 205 N; control mean = 110 N, P < .001). When the control and OsteoCrete load-to-failure values were compared using Pearson correlation, a significantly strong positive correlation (r = 0.66, P = 0.02) was detected. When the control load-to-failure values were compared with its percent increase value when OsteoCrete was used, there was a significantly very strong negative correlation (r = −0.90, P < .001).
Table 1. Cadaveric Lateral Row Rotator Cuff Anchor Pull-To-Failure; Testing Occurred 15 Minutes Post-Injection
| Humerus No. | Control (N) | OsteoCrete (N)a | Percent Increase |
| 1-Right (PA) | 197.28 | 278.73 | 41% |
| 1-Left (AP) | 152.62 | 241.72 | 58% |
| 2-Right (PA) | 178.60 | 196.03 | 10% |
| 2-Left (AP) | 170.10 | 175.57 | 3% |
| 3-Right (PA) | 67.70 | 158.31 | 134% |
| 3-Left (AP) | 74.24 | 173.08 | 133% |
| 4-Right (PA) | 195.81 | 248.12 | 27% |
| 4-Left (AP) | 201.95 | 209.42 | 4% |
| 5-Right (PA) | 173.30 | 220.59 | 27% |
| 5-Left (AP) | 146.61 | 247.37 | 69% |
| 6-Right (PA) | 171.03 | 266.14 | 56% |
| 6-Left (AP) | 199.99 | 286.91 | 43% |
| Average | 160.77 + 45.60 | 225.17 + 43.08 | 50% + 44 |
aOsteoCrete (Bone Solutions Incorporated) resulted in significantly increased (P < 0.001) pull-to-failure. Abbreviations: AP, control anchor located in anterior position, OsteoCrete anchor located in posterior position; PA, control anchor located in posterior position, OsteoCrete anchor located in anterior position.
Continue to: IN VIVO RESULTS
IN VIVO RESULT
No intraoperative or postoperative complications were noted. All repairs were found to be intact based on the gross assessment and the completed biomechanical testing without failure. No statistically significant (P > 0.3) biomechanical differences were found between the techniques (Table 2). Histologic assessments showed low-to-mild pathology scores for all sites with no statistically significant (P > 0.3) differences between the techniques (Table 2). Both control and OsteoCrete rotator cuff repairs demonstrated tendon-to-bone integration via fibrous connective tissue attachment to bone. All anchors were in place with no evidence for loosening, tunnel expansion, or cyst formation. OsteoCrete-augmented anchor repairs were associated with cement remaining within their lumens along with a thin layer of cement interposed between the anchor and the bone interface around their entire periphery. The cement-bone interface was discrete with typical inflammatory cell infiltrate without evidence for infection, membrane or cyst formation, or other untoward pathologic responses. In the OsteoCrete biceps tenodesis group, the tendons filled the tunnels with a thin layer of cement remaining interposed between the tendon and the bone interface around the entire periphery. The tendon-cement-bone interface was discrete with typical inflammatory cell infiltrates and without evidence for infection, membrane or cyst formation, or other untoward pathologic responses. Tendon-to-bone integration was not observed in the control or OsteoCrete biceps tenodesis groups at the 12-week study endpoint. Representative histologic images of the rotator cuff tendon repairs and biceps tenodesis procedures are shown in Figures 3A, 3B and Figures 4A, 4B, respectively.
Table 2. Biomechanical Testing And Histologic Scoring Of Rotator Cuff And Biceps Tendon Repairs In A Preclinical Model
| Procedure | Force (N) at 1 mm | Force (N) at 2 mm | Force (N) at 3 mm | Stiffness (N/mm) | Histologic Score |
| Rotator Cuff - Control | 14.0 + 3.3 | 19.3 + 5.5 | 25.0 + 7.0 | 5.4 + 2.0 | 4.6 + 1.1 |
| Rotator Cuff - OsteoCrete (Bone Solutions Incorporated) | 14.8 + 3.7 | 20.4 + 6.0 | 26.4 + 8.5 | 6.3 + 2.5 | 3.9 + 1.7 |
| Biceps - Control | 23.1 + 6.2 | 35.5 + 8.5 | 52.6 + 15.0 | 17.8 + 6.4 | 3.4 + 1.2 |
| Biceps - OsteoCrete | 22.4 + 7.3 | 36.8 + 10.1 | 57.8 + 16.0 | 21.1 + 8.5 | 3.4 + 0.7 |
There were no significant differences (P < 0.05) between groups. Histologic scoring based on a 15-point scale with higher scores indicating more pathology.
DISCUSSION
The results of this study highlight the safety and efficacy of OsteoCrete in applications for the augmentation of anchor and tendon fixation in rotator cuff repair and biceps tenodesis procedures, respectively. Anchors augmented with OsteoCrete resulted in significantly increased load-to-failure pull-out strength 15 minutes after insertion. In addition, a very strong negative correlation was found between the percentage of improved load-to-failure after OsteoCrete injection and the bone quality of the humerus, which was based on the control load-to-failure values. In the validated preclinical model used in this study, OsteoCrete-based fixation was found to be noninferior to current standard-of-care techniques and was not associated with any untoward pathologic responses of humeral bone, rotator cuff tendon, or biceps tendon based on the biomechanical and histologic analyses. These data highlight the functional efficacy and biocompatibility of OsteoCrete when used for these common indications.
More than 270,000 rotator cuff procedures have been reported to be performed in the US annually (average patient age: 61 years for women, 56 years for men).22 Rotator cuff repair procedures have been associated with a 20% failure rate, with one of the causes being related to an inability for the tendon to heal, even with strong initial fixation.23 Rotator cuff repair techniques are being continuously optimized with the goal of improving patient outcomes. This goal is being realized, primarily with respect to re-tear rates.24,25 However, even with advanced techniques, there are still relatively high rates of failure reported, with increasing patient age serving as one of the primary negative prognostic factors.26 An older patient population is associated with decreased bone mass and strength, and postmenopausal females have decreased bone quality; these factors are associated with higher rotator cuff failure rates due to poor tendon healing, with anchor fixation failure also playing a role.27-29 Therefore, it is critically important to develop methods for augmenting implant and tendon fixation to bone to achieve functional healing. The results of this study suggest that OsteoCrete provides a valid method for accomplishing this goal based on the observation that proximal humeral anchor fixation was improved by 50% in load-to-failure 15 minutes post-injection with an even more profound impact on the anchors placed in poor-quality bone (99% increased load-to-failure 15 minutes post-injection). It is probable that the degree of improvement in fixation strength would be even greater 1 day after fixation, since the strength of OsteoCrete continues to increase over the first 30 hours of curing.
Based on the preclinical animal model data of this study, OsteoCrete augmentation of rotator cuff anchor fixation had no untoward effects on tendon healing or function and can be considered as safe for use. Previously published data also suggest that OsteoCrete may improve osseous replacement of anchors as a result of magnesium ion release, which can drive adjacent attachment and growth of osteoblasts, leading to enhanced new bone formation.9-16,18 As such, surgeons may consider this means of anchor augmentation in situations of questionable or poor-quality bone and/or when accelerated postoperative rehabilitation protocols are desired.
A very low early incidence failure rate (1.2%) has been reported when a distal biceps tendon rupture is repaired using cortical suspensory fixation in conjunction with an interference screw.30 When an early re-rupture does occur, the most common explanation for failure tends to be a lack of patient compliance, with excessive force being placed on the repair.31 This study was not meant to investigate the methods to increase the strength of a biceps tendon repair using OsteoCrete but instead to replace the interference screw with OsteoCrete in a safe and noninferior manner. Primary fixation was still dependent on cortical suspensory fixation; however, OsteoCrete was used to help aid in stabilization of the tendon without the need for interference screw fixation. Although rare, osteolysis and perianchor cyst formation have been reported adjacent to nonbiodegradable anchors (PEEK), along with several types of biodegradable anchors (PLLA, hydroxyapatite plus PLLA, β-tricalcium phosphate plus PLLA, and polyglycolic acid; the latter of the 3 resulted in the lowest incidence of perianchor cyst formation) in the shoulder and elbow.32-34 Whenever osteolysis or cyst formation occurs around an anchor, it leads to decreased bone volume and potential adjacent bone weakness, which may act as a stress riser, thus increasing the risk for fracture. This potential is probably more of a concern within the proximal radius where there is a decreased amount of bone stock around the anchor.34
Continue to: In this study...
In this study, a short-term 12-week analysis revealed no significant differences in the nondestructive biomechanical testing and histologic analysis results between the use of OsteoCrete and the use of a tenodesis anchor. These results indicate the potential for using OsteoCrete as an anchor replacement. The biceps tendon did not react negatively to the OsteoCrete material, which indicated that OsteoCrete can be used adjacent to tendons without the concern of weakening the tendon due to an inflammatory reaction. This being said, tendon-to-bone integration was not evident at this early time point. It would be helpful to further explore the potential of this technique with a longer-term study investigating tendon-to-bone integration in more detail. Ideally, a long-term study would reveal an increased amount of new bone formation within the socket when compared to that with the anchor comparison, similar to the results reported by Gulotta and colleagues16 when using a tendon for ACL reconstruction with OsteoCrete.
We do note several limitations in this study. The dogs used in this study were healthy with normal bone and tendon morphology, the tendons were transected and repaired during the course of the same surgery, and only 1 early time point was evaluated. Additional investigations continuing the characterization of these clinical applications using an osteopenic or osteoporotic preclinical model with chronic tendon pathology and longer-term evaluation are now warranted based on the positive findings of this initial work.
CONCLUSION
OsteoCrete augmentation significantly improved initial rotator cuff anchor fixation (human in vitro) and was safe and effective for anchor and tendon fixation in rotator cuff tendon repair and biceps tenodesis procedures (canine in vivo), respectively, when compared with the current standard-of-care. Of note, the significant improvements associated with OsteoCrete were the greatest in poor-quality bone. Based on these results and considering the previously discussed limitations, it can be concluded that OsteoCrete has the potential for safely providing improved suture anchor and tissue fixation in patients with poor bone or tissue quality. Further in vivo study toward potential clinical applications is warranted.
1. Russell TA, Leighton RK, Group A-BTPFS. Comparison of autogenous bone graft and endothermic calcium phosphate cement for defect augmentation in tibial plateau fractures. A multicenter, prospective, randomized study. J Bone Joint Surg Am. 2008; 90(10):2057-2061. doi:10.2106/JBJS.G.01191.
2. Egol KA, Sugi MT, Ong CC, Montero N, Davidovitch R, Zuckerman JD. Fracture site augmentation with calcium phosphate cement reduces screw penetration after open reduction-internal fixation of proximal humeral fractures. J Shoulder Elbow Surg. 2012; 21(6):741-748. doi:10.1016/j.jse.2011.09.017.
3. Cassidy C, Jupiter JB, Cohen M, et al. Norian SRS cement compared with conventional fixation in distal radial fractures. A randomized study. J Bone Joint Surg Am. 2003;85-A(11):2127-2137.
4. Mattsson P, Alberts A, Dahlberg G, Sohlman M, Hyldahl HC, Larsson S. Resorbable cement for the augmentation of internally-fixed unstable trochanteric fractures. A prospective, randomised multicentre study. J Bone Joint Surg Br. 2005;87(9):1203-1209.
5. Cohen SB, Sharkey PF. Subchondroplasty for treating bone marrow lesions. J Knee Surg. 2016;29(07):555-563. doi:10.1302/0301-620X.87B9.15792.
6. Guida P, Ragozzino R, Sorrentino B, et al. Three-in-One minimally invasive approach to surgical treatment of pediatric pathological fractures with wide bone loss through bone cysts: ESIN, curettage and packing with injectable HA bone substitute. A retrospective series of 116 cases. Injury. 2016;47(6):1222-1228. doi:10.1016/j.injury.2016.01.006.
7. Maestretti G, Sutter P, Monnard E, et al. A prospective study of percutaneous balloon kyphoplasty with calcium phosphate cement in traumatic vertebral fractures: 10-year results. Eur Spine J. 2014;23(6):1354-1360. doi:10.1007/s00586-014-3206-1.
8. Nakano M, Hirano N, Zukawa M, et al. Vertebroplasty using calcium phosphate cement for osteoporotic vertebral fractures: study of outcomes at a minimum follow-up of two years. Asian Spine J. 2012;6(1):34-42. doi:10.4184/asj.2012.6.1.34.
9. Jia J, Zhou H, Wei J, et al. Development of magnesium calcium phosphate biocement for bone regeneration. J R Soc Interface. 2010;7(49):1171-1180. doi:10.1098/rsif.2009.0559.
10. Wu F, Wei J, Guo H, Chen F, Hong H, Liu C. Self-setting bioactive calcium-magnesium phosphate cement with high strength and degradability for bone regeneration. Acta Biomater. 2008;4(6):1873-1884. doi:10.1016/j.actbio.2008.06.020.
11. Zeng D, Xia L, Zhang W, et al. Maxillary sinus floor elevation using a tissue-engineered bone with calcium-magnesium phosphate cement and bone marrow stromal cells in rabbits. Tissue Eng Part A. 2012;18(7-8):870-881. doi:10.1089/ten.TEA.2011.0379.
12. Yoshizawa S, Brown A, Barchowsky A, Sfeir C. Magnesium ion stimulation of bone marrow stromal cells enhances osteogenic activity, simulating the effect of magnesium alloy degradation. Acta Biomater. 2014;10(6):2834-2842. doi:10.1016/j.actbio.2014.02.002.
13. Liao J, Qu Y, Chu B, Zhang X, Qian Z. Biodegradable CSMA/PECA/Graphene porous hybrid scaffold for cartilage tissue engineering. Sci Rep. 2015;5:9879. doi:10.1038/srep09879.
14. Hirvinen LJ, Litsky AS, Samii VF, Weisbrode SE, Bertone AL. Influence of bone cements on bone-screw interfaces in the third metacarpal and third metatarsal bones of horses. Am J Vet Res. 2009;70(8):964-972. doi:10.2460/ajvr.70.8.964.
15. Waselau M, Samii VF, Weisbrode SE, Litsky AS, Bertone AL. Effects of a magnesium adhesive cement on bone stability and healing following a metatarsal osteotomy in horses. Am J Vet Res. 2007;68(4):370-378. doi:10.2460/ajvr.68.4.370.
16. Gulotta LV, Kovacevic D, Ying L, Ehteshami JR, Montgomery S, Rodeo SA. Augmentation of tendon-to-bone healing with a magnesium-based bone adhesive. Am J Sports Med. 2008;36(7):1290-1297. doi:10.1177/0363546508314396.
17. Kim MS, Kovacevic D, Milks RA, et al. Bone graft substitute provides metaphyseal fixation for a stemless humeral implant. Orthopedics. 2015;38(7):e597-e603. doi:10.3928/01477447-20150701-58.
18. Schendel SA, Peauroi J. Magnesium-based bone cement and bone void filler: preliminary experimental studies. J Craniofac Surg. 2009;20(2):461-464. doi:10.1097/SCS.0b013e31819b9819.
19. Pfeiffer FM, Smith MJ, Cook JL, Kuroki K. The histologic and biomechanical response of two commercially available small glenoid anchors for use in labral repairs. J Shoulder Elbow Surg. 2014;23(8):1156-1161. doi:10.1016/j.jse.2013.12.036.
20. Smith MJ, Cook JL, Kuroki K, et al. Comparison of a novel bone-tendon allograft with a human dermis-derived patch for repair of chronic large rotator cuff tears using a canine model. Arthroscopy. 2012;28(2):169-177. doi:10.1016/j.arthro.2011.08.296.
21. Fearon A, Dahlstrom JE, Twin J, Cook J, Scott A. The Bonar score revisited: region of evaluation significantly influences the standardized assessment of tendon degeneration. J Sci Med Sport. 2014;17(4):346-350. doi:10.1016/j.jsams.2013.07.008.
22. Colvin AC, Egorova N, Harrison AK, Moskowitz A, Flatow EL. National trends in rotator cuff repair. J Bone Joint Surg Am. 2012;94(3):227-233. doi:10.2106/JBJS.J.00739.
23. Lädermann A, Denard PJ, Burkhart SS. Management of failed rotator cuff repair: a systematic review. J ISAKOS. 2016;1(1):32-37. doi:10.1136/jisakos-2015-000027.
24. Franceschi F, Papalia R, Franceschetti E, et al. Double-Row repair lowers the retear risk after accelerated rehabilitation. Am J Sports Med. 2016;44(4):948-956. doi:10.1177/0363546515623031.
25. Wang E, Wang L, Gao P, Li Z, Zhou X, Wang S. Single-versus double-row arthroscopic rotator cuff repair in massive tears. Med Sci Monit. 2015;21:1556-1561. doi:10.12659/MSM.893058.
26. Abtahi AM, Granger EK, Tashjian RZ. Factors affecting healing after arthroscopic rotator cuff repair. World J Orthop. 2015;6(2):211-220. doi:10.5312/wjo.v6.i2.211.
27. Chung SW, Oh JH, Gong HS, Kim JY, Kim SH. Factors affecting rotator cuff healing after arthroscopic repair: osteoporosis as one of the independent risk factors. Am J Sports Med. 2011;39(10):2099-2107. doi:10.1177/0363546511415659.
28. Tsiouri C, Mok DH. Early pullout of lateral row knotless anchor in rotator cuff repair. Int J Shoulder Surg. 2009;3(3):63-65. doi:10.4103/0973-6042.59972.
29. Boskey AL, Coleman R. Aging and bone. J Dent Res. 2010;89(12):1333-1348. doi:10.1177/0022034510377791.
30. Cusick MC, Cottrell BJ, Cain RA, Mighell MA. Low incidence of tendon rerupture after distal biceps repair by cortical button and interference screw. J Shoulder Elbow Surg. 2014;23(10):1532-1536. doi:10.1016/j.jse.2014.04.013.
31. Hinchey JW, Aronowitz JG, Sanchez-Sotelo J, Morrey BF. Re-rupture rate of primarily repaired distal biceps tendon injuries. J Shoulder Elbow Surg. 2014;23(6):850-854. doi:10.1016/j.jse.2014.02.006.
32. Shahrulazua A, Duckworth D, Bokor DJ. Perianchor radiolucency following PEEK suture anchor application associated with recurrent shoulder dislocation: a case report. Clin Ter. 2014;165(1):31-34. doi:10.7471/CT.2014.1658.
33. Kim SH, Kim dY, Kwon JE, Park JS, Oh JH. Perianchor cyst formation around biocomposite biodegradable suture anchors after rotator cuff repair. Am J Sports Med. 2015;43(12):2907-2912. doi:10.1177/0363546515608484
34. Potapov A, Laflamme YG, Gagnon S, Canet F, Rouleau DM. Progressive osteolysis of the radius after distal biceps tendon repair with the bioabsorbable screw. J Shoulder Elbow Surg. 2011;20(5):819-826. doi:10.1016/j.jse.2011.02.021.
ABSTRACT
The aim of this study was to assess the efficacy and safety of a novel magnesium-based resorbable bone cement (OsteoCrete, Bone Solutions Incorporated) for anchor and tendon fixation.
Cadaveric humeral testing involved straight pull-to-failure of rotator cuff suture anchors; OsteoCrete was injected through one anchor, and a second anchor served as the uninjected control. Testing was conducted 15 minutes post-injection. A canine preclinical model was used to evaluate the safety of the following parameters: Rotator cuff repair: A double-row technique was used to repair transected infraspinatus tendons; OsteoCrete was injected through both anchors in one limb, and the contralateral limb served as the uninjected control. Biceps tenodesis: The transected biceps tendon was implanted into a proximal humeral socket with a transcortical button; OsteoCrete was injected into the socket of one limb, and a screw was used for final fixation in the contralateral control limb. Nondestructive biomechanical testing and histologic assessment were performed after 12 weeks.
OsteoCrete-augmented anchors showed significantly higher load-to-failure compared to that with uninjected controls. In cadaveric humeri with reduced bone quality, OsteoCrete increased the mean load-to-failure by 99%. Within the preclinical model, there were no complications or statistically significant biomechanical/histologic differences between the techniques.
OsteoCrete has the potential for safely providing improved suture anchor and tissue fixation in patients with poor bone or tissue quality.
Continue to: Calcium phosphate bone void fillers...
Calcium phosphate bone void fillers have been commonly used in orthopedic surgery for several applications, including, but not limited to, a variety of fracture fixation or augmentation procedures.1-8 Continuing research on calcium phosphates has evidenced that the addition of magnesium phosphate to the formulation results in improved reactivity of the bone void filler. An in vitro study demonstrated enhanced attachment and proliferation of MG63 osteoblast-like cells on calcium magnesium phosphate cement (CMPC), in comparison with calcium phosphate cement (CPC), along with increased cellular alkaline phosphatase activity.9 The authors further explored the proliferation rates of MG63 cells by comparing CMPC with CPC and magnesium phosphate cement (MPC), and observed significantly increased proliferation of cells on CMPC. They also compared CMPC and CPC using a rabbit bone void model and observed substantial CMPC resorption with new bone formation at the 3-month time point and further reported that the majority of the defect had filled with new bone at 6 months, whereas CPC resulted in <10% new bone formation after 6 months.10 The authors continued to study the differences between CPC, MPC, and CMPC and identified increased proliferation of bone marrow stromal cells (bMSCs), when the cells were associated with CMPC and MPC, and when compared to that with CPC. The osteogenic differentiation of bMSCs was highest in the CMPC and CPC groups, when compared to that in the MPC group, with no significant difference between the CMPC and CPC groups. The authors also compared these 3 different formulations using a rabbit maxillary sinus floor elevation model, in which CMPC resulted in increased new bone formation and mineralization compared to that with CPC and MPC, which was further enhanced with the addition of bMSCs.11
These studies highlight the importance of having both a magnesium phosphate and a calcium phosphate component for a resorbable cement intended for use as a bone void filler. The rationale behind this strategy is related to the release of magnesium ions from the magnesium phosphate component. Magnesium has been shown to increase the proliferation of bMSCs, improve the attachment and growth of osteoblasts, stimulate the proteins involved in bone regeneration, enhance new bone formation, and boost bone mineralization.12,13
OsteoCrete (Bone Solutions Incorporation) is a novel CMPC composed of magnesium oxide, monopotassium phosphate, monosodium phosphate, hydroxyapatite, and sucrose. OsteoCrete has been demonstrated to significantly increase peak torque-to-failure of stainless-steel cortical bone screw fixation, when compared with screw fixation without augmentation and screw fixation with calcium phosphate augmentation using an in vivo equine model. In the same study, the authors showed that OsteoCrete resulted in an interface toughness that was significantly increased compared to that with no treatment, CPC augmentation, and polymethylmethacrylate (PMMA) augmentation. At 6 months after implantation, woven bone had replaced 69% of the OsteoCrete at the screw interface, compared to 44% of that with CPC.14 An equine study examined the effects of OsteoCrete on bone stability and healing using a metatarsal osteotomy model; the study reported significantly improved radiographic callus formation and a greater amount of new bone formation within the fracture gap when compared to that with CPC augmentation or no augmentation. OsteoCrete also secured the fragment significantly better than the CPC and control groups based on a decreased fracture gap over time.15 Another study using a preclinical anterior cruciate ligament (ACL) reconstruction model reported that OsteoCrete resulted in significantly better new bone formation in the tibial tunnel, a smaller amount of fibrous tissue, more cartilage formation at the tendon-bone interface, and a higher ultimate load-to-failure compared to that with standard ACL reconstruction in the contralateral limb after 6 weeks.16 OsteoCrete and PMMA were evaluated in terms of biomechanical fixation of a stemless humeral prosthesis, with data showing that both groups have higher failure loads, failure displacements, and failure cycles when compared to those with the control, nonaugmented group.17 Another preclinical model evaluated cranial bone flap augmentation with 2 resorbable cements and highlighted faster cement resorption and replacement with bone, along with superior stability within the OsteoCrete group compared to that with CPC.18 In a preclinical bone void study conducted for obtaining US Food and Drug Administration 510(k) clearance, OsteoCrete resulted in 83% greater resorption than that with CPC after 12 weeks and 35% greater resorption at 26 weeks, with 84% of OsteoCrete being resorbed and replaced with woven or lamellar mineralized bone of normal morphology at the 26-week time point (unpublished data provided by Bone Solutions Incorporated [BSI]).
These data indicate that CMPCs such as OsteoCrete appear to have potential benefits for augmenting the healing of bone implants and bone soft tissue. Therefore, the objective of this study was to assess the safety and efficacy of OsteoCrete in applications for the augmentation of anchor and tendon fixation in rotator cuff repair and biceps tenodesis procedures, respectively. Improving healing for these 2 commonly performed procedures would be of great benefit in improving the functional outcomes and mitigating the complications and morbidity.
MATERIALS AND METHODS
IN VITRO STUDY METHODS
Cadaveric humeri (N = 12, six matched pairs) of females (age, 70-75 years) were warmed to 37°C prior to testing. Two 4.75-mm vented anchors (SwiveLock, Arthrex) with FiberTape were implanted into a lateral row position (anterior and posterior anchor positioning) of a double-row rotator cuff repair within the greater tuberosity. One anchor was injected with 1 ml of OsteoCrete–after preparation according to the manufacturer’s instructions–through the cannulation channel after placement, and the other anchor served as the uninjected control for each humerus. For the six matched pairs, the OsteoCrete group and the control group were rotated with respect to anterior vs posterior location within the lateral row position. After 15 minutes of the injection, straight pull-to-failure (12 in/min) was performed. Data were compared between the groups for significant (P < .05) differences using t-tests and Pearson correlation.
Continue to: IN VIVO STUDY METHODS
IN VIVO STUDY METHODS
With Institutional Animal Care and Use Committee approval, adult (age, 2-4 years) purpose-bred dogs (N = 8) underwent aseptic surgery of both forelimbs for rotator cuff (infraspinatus) tendon repair (Figure 1) and biceps tenodesis (Figure 2). For the rotator cuff repair, two 4.75-mm vented anchors (1 medial and 1 lateral) with FiberTape were used in a modified double-row technique to repair the acutely transected infraspinatus tendon. In one limb, 1 ml of OsteoCrete was injected through both anchors; the other limb served as the uninjected control. For the biceps tenodesis procedure, the long head of the biceps tendon was transected at its origin and whip-stitched. The tendon was transposed and inserted into a 7-mm diameter socket drilled into the proximal humerus using a tension-slide technique with a transcortical button for fixation. In one limb, 1 ml of OsteoCrete was injected into the socket prior to final tensioning and tying. In the contralateral limb, a 7-mm interference screw (Bio-Tenodesis™ Screw, Arthrex) was inserted into the socket after tensioning and tying. The dogs were allowed to perform out-of-kennel monitored exercise daily for a period of 12 weeks after surgery and were then sacrificed.
The infraspinatus and biceps bone-tendon-muscle units were excised en bloc. Custom-designed jigs were used for biomechanical testing of the bone-tendon-muscle units along the anatomical vector of muscle contraction. Optical markers were mounted at standardized anatomical locations. Elongation of the repair site was defined as the change in distance between markers and was measured to 0.01-mm resolution using an optical tracking system (Optotrak Certus, NDI), synchronized with measurement of the applied tension load. The bone-tendon-muscle units were loaded in tension to 3-mm elongation at a displacement controlled rate of 0.01 mm/s. Load at 1-mm, 2-mm, and 3-mm displacement of the tendon-bone junction was extracted from the load vs the displacement curve of each sample. Stiffness was calculated as the slope of the linear portion of the load vs the displacement curve.19,20
For histologic assessments, sections of each treatment site were obtained using a microsaw and alternated between decalcified and non-decalcified processing. For decalcified bone processing, formalin-fixed tissues were placed in 10% ethylenediaminetetraacetic acid with phosphate-buffered saline for 39 days and then processed routinely for the assessment of sections stained with hematoxylin and eosin (H&E), toluidine blue, and picrosirius red. For non-decalcified bone processing, the tissues were dehydrated through a series of graded ethyl alcohol solutions, embedded in PMMA, sectioned, and stained with toluidine blue and Goldner’s trichrome. Two pathologists who were blinded to the clinical application and the differences between techniques assessed the histologic sections and scored each section using the modified Bonar score that assesses cell morphology, collagen arrangement, cellularity, vascularity, and extracellular matrix using a 15-point scale, where a higher score indicates more pathology.21
Categorical data were compared for detecting statistically significant differences using the rank sum test. Continuous data were compared for identifying statistically significant differences using the t-test or one-way ANOVA. Significance was set at P < .05.
RESULTS
IN VITRO RESULTS
OsteoCrete-augmented anchors (mean = 225 N; range, 158-287 N) had significantly (P < .001) higher pull-out load-to-failure compared to that in the uninjected controls (mean = 161 N; range, 68-202 N), which translated to a 50% mean increase (range, 3%-134%) in load-to-failure (Table 1). For humeri with reduced bone quality (control anchors that failed at <160 N, 4 humeri), the mean increase in load-to-failure for OsteoCrete-augmented anchors was 99% (range, 58%-135%), with the difference between mean values being again significantly different (OsteoCrete mean = 205 N; control mean = 110 N, P < .001). When the control and OsteoCrete load-to-failure values were compared using Pearson correlation, a significantly strong positive correlation (r = 0.66, P = 0.02) was detected. When the control load-to-failure values were compared with its percent increase value when OsteoCrete was used, there was a significantly very strong negative correlation (r = −0.90, P < .001).
Table 1. Cadaveric Lateral Row Rotator Cuff Anchor Pull-To-Failure; Testing Occurred 15 Minutes Post-Injection
| Humerus No. | Control (N) | OsteoCrete (N)a | Percent Increase |
| 1-Right (PA) | 197.28 | 278.73 | 41% |
| 1-Left (AP) | 152.62 | 241.72 | 58% |
| 2-Right (PA) | 178.60 | 196.03 | 10% |
| 2-Left (AP) | 170.10 | 175.57 | 3% |
| 3-Right (PA) | 67.70 | 158.31 | 134% |
| 3-Left (AP) | 74.24 | 173.08 | 133% |
| 4-Right (PA) | 195.81 | 248.12 | 27% |
| 4-Left (AP) | 201.95 | 209.42 | 4% |
| 5-Right (PA) | 173.30 | 220.59 | 27% |
| 5-Left (AP) | 146.61 | 247.37 | 69% |
| 6-Right (PA) | 171.03 | 266.14 | 56% |
| 6-Left (AP) | 199.99 | 286.91 | 43% |
| Average | 160.77 + 45.60 | 225.17 + 43.08 | 50% + 44 |
aOsteoCrete (Bone Solutions Incorporated) resulted in significantly increased (P < 0.001) pull-to-failure. Abbreviations: AP, control anchor located in anterior position, OsteoCrete anchor located in posterior position; PA, control anchor located in posterior position, OsteoCrete anchor located in anterior position.
Continue to: IN VIVO RESULTS
IN VIVO RESULT
No intraoperative or postoperative complications were noted. All repairs were found to be intact based on the gross assessment and the completed biomechanical testing without failure. No statistically significant (P > 0.3) biomechanical differences were found between the techniques (Table 2). Histologic assessments showed low-to-mild pathology scores for all sites with no statistically significant (P > 0.3) differences between the techniques (Table 2). Both control and OsteoCrete rotator cuff repairs demonstrated tendon-to-bone integration via fibrous connective tissue attachment to bone. All anchors were in place with no evidence for loosening, tunnel expansion, or cyst formation. OsteoCrete-augmented anchor repairs were associated with cement remaining within their lumens along with a thin layer of cement interposed between the anchor and the bone interface around their entire periphery. The cement-bone interface was discrete with typical inflammatory cell infiltrate without evidence for infection, membrane or cyst formation, or other untoward pathologic responses. In the OsteoCrete biceps tenodesis group, the tendons filled the tunnels with a thin layer of cement remaining interposed between the tendon and the bone interface around the entire periphery. The tendon-cement-bone interface was discrete with typical inflammatory cell infiltrates and without evidence for infection, membrane or cyst formation, or other untoward pathologic responses. Tendon-to-bone integration was not observed in the control or OsteoCrete biceps tenodesis groups at the 12-week study endpoint. Representative histologic images of the rotator cuff tendon repairs and biceps tenodesis procedures are shown in Figures 3A, 3B and Figures 4A, 4B, respectively.
Table 2. Biomechanical Testing And Histologic Scoring Of Rotator Cuff And Biceps Tendon Repairs In A Preclinical Model
| Procedure | Force (N) at 1 mm | Force (N) at 2 mm | Force (N) at 3 mm | Stiffness (N/mm) | Histologic Score |
| Rotator Cuff - Control | 14.0 + 3.3 | 19.3 + 5.5 | 25.0 + 7.0 | 5.4 + 2.0 | 4.6 + 1.1 |
| Rotator Cuff - OsteoCrete (Bone Solutions Incorporated) | 14.8 + 3.7 | 20.4 + 6.0 | 26.4 + 8.5 | 6.3 + 2.5 | 3.9 + 1.7 |
| Biceps - Control | 23.1 + 6.2 | 35.5 + 8.5 | 52.6 + 15.0 | 17.8 + 6.4 | 3.4 + 1.2 |
| Biceps - OsteoCrete | 22.4 + 7.3 | 36.8 + 10.1 | 57.8 + 16.0 | 21.1 + 8.5 | 3.4 + 0.7 |
There were no significant differences (P < 0.05) between groups. Histologic scoring based on a 15-point scale with higher scores indicating more pathology.
DISCUSSION
The results of this study highlight the safety and efficacy of OsteoCrete in applications for the augmentation of anchor and tendon fixation in rotator cuff repair and biceps tenodesis procedures, respectively. Anchors augmented with OsteoCrete resulted in significantly increased load-to-failure pull-out strength 15 minutes after insertion. In addition, a very strong negative correlation was found between the percentage of improved load-to-failure after OsteoCrete injection and the bone quality of the humerus, which was based on the control load-to-failure values. In the validated preclinical model used in this study, OsteoCrete-based fixation was found to be noninferior to current standard-of-care techniques and was not associated with any untoward pathologic responses of humeral bone, rotator cuff tendon, or biceps tendon based on the biomechanical and histologic analyses. These data highlight the functional efficacy and biocompatibility of OsteoCrete when used for these common indications.
More than 270,000 rotator cuff procedures have been reported to be performed in the US annually (average patient age: 61 years for women, 56 years for men).22 Rotator cuff repair procedures have been associated with a 20% failure rate, with one of the causes being related to an inability for the tendon to heal, even with strong initial fixation.23 Rotator cuff repair techniques are being continuously optimized with the goal of improving patient outcomes. This goal is being realized, primarily with respect to re-tear rates.24,25 However, even with advanced techniques, there are still relatively high rates of failure reported, with increasing patient age serving as one of the primary negative prognostic factors.26 An older patient population is associated with decreased bone mass and strength, and postmenopausal females have decreased bone quality; these factors are associated with higher rotator cuff failure rates due to poor tendon healing, with anchor fixation failure also playing a role.27-29 Therefore, it is critically important to develop methods for augmenting implant and tendon fixation to bone to achieve functional healing. The results of this study suggest that OsteoCrete provides a valid method for accomplishing this goal based on the observation that proximal humeral anchor fixation was improved by 50% in load-to-failure 15 minutes post-injection with an even more profound impact on the anchors placed in poor-quality bone (99% increased load-to-failure 15 minutes post-injection). It is probable that the degree of improvement in fixation strength would be even greater 1 day after fixation, since the strength of OsteoCrete continues to increase over the first 30 hours of curing.
Based on the preclinical animal model data of this study, OsteoCrete augmentation of rotator cuff anchor fixation had no untoward effects on tendon healing or function and can be considered as safe for use. Previously published data also suggest that OsteoCrete may improve osseous replacement of anchors as a result of magnesium ion release, which can drive adjacent attachment and growth of osteoblasts, leading to enhanced new bone formation.9-16,18 As such, surgeons may consider this means of anchor augmentation in situations of questionable or poor-quality bone and/or when accelerated postoperative rehabilitation protocols are desired.
A very low early incidence failure rate (1.2%) has been reported when a distal biceps tendon rupture is repaired using cortical suspensory fixation in conjunction with an interference screw.30 When an early re-rupture does occur, the most common explanation for failure tends to be a lack of patient compliance, with excessive force being placed on the repair.31 This study was not meant to investigate the methods to increase the strength of a biceps tendon repair using OsteoCrete but instead to replace the interference screw with OsteoCrete in a safe and noninferior manner. Primary fixation was still dependent on cortical suspensory fixation; however, OsteoCrete was used to help aid in stabilization of the tendon without the need for interference screw fixation. Although rare, osteolysis and perianchor cyst formation have been reported adjacent to nonbiodegradable anchors (PEEK), along with several types of biodegradable anchors (PLLA, hydroxyapatite plus PLLA, β-tricalcium phosphate plus PLLA, and polyglycolic acid; the latter of the 3 resulted in the lowest incidence of perianchor cyst formation) in the shoulder and elbow.32-34 Whenever osteolysis or cyst formation occurs around an anchor, it leads to decreased bone volume and potential adjacent bone weakness, which may act as a stress riser, thus increasing the risk for fracture. This potential is probably more of a concern within the proximal radius where there is a decreased amount of bone stock around the anchor.34
Continue to: In this study...
In this study, a short-term 12-week analysis revealed no significant differences in the nondestructive biomechanical testing and histologic analysis results between the use of OsteoCrete and the use of a tenodesis anchor. These results indicate the potential for using OsteoCrete as an anchor replacement. The biceps tendon did not react negatively to the OsteoCrete material, which indicated that OsteoCrete can be used adjacent to tendons without the concern of weakening the tendon due to an inflammatory reaction. This being said, tendon-to-bone integration was not evident at this early time point. It would be helpful to further explore the potential of this technique with a longer-term study investigating tendon-to-bone integration in more detail. Ideally, a long-term study would reveal an increased amount of new bone formation within the socket when compared to that with the anchor comparison, similar to the results reported by Gulotta and colleagues16 when using a tendon for ACL reconstruction with OsteoCrete.
We do note several limitations in this study. The dogs used in this study were healthy with normal bone and tendon morphology, the tendons were transected and repaired during the course of the same surgery, and only 1 early time point was evaluated. Additional investigations continuing the characterization of these clinical applications using an osteopenic or osteoporotic preclinical model with chronic tendon pathology and longer-term evaluation are now warranted based on the positive findings of this initial work.
CONCLUSION
OsteoCrete augmentation significantly improved initial rotator cuff anchor fixation (human in vitro) and was safe and effective for anchor and tendon fixation in rotator cuff tendon repair and biceps tenodesis procedures (canine in vivo), respectively, when compared with the current standard-of-care. Of note, the significant improvements associated with OsteoCrete were the greatest in poor-quality bone. Based on these results and considering the previously discussed limitations, it can be concluded that OsteoCrete has the potential for safely providing improved suture anchor and tissue fixation in patients with poor bone or tissue quality. Further in vivo study toward potential clinical applications is warranted.
ABSTRACT
The aim of this study was to assess the efficacy and safety of a novel magnesium-based resorbable bone cement (OsteoCrete, Bone Solutions Incorporated) for anchor and tendon fixation.
Cadaveric humeral testing involved straight pull-to-failure of rotator cuff suture anchors; OsteoCrete was injected through one anchor, and a second anchor served as the uninjected control. Testing was conducted 15 minutes post-injection. A canine preclinical model was used to evaluate the safety of the following parameters: Rotator cuff repair: A double-row technique was used to repair transected infraspinatus tendons; OsteoCrete was injected through both anchors in one limb, and the contralateral limb served as the uninjected control. Biceps tenodesis: The transected biceps tendon was implanted into a proximal humeral socket with a transcortical button; OsteoCrete was injected into the socket of one limb, and a screw was used for final fixation in the contralateral control limb. Nondestructive biomechanical testing and histologic assessment were performed after 12 weeks.
OsteoCrete-augmented anchors showed significantly higher load-to-failure compared to that with uninjected controls. In cadaveric humeri with reduced bone quality, OsteoCrete increased the mean load-to-failure by 99%. Within the preclinical model, there were no complications or statistically significant biomechanical/histologic differences between the techniques.
OsteoCrete has the potential for safely providing improved suture anchor and tissue fixation in patients with poor bone or tissue quality.
Continue to: Calcium phosphate bone void fillers...
Calcium phosphate bone void fillers have been commonly used in orthopedic surgery for several applications, including, but not limited to, a variety of fracture fixation or augmentation procedures.1-8 Continuing research on calcium phosphates has evidenced that the addition of magnesium phosphate to the formulation results in improved reactivity of the bone void filler. An in vitro study demonstrated enhanced attachment and proliferation of MG63 osteoblast-like cells on calcium magnesium phosphate cement (CMPC), in comparison with calcium phosphate cement (CPC), along with increased cellular alkaline phosphatase activity.9 The authors further explored the proliferation rates of MG63 cells by comparing CMPC with CPC and magnesium phosphate cement (MPC), and observed significantly increased proliferation of cells on CMPC. They also compared CMPC and CPC using a rabbit bone void model and observed substantial CMPC resorption with new bone formation at the 3-month time point and further reported that the majority of the defect had filled with new bone at 6 months, whereas CPC resulted in <10% new bone formation after 6 months.10 The authors continued to study the differences between CPC, MPC, and CMPC and identified increased proliferation of bone marrow stromal cells (bMSCs), when the cells were associated with CMPC and MPC, and when compared to that with CPC. The osteogenic differentiation of bMSCs was highest in the CMPC and CPC groups, when compared to that in the MPC group, with no significant difference between the CMPC and CPC groups. The authors also compared these 3 different formulations using a rabbit maxillary sinus floor elevation model, in which CMPC resulted in increased new bone formation and mineralization compared to that with CPC and MPC, which was further enhanced with the addition of bMSCs.11
These studies highlight the importance of having both a magnesium phosphate and a calcium phosphate component for a resorbable cement intended for use as a bone void filler. The rationale behind this strategy is related to the release of magnesium ions from the magnesium phosphate component. Magnesium has been shown to increase the proliferation of bMSCs, improve the attachment and growth of osteoblasts, stimulate the proteins involved in bone regeneration, enhance new bone formation, and boost bone mineralization.12,13
OsteoCrete (Bone Solutions Incorporation) is a novel CMPC composed of magnesium oxide, monopotassium phosphate, monosodium phosphate, hydroxyapatite, and sucrose. OsteoCrete has been demonstrated to significantly increase peak torque-to-failure of stainless-steel cortical bone screw fixation, when compared with screw fixation without augmentation and screw fixation with calcium phosphate augmentation using an in vivo equine model. In the same study, the authors showed that OsteoCrete resulted in an interface toughness that was significantly increased compared to that with no treatment, CPC augmentation, and polymethylmethacrylate (PMMA) augmentation. At 6 months after implantation, woven bone had replaced 69% of the OsteoCrete at the screw interface, compared to 44% of that with CPC.14 An equine study examined the effects of OsteoCrete on bone stability and healing using a metatarsal osteotomy model; the study reported significantly improved radiographic callus formation and a greater amount of new bone formation within the fracture gap when compared to that with CPC augmentation or no augmentation. OsteoCrete also secured the fragment significantly better than the CPC and control groups based on a decreased fracture gap over time.15 Another study using a preclinical anterior cruciate ligament (ACL) reconstruction model reported that OsteoCrete resulted in significantly better new bone formation in the tibial tunnel, a smaller amount of fibrous tissue, more cartilage formation at the tendon-bone interface, and a higher ultimate load-to-failure compared to that with standard ACL reconstruction in the contralateral limb after 6 weeks.16 OsteoCrete and PMMA were evaluated in terms of biomechanical fixation of a stemless humeral prosthesis, with data showing that both groups have higher failure loads, failure displacements, and failure cycles when compared to those with the control, nonaugmented group.17 Another preclinical model evaluated cranial bone flap augmentation with 2 resorbable cements and highlighted faster cement resorption and replacement with bone, along with superior stability within the OsteoCrete group compared to that with CPC.18 In a preclinical bone void study conducted for obtaining US Food and Drug Administration 510(k) clearance, OsteoCrete resulted in 83% greater resorption than that with CPC after 12 weeks and 35% greater resorption at 26 weeks, with 84% of OsteoCrete being resorbed and replaced with woven or lamellar mineralized bone of normal morphology at the 26-week time point (unpublished data provided by Bone Solutions Incorporated [BSI]).
These data indicate that CMPCs such as OsteoCrete appear to have potential benefits for augmenting the healing of bone implants and bone soft tissue. Therefore, the objective of this study was to assess the safety and efficacy of OsteoCrete in applications for the augmentation of anchor and tendon fixation in rotator cuff repair and biceps tenodesis procedures, respectively. Improving healing for these 2 commonly performed procedures would be of great benefit in improving the functional outcomes and mitigating the complications and morbidity.
MATERIALS AND METHODS
IN VITRO STUDY METHODS
Cadaveric humeri (N = 12, six matched pairs) of females (age, 70-75 years) were warmed to 37°C prior to testing. Two 4.75-mm vented anchors (SwiveLock, Arthrex) with FiberTape were implanted into a lateral row position (anterior and posterior anchor positioning) of a double-row rotator cuff repair within the greater tuberosity. One anchor was injected with 1 ml of OsteoCrete–after preparation according to the manufacturer’s instructions–through the cannulation channel after placement, and the other anchor served as the uninjected control for each humerus. For the six matched pairs, the OsteoCrete group and the control group were rotated with respect to anterior vs posterior location within the lateral row position. After 15 minutes of the injection, straight pull-to-failure (12 in/min) was performed. Data were compared between the groups for significant (P < .05) differences using t-tests and Pearson correlation.
Continue to: IN VIVO STUDY METHODS
IN VIVO STUDY METHODS
With Institutional Animal Care and Use Committee approval, adult (age, 2-4 years) purpose-bred dogs (N = 8) underwent aseptic surgery of both forelimbs for rotator cuff (infraspinatus) tendon repair (Figure 1) and biceps tenodesis (Figure 2). For the rotator cuff repair, two 4.75-mm vented anchors (1 medial and 1 lateral) with FiberTape were used in a modified double-row technique to repair the acutely transected infraspinatus tendon. In one limb, 1 ml of OsteoCrete was injected through both anchors; the other limb served as the uninjected control. For the biceps tenodesis procedure, the long head of the biceps tendon was transected at its origin and whip-stitched. The tendon was transposed and inserted into a 7-mm diameter socket drilled into the proximal humerus using a tension-slide technique with a transcortical button for fixation. In one limb, 1 ml of OsteoCrete was injected into the socket prior to final tensioning and tying. In the contralateral limb, a 7-mm interference screw (Bio-Tenodesis™ Screw, Arthrex) was inserted into the socket after tensioning and tying. The dogs were allowed to perform out-of-kennel monitored exercise daily for a period of 12 weeks after surgery and were then sacrificed.
The infraspinatus and biceps bone-tendon-muscle units were excised en bloc. Custom-designed jigs were used for biomechanical testing of the bone-tendon-muscle units along the anatomical vector of muscle contraction. Optical markers were mounted at standardized anatomical locations. Elongation of the repair site was defined as the change in distance between markers and was measured to 0.01-mm resolution using an optical tracking system (Optotrak Certus, NDI), synchronized with measurement of the applied tension load. The bone-tendon-muscle units were loaded in tension to 3-mm elongation at a displacement controlled rate of 0.01 mm/s. Load at 1-mm, 2-mm, and 3-mm displacement of the tendon-bone junction was extracted from the load vs the displacement curve of each sample. Stiffness was calculated as the slope of the linear portion of the load vs the displacement curve.19,20
For histologic assessments, sections of each treatment site were obtained using a microsaw and alternated between decalcified and non-decalcified processing. For decalcified bone processing, formalin-fixed tissues were placed in 10% ethylenediaminetetraacetic acid with phosphate-buffered saline for 39 days and then processed routinely for the assessment of sections stained with hematoxylin and eosin (H&E), toluidine blue, and picrosirius red. For non-decalcified bone processing, the tissues were dehydrated through a series of graded ethyl alcohol solutions, embedded in PMMA, sectioned, and stained with toluidine blue and Goldner’s trichrome. Two pathologists who were blinded to the clinical application and the differences between techniques assessed the histologic sections and scored each section using the modified Bonar score that assesses cell morphology, collagen arrangement, cellularity, vascularity, and extracellular matrix using a 15-point scale, where a higher score indicates more pathology.21
Categorical data were compared for detecting statistically significant differences using the rank sum test. Continuous data were compared for identifying statistically significant differences using the t-test or one-way ANOVA. Significance was set at P < .05.
RESULTS
IN VITRO RESULTS
OsteoCrete-augmented anchors (mean = 225 N; range, 158-287 N) had significantly (P < .001) higher pull-out load-to-failure compared to that in the uninjected controls (mean = 161 N; range, 68-202 N), which translated to a 50% mean increase (range, 3%-134%) in load-to-failure (Table 1). For humeri with reduced bone quality (control anchors that failed at <160 N, 4 humeri), the mean increase in load-to-failure for OsteoCrete-augmented anchors was 99% (range, 58%-135%), with the difference between mean values being again significantly different (OsteoCrete mean = 205 N; control mean = 110 N, P < .001). When the control and OsteoCrete load-to-failure values were compared using Pearson correlation, a significantly strong positive correlation (r = 0.66, P = 0.02) was detected. When the control load-to-failure values were compared with its percent increase value when OsteoCrete was used, there was a significantly very strong negative correlation (r = −0.90, P < .001).
Table 1. Cadaveric Lateral Row Rotator Cuff Anchor Pull-To-Failure; Testing Occurred 15 Minutes Post-Injection
| Humerus No. | Control (N) | OsteoCrete (N)a | Percent Increase |
| 1-Right (PA) | 197.28 | 278.73 | 41% |
| 1-Left (AP) | 152.62 | 241.72 | 58% |
| 2-Right (PA) | 178.60 | 196.03 | 10% |
| 2-Left (AP) | 170.10 | 175.57 | 3% |
| 3-Right (PA) | 67.70 | 158.31 | 134% |
| 3-Left (AP) | 74.24 | 173.08 | 133% |
| 4-Right (PA) | 195.81 | 248.12 | 27% |
| 4-Left (AP) | 201.95 | 209.42 | 4% |
| 5-Right (PA) | 173.30 | 220.59 | 27% |
| 5-Left (AP) | 146.61 | 247.37 | 69% |
| 6-Right (PA) | 171.03 | 266.14 | 56% |
| 6-Left (AP) | 199.99 | 286.91 | 43% |
| Average | 160.77 + 45.60 | 225.17 + 43.08 | 50% + 44 |
aOsteoCrete (Bone Solutions Incorporated) resulted in significantly increased (P < 0.001) pull-to-failure. Abbreviations: AP, control anchor located in anterior position, OsteoCrete anchor located in posterior position; PA, control anchor located in posterior position, OsteoCrete anchor located in anterior position.
Continue to: IN VIVO RESULTS
IN VIVO RESULT
No intraoperative or postoperative complications were noted. All repairs were found to be intact based on the gross assessment and the completed biomechanical testing without failure. No statistically significant (P > 0.3) biomechanical differences were found between the techniques (Table 2). Histologic assessments showed low-to-mild pathology scores for all sites with no statistically significant (P > 0.3) differences between the techniques (Table 2). Both control and OsteoCrete rotator cuff repairs demonstrated tendon-to-bone integration via fibrous connective tissue attachment to bone. All anchors were in place with no evidence for loosening, tunnel expansion, or cyst formation. OsteoCrete-augmented anchor repairs were associated with cement remaining within their lumens along with a thin layer of cement interposed between the anchor and the bone interface around their entire periphery. The cement-bone interface was discrete with typical inflammatory cell infiltrate without evidence for infection, membrane or cyst formation, or other untoward pathologic responses. In the OsteoCrete biceps tenodesis group, the tendons filled the tunnels with a thin layer of cement remaining interposed between the tendon and the bone interface around the entire periphery. The tendon-cement-bone interface was discrete with typical inflammatory cell infiltrates and without evidence for infection, membrane or cyst formation, or other untoward pathologic responses. Tendon-to-bone integration was not observed in the control or OsteoCrete biceps tenodesis groups at the 12-week study endpoint. Representative histologic images of the rotator cuff tendon repairs and biceps tenodesis procedures are shown in Figures 3A, 3B and Figures 4A, 4B, respectively.
Table 2. Biomechanical Testing And Histologic Scoring Of Rotator Cuff And Biceps Tendon Repairs In A Preclinical Model
| Procedure | Force (N) at 1 mm | Force (N) at 2 mm | Force (N) at 3 mm | Stiffness (N/mm) | Histologic Score |
| Rotator Cuff - Control | 14.0 + 3.3 | 19.3 + 5.5 | 25.0 + 7.0 | 5.4 + 2.0 | 4.6 + 1.1 |
| Rotator Cuff - OsteoCrete (Bone Solutions Incorporated) | 14.8 + 3.7 | 20.4 + 6.0 | 26.4 + 8.5 | 6.3 + 2.5 | 3.9 + 1.7 |
| Biceps - Control | 23.1 + 6.2 | 35.5 + 8.5 | 52.6 + 15.0 | 17.8 + 6.4 | 3.4 + 1.2 |
| Biceps - OsteoCrete | 22.4 + 7.3 | 36.8 + 10.1 | 57.8 + 16.0 | 21.1 + 8.5 | 3.4 + 0.7 |
There were no significant differences (P < 0.05) between groups. Histologic scoring based on a 15-point scale with higher scores indicating more pathology.
DISCUSSION
The results of this study highlight the safety and efficacy of OsteoCrete in applications for the augmentation of anchor and tendon fixation in rotator cuff repair and biceps tenodesis procedures, respectively. Anchors augmented with OsteoCrete resulted in significantly increased load-to-failure pull-out strength 15 minutes after insertion. In addition, a very strong negative correlation was found between the percentage of improved load-to-failure after OsteoCrete injection and the bone quality of the humerus, which was based on the control load-to-failure values. In the validated preclinical model used in this study, OsteoCrete-based fixation was found to be noninferior to current standard-of-care techniques and was not associated with any untoward pathologic responses of humeral bone, rotator cuff tendon, or biceps tendon based on the biomechanical and histologic analyses. These data highlight the functional efficacy and biocompatibility of OsteoCrete when used for these common indications.
More than 270,000 rotator cuff procedures have been reported to be performed in the US annually (average patient age: 61 years for women, 56 years for men).22 Rotator cuff repair procedures have been associated with a 20% failure rate, with one of the causes being related to an inability for the tendon to heal, even with strong initial fixation.23 Rotator cuff repair techniques are being continuously optimized with the goal of improving patient outcomes. This goal is being realized, primarily with respect to re-tear rates.24,25 However, even with advanced techniques, there are still relatively high rates of failure reported, with increasing patient age serving as one of the primary negative prognostic factors.26 An older patient population is associated with decreased bone mass and strength, and postmenopausal females have decreased bone quality; these factors are associated with higher rotator cuff failure rates due to poor tendon healing, with anchor fixation failure also playing a role.27-29 Therefore, it is critically important to develop methods for augmenting implant and tendon fixation to bone to achieve functional healing. The results of this study suggest that OsteoCrete provides a valid method for accomplishing this goal based on the observation that proximal humeral anchor fixation was improved by 50% in load-to-failure 15 minutes post-injection with an even more profound impact on the anchors placed in poor-quality bone (99% increased load-to-failure 15 minutes post-injection). It is probable that the degree of improvement in fixation strength would be even greater 1 day after fixation, since the strength of OsteoCrete continues to increase over the first 30 hours of curing.
Based on the preclinical animal model data of this study, OsteoCrete augmentation of rotator cuff anchor fixation had no untoward effects on tendon healing or function and can be considered as safe for use. Previously published data also suggest that OsteoCrete may improve osseous replacement of anchors as a result of magnesium ion release, which can drive adjacent attachment and growth of osteoblasts, leading to enhanced new bone formation.9-16,18 As such, surgeons may consider this means of anchor augmentation in situations of questionable or poor-quality bone and/or when accelerated postoperative rehabilitation protocols are desired.
A very low early incidence failure rate (1.2%) has been reported when a distal biceps tendon rupture is repaired using cortical suspensory fixation in conjunction with an interference screw.30 When an early re-rupture does occur, the most common explanation for failure tends to be a lack of patient compliance, with excessive force being placed on the repair.31 This study was not meant to investigate the methods to increase the strength of a biceps tendon repair using OsteoCrete but instead to replace the interference screw with OsteoCrete in a safe and noninferior manner. Primary fixation was still dependent on cortical suspensory fixation; however, OsteoCrete was used to help aid in stabilization of the tendon without the need for interference screw fixation. Although rare, osteolysis and perianchor cyst formation have been reported adjacent to nonbiodegradable anchors (PEEK), along with several types of biodegradable anchors (PLLA, hydroxyapatite plus PLLA, β-tricalcium phosphate plus PLLA, and polyglycolic acid; the latter of the 3 resulted in the lowest incidence of perianchor cyst formation) in the shoulder and elbow.32-34 Whenever osteolysis or cyst formation occurs around an anchor, it leads to decreased bone volume and potential adjacent bone weakness, which may act as a stress riser, thus increasing the risk for fracture. This potential is probably more of a concern within the proximal radius where there is a decreased amount of bone stock around the anchor.34
Continue to: In this study...
In this study, a short-term 12-week analysis revealed no significant differences in the nondestructive biomechanical testing and histologic analysis results between the use of OsteoCrete and the use of a tenodesis anchor. These results indicate the potential for using OsteoCrete as an anchor replacement. The biceps tendon did not react negatively to the OsteoCrete material, which indicated that OsteoCrete can be used adjacent to tendons without the concern of weakening the tendon due to an inflammatory reaction. This being said, tendon-to-bone integration was not evident at this early time point. It would be helpful to further explore the potential of this technique with a longer-term study investigating tendon-to-bone integration in more detail. Ideally, a long-term study would reveal an increased amount of new bone formation within the socket when compared to that with the anchor comparison, similar to the results reported by Gulotta and colleagues16 when using a tendon for ACL reconstruction with OsteoCrete.
We do note several limitations in this study. The dogs used in this study were healthy with normal bone and tendon morphology, the tendons were transected and repaired during the course of the same surgery, and only 1 early time point was evaluated. Additional investigations continuing the characterization of these clinical applications using an osteopenic or osteoporotic preclinical model with chronic tendon pathology and longer-term evaluation are now warranted based on the positive findings of this initial work.
CONCLUSION
OsteoCrete augmentation significantly improved initial rotator cuff anchor fixation (human in vitro) and was safe and effective for anchor and tendon fixation in rotator cuff tendon repair and biceps tenodesis procedures (canine in vivo), respectively, when compared with the current standard-of-care. Of note, the significant improvements associated with OsteoCrete were the greatest in poor-quality bone. Based on these results and considering the previously discussed limitations, it can be concluded that OsteoCrete has the potential for safely providing improved suture anchor and tissue fixation in patients with poor bone or tissue quality. Further in vivo study toward potential clinical applications is warranted.
1. Russell TA, Leighton RK, Group A-BTPFS. Comparison of autogenous bone graft and endothermic calcium phosphate cement for defect augmentation in tibial plateau fractures. A multicenter, prospective, randomized study. J Bone Joint Surg Am. 2008; 90(10):2057-2061. doi:10.2106/JBJS.G.01191.
2. Egol KA, Sugi MT, Ong CC, Montero N, Davidovitch R, Zuckerman JD. Fracture site augmentation with calcium phosphate cement reduces screw penetration after open reduction-internal fixation of proximal humeral fractures. J Shoulder Elbow Surg. 2012; 21(6):741-748. doi:10.1016/j.jse.2011.09.017.
3. Cassidy C, Jupiter JB, Cohen M, et al. Norian SRS cement compared with conventional fixation in distal radial fractures. A randomized study. J Bone Joint Surg Am. 2003;85-A(11):2127-2137.
4. Mattsson P, Alberts A, Dahlberg G, Sohlman M, Hyldahl HC, Larsson S. Resorbable cement for the augmentation of internally-fixed unstable trochanteric fractures. A prospective, randomised multicentre study. J Bone Joint Surg Br. 2005;87(9):1203-1209.
5. Cohen SB, Sharkey PF. Subchondroplasty for treating bone marrow lesions. J Knee Surg. 2016;29(07):555-563. doi:10.1302/0301-620X.87B9.15792.
6. Guida P, Ragozzino R, Sorrentino B, et al. Three-in-One minimally invasive approach to surgical treatment of pediatric pathological fractures with wide bone loss through bone cysts: ESIN, curettage and packing with injectable HA bone substitute. A retrospective series of 116 cases. Injury. 2016;47(6):1222-1228. doi:10.1016/j.injury.2016.01.006.
7. Maestretti G, Sutter P, Monnard E, et al. A prospective study of percutaneous balloon kyphoplasty with calcium phosphate cement in traumatic vertebral fractures: 10-year results. Eur Spine J. 2014;23(6):1354-1360. doi:10.1007/s00586-014-3206-1.
8. Nakano M, Hirano N, Zukawa M, et al. Vertebroplasty using calcium phosphate cement for osteoporotic vertebral fractures: study of outcomes at a minimum follow-up of two years. Asian Spine J. 2012;6(1):34-42. doi:10.4184/asj.2012.6.1.34.
9. Jia J, Zhou H, Wei J, et al. Development of magnesium calcium phosphate biocement for bone regeneration. J R Soc Interface. 2010;7(49):1171-1180. doi:10.1098/rsif.2009.0559.
10. Wu F, Wei J, Guo H, Chen F, Hong H, Liu C. Self-setting bioactive calcium-magnesium phosphate cement with high strength and degradability for bone regeneration. Acta Biomater. 2008;4(6):1873-1884. doi:10.1016/j.actbio.2008.06.020.
11. Zeng D, Xia L, Zhang W, et al. Maxillary sinus floor elevation using a tissue-engineered bone with calcium-magnesium phosphate cement and bone marrow stromal cells in rabbits. Tissue Eng Part A. 2012;18(7-8):870-881. doi:10.1089/ten.TEA.2011.0379.
12. Yoshizawa S, Brown A, Barchowsky A, Sfeir C. Magnesium ion stimulation of bone marrow stromal cells enhances osteogenic activity, simulating the effect of magnesium alloy degradation. Acta Biomater. 2014;10(6):2834-2842. doi:10.1016/j.actbio.2014.02.002.
13. Liao J, Qu Y, Chu B, Zhang X, Qian Z. Biodegradable CSMA/PECA/Graphene porous hybrid scaffold for cartilage tissue engineering. Sci Rep. 2015;5:9879. doi:10.1038/srep09879.
14. Hirvinen LJ, Litsky AS, Samii VF, Weisbrode SE, Bertone AL. Influence of bone cements on bone-screw interfaces in the third metacarpal and third metatarsal bones of horses. Am J Vet Res. 2009;70(8):964-972. doi:10.2460/ajvr.70.8.964.
15. Waselau M, Samii VF, Weisbrode SE, Litsky AS, Bertone AL. Effects of a magnesium adhesive cement on bone stability and healing following a metatarsal osteotomy in horses. Am J Vet Res. 2007;68(4):370-378. doi:10.2460/ajvr.68.4.370.
16. Gulotta LV, Kovacevic D, Ying L, Ehteshami JR, Montgomery S, Rodeo SA. Augmentation of tendon-to-bone healing with a magnesium-based bone adhesive. Am J Sports Med. 2008;36(7):1290-1297. doi:10.1177/0363546508314396.
17. Kim MS, Kovacevic D, Milks RA, et al. Bone graft substitute provides metaphyseal fixation for a stemless humeral implant. Orthopedics. 2015;38(7):e597-e603. doi:10.3928/01477447-20150701-58.
18. Schendel SA, Peauroi J. Magnesium-based bone cement and bone void filler: preliminary experimental studies. J Craniofac Surg. 2009;20(2):461-464. doi:10.1097/SCS.0b013e31819b9819.
19. Pfeiffer FM, Smith MJ, Cook JL, Kuroki K. The histologic and biomechanical response of two commercially available small glenoid anchors for use in labral repairs. J Shoulder Elbow Surg. 2014;23(8):1156-1161. doi:10.1016/j.jse.2013.12.036.
20. Smith MJ, Cook JL, Kuroki K, et al. Comparison of a novel bone-tendon allograft with a human dermis-derived patch for repair of chronic large rotator cuff tears using a canine model. Arthroscopy. 2012;28(2):169-177. doi:10.1016/j.arthro.2011.08.296.
21. Fearon A, Dahlstrom JE, Twin J, Cook J, Scott A. The Bonar score revisited: region of evaluation significantly influences the standardized assessment of tendon degeneration. J Sci Med Sport. 2014;17(4):346-350. doi:10.1016/j.jsams.2013.07.008.
22. Colvin AC, Egorova N, Harrison AK, Moskowitz A, Flatow EL. National trends in rotator cuff repair. J Bone Joint Surg Am. 2012;94(3):227-233. doi:10.2106/JBJS.J.00739.
23. Lädermann A, Denard PJ, Burkhart SS. Management of failed rotator cuff repair: a systematic review. J ISAKOS. 2016;1(1):32-37. doi:10.1136/jisakos-2015-000027.
24. Franceschi F, Papalia R, Franceschetti E, et al. Double-Row repair lowers the retear risk after accelerated rehabilitation. Am J Sports Med. 2016;44(4):948-956. doi:10.1177/0363546515623031.
25. Wang E, Wang L, Gao P, Li Z, Zhou X, Wang S. Single-versus double-row arthroscopic rotator cuff repair in massive tears. Med Sci Monit. 2015;21:1556-1561. doi:10.12659/MSM.893058.
26. Abtahi AM, Granger EK, Tashjian RZ. Factors affecting healing after arthroscopic rotator cuff repair. World J Orthop. 2015;6(2):211-220. doi:10.5312/wjo.v6.i2.211.
27. Chung SW, Oh JH, Gong HS, Kim JY, Kim SH. Factors affecting rotator cuff healing after arthroscopic repair: osteoporosis as one of the independent risk factors. Am J Sports Med. 2011;39(10):2099-2107. doi:10.1177/0363546511415659.
28. Tsiouri C, Mok DH. Early pullout of lateral row knotless anchor in rotator cuff repair. Int J Shoulder Surg. 2009;3(3):63-65. doi:10.4103/0973-6042.59972.
29. Boskey AL, Coleman R. Aging and bone. J Dent Res. 2010;89(12):1333-1348. doi:10.1177/0022034510377791.
30. Cusick MC, Cottrell BJ, Cain RA, Mighell MA. Low incidence of tendon rerupture after distal biceps repair by cortical button and interference screw. J Shoulder Elbow Surg. 2014;23(10):1532-1536. doi:10.1016/j.jse.2014.04.013.
31. Hinchey JW, Aronowitz JG, Sanchez-Sotelo J, Morrey BF. Re-rupture rate of primarily repaired distal biceps tendon injuries. J Shoulder Elbow Surg. 2014;23(6):850-854. doi:10.1016/j.jse.2014.02.006.
32. Shahrulazua A, Duckworth D, Bokor DJ. Perianchor radiolucency following PEEK suture anchor application associated with recurrent shoulder dislocation: a case report. Clin Ter. 2014;165(1):31-34. doi:10.7471/CT.2014.1658.
33. Kim SH, Kim dY, Kwon JE, Park JS, Oh JH. Perianchor cyst formation around biocomposite biodegradable suture anchors after rotator cuff repair. Am J Sports Med. 2015;43(12):2907-2912. doi:10.1177/0363546515608484
34. Potapov A, Laflamme YG, Gagnon S, Canet F, Rouleau DM. Progressive osteolysis of the radius after distal biceps tendon repair with the bioabsorbable screw. J Shoulder Elbow Surg. 2011;20(5):819-826. doi:10.1016/j.jse.2011.02.021.
1. Russell TA, Leighton RK, Group A-BTPFS. Comparison of autogenous bone graft and endothermic calcium phosphate cement for defect augmentation in tibial plateau fractures. A multicenter, prospective, randomized study. J Bone Joint Surg Am. 2008; 90(10):2057-2061. doi:10.2106/JBJS.G.01191.
2. Egol KA, Sugi MT, Ong CC, Montero N, Davidovitch R, Zuckerman JD. Fracture site augmentation with calcium phosphate cement reduces screw penetration after open reduction-internal fixation of proximal humeral fractures. J Shoulder Elbow Surg. 2012; 21(6):741-748. doi:10.1016/j.jse.2011.09.017.
3. Cassidy C, Jupiter JB, Cohen M, et al. Norian SRS cement compared with conventional fixation in distal radial fractures. A randomized study. J Bone Joint Surg Am. 2003;85-A(11):2127-2137.
4. Mattsson P, Alberts A, Dahlberg G, Sohlman M, Hyldahl HC, Larsson S. Resorbable cement for the augmentation of internally-fixed unstable trochanteric fractures. A prospective, randomised multicentre study. J Bone Joint Surg Br. 2005;87(9):1203-1209.
5. Cohen SB, Sharkey PF. Subchondroplasty for treating bone marrow lesions. J Knee Surg. 2016;29(07):555-563. doi:10.1302/0301-620X.87B9.15792.
6. Guida P, Ragozzino R, Sorrentino B, et al. Three-in-One minimally invasive approach to surgical treatment of pediatric pathological fractures with wide bone loss through bone cysts: ESIN, curettage and packing with injectable HA bone substitute. A retrospective series of 116 cases. Injury. 2016;47(6):1222-1228. doi:10.1016/j.injury.2016.01.006.
7. Maestretti G, Sutter P, Monnard E, et al. A prospective study of percutaneous balloon kyphoplasty with calcium phosphate cement in traumatic vertebral fractures: 10-year results. Eur Spine J. 2014;23(6):1354-1360. doi:10.1007/s00586-014-3206-1.
8. Nakano M, Hirano N, Zukawa M, et al. Vertebroplasty using calcium phosphate cement for osteoporotic vertebral fractures: study of outcomes at a minimum follow-up of two years. Asian Spine J. 2012;6(1):34-42. doi:10.4184/asj.2012.6.1.34.
9. Jia J, Zhou H, Wei J, et al. Development of magnesium calcium phosphate biocement for bone regeneration. J R Soc Interface. 2010;7(49):1171-1180. doi:10.1098/rsif.2009.0559.
10. Wu F, Wei J, Guo H, Chen F, Hong H, Liu C. Self-setting bioactive calcium-magnesium phosphate cement with high strength and degradability for bone regeneration. Acta Biomater. 2008;4(6):1873-1884. doi:10.1016/j.actbio.2008.06.020.
11. Zeng D, Xia L, Zhang W, et al. Maxillary sinus floor elevation using a tissue-engineered bone with calcium-magnesium phosphate cement and bone marrow stromal cells in rabbits. Tissue Eng Part A. 2012;18(7-8):870-881. doi:10.1089/ten.TEA.2011.0379.
12. Yoshizawa S, Brown A, Barchowsky A, Sfeir C. Magnesium ion stimulation of bone marrow stromal cells enhances osteogenic activity, simulating the effect of magnesium alloy degradation. Acta Biomater. 2014;10(6):2834-2842. doi:10.1016/j.actbio.2014.02.002.
13. Liao J, Qu Y, Chu B, Zhang X, Qian Z. Biodegradable CSMA/PECA/Graphene porous hybrid scaffold for cartilage tissue engineering. Sci Rep. 2015;5:9879. doi:10.1038/srep09879.
14. Hirvinen LJ, Litsky AS, Samii VF, Weisbrode SE, Bertone AL. Influence of bone cements on bone-screw interfaces in the third metacarpal and third metatarsal bones of horses. Am J Vet Res. 2009;70(8):964-972. doi:10.2460/ajvr.70.8.964.
15. Waselau M, Samii VF, Weisbrode SE, Litsky AS, Bertone AL. Effects of a magnesium adhesive cement on bone stability and healing following a metatarsal osteotomy in horses. Am J Vet Res. 2007;68(4):370-378. doi:10.2460/ajvr.68.4.370.
16. Gulotta LV, Kovacevic D, Ying L, Ehteshami JR, Montgomery S, Rodeo SA. Augmentation of tendon-to-bone healing with a magnesium-based bone adhesive. Am J Sports Med. 2008;36(7):1290-1297. doi:10.1177/0363546508314396.
17. Kim MS, Kovacevic D, Milks RA, et al. Bone graft substitute provides metaphyseal fixation for a stemless humeral implant. Orthopedics. 2015;38(7):e597-e603. doi:10.3928/01477447-20150701-58.
18. Schendel SA, Peauroi J. Magnesium-based bone cement and bone void filler: preliminary experimental studies. J Craniofac Surg. 2009;20(2):461-464. doi:10.1097/SCS.0b013e31819b9819.
19. Pfeiffer FM, Smith MJ, Cook JL, Kuroki K. The histologic and biomechanical response of two commercially available small glenoid anchors for use in labral repairs. J Shoulder Elbow Surg. 2014;23(8):1156-1161. doi:10.1016/j.jse.2013.12.036.
20. Smith MJ, Cook JL, Kuroki K, et al. Comparison of a novel bone-tendon allograft with a human dermis-derived patch for repair of chronic large rotator cuff tears using a canine model. Arthroscopy. 2012;28(2):169-177. doi:10.1016/j.arthro.2011.08.296.
21. Fearon A, Dahlstrom JE, Twin J, Cook J, Scott A. The Bonar score revisited: region of evaluation significantly influences the standardized assessment of tendon degeneration. J Sci Med Sport. 2014;17(4):346-350. doi:10.1016/j.jsams.2013.07.008.
22. Colvin AC, Egorova N, Harrison AK, Moskowitz A, Flatow EL. National trends in rotator cuff repair. J Bone Joint Surg Am. 2012;94(3):227-233. doi:10.2106/JBJS.J.00739.
23. Lädermann A, Denard PJ, Burkhart SS. Management of failed rotator cuff repair: a systematic review. J ISAKOS. 2016;1(1):32-37. doi:10.1136/jisakos-2015-000027.
24. Franceschi F, Papalia R, Franceschetti E, et al. Double-Row repair lowers the retear risk after accelerated rehabilitation. Am J Sports Med. 2016;44(4):948-956. doi:10.1177/0363546515623031.
25. Wang E, Wang L, Gao P, Li Z, Zhou X, Wang S. Single-versus double-row arthroscopic rotator cuff repair in massive tears. Med Sci Monit. 2015;21:1556-1561. doi:10.12659/MSM.893058.
26. Abtahi AM, Granger EK, Tashjian RZ. Factors affecting healing after arthroscopic rotator cuff repair. World J Orthop. 2015;6(2):211-220. doi:10.5312/wjo.v6.i2.211.
27. Chung SW, Oh JH, Gong HS, Kim JY, Kim SH. Factors affecting rotator cuff healing after arthroscopic repair: osteoporosis as one of the independent risk factors. Am J Sports Med. 2011;39(10):2099-2107. doi:10.1177/0363546511415659.
28. Tsiouri C, Mok DH. Early pullout of lateral row knotless anchor in rotator cuff repair. Int J Shoulder Surg. 2009;3(3):63-65. doi:10.4103/0973-6042.59972.
29. Boskey AL, Coleman R. Aging and bone. J Dent Res. 2010;89(12):1333-1348. doi:10.1177/0022034510377791.
30. Cusick MC, Cottrell BJ, Cain RA, Mighell MA. Low incidence of tendon rerupture after distal biceps repair by cortical button and interference screw. J Shoulder Elbow Surg. 2014;23(10):1532-1536. doi:10.1016/j.jse.2014.04.013.
31. Hinchey JW, Aronowitz JG, Sanchez-Sotelo J, Morrey BF. Re-rupture rate of primarily repaired distal biceps tendon injuries. J Shoulder Elbow Surg. 2014;23(6):850-854. doi:10.1016/j.jse.2014.02.006.
32. Shahrulazua A, Duckworth D, Bokor DJ. Perianchor radiolucency following PEEK suture anchor application associated with recurrent shoulder dislocation: a case report. Clin Ter. 2014;165(1):31-34. doi:10.7471/CT.2014.1658.
33. Kim SH, Kim dY, Kwon JE, Park JS, Oh JH. Perianchor cyst formation around biocomposite biodegradable suture anchors after rotator cuff repair. Am J Sports Med. 2015;43(12):2907-2912. doi:10.1177/0363546515608484
34. Potapov A, Laflamme YG, Gagnon S, Canet F, Rouleau DM. Progressive osteolysis of the radius after distal biceps tendon repair with the bioabsorbable screw. J Shoulder Elbow Surg. 2011;20(5):819-826. doi:10.1016/j.jse.2011.02.021.
TAKE-HOME POINTS
- OsteoCrete, a magnesium-based resorbable bone cement, has potential to safely and effectively augment suture anchor fixation.
- OsteoCrete increases anchor pull-out strength within 15 minutes of injection.
- OsteoCrete has a more profound impact on anchors when used within bone of decreased density and quality.
- OsteoCrete does not result in any untoward effect when placed near, or in contact with, rotator cuff or biceps tendons during fixation procedures.
- OsteoCrete can potentially be used to replace the anchor within tenodesis procedures that utilize transcortical button fixation in addition to anchor fixation.
Patient-Specific Implants in Severe Glenoid Bone Loss
ABSTRACT
Complex glenoid bone deformities present the treating surgeon with a complex reconstructive challenge. Although glenoid bone loss can be encountered in the primary setting (degenerative, congenital, post-traumatic), severe glenoid bone loss is encountered in most revision total shoulder arthroplasties. Severe glenoid bone loss is treated with various techniques including hemiarthroplasty, eccentric reaming, and glenoid reconstruction with bone autografts and allografts. Despite encouraging short- to mid-term results reported with these reconstruction techniques, the clinical and radiographic outcomes remain inconsistent and the high number of complications is a concern. To overcome this problem, more recently augmented components and patient specific implants were introduced. Using the computer-aided design and computer-aided manufacturing technology patient-specific implants have been created to reconstruct the glenoid vault in cases of severe glenoid bone loss.
In this article we describe a patient specific glenoid implant, its indication, technical aspects and surgical technique, based on the author's experience as well as a review of the current literature on custom glenoid implants.
Continue to: Total shoulder arthroplasty...
Total shoulder arthroplasty (TSA) is an effective operation for providing pain relief and improving function in patients with end-stage degenerative shoulder disease that is nonresponsive to nonoperative treatments.1-4 With the increasing number of arthroplasties performed, and the expanding indication for shoulder arthroplasty, the number of revision shoulder arthroplasties is also increasing.5-14 Complex glenoid bone deformities present the treating surgeon with a complex reconstructive challenge. Although glenoid bone loss can be seen in the primary setting (degenerative, congenital, and post-traumatic), severe glenoid bone loss is encountered mostly in revision TSAs.
Historically, patients with severe glenoid bone loss were treated with a hemiarthroplasty.15-17 However, due to inferior outcomes associated with the use of shoulder hemiarthroplasties compared with TSA in these cases,18-20 various techniques were developed with the aim of realigning the glenoid axis and securing the implants into the deficient glenoid vault.21-25 Options have included eccentric reaming, glenoid reconstruction with bone autografts and allografts, and more recently augmented components and patient-specific implants. Studies with eccentric reaming and reconstruction with bone graft during complex shoulder arthroplasty have reported encouraging short- to mid-term results, but the clinical and radiographic outcomes remain inconsistent, and the high number of complications is a concern.25-28
Complications with these techniques include component loosening, graft resorption, nonunion, failure of graft incorporation, infection, and instability.25-28
Computer-aided design and computer-aided manufacturing (CAD/CAM) of patient-specific implants have been used successfully by hip arthroplasty surgeons to deal with complex acetabular reconstructions in the setting of severe bone loss. More recently, the same technology has been used to reconstruct the glenoid vault in cases of severe glenoid bone loss.
In this article, we describe a patient-specific glenoid implant, its indication, and both technical aspects and the surgical technique, based on the authors’ experience as well as a review of the current literature on custom glenoid implants.
Continue to: PATIENT-SPECIFIC GLENOID COMPONENT
PATIENT-SPECIFIC GLENOID COMPONENT
The Vault Reconstruction System ([VRS], Zimmer Biomet) is a patient-specific glenoid vault reconstruction system developed with the use of CAD/CAM to address severe glenoid bone loss encountered during shoulder arthroplasty. For several years, the VRS was available only as a custom implant according to the US Food and Drug Administration rules, and therefore its use was limited to a few cases per year. Recently, a 510(k) envelope clearance was granted to use the VRS in reverse TSA to address significant glenoid bone defects.
The VRS is made of porous plasma spray titanium to provide high strength and flexibility, and allows for biologic fixation. This system can accommodate a restricted bone loss envelope of about 50 mm × 50 mm × 35 mm according to the previous experience of the manufacturer in the custom scenario, covering 96% of defects previously addressed. One 6.5-mm nonlocking central screw and a minimum of four 4.75-mm nonlocking or locking peripheral screws are required for optimal fixation of the implant in the native scapula. A custom boss can be added in to enhance fixation in the native scapula when the bone is sufficient. To facilitate the surgical procedure, a trial implant, a bone model of the scapula, and a custom boss reaming guide are 3-dimensional (3-D) and printed in sterilizable material. These are all provided as single-use disposable instruments and can be available for surgeons during both the initial plan review and surgery.
PREOPERATIVE PLANNING
Patients undergo a preoperative fine-cut 2-dimensional computed tomography scan of the scapula and adjacent humerus following a predefined protocol with a slice thickness of 2 mm to 3 mm. An accurate 3-D bone model of the scapula is obtained using a 3-D image processing software system (Figure 1). The 3-D scapular model is used to create a patient-specific glenoid implant proposal that is approved by the surgeon (Figure 2). Implant position, orientation, size, screw trajectory, and recommended bone removal, if necessary, are determined to create a more normal glenohumeral center of rotation and to secure a glenoid implant in severely deficient glenoid bone (Figure 3). Once the implant design is approved by the surgeon, the final patient-specific implant is manufactured.
SURGICAL TECHNIQUE
The exposure of the glenoid is a critical step for the successful implantation of the patient-specific glenoid implant. Soft tissue and scar tissue around the glenoid must be removed to allow for optimal fit of the custom-made reaming guide. Also, removal of the entire capsulolabral complex on the anteroinferior rim of the glenoid is essential to both enhance glenoid exposure and to allow a perfect fit of the guide to the pathologic bone stock. Attention should be paid during débridement and/or implant removal in case of revision, to make sure that no excessive bone is removed because the patient-specific guide is referenced to this anatomy. Excessive bone removal can change the orientation of the patient-specific guide and ultimately the fixation of the implant. Once the custom-made patient-specific guide is positioned, a 3.2-mm Steinmann pin is placed through the inserter for temporary fixation. The pin should engage or perforate the medial cortical wall to ensure that the subsequent reamer has a stable cannula over which to ream. After the glenoid is reamed, the final implant can be placed in the ideal position according to the preoperative planning. A central 6.5-mm nonlocking central screw and 4.75-mm nonlocking or locking peripheral screws are required to complete the fixation of the implant in the native scapula. Once the patient-specific glenoid component is positioned and strongly fixed to the bone, the glenosphere can be positioned according to the preoperative planning, and the reverse shoulder arthroplasty can be completed in the usual fashion.
CASE EXAMPLES
A 68-year-old woman underwent a TSA for end-stage osteoarthritis in 2000. The implant failed due to a cuff failure. The patient underwent several surgeries, including an open cuff repair, with no success. She had no active elevation preoperatively. Because of the significant glenoid bone loss, a patient-specific glenoid reconstruction was planned. Within 24 months after this surgery, the patient was able to get her hand to her head and elevate to 90º (Figures 4A-4F).
Continue to: In October 2013...
In October 2013, a 68-year-old man underwent a TSA for end-stage osteoarthritis. After 18 months, the implant failed due to active Propionibacterium acnes infection, which required excisional arthroplasty with insertion of an antibiotic spacer. Significant glenoid bone loss (Figure 5) and global soft-tissue deficiency caused substantial disability and led to an indication for a reverse TSA with a patient-specific glenoid vault reconstruction (Figures 6A-6D) after infection eradication. Within 20 months after this surgery, the patient had resumed a satisfactory range of motion (130º forward elevation, 20º external rotation) and outcome.
DISCUSSION
Although glenoid bone loss is often seen in the primary setting (degenerative, congenital, and post-traumatic), severe glenoid bone loss is encountered in most revision TSAs. The best treatment method for massive glenoid bone defects during complex shoulder arthroplasty remains uncertain. Options have included eccentric reaming, glenoid reconstruction with bone allograft and autograft, and more recently augmented components and patient-specific implants.21-25 The advent and availability of CAD/CAM technology have enabled shoulder surgeons to create patient-specific metal solutions to these challenging cases. Currently, only a few reports exist in the literature on patient-specific glenoid components in the setting of severe bone loss.29-32
Chammaa and colleagues29 reported the outcomes of 37 patients with a hip-inspired glenoid component (Total Shoulder Replacement, Stanmore Implants Worldwide). The 5-year results with this implant were promising, with a 16% revision rate and only 1 case of glenoid loosening.
Stoffelen and colleagues30 recently described the successful use of a patient-specific anatomic metal-backed glenoid component for the management of severe glenoid bone loss with excellent results at 2.5 years of follow-up. A different approach was pursued by Gunther and Lynch,31 who reported on 7 patients with a custom inset glenoid implant for deficient glenoid vaults. These circular anatomic, custom-made glenoid components were created with the intention of placing the implants partially inside the glenoid vault and relying partially on sclerotic cortical bone. Despite excellent results at 3 years of follow-up, their use is limited to specific defect geometries and cannot be used in cases of extreme bone loss.
CONCLUSION
We have described the use of a patient-specific glenoid component in 2 patients with severe glenoid bone loss. Despite the satisfactory clinical and short-term radiographic results, we acknowledge that longer-term follow-up is needed to confirm the efficacy of this type of reconstruction. We believe that patient-specific glenoid components represent a valuable addition to the armamentarium of shoulder surgeons who address complex glenoid bone deformities.
1. Chalmers PN, Gupta AK, Rahman Z, Bruce B, Romeo AA, Nicholson GP. Predictors of early complications of total shoulder arthroplasty. J Arthroplasty. 2014;29(4):856-860. doi:10.1016/j.arth.2013.07.002.
2. Deshmukh AV, Koris M, Zurakowski D, Thornhill TS. Total shoulder arthroplasty: long-term survivorship, functional outcome, and quality of life. J Shoulder Elbow Surg. 2005;14(5):471-479. doi:10.1016/j.jse.2005.02.009.
3. Montoya F, Magosch P, Scheiderer B, Lichtenberg S, Melean P, Habermeyer P. Midterm results of a total shoulder prosthesis fixed with a cementless glenoid component. J Shoulder Elbow Surg. 2013;22(5):628-635. doi:10.1016/j.jse.2012.07.005.
4. Torchia ME, Cofield RH, Settergren CR. Total shoulder arthroplasty with the Neer prosthesis: long-term results. J Shoulder Elbow Surg. 1997;6(6):495-505.
5. Antuna SA, Sperling JW, Cofield RH, Rowland CM. Glenoid revision surgery after total shoulder arthroplasty. J Shoulder Elbow Surg. 2001;10(3):217-224. doi:10.1067/mse.2001.113961.
6. Chalmers PN, Rahman Z, Romeo AA, Nicholson GP. Early dislocation after reverse total shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(5):737-744. doi:10.1016/j.jse.2013.08.015.
7. Farng E, Zingmond D, Krenek L, Soohoo NF. Factors predicting complication rates after primary shoulder arthroplasty. J Shoulder Elbow Surg. 2011;20(4):557-563. doi:10.1016/j.jse.2010.11.005.
8. Farshad M, Grogli M, Catanzaro S, Gerber C. Revision of reversed total shoulder arthroplasty. Indications and outcome. BMC Musculoskelet Disord. 2012;13(1):160. doi:10.1186/1471-2474-13-160.
9. Fevang BT, Lie SA, Havelin LI, Skredderstuen A, Furnes O. Risk factors for revision after shoulder arthroplasty: 1,825 shoulder arthroplasties from the Norwegian Arthroplasty Register. Acta Orthop. 2009;80(1):83-91.
10. Fox TJ, Cil A, Sperling JW, Sanchez-Sotelo J, Schleck CD, Cofield RH. Survival of the glenoid component in shoulder arthroplasty. J Shoulder Elbow Surg. 2009;18(6):859-863. doi:10.1016/j.jse.2008.11.020.
11. Rasmussen JV. Outcome and risk of revision following shoulder replacement in patients with glenohumeral osteoarthritis. Acta Orthop Suppl. 2014;85(355 suppl):1-23. doi:10.3109/17453674.2014.922007.
12. Rasmussen JV, Polk A, Brorson S, Sorensen AK, Olsen BS. Patient-reported outcome and risk of revision after shoulder replacement for osteoarthritis. 1,209 cases from the Danish Shoulder Arthroplasty Registry, 2006-2010. Acta Orthop. 2014;85(2):117-122. doi:10.3109/17453674.2014.893497.
13. Sajadi KR, Kwon YW, Zuckerman JD. Revision shoulder arthroplasty: an analysis of indications and outcomes. J Shoulder Elbow Surg. 2010;19(2):308-313. doi:10.1016/j.jse.2009.05.016.
14. Singh JA, Sperling JW, Cofield RH. Revision surgery following total shoulder arthroplasty: analysis of 2588 shoulders over three decades (1976 to 2008). J Bone Joint Surg Br. 2011;93(11):1513-1517. doi:10.1302/0301-620X.93B11.26938.
15. Levine WN, Djurasovic M, Glasson JM, Pollock RG, Flatow EL, Bigliani LU. Hemiarthroplasty for glenohumeral osteoarthritis: results correlated to degree of glenoid wear. J Shoulder Elbow Surg. 1997;6(5):449-454.
16. Levine WN, Fischer CR, Nguyen D, Flatow EL, Ahmad CS, Bigliani LU. Long-term follow-up of shoulder hemiarthroplasty for glenohumeral osteoarthritis. J Bone Joint Surg Am. 2012;94(22):e164. doi:10.2106/JBJS.K.00603.
17. Lynch JR, Franta AK, Montgomery WH, Lenters TR, Mounce D, Matsen FA. Self-assessed outcome at two to four years after shoulder hemiarthroplasty with concentric glenoid reaming. J Bone Joint Surg Am. 2007;89(6):1284-1292. doi:10.2106/JBJS.E.00942.
18. Iannotti JP, Norris TR. Influence of preoperative factors on outcome of shoulder arthroplasty for glenohumeral osteoarthritis. J Bone Joint Surg Am. 2003;85-A(2):251-258.
19. Sperling JW, Cofield RH, Rowland CM. Neer hemiarthroplasty and Neer total shoulder arthroplasty in patients fifty years old or less. Long-term results. J Bone Joint Surg Am. 1998;80(4):464-473.
20. Strauss EJ, Roche C, Flurin PH, Wright T, Zuckerman JD. The glenoid in shoulder arthroplasty. J Shoulder Elbow Surg. 2009;18(5):819-833. doi:10.1016/j.jse.2009.05.008.
21. Cil A, Sperling JW, Cofield RH. Nonstandard glenoid components for bone deficiencies in shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(7):e149-e157. doi:10.1016/j.jse.2013.09.023.
22. Denard PJ, Walch G. Current concepts in the surgical management of primary glenohumeral arthritis with a biconcave glenoid. J Shoulder Elbow Surg. 2013;22(11):1589-1598. doi:10.1016/j.jse.2013.06.017.
23. Gunther SB, Lynch TL. Total shoulder replacement surgery with custom glenoid implants for severe bone deficiency. J Shoulder Elbow Surg. 2012;21(5):675-684. doi:10.1016/j.jse.2011.03.023.
24. Neer CS, Morrison DS. Glenoid bone-grafting in total shoulder arthroplasty. J Bone Joint Surg Am. 1988;70(8):1154-1162.
25. Steinmann SP, Cofield RH. Bone grafting for glenoid deficiency in total shoulder replacement. J Shoulder Elbow Surg. 2000;9(5):361-367. doi:10.1067/mse.2000.106921.
26. Iannotti JP, Frangiamore SJ. Fate of large structural allograft for treatment of severe uncontained glenoid bone deficiency. J Shoulder Elbow Surg. 2012:21(6):765-771. doi:10.1016/j.jse.2011.08.069.
27. Hill JM, Norris TR. Long-term results of total shoulder arthroplasty following bone-grafting of the glenoid. J Bone Joint Surg Am. 2001;83-A(6):877-883.
28. Hsu JE, Ricchetti ET, Huffman GR, Iannotti JP, Glaser DL. Addressing glenoid bone deficiency and asymptomatic posterior erosion in shoulder arthroplasty. J Shoulder Elbow Surg. 2013;22(9):1298-1308.
29. Chammaa R, Uri O, Lambert S. Primary shoulder arthroplasty using a custom-made hip-inspired implant for the treatment of advanced glenohumeral arthritis in the presence of severe glenoid bone loss. J Shoulder Elbow Surg. 2017;26(1):101-107. doi:10.1016/j.jse.2016.05.027.
30. Stoffelen DV, Eraly K, Debeer P. The use of 3D printing technology in reconstruction of a severe glenoid defect: a case report with 2.5 years of follow-up. J Shoulder Elbow Surg. 2015;24(8):e218-e222. doi:10.1016/j.jse.2015.04.006.
31. Gunther SB, Lynch TL. Total shoulder replacement surgery with custom glenoid implants for severe bone deficiency. J Shoulder Elbow Surg. 2012;21(5):675-684. doi:10.1016/j.jse.2011.03.023.
32. Dines DM, Gulotta L, Craig EV, Dines JS. Novel solution for massive glenoid defects in shoulder arthroplasty: a patient-specific glenoid vault reconstruction system. Am J Orthop. 2017;46(2):104-108.
ABSTRACT
Complex glenoid bone deformities present the treating surgeon with a complex reconstructive challenge. Although glenoid bone loss can be encountered in the primary setting (degenerative, congenital, post-traumatic), severe glenoid bone loss is encountered in most revision total shoulder arthroplasties. Severe glenoid bone loss is treated with various techniques including hemiarthroplasty, eccentric reaming, and glenoid reconstruction with bone autografts and allografts. Despite encouraging short- to mid-term results reported with these reconstruction techniques, the clinical and radiographic outcomes remain inconsistent and the high number of complications is a concern. To overcome this problem, more recently augmented components and patient specific implants were introduced. Using the computer-aided design and computer-aided manufacturing technology patient-specific implants have been created to reconstruct the glenoid vault in cases of severe glenoid bone loss.
In this article we describe a patient specific glenoid implant, its indication, technical aspects and surgical technique, based on the author's experience as well as a review of the current literature on custom glenoid implants.
Continue to: Total shoulder arthroplasty...
Total shoulder arthroplasty (TSA) is an effective operation for providing pain relief and improving function in patients with end-stage degenerative shoulder disease that is nonresponsive to nonoperative treatments.1-4 With the increasing number of arthroplasties performed, and the expanding indication for shoulder arthroplasty, the number of revision shoulder arthroplasties is also increasing.5-14 Complex glenoid bone deformities present the treating surgeon with a complex reconstructive challenge. Although glenoid bone loss can be seen in the primary setting (degenerative, congenital, and post-traumatic), severe glenoid bone loss is encountered mostly in revision TSAs.
Historically, patients with severe glenoid bone loss were treated with a hemiarthroplasty.15-17 However, due to inferior outcomes associated with the use of shoulder hemiarthroplasties compared with TSA in these cases,18-20 various techniques were developed with the aim of realigning the glenoid axis and securing the implants into the deficient glenoid vault.21-25 Options have included eccentric reaming, glenoid reconstruction with bone autografts and allografts, and more recently augmented components and patient-specific implants. Studies with eccentric reaming and reconstruction with bone graft during complex shoulder arthroplasty have reported encouraging short- to mid-term results, but the clinical and radiographic outcomes remain inconsistent, and the high number of complications is a concern.25-28
Complications with these techniques include component loosening, graft resorption, nonunion, failure of graft incorporation, infection, and instability.25-28
Computer-aided design and computer-aided manufacturing (CAD/CAM) of patient-specific implants have been used successfully by hip arthroplasty surgeons to deal with complex acetabular reconstructions in the setting of severe bone loss. More recently, the same technology has been used to reconstruct the glenoid vault in cases of severe glenoid bone loss.
In this article, we describe a patient-specific glenoid implant, its indication, and both technical aspects and the surgical technique, based on the authors’ experience as well as a review of the current literature on custom glenoid implants.
Continue to: PATIENT-SPECIFIC GLENOID COMPONENT
PATIENT-SPECIFIC GLENOID COMPONENT
The Vault Reconstruction System ([VRS], Zimmer Biomet) is a patient-specific glenoid vault reconstruction system developed with the use of CAD/CAM to address severe glenoid bone loss encountered during shoulder arthroplasty. For several years, the VRS was available only as a custom implant according to the US Food and Drug Administration rules, and therefore its use was limited to a few cases per year. Recently, a 510(k) envelope clearance was granted to use the VRS in reverse TSA to address significant glenoid bone defects.
The VRS is made of porous plasma spray titanium to provide high strength and flexibility, and allows for biologic fixation. This system can accommodate a restricted bone loss envelope of about 50 mm × 50 mm × 35 mm according to the previous experience of the manufacturer in the custom scenario, covering 96% of defects previously addressed. One 6.5-mm nonlocking central screw and a minimum of four 4.75-mm nonlocking or locking peripheral screws are required for optimal fixation of the implant in the native scapula. A custom boss can be added in to enhance fixation in the native scapula when the bone is sufficient. To facilitate the surgical procedure, a trial implant, a bone model of the scapula, and a custom boss reaming guide are 3-dimensional (3-D) and printed in sterilizable material. These are all provided as single-use disposable instruments and can be available for surgeons during both the initial plan review and surgery.
PREOPERATIVE PLANNING
Patients undergo a preoperative fine-cut 2-dimensional computed tomography scan of the scapula and adjacent humerus following a predefined protocol with a slice thickness of 2 mm to 3 mm. An accurate 3-D bone model of the scapula is obtained using a 3-D image processing software system (Figure 1). The 3-D scapular model is used to create a patient-specific glenoid implant proposal that is approved by the surgeon (Figure 2). Implant position, orientation, size, screw trajectory, and recommended bone removal, if necessary, are determined to create a more normal glenohumeral center of rotation and to secure a glenoid implant in severely deficient glenoid bone (Figure 3). Once the implant design is approved by the surgeon, the final patient-specific implant is manufactured.
SURGICAL TECHNIQUE
The exposure of the glenoid is a critical step for the successful implantation of the patient-specific glenoid implant. Soft tissue and scar tissue around the glenoid must be removed to allow for optimal fit of the custom-made reaming guide. Also, removal of the entire capsulolabral complex on the anteroinferior rim of the glenoid is essential to both enhance glenoid exposure and to allow a perfect fit of the guide to the pathologic bone stock. Attention should be paid during débridement and/or implant removal in case of revision, to make sure that no excessive bone is removed because the patient-specific guide is referenced to this anatomy. Excessive bone removal can change the orientation of the patient-specific guide and ultimately the fixation of the implant. Once the custom-made patient-specific guide is positioned, a 3.2-mm Steinmann pin is placed through the inserter for temporary fixation. The pin should engage or perforate the medial cortical wall to ensure that the subsequent reamer has a stable cannula over which to ream. After the glenoid is reamed, the final implant can be placed in the ideal position according to the preoperative planning. A central 6.5-mm nonlocking central screw and 4.75-mm nonlocking or locking peripheral screws are required to complete the fixation of the implant in the native scapula. Once the patient-specific glenoid component is positioned and strongly fixed to the bone, the glenosphere can be positioned according to the preoperative planning, and the reverse shoulder arthroplasty can be completed in the usual fashion.
CASE EXAMPLES
A 68-year-old woman underwent a TSA for end-stage osteoarthritis in 2000. The implant failed due to a cuff failure. The patient underwent several surgeries, including an open cuff repair, with no success. She had no active elevation preoperatively. Because of the significant glenoid bone loss, a patient-specific glenoid reconstruction was planned. Within 24 months after this surgery, the patient was able to get her hand to her head and elevate to 90º (Figures 4A-4F).
Continue to: In October 2013...
In October 2013, a 68-year-old man underwent a TSA for end-stage osteoarthritis. After 18 months, the implant failed due to active Propionibacterium acnes infection, which required excisional arthroplasty with insertion of an antibiotic spacer. Significant glenoid bone loss (Figure 5) and global soft-tissue deficiency caused substantial disability and led to an indication for a reverse TSA with a patient-specific glenoid vault reconstruction (Figures 6A-6D) after infection eradication. Within 20 months after this surgery, the patient had resumed a satisfactory range of motion (130º forward elevation, 20º external rotation) and outcome.
DISCUSSION
Although glenoid bone loss is often seen in the primary setting (degenerative, congenital, and post-traumatic), severe glenoid bone loss is encountered in most revision TSAs. The best treatment method for massive glenoid bone defects during complex shoulder arthroplasty remains uncertain. Options have included eccentric reaming, glenoid reconstruction with bone allograft and autograft, and more recently augmented components and patient-specific implants.21-25 The advent and availability of CAD/CAM technology have enabled shoulder surgeons to create patient-specific metal solutions to these challenging cases. Currently, only a few reports exist in the literature on patient-specific glenoid components in the setting of severe bone loss.29-32
Chammaa and colleagues29 reported the outcomes of 37 patients with a hip-inspired glenoid component (Total Shoulder Replacement, Stanmore Implants Worldwide). The 5-year results with this implant were promising, with a 16% revision rate and only 1 case of glenoid loosening.
Stoffelen and colleagues30 recently described the successful use of a patient-specific anatomic metal-backed glenoid component for the management of severe glenoid bone loss with excellent results at 2.5 years of follow-up. A different approach was pursued by Gunther and Lynch,31 who reported on 7 patients with a custom inset glenoid implant for deficient glenoid vaults. These circular anatomic, custom-made glenoid components were created with the intention of placing the implants partially inside the glenoid vault and relying partially on sclerotic cortical bone. Despite excellent results at 3 years of follow-up, their use is limited to specific defect geometries and cannot be used in cases of extreme bone loss.
CONCLUSION
We have described the use of a patient-specific glenoid component in 2 patients with severe glenoid bone loss. Despite the satisfactory clinical and short-term radiographic results, we acknowledge that longer-term follow-up is needed to confirm the efficacy of this type of reconstruction. We believe that patient-specific glenoid components represent a valuable addition to the armamentarium of shoulder surgeons who address complex glenoid bone deformities.
ABSTRACT
Complex glenoid bone deformities present the treating surgeon with a complex reconstructive challenge. Although glenoid bone loss can be encountered in the primary setting (degenerative, congenital, post-traumatic), severe glenoid bone loss is encountered in most revision total shoulder arthroplasties. Severe glenoid bone loss is treated with various techniques including hemiarthroplasty, eccentric reaming, and glenoid reconstruction with bone autografts and allografts. Despite encouraging short- to mid-term results reported with these reconstruction techniques, the clinical and radiographic outcomes remain inconsistent and the high number of complications is a concern. To overcome this problem, more recently augmented components and patient specific implants were introduced. Using the computer-aided design and computer-aided manufacturing technology patient-specific implants have been created to reconstruct the glenoid vault in cases of severe glenoid bone loss.
In this article we describe a patient specific glenoid implant, its indication, technical aspects and surgical technique, based on the author's experience as well as a review of the current literature on custom glenoid implants.
Continue to: Total shoulder arthroplasty...
Total shoulder arthroplasty (TSA) is an effective operation for providing pain relief and improving function in patients with end-stage degenerative shoulder disease that is nonresponsive to nonoperative treatments.1-4 With the increasing number of arthroplasties performed, and the expanding indication for shoulder arthroplasty, the number of revision shoulder arthroplasties is also increasing.5-14 Complex glenoid bone deformities present the treating surgeon with a complex reconstructive challenge. Although glenoid bone loss can be seen in the primary setting (degenerative, congenital, and post-traumatic), severe glenoid bone loss is encountered mostly in revision TSAs.
Historically, patients with severe glenoid bone loss were treated with a hemiarthroplasty.15-17 However, due to inferior outcomes associated with the use of shoulder hemiarthroplasties compared with TSA in these cases,18-20 various techniques were developed with the aim of realigning the glenoid axis and securing the implants into the deficient glenoid vault.21-25 Options have included eccentric reaming, glenoid reconstruction with bone autografts and allografts, and more recently augmented components and patient-specific implants. Studies with eccentric reaming and reconstruction with bone graft during complex shoulder arthroplasty have reported encouraging short- to mid-term results, but the clinical and radiographic outcomes remain inconsistent, and the high number of complications is a concern.25-28
Complications with these techniques include component loosening, graft resorption, nonunion, failure of graft incorporation, infection, and instability.25-28
Computer-aided design and computer-aided manufacturing (CAD/CAM) of patient-specific implants have been used successfully by hip arthroplasty surgeons to deal with complex acetabular reconstructions in the setting of severe bone loss. More recently, the same technology has been used to reconstruct the glenoid vault in cases of severe glenoid bone loss.
In this article, we describe a patient-specific glenoid implant, its indication, and both technical aspects and the surgical technique, based on the authors’ experience as well as a review of the current literature on custom glenoid implants.
Continue to: PATIENT-SPECIFIC GLENOID COMPONENT
PATIENT-SPECIFIC GLENOID COMPONENT
The Vault Reconstruction System ([VRS], Zimmer Biomet) is a patient-specific glenoid vault reconstruction system developed with the use of CAD/CAM to address severe glenoid bone loss encountered during shoulder arthroplasty. For several years, the VRS was available only as a custom implant according to the US Food and Drug Administration rules, and therefore its use was limited to a few cases per year. Recently, a 510(k) envelope clearance was granted to use the VRS in reverse TSA to address significant glenoid bone defects.
The VRS is made of porous plasma spray titanium to provide high strength and flexibility, and allows for biologic fixation. This system can accommodate a restricted bone loss envelope of about 50 mm × 50 mm × 35 mm according to the previous experience of the manufacturer in the custom scenario, covering 96% of defects previously addressed. One 6.5-mm nonlocking central screw and a minimum of four 4.75-mm nonlocking or locking peripheral screws are required for optimal fixation of the implant in the native scapula. A custom boss can be added in to enhance fixation in the native scapula when the bone is sufficient. To facilitate the surgical procedure, a trial implant, a bone model of the scapula, and a custom boss reaming guide are 3-dimensional (3-D) and printed in sterilizable material. These are all provided as single-use disposable instruments and can be available for surgeons during both the initial plan review and surgery.
PREOPERATIVE PLANNING
Patients undergo a preoperative fine-cut 2-dimensional computed tomography scan of the scapula and adjacent humerus following a predefined protocol with a slice thickness of 2 mm to 3 mm. An accurate 3-D bone model of the scapula is obtained using a 3-D image processing software system (Figure 1). The 3-D scapular model is used to create a patient-specific glenoid implant proposal that is approved by the surgeon (Figure 2). Implant position, orientation, size, screw trajectory, and recommended bone removal, if necessary, are determined to create a more normal glenohumeral center of rotation and to secure a glenoid implant in severely deficient glenoid bone (Figure 3). Once the implant design is approved by the surgeon, the final patient-specific implant is manufactured.
SURGICAL TECHNIQUE
The exposure of the glenoid is a critical step for the successful implantation of the patient-specific glenoid implant. Soft tissue and scar tissue around the glenoid must be removed to allow for optimal fit of the custom-made reaming guide. Also, removal of the entire capsulolabral complex on the anteroinferior rim of the glenoid is essential to both enhance glenoid exposure and to allow a perfect fit of the guide to the pathologic bone stock. Attention should be paid during débridement and/or implant removal in case of revision, to make sure that no excessive bone is removed because the patient-specific guide is referenced to this anatomy. Excessive bone removal can change the orientation of the patient-specific guide and ultimately the fixation of the implant. Once the custom-made patient-specific guide is positioned, a 3.2-mm Steinmann pin is placed through the inserter for temporary fixation. The pin should engage or perforate the medial cortical wall to ensure that the subsequent reamer has a stable cannula over which to ream. After the glenoid is reamed, the final implant can be placed in the ideal position according to the preoperative planning. A central 6.5-mm nonlocking central screw and 4.75-mm nonlocking or locking peripheral screws are required to complete the fixation of the implant in the native scapula. Once the patient-specific glenoid component is positioned and strongly fixed to the bone, the glenosphere can be positioned according to the preoperative planning, and the reverse shoulder arthroplasty can be completed in the usual fashion.
CASE EXAMPLES
A 68-year-old woman underwent a TSA for end-stage osteoarthritis in 2000. The implant failed due to a cuff failure. The patient underwent several surgeries, including an open cuff repair, with no success. She had no active elevation preoperatively. Because of the significant glenoid bone loss, a patient-specific glenoid reconstruction was planned. Within 24 months after this surgery, the patient was able to get her hand to her head and elevate to 90º (Figures 4A-4F).
Continue to: In October 2013...
In October 2013, a 68-year-old man underwent a TSA for end-stage osteoarthritis. After 18 months, the implant failed due to active Propionibacterium acnes infection, which required excisional arthroplasty with insertion of an antibiotic spacer. Significant glenoid bone loss (Figure 5) and global soft-tissue deficiency caused substantial disability and led to an indication for a reverse TSA with a patient-specific glenoid vault reconstruction (Figures 6A-6D) after infection eradication. Within 20 months after this surgery, the patient had resumed a satisfactory range of motion (130º forward elevation, 20º external rotation) and outcome.
DISCUSSION
Although glenoid bone loss is often seen in the primary setting (degenerative, congenital, and post-traumatic), severe glenoid bone loss is encountered in most revision TSAs. The best treatment method for massive glenoid bone defects during complex shoulder arthroplasty remains uncertain. Options have included eccentric reaming, glenoid reconstruction with bone allograft and autograft, and more recently augmented components and patient-specific implants.21-25 The advent and availability of CAD/CAM technology have enabled shoulder surgeons to create patient-specific metal solutions to these challenging cases. Currently, only a few reports exist in the literature on patient-specific glenoid components in the setting of severe bone loss.29-32
Chammaa and colleagues29 reported the outcomes of 37 patients with a hip-inspired glenoid component (Total Shoulder Replacement, Stanmore Implants Worldwide). The 5-year results with this implant were promising, with a 16% revision rate and only 1 case of glenoid loosening.
Stoffelen and colleagues30 recently described the successful use of a patient-specific anatomic metal-backed glenoid component for the management of severe glenoid bone loss with excellent results at 2.5 years of follow-up. A different approach was pursued by Gunther and Lynch,31 who reported on 7 patients with a custom inset glenoid implant for deficient glenoid vaults. These circular anatomic, custom-made glenoid components were created with the intention of placing the implants partially inside the glenoid vault and relying partially on sclerotic cortical bone. Despite excellent results at 3 years of follow-up, their use is limited to specific defect geometries and cannot be used in cases of extreme bone loss.
CONCLUSION
We have described the use of a patient-specific glenoid component in 2 patients with severe glenoid bone loss. Despite the satisfactory clinical and short-term radiographic results, we acknowledge that longer-term follow-up is needed to confirm the efficacy of this type of reconstruction. We believe that patient-specific glenoid components represent a valuable addition to the armamentarium of shoulder surgeons who address complex glenoid bone deformities.
1. Chalmers PN, Gupta AK, Rahman Z, Bruce B, Romeo AA, Nicholson GP. Predictors of early complications of total shoulder arthroplasty. J Arthroplasty. 2014;29(4):856-860. doi:10.1016/j.arth.2013.07.002.
2. Deshmukh AV, Koris M, Zurakowski D, Thornhill TS. Total shoulder arthroplasty: long-term survivorship, functional outcome, and quality of life. J Shoulder Elbow Surg. 2005;14(5):471-479. doi:10.1016/j.jse.2005.02.009.
3. Montoya F, Magosch P, Scheiderer B, Lichtenberg S, Melean P, Habermeyer P. Midterm results of a total shoulder prosthesis fixed with a cementless glenoid component. J Shoulder Elbow Surg. 2013;22(5):628-635. doi:10.1016/j.jse.2012.07.005.
4. Torchia ME, Cofield RH, Settergren CR. Total shoulder arthroplasty with the Neer prosthesis: long-term results. J Shoulder Elbow Surg. 1997;6(6):495-505.
5. Antuna SA, Sperling JW, Cofield RH, Rowland CM. Glenoid revision surgery after total shoulder arthroplasty. J Shoulder Elbow Surg. 2001;10(3):217-224. doi:10.1067/mse.2001.113961.
6. Chalmers PN, Rahman Z, Romeo AA, Nicholson GP. Early dislocation after reverse total shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(5):737-744. doi:10.1016/j.jse.2013.08.015.
7. Farng E, Zingmond D, Krenek L, Soohoo NF. Factors predicting complication rates after primary shoulder arthroplasty. J Shoulder Elbow Surg. 2011;20(4):557-563. doi:10.1016/j.jse.2010.11.005.
8. Farshad M, Grogli M, Catanzaro S, Gerber C. Revision of reversed total shoulder arthroplasty. Indications and outcome. BMC Musculoskelet Disord. 2012;13(1):160. doi:10.1186/1471-2474-13-160.
9. Fevang BT, Lie SA, Havelin LI, Skredderstuen A, Furnes O. Risk factors for revision after shoulder arthroplasty: 1,825 shoulder arthroplasties from the Norwegian Arthroplasty Register. Acta Orthop. 2009;80(1):83-91.
10. Fox TJ, Cil A, Sperling JW, Sanchez-Sotelo J, Schleck CD, Cofield RH. Survival of the glenoid component in shoulder arthroplasty. J Shoulder Elbow Surg. 2009;18(6):859-863. doi:10.1016/j.jse.2008.11.020.
11. Rasmussen JV. Outcome and risk of revision following shoulder replacement in patients with glenohumeral osteoarthritis. Acta Orthop Suppl. 2014;85(355 suppl):1-23. doi:10.3109/17453674.2014.922007.
12. Rasmussen JV, Polk A, Brorson S, Sorensen AK, Olsen BS. Patient-reported outcome and risk of revision after shoulder replacement for osteoarthritis. 1,209 cases from the Danish Shoulder Arthroplasty Registry, 2006-2010. Acta Orthop. 2014;85(2):117-122. doi:10.3109/17453674.2014.893497.
13. Sajadi KR, Kwon YW, Zuckerman JD. Revision shoulder arthroplasty: an analysis of indications and outcomes. J Shoulder Elbow Surg. 2010;19(2):308-313. doi:10.1016/j.jse.2009.05.016.
14. Singh JA, Sperling JW, Cofield RH. Revision surgery following total shoulder arthroplasty: analysis of 2588 shoulders over three decades (1976 to 2008). J Bone Joint Surg Br. 2011;93(11):1513-1517. doi:10.1302/0301-620X.93B11.26938.
15. Levine WN, Djurasovic M, Glasson JM, Pollock RG, Flatow EL, Bigliani LU. Hemiarthroplasty for glenohumeral osteoarthritis: results correlated to degree of glenoid wear. J Shoulder Elbow Surg. 1997;6(5):449-454.
16. Levine WN, Fischer CR, Nguyen D, Flatow EL, Ahmad CS, Bigliani LU. Long-term follow-up of shoulder hemiarthroplasty for glenohumeral osteoarthritis. J Bone Joint Surg Am. 2012;94(22):e164. doi:10.2106/JBJS.K.00603.
17. Lynch JR, Franta AK, Montgomery WH, Lenters TR, Mounce D, Matsen FA. Self-assessed outcome at two to four years after shoulder hemiarthroplasty with concentric glenoid reaming. J Bone Joint Surg Am. 2007;89(6):1284-1292. doi:10.2106/JBJS.E.00942.
18. Iannotti JP, Norris TR. Influence of preoperative factors on outcome of shoulder arthroplasty for glenohumeral osteoarthritis. J Bone Joint Surg Am. 2003;85-A(2):251-258.
19. Sperling JW, Cofield RH, Rowland CM. Neer hemiarthroplasty and Neer total shoulder arthroplasty in patients fifty years old or less. Long-term results. J Bone Joint Surg Am. 1998;80(4):464-473.
20. Strauss EJ, Roche C, Flurin PH, Wright T, Zuckerman JD. The glenoid in shoulder arthroplasty. J Shoulder Elbow Surg. 2009;18(5):819-833. doi:10.1016/j.jse.2009.05.008.
21. Cil A, Sperling JW, Cofield RH. Nonstandard glenoid components for bone deficiencies in shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(7):e149-e157. doi:10.1016/j.jse.2013.09.023.
22. Denard PJ, Walch G. Current concepts in the surgical management of primary glenohumeral arthritis with a biconcave glenoid. J Shoulder Elbow Surg. 2013;22(11):1589-1598. doi:10.1016/j.jse.2013.06.017.
23. Gunther SB, Lynch TL. Total shoulder replacement surgery with custom glenoid implants for severe bone deficiency. J Shoulder Elbow Surg. 2012;21(5):675-684. doi:10.1016/j.jse.2011.03.023.
24. Neer CS, Morrison DS. Glenoid bone-grafting in total shoulder arthroplasty. J Bone Joint Surg Am. 1988;70(8):1154-1162.
25. Steinmann SP, Cofield RH. Bone grafting for glenoid deficiency in total shoulder replacement. J Shoulder Elbow Surg. 2000;9(5):361-367. doi:10.1067/mse.2000.106921.
26. Iannotti JP, Frangiamore SJ. Fate of large structural allograft for treatment of severe uncontained glenoid bone deficiency. J Shoulder Elbow Surg. 2012:21(6):765-771. doi:10.1016/j.jse.2011.08.069.
27. Hill JM, Norris TR. Long-term results of total shoulder arthroplasty following bone-grafting of the glenoid. J Bone Joint Surg Am. 2001;83-A(6):877-883.
28. Hsu JE, Ricchetti ET, Huffman GR, Iannotti JP, Glaser DL. Addressing glenoid bone deficiency and asymptomatic posterior erosion in shoulder arthroplasty. J Shoulder Elbow Surg. 2013;22(9):1298-1308.
29. Chammaa R, Uri O, Lambert S. Primary shoulder arthroplasty using a custom-made hip-inspired implant for the treatment of advanced glenohumeral arthritis in the presence of severe glenoid bone loss. J Shoulder Elbow Surg. 2017;26(1):101-107. doi:10.1016/j.jse.2016.05.027.
30. Stoffelen DV, Eraly K, Debeer P. The use of 3D printing technology in reconstruction of a severe glenoid defect: a case report with 2.5 years of follow-up. J Shoulder Elbow Surg. 2015;24(8):e218-e222. doi:10.1016/j.jse.2015.04.006.
31. Gunther SB, Lynch TL. Total shoulder replacement surgery with custom glenoid implants for severe bone deficiency. J Shoulder Elbow Surg. 2012;21(5):675-684. doi:10.1016/j.jse.2011.03.023.
32. Dines DM, Gulotta L, Craig EV, Dines JS. Novel solution for massive glenoid defects in shoulder arthroplasty: a patient-specific glenoid vault reconstruction system. Am J Orthop. 2017;46(2):104-108.
1. Chalmers PN, Gupta AK, Rahman Z, Bruce B, Romeo AA, Nicholson GP. Predictors of early complications of total shoulder arthroplasty. J Arthroplasty. 2014;29(4):856-860. doi:10.1016/j.arth.2013.07.002.
2. Deshmukh AV, Koris M, Zurakowski D, Thornhill TS. Total shoulder arthroplasty: long-term survivorship, functional outcome, and quality of life. J Shoulder Elbow Surg. 2005;14(5):471-479. doi:10.1016/j.jse.2005.02.009.
3. Montoya F, Magosch P, Scheiderer B, Lichtenberg S, Melean P, Habermeyer P. Midterm results of a total shoulder prosthesis fixed with a cementless glenoid component. J Shoulder Elbow Surg. 2013;22(5):628-635. doi:10.1016/j.jse.2012.07.005.
4. Torchia ME, Cofield RH, Settergren CR. Total shoulder arthroplasty with the Neer prosthesis: long-term results. J Shoulder Elbow Surg. 1997;6(6):495-505.
5. Antuna SA, Sperling JW, Cofield RH, Rowland CM. Glenoid revision surgery after total shoulder arthroplasty. J Shoulder Elbow Surg. 2001;10(3):217-224. doi:10.1067/mse.2001.113961.
6. Chalmers PN, Rahman Z, Romeo AA, Nicholson GP. Early dislocation after reverse total shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(5):737-744. doi:10.1016/j.jse.2013.08.015.
7. Farng E, Zingmond D, Krenek L, Soohoo NF. Factors predicting complication rates after primary shoulder arthroplasty. J Shoulder Elbow Surg. 2011;20(4):557-563. doi:10.1016/j.jse.2010.11.005.
8. Farshad M, Grogli M, Catanzaro S, Gerber C. Revision of reversed total shoulder arthroplasty. Indications and outcome. BMC Musculoskelet Disord. 2012;13(1):160. doi:10.1186/1471-2474-13-160.
9. Fevang BT, Lie SA, Havelin LI, Skredderstuen A, Furnes O. Risk factors for revision after shoulder arthroplasty: 1,825 shoulder arthroplasties from the Norwegian Arthroplasty Register. Acta Orthop. 2009;80(1):83-91.
10. Fox TJ, Cil A, Sperling JW, Sanchez-Sotelo J, Schleck CD, Cofield RH. Survival of the glenoid component in shoulder arthroplasty. J Shoulder Elbow Surg. 2009;18(6):859-863. doi:10.1016/j.jse.2008.11.020.
11. Rasmussen JV. Outcome and risk of revision following shoulder replacement in patients with glenohumeral osteoarthritis. Acta Orthop Suppl. 2014;85(355 suppl):1-23. doi:10.3109/17453674.2014.922007.
12. Rasmussen JV, Polk A, Brorson S, Sorensen AK, Olsen BS. Patient-reported outcome and risk of revision after shoulder replacement for osteoarthritis. 1,209 cases from the Danish Shoulder Arthroplasty Registry, 2006-2010. Acta Orthop. 2014;85(2):117-122. doi:10.3109/17453674.2014.893497.
13. Sajadi KR, Kwon YW, Zuckerman JD. Revision shoulder arthroplasty: an analysis of indications and outcomes. J Shoulder Elbow Surg. 2010;19(2):308-313. doi:10.1016/j.jse.2009.05.016.
14. Singh JA, Sperling JW, Cofield RH. Revision surgery following total shoulder arthroplasty: analysis of 2588 shoulders over three decades (1976 to 2008). J Bone Joint Surg Br. 2011;93(11):1513-1517. doi:10.1302/0301-620X.93B11.26938.
15. Levine WN, Djurasovic M, Glasson JM, Pollock RG, Flatow EL, Bigliani LU. Hemiarthroplasty for glenohumeral osteoarthritis: results correlated to degree of glenoid wear. J Shoulder Elbow Surg. 1997;6(5):449-454.
16. Levine WN, Fischer CR, Nguyen D, Flatow EL, Ahmad CS, Bigliani LU. Long-term follow-up of shoulder hemiarthroplasty for glenohumeral osteoarthritis. J Bone Joint Surg Am. 2012;94(22):e164. doi:10.2106/JBJS.K.00603.
17. Lynch JR, Franta AK, Montgomery WH, Lenters TR, Mounce D, Matsen FA. Self-assessed outcome at two to four years after shoulder hemiarthroplasty with concentric glenoid reaming. J Bone Joint Surg Am. 2007;89(6):1284-1292. doi:10.2106/JBJS.E.00942.
18. Iannotti JP, Norris TR. Influence of preoperative factors on outcome of shoulder arthroplasty for glenohumeral osteoarthritis. J Bone Joint Surg Am. 2003;85-A(2):251-258.
19. Sperling JW, Cofield RH, Rowland CM. Neer hemiarthroplasty and Neer total shoulder arthroplasty in patients fifty years old or less. Long-term results. J Bone Joint Surg Am. 1998;80(4):464-473.
20. Strauss EJ, Roche C, Flurin PH, Wright T, Zuckerman JD. The glenoid in shoulder arthroplasty. J Shoulder Elbow Surg. 2009;18(5):819-833. doi:10.1016/j.jse.2009.05.008.
21. Cil A, Sperling JW, Cofield RH. Nonstandard glenoid components for bone deficiencies in shoulder arthroplasty. J Shoulder Elbow Surg. 2014;23(7):e149-e157. doi:10.1016/j.jse.2013.09.023.
22. Denard PJ, Walch G. Current concepts in the surgical management of primary glenohumeral arthritis with a biconcave glenoid. J Shoulder Elbow Surg. 2013;22(11):1589-1598. doi:10.1016/j.jse.2013.06.017.
23. Gunther SB, Lynch TL. Total shoulder replacement surgery with custom glenoid implants for severe bone deficiency. J Shoulder Elbow Surg. 2012;21(5):675-684. doi:10.1016/j.jse.2011.03.023.
24. Neer CS, Morrison DS. Glenoid bone-grafting in total shoulder arthroplasty. J Bone Joint Surg Am. 1988;70(8):1154-1162.
25. Steinmann SP, Cofield RH. Bone grafting for glenoid deficiency in total shoulder replacement. J Shoulder Elbow Surg. 2000;9(5):361-367. doi:10.1067/mse.2000.106921.
26. Iannotti JP, Frangiamore SJ. Fate of large structural allograft for treatment of severe uncontained glenoid bone deficiency. J Shoulder Elbow Surg. 2012:21(6):765-771. doi:10.1016/j.jse.2011.08.069.
27. Hill JM, Norris TR. Long-term results of total shoulder arthroplasty following bone-grafting of the glenoid. J Bone Joint Surg Am. 2001;83-A(6):877-883.
28. Hsu JE, Ricchetti ET, Huffman GR, Iannotti JP, Glaser DL. Addressing glenoid bone deficiency and asymptomatic posterior erosion in shoulder arthroplasty. J Shoulder Elbow Surg. 2013;22(9):1298-1308.
29. Chammaa R, Uri O, Lambert S. Primary shoulder arthroplasty using a custom-made hip-inspired implant for the treatment of advanced glenohumeral arthritis in the presence of severe glenoid bone loss. J Shoulder Elbow Surg. 2017;26(1):101-107. doi:10.1016/j.jse.2016.05.027.
30. Stoffelen DV, Eraly K, Debeer P. The use of 3D printing technology in reconstruction of a severe glenoid defect: a case report with 2.5 years of follow-up. J Shoulder Elbow Surg. 2015;24(8):e218-e222. doi:10.1016/j.jse.2015.04.006.
31. Gunther SB, Lynch TL. Total shoulder replacement surgery with custom glenoid implants for severe bone deficiency. J Shoulder Elbow Surg. 2012;21(5):675-684. doi:10.1016/j.jse.2011.03.023.
32. Dines DM, Gulotta L, Craig EV, Dines JS. Novel solution for massive glenoid defects in shoulder arthroplasty: a patient-specific glenoid vault reconstruction system. Am J Orthop. 2017;46(2):104-108.
TAKE-HOME POINTS
- With the increasing number of arthroplasties performed, and the expanding indication for shoulder arthroplasty, the number of revision shoulder arthroplasties is also increasing.
- Complex glenoid bone defects are sometimes encountered in revision shoulder arthroplasties.
- Glenoid reconstructions with bone graft have reported encouraging short- to mid-term results, but the high number of complications is a concern.
- Using the CAD/CAM technology patient-specific glenoid components have been created to reconstruct the glenoid vault in cases of severe glenoid bone loss.
- Short-term clinical and radiographic results of patient-specific glenoid components are encouraging, however longer-term follow-up are needed to confirm the efficacy of this type of reconstruction.
Convertible Glenoid Components Facilitate Revisions to Reverse Shoulder Arthroplasty Easier: Retrospective Review of 13 Cases
ABSTRACT
Removal of a cemented glenoid component often leads to massive glenoid bone loss, which makes it difficult to implant a new glenoid baseplate. The purpose of this study was to demonstrate the feasibility of revisions with a completely convertible system and to report clinical and radiographic results of a retrospective review of 13 cases.
Between 2003 and 2011, 104 primary total shoulder arthroplasties (TSAs) were performed with an uncemented glenoid component in our group. Of these patients, 13 (average age, 64 years) were revised to reverse shoulder arthroplasty (RSA) using a modular convertible platform system and were included in this study. Average follow-up after revision was 22 months. Outcome measures included pain, range of motion, Constant-Murley scores, Simple Shoulder Tests, and subjective shoulder values. Active flexion increased significantly from a mean of 93° (range, 30°-120°) to 138° (range, 95°-170°) (P = 0.021), and active external rotation increased significantly from 8° (range, −20°-15°) to 25° (range, −10°-60°). Mean pain scores significantly improved from 4.2 to 13.3 points. The mean Constant Scores improved from 21 (range, 18-32) to 63 (range, 43-90). Subjectively, 12 patients rated their shoulder as better or much better than preoperatively. This retrospective study shows that a complete convertible system facilitates conversion of TSAs to RSAs with excellent pain relief and a significant improvement in shoulder function.
Continue to: Polyethylene glenoid components...
Polyethylene glenoid components are the gold standard in anatomic total shoulder arthroplasty (TSA). However, even though TSA survivorship exceeds 95% at 10-year follow-up,1 glenoid component loosening remains the main complication and the weak link in these implants. This complication accounts for 25% of all complications related to TSA in the literature.2 In most cases, glenoid component loosening is not isolated but combined with a rotator cuff tear, glenohumeral instability, or component malposition.
We hypothesized that a completely convertible platform system on both the humeral and the glenoid side could facilitate the revision of a failed TSA to a RSA. This would enable the surgeon to leave the humeral stem and the glenoid baseplate in place, avoiding the difficulty of stem removal and the reimplantation of a glenoid component, especially in osteoporotic glenoid bone and elderly patients. The revision procedure would then only consist of replacing the humeral head by a metallic tray and polyethylene bearing on the humeral side and by impacting a glenosphere on the glenoid baseplate (Figures 2A, 2B).
The purpose of this study was to demonstrate the feasibility of revisions with this completely convertible system and to report clinical and radiographic results of a retrospective review of 13 cases.
MATERIALS AND METHODS
PATIENT SELECTION
Between 2003 and 2011, 104 primary TSAs were performed with an uncemented glenoid component in our group. Of these patients, 18 underwent revision (17.3%). Among these 18 patients, 13 were revised to RSA using a modular convertible platform system and were included in this study, while 5 patients were revised to another TSA (2 dissociations of the polyethylene glenoid implant, 2 excessively low implantations of the glenoid baseplate, and 1 glenoid loosening). The mean age of the 13 patients (9 women, 4 men) included in this retrospective study at the time of revision was 64 years (range, 50-75 years). The reasons for revision surgery were rotator cuff tear (5, among which 2 were posterosuperior tears, and 3 were tears of the subscapularis), dislocations (5 posterior and 1 anterior, among which 4 had a B2 or C glenoid), suprascapular nerve paralysis (1), and dissociation of the polyethylene (1). The initial TSA was indicated for primary osteoarthritis with a normal cuff (9), primary osteoarthritis with a reparable cuff tear (2), posttraumatic osteoarthritis (1), and chronic dislocation (1). The right dominant shoulder was involved in 10 cases. The mean time interval between the primary TSA and the revision was 15 months (range, 1-61 months).
OPERATIVE TECHNIQUE
PREOPERATIVE PLANNING
Revision of a failed TSA is always a difficult challenge, and evaluation of bone loss on both the humeral and the glenoid sides, as well as the status of the cuff, is mandatory, even with a completely convertible arthroplasty system. The surgeon must be prepared to remove the humeral stem in case reduction of the joint is impossible. We systematically performed standard radiographs (anteroposterior, axillary, and outlet views) and computed tomography (CT) scans in order to assess both the version and positioning, as well as potential signs of loosening of the implants and the status of the cuff (continuity, degree of muscle trophicity, and fatty infiltration). A preoperative leucocyte count, sedimentation rate, and C-reactive protein rates were requested in every revision case, even if a mechanical etiology was strongly suspected.
Continue to: REVISION PROCEDURE
REVISION PROCEDURE
All the implants that had been used in the primary TSAs were Arrow Universal Shoulder Prostheses (FH Orthopedics). All revisions were performed through the previous deltopectoral approach in the beach chair position under general anesthesia with an interscalene block. Adhesions of the deep part of the deltoid were carefully released. The conjoint tendon was released, and the location of the musculocutaneous and axillary nerves was identified before any retractor was placed. In the 10 cases where the subscapularis was intact, it was peeled off the medial border of the bicipital groove to obtain sufficient length for a tension-free reinsertion.
The anatomical head of the humeral implant was disconnected from the stem and removed. All stems were found to be well fixed; there were no cases of loosening or evidence of infection. A circumferential capsular release was systematically carried out. The polyethylene glenoid onlay was then unlocked from the baseplate.
The quality of the fixation of the glenoid baseplate was systematically evaluated; no screw was found to be loose, and the fixation of all baseplates was stable. Therefore, there was no need to revise the glenoid baseplate, even when its position was considered excessively retroverted (Glenoid B2) or high. A glenosphere was impacted on the baseplate, and a polyethylene humeral bearing was then implanted on the humeral stem. The thinnest polyethylene bearing available (number 0) was chosen in all cases, and a size 36 glenosphere was chosen in 12 out of 13 cases. Intraoperative stability of the implant was satisfactory, and no impingement was found posteriorly, anteriorly, or inferiorly.
In one case, the humeral stem was a first-generation humeral implant which was not compatible with the new-generation humeral bearing, and the humeral stem had to be replaced.
In 2 cases, reduction of the RSA was either impossible or felt to be too tight, even after extensive soft-tissue release and resection of the remaining supraspinatus. The main reason for this was an excessively proud humeral stem because of an onlay polyethylene humeral bearing instead of an inlay design. However, removal of the uncemented humeral stem was always possible with no osteotomy or cortical window of the humeral shaft as the humeral stem has been designed with a bone ingrowth surface only on the metaphyseal part with a smooth surface on diaphyseal part. After removal of the stem, a small amount of humeral metaphysis was cut, and a new humeral stem was press-fit in a lower position. This allowed restoration of an appropriate tension of the soft tissue and, therefore, an easier reduction. The subscapularis was medialized and reinserted transosseously when possible with a double-row repair. In 3 cases, the subscapularis was torn and retracted at the level of the glenoid, or impossible to identify to allow its reinsertion.
Continue to: According to our infectious disease department...
According to our infectious disease department, we made a minimum of 5 cultures for each revision case looking for a possible low-grade infection. All cultures in our group are held for 14 days to assess for Propionibacterium acnes.
POSTOPERATIVE MANAGEMENT
A shoulder splint in neutral rotation was used for the first 4 weeks. Passive range of motion (ROM) was started immediately with pendulum exercises and passive anterior elevation. Active assisted and active ROM were allowed after 4 weeks, and physiotherapy was continued for 6 months. Elderly patients were referred to a center of rehabilitation. We found only 1 or 2 positive cultures (Propionibacterium acnes) for 4 patients, and we decided to consider them as a contamination. None of the patients were treated with antibiotics.
CLINICAL AND RADIOLOGICAL ASSESSMENT
Clinical evaluation included pre- and postoperative pain scores (visual analog scale [VAS]), ROM, the Constant-Murley13 score, the Simple Shoulder Test (SST),14 and the subjective shoulder value.15 Subjective satisfaction was assessed by asking the patients at follow-up how they felt compared with before surgery and was graded using a 4-point scale: 1, much better; 2, better; 3, the same; and 4, worse. Radiographic evaluation was performed on pre- and postoperative standard anteroposterior, outlet, and axillary views. Radiographs were reviewed to determine the presence of glenohumeral subluxation, periprosthetic lucency, component shift in position, and scapular notching.
STATISTICAL ANALYSIS
Descriptive statistics are reported as mean (range) for continuous measures and number (percentage) for discrete variables. The Wilcoxon signed-rank test was used for preoperative vs postoperative changes. The alpha level for all tests was set at 0.05 for statistical significance.
RESULTS
CLINICAL OUTCOME
At a mean of 22 months (range, 7-38 months) follow-up after revision, active ROM was significantly improved. Active flexion increased significantly from a mean of 93° (range, 30°-120°) to 138° (range, 95°-170°) (P = 0.021). Active external rotation with the elbow on the side increased significantly from 8° (range, −20°-15°) to 25° (range, −10°-60°) (P = 0.034), and increased with the arm held at 90° abduction from 13° (range, 0°-20°) to 49° (range, 0°-80°) (P = 0.025). Mean pain scores improved from 4.2 to 13.3 points (P < 0.001). VAS improved significantly from 9 to 1 (P < 0.0001). The mean Constant Scores improved from 21 (range, 18-32) to 63 (range, 43-90) (P = 0.006). The final SST was 7 per 12. Subjectively, 4 patients rated their shoulder as much better, 8 as better, and 1 as the same as preoperatively. No intra- or postoperative complications, including infections, were observed. The mean duration of the procedure was 60 minutes (range, 30-75 minutes).
Continue to: RADIOLOGICAL OUTCOME
RADIOLOGICAL OUTCOME
No periprosthetic lucency or shift in component was observed at the last follow-up. There was no scapular notching. No resorption of the tuberosities, and no fractures of the acromion or the scapular spine were observed.
DISCUSSION
In this retrospective study, failure of TSA with a metal-backed glenoid implant was successfully revised to RSA. In 10 patients, the use of a universal platform system allowed an easier conversion without removal of the humeral stem or the glenoid component (Figures 3A-3D). Twelve of the 13 patients were satisfied or very satisfied at the last follow-up. None of the patients were in pain, and the mean Constant score was 63. In all the cases, the glenoid baseplate was not changed. In 3 cases the humeral stem was changed without any fracture of the tuberosities of need for an osteotomy. This greatly simplified the revision procedure, as glenoid revisions can be very challenging. Indeed, it is often difficult to assess precisely preoperatively the remaining glenoid bone stock after removal of the glenoid component and the cement. Many therapeutic options to deal with glenoid loosening have been reported in the literature: glenoid bone reconstruction after glenoid component removal and revision to a hemiarthroplasty (HA),10,16-18 glenoid bone reconstruction after glenoid component removal and revision to a new TSA with a cemented glenoid implant,16,17,19,20 and glenoid reconstruction after glenoid component removal and revision to a RSA.12,21 These authors reported that glenoid reconstruction frequently necessitates an iliac bone graft associated with a special design of the baseplate with a long post fixed into the native glenoid bone. However, sometimes implantation of an uncemented glenoid component can be unstable with a high risk of early mobilization of the implant, and 2 steps may be necessary. Conversion to a HA,10,16-18 or a TSA16,17,19,20 with a new cemented implant have both been associated with poor clinical outcome, with a high rate of recurrent glenoid loosening for the TSAs.
In our retrospective study, we reported no intra- or postoperative complications. Flury and colleagues22 reported a complication rate of 38% in 21 patients after conversion from a TSA to a RSA with a mean follow-up of 46 months. They removed all the components of the prosthesis with a crack or fracture of the humerus and/or the glenoid. Ortmaier and colleagues23 reported a rate of complication of 22.7% during the conversion of TSA to RSA. They did an osteotomy of the humeral diaphysis to extract the stem in 40% of cases and had to remove the glenoid cement in 86% of cases with severe damage of the glenoid bone in 10% of cases. Fewer complications were found in our study, as we did not need any procedure such as humeral osteotomy, cerclage, bone grafting, and/or reconstruction of the glenoid. The short operative time and the absence of extensive soft-tissue dissection, thanks to a standard deltopectoral approach, could explain the absence of infection in our series.
Other authors shared our strategy of a universal convertible system and reported their results in the literature. Castagna and colleagues24 in 2013 reported the clinical and radiological results of conversions of HA or TSA to RSA using a modular, convertible system (SMR Shoulder System, Lima Corporate). In their series, only 8 cases of TSAs were converted to RSA. They preserved, in each case, the humeral stem and the glenoid baseplate. There were no intra- or postoperative complications. The mean VAS score decreased from 8 to 2. Weber-Spickschen and colleague25 reported recently in 2015 the same experience with the same system (SMR Shoulder System). They reviewed 15 conversions of TSAs to RSAs without any removal of the implants at a mean 43-month follow-up. They reported excellent pain relief (VAS decreased from 8 to 1) and improvement in shoulder function with a low rate of complications.
Kany and colleagues26 in 2015 had already reported the advantages of a shoulder platform system for revisions. In their series, the authors included cases of failure of HAs and TSAs with loose cemented glenoids and metal-backed glenoids. The clinical and radiological results were similar, with a final Constant score of 60 (range, 42-85) and a similar rate of humeral stems which had to be changed (24%). These stems were replaced either because they were too proud or because there was not enough space to add an onlay polyethylene socket.
Continue to: Despite the encouraging results...
Despite the encouraging results reported in this study, there are some limitations. Firstly, no control group was used. Attempting to address this issue, we compared our results with the literature. Secondly, the number of patients in our study was small. Finally, the follow-up duration (mean 22 months) did not provide long-term outcomes.
CONCLUSION
This retrospective study shows that a complete convertible system facilitates conversion of TSAs to RSAs with excellent pain relief and a significant improvement in shoulder function. A platform system on both the humeral and the glenoid side reduces the operative time of the conversion with a low risk of complications.
1. Brenner BC, Ferlic DC, Clayton ML, Dennis DA. Survivorship of unconstrained total shoulder arthroplasty. J Bone Joint Surg Am. 1989;71(9):1289-1296.
2. Budge MD, Nolan EM, Heisey MH, Baker K, Wiater JM. Results of total shoulder arthroplasty with a monoblock porous tantalum glenoid component: a prospective minimum 2-year follow-up study. J Shoulder Elbow Surg. 2013;22(4):535-541. doi:10.1016/j.jse.2012.06.001.
3. Chin PY, Sperling JW, Cofield RH, Schleck C. Complications of total shoulder arthroplasty: are they fewer or different? J Shoulder Elbow Surg. 2006;15(1):19-22. doi:10.1016/j.jse.2005.05.005.
4. Torchia ME, Cofield RH, Settergren CR. Total shoulder arthroplasty with the Neer prosthesis: long-term results. J Shoulder Elbow Surg. 1997;6(6):495-505.
5. Wirth MA, Rockwood CA Jr. Complications of total shoulder-replacement surgery. J Bone Joint Surg Am. 1996;78(4):603-616.
6. Gohlke F, Rolf O. Revision of failed fracture hemiarthroplasties to reverse total shoulder prosthesis through the transhumeral approach: method incorporating a pectoralis-major-pedicled bone window. Oper Orthop Traumatol. 2007;19(2):185-208. doi:10.1007/s00064-007-1202-x.
7. Goldberg SH, Cohen MS, Young M, Bradnock B. Thermal tissue damage caused by ultrasonic cement removal from the humerus. J Bone Joint Surg Am. 2005;87(3):583-591. doi:10.2106/JBJS.D.01966.
8. Sperling JW, Cofield RH. Humeral windows in revision shoulder arthroplasty. J Shoulder Elbow Surg. 2005;14(3):258-263. doi:10.1016/j.jse.2004.09.004.
9. Chacon A, Virani N, Shannon R, Levy JC, Pupello D, Frankle M. Revision arthroplasty with use of a reverse shoulder prosthesis-allograft composite. J Bone Joint Surg Am. 2009;91(1):119-127. doi:10.2106/JBJS.H.00094.
10. Iannotti JP, Frangiamore SJ. Fate of large structural allograft for treatment of severe uncontained glenoid bone deficiency. J Shoulder Elbow Surg. 2012;21(6):765-771. doi:10.1016/j.jse.2011.08.069.
11. Kelly JD 2nd, Zhao JX, Hobgood ER, Norris TR. Clinical results of revision shoulder arthroplasty using the reverse prosthesis. J Shoulder Elbow Surg. 2012;21(11):1516-1525. doi:10.1016/j.jse.2011.11.021.
12. Melis B, Bonnevialle N, Neyton L, et al. Glenoid loosening and failure in anatomical total shoulder arthroplasty: is revision with a reverse shoulder arthroplasty a reliable option? J Shoulder Elbow Surg. 2012;21(3):342-349. doi:10.1016/j.jse.2011.05.021.
13. Constant CR, Murley AH. A clinical method of functional assessment of the shoulder. Clin Orthop Relat Res. 1987;(214):160-164.
14. Matsen FA 3rd, Ziegler DW, DeBartolo SE. Patient self-assessment of health status and function in glenohumeral degenerative joint disease. J Shoulder Elbow Surg. 1995;4(5):345-351.
15. Gilbart MK, Gerber C. Comparison of the subjective shoulder value and the Constant score. J Shoulder Elbow Surg. 2007;16(6):717-721. doi:10.1016/j.jse.2007.02.123.
16. Antuna SA, Sperling JW, Cofield RH, Rowland CM. Glenoid revision surgery after total shoulder arthroplasty. J Shoulder Elbow Surg. 2001;10(3):217-224. doi:10.1067/mse.2001.113961.
17. Cofield RH, Edgerton BC. Total shoulder arthroplasty: complications and revision surgery. Instr Course Lect. 1990;39:449-462.
18. Neyton L, Walch G, Nove-Josserand L, Edwards TB. Glenoid corticocancellous bone grafting after glenoid component removal in the treatment of glenoid loosening. J Shoulder Elbow Surg. 2006;15(2):173-179. doi:10.1016/j.jse.2005.07.010.
19. Bonnevialle N, Melis B, Neyton L, et al. Aseptic glenoid loosening or failure in total shoulder arthroplasty: revision with glenoid reimplantation. J Shoulder Elbow Surg. 2013;22(6):745-751. doi:10.1016/j.jse.2012.08.009.
20. Rodosky MW, Bigliani LU. Indications for glenoid resurfacing in shoulder arthroplasty. J Shoulder Elbow Surg. 1996;5(3):231-248.
21. Bateman E, Donald SM. Reconstruction of massive uncontained glenoid defects using a combined autograft-allograft construct with reverse shoulder arthroplasty: preliminary results. J Shoulder Elbow Surg. 2012;21(7):925-934. doi:10.1016/j.jse.2011.07.009.
22. Flury MP, Frey P, Goldhahn J, Schwyzer HK, Simmen BR. Reverse shoulder arthroplasty as a salvage procedure for failed conventional shoulder replacement due to cuff failure--midterm results. Int Orthop. 2011;35(1):53-60. doi:10.1007/s00264-010-0990-z.
23. Ortmaier R, Resch H, Hitzl W, et al. Reverse shoulder arthroplasty combined with latissimus dorsi transfer using the bone-chip technique. Int Orthop. 2013;38(3):1-7. doi:10.1007/s00264-013-2139-3.
24. Castagna A, Delcogliano M, de Caro F, et al. Conversion of shoulder arthroplasty to reverse implants: clinical and radiological results using a modular system. Int Orthop. 2013;37(7):1297-1305. doi:10.1007/s00264-013-1907-4.
25. Weber-Spickschen TS, Alfke D, Agneskirchner JD. The use of a modular system to convert an anatomical total shoulder arthroplasty to a reverse shoulder arthroplasty: Clinical and radiological results. Bone Joint J. 2015;97-B(12):1662-1667. doi:10.1302/0301-620X.97B12.35176.
26. Kany J, Amouyel T, Flamand O, Katz D, Valenti P. A convertible shoulder system: is it useful in total shoulder arthroplasty revisions? Int Orthop. 2015;39(2):299-304. doi:10.1007/s00264-014-2563-z.
ABSTRACT
Removal of a cemented glenoid component often leads to massive glenoid bone loss, which makes it difficult to implant a new glenoid baseplate. The purpose of this study was to demonstrate the feasibility of revisions with a completely convertible system and to report clinical and radiographic results of a retrospective review of 13 cases.
Between 2003 and 2011, 104 primary total shoulder arthroplasties (TSAs) were performed with an uncemented glenoid component in our group. Of these patients, 13 (average age, 64 years) were revised to reverse shoulder arthroplasty (RSA) using a modular convertible platform system and were included in this study. Average follow-up after revision was 22 months. Outcome measures included pain, range of motion, Constant-Murley scores, Simple Shoulder Tests, and subjective shoulder values. Active flexion increased significantly from a mean of 93° (range, 30°-120°) to 138° (range, 95°-170°) (P = 0.021), and active external rotation increased significantly from 8° (range, −20°-15°) to 25° (range, −10°-60°). Mean pain scores significantly improved from 4.2 to 13.3 points. The mean Constant Scores improved from 21 (range, 18-32) to 63 (range, 43-90). Subjectively, 12 patients rated their shoulder as better or much better than preoperatively. This retrospective study shows that a complete convertible system facilitates conversion of TSAs to RSAs with excellent pain relief and a significant improvement in shoulder function.
Continue to: Polyethylene glenoid components...
Polyethylene glenoid components are the gold standard in anatomic total shoulder arthroplasty (TSA). However, even though TSA survivorship exceeds 95% at 10-year follow-up,1 glenoid component loosening remains the main complication and the weak link in these implants. This complication accounts for 25% of all complications related to TSA in the literature.2 In most cases, glenoid component loosening is not isolated but combined with a rotator cuff tear, glenohumeral instability, or component malposition.
We hypothesized that a completely convertible platform system on both the humeral and the glenoid side could facilitate the revision of a failed TSA to a RSA. This would enable the surgeon to leave the humeral stem and the glenoid baseplate in place, avoiding the difficulty of stem removal and the reimplantation of a glenoid component, especially in osteoporotic glenoid bone and elderly patients. The revision procedure would then only consist of replacing the humeral head by a metallic tray and polyethylene bearing on the humeral side and by impacting a glenosphere on the glenoid baseplate (Figures 2A, 2B).
The purpose of this study was to demonstrate the feasibility of revisions with this completely convertible system and to report clinical and radiographic results of a retrospective review of 13 cases.
MATERIALS AND METHODS
PATIENT SELECTION
Between 2003 and 2011, 104 primary TSAs were performed with an uncemented glenoid component in our group. Of these patients, 18 underwent revision (17.3%). Among these 18 patients, 13 were revised to RSA using a modular convertible platform system and were included in this study, while 5 patients were revised to another TSA (2 dissociations of the polyethylene glenoid implant, 2 excessively low implantations of the glenoid baseplate, and 1 glenoid loosening). The mean age of the 13 patients (9 women, 4 men) included in this retrospective study at the time of revision was 64 years (range, 50-75 years). The reasons for revision surgery were rotator cuff tear (5, among which 2 were posterosuperior tears, and 3 were tears of the subscapularis), dislocations (5 posterior and 1 anterior, among which 4 had a B2 or C glenoid), suprascapular nerve paralysis (1), and dissociation of the polyethylene (1). The initial TSA was indicated for primary osteoarthritis with a normal cuff (9), primary osteoarthritis with a reparable cuff tear (2), posttraumatic osteoarthritis (1), and chronic dislocation (1). The right dominant shoulder was involved in 10 cases. The mean time interval between the primary TSA and the revision was 15 months (range, 1-61 months).
OPERATIVE TECHNIQUE
PREOPERATIVE PLANNING
Revision of a failed TSA is always a difficult challenge, and evaluation of bone loss on both the humeral and the glenoid sides, as well as the status of the cuff, is mandatory, even with a completely convertible arthroplasty system. The surgeon must be prepared to remove the humeral stem in case reduction of the joint is impossible. We systematically performed standard radiographs (anteroposterior, axillary, and outlet views) and computed tomography (CT) scans in order to assess both the version and positioning, as well as potential signs of loosening of the implants and the status of the cuff (continuity, degree of muscle trophicity, and fatty infiltration). A preoperative leucocyte count, sedimentation rate, and C-reactive protein rates were requested in every revision case, even if a mechanical etiology was strongly suspected.
Continue to: REVISION PROCEDURE
REVISION PROCEDURE
All the implants that had been used in the primary TSAs were Arrow Universal Shoulder Prostheses (FH Orthopedics). All revisions were performed through the previous deltopectoral approach in the beach chair position under general anesthesia with an interscalene block. Adhesions of the deep part of the deltoid were carefully released. The conjoint tendon was released, and the location of the musculocutaneous and axillary nerves was identified before any retractor was placed. In the 10 cases where the subscapularis was intact, it was peeled off the medial border of the bicipital groove to obtain sufficient length for a tension-free reinsertion.
The anatomical head of the humeral implant was disconnected from the stem and removed. All stems were found to be well fixed; there were no cases of loosening or evidence of infection. A circumferential capsular release was systematically carried out. The polyethylene glenoid onlay was then unlocked from the baseplate.
The quality of the fixation of the glenoid baseplate was systematically evaluated; no screw was found to be loose, and the fixation of all baseplates was stable. Therefore, there was no need to revise the glenoid baseplate, even when its position was considered excessively retroverted (Glenoid B2) or high. A glenosphere was impacted on the baseplate, and a polyethylene humeral bearing was then implanted on the humeral stem. The thinnest polyethylene bearing available (number 0) was chosen in all cases, and a size 36 glenosphere was chosen in 12 out of 13 cases. Intraoperative stability of the implant was satisfactory, and no impingement was found posteriorly, anteriorly, or inferiorly.
In one case, the humeral stem was a first-generation humeral implant which was not compatible with the new-generation humeral bearing, and the humeral stem had to be replaced.
In 2 cases, reduction of the RSA was either impossible or felt to be too tight, even after extensive soft-tissue release and resection of the remaining supraspinatus. The main reason for this was an excessively proud humeral stem because of an onlay polyethylene humeral bearing instead of an inlay design. However, removal of the uncemented humeral stem was always possible with no osteotomy or cortical window of the humeral shaft as the humeral stem has been designed with a bone ingrowth surface only on the metaphyseal part with a smooth surface on diaphyseal part. After removal of the stem, a small amount of humeral metaphysis was cut, and a new humeral stem was press-fit in a lower position. This allowed restoration of an appropriate tension of the soft tissue and, therefore, an easier reduction. The subscapularis was medialized and reinserted transosseously when possible with a double-row repair. In 3 cases, the subscapularis was torn and retracted at the level of the glenoid, or impossible to identify to allow its reinsertion.
Continue to: According to our infectious disease department...
According to our infectious disease department, we made a minimum of 5 cultures for each revision case looking for a possible low-grade infection. All cultures in our group are held for 14 days to assess for Propionibacterium acnes.
POSTOPERATIVE MANAGEMENT
A shoulder splint in neutral rotation was used for the first 4 weeks. Passive range of motion (ROM) was started immediately with pendulum exercises and passive anterior elevation. Active assisted and active ROM were allowed after 4 weeks, and physiotherapy was continued for 6 months. Elderly patients were referred to a center of rehabilitation. We found only 1 or 2 positive cultures (Propionibacterium acnes) for 4 patients, and we decided to consider them as a contamination. None of the patients were treated with antibiotics.
CLINICAL AND RADIOLOGICAL ASSESSMENT
Clinical evaluation included pre- and postoperative pain scores (visual analog scale [VAS]), ROM, the Constant-Murley13 score, the Simple Shoulder Test (SST),14 and the subjective shoulder value.15 Subjective satisfaction was assessed by asking the patients at follow-up how they felt compared with before surgery and was graded using a 4-point scale: 1, much better; 2, better; 3, the same; and 4, worse. Radiographic evaluation was performed on pre- and postoperative standard anteroposterior, outlet, and axillary views. Radiographs were reviewed to determine the presence of glenohumeral subluxation, periprosthetic lucency, component shift in position, and scapular notching.
STATISTICAL ANALYSIS
Descriptive statistics are reported as mean (range) for continuous measures and number (percentage) for discrete variables. The Wilcoxon signed-rank test was used for preoperative vs postoperative changes. The alpha level for all tests was set at 0.05 for statistical significance.
RESULTS
CLINICAL OUTCOME
At a mean of 22 months (range, 7-38 months) follow-up after revision, active ROM was significantly improved. Active flexion increased significantly from a mean of 93° (range, 30°-120°) to 138° (range, 95°-170°) (P = 0.021). Active external rotation with the elbow on the side increased significantly from 8° (range, −20°-15°) to 25° (range, −10°-60°) (P = 0.034), and increased with the arm held at 90° abduction from 13° (range, 0°-20°) to 49° (range, 0°-80°) (P = 0.025). Mean pain scores improved from 4.2 to 13.3 points (P < 0.001). VAS improved significantly from 9 to 1 (P < 0.0001). The mean Constant Scores improved from 21 (range, 18-32) to 63 (range, 43-90) (P = 0.006). The final SST was 7 per 12. Subjectively, 4 patients rated their shoulder as much better, 8 as better, and 1 as the same as preoperatively. No intra- or postoperative complications, including infections, were observed. The mean duration of the procedure was 60 minutes (range, 30-75 minutes).
Continue to: RADIOLOGICAL OUTCOME
RADIOLOGICAL OUTCOME
No periprosthetic lucency or shift in component was observed at the last follow-up. There was no scapular notching. No resorption of the tuberosities, and no fractures of the acromion or the scapular spine were observed.
DISCUSSION
In this retrospective study, failure of TSA with a metal-backed glenoid implant was successfully revised to RSA. In 10 patients, the use of a universal platform system allowed an easier conversion without removal of the humeral stem or the glenoid component (Figures 3A-3D). Twelve of the 13 patients were satisfied or very satisfied at the last follow-up. None of the patients were in pain, and the mean Constant score was 63. In all the cases, the glenoid baseplate was not changed. In 3 cases the humeral stem was changed without any fracture of the tuberosities of need for an osteotomy. This greatly simplified the revision procedure, as glenoid revisions can be very challenging. Indeed, it is often difficult to assess precisely preoperatively the remaining glenoid bone stock after removal of the glenoid component and the cement. Many therapeutic options to deal with glenoid loosening have been reported in the literature: glenoid bone reconstruction after glenoid component removal and revision to a hemiarthroplasty (HA),10,16-18 glenoid bone reconstruction after glenoid component removal and revision to a new TSA with a cemented glenoid implant,16,17,19,20 and glenoid reconstruction after glenoid component removal and revision to a RSA.12,21 These authors reported that glenoid reconstruction frequently necessitates an iliac bone graft associated with a special design of the baseplate with a long post fixed into the native glenoid bone. However, sometimes implantation of an uncemented glenoid component can be unstable with a high risk of early mobilization of the implant, and 2 steps may be necessary. Conversion to a HA,10,16-18 or a TSA16,17,19,20 with a new cemented implant have both been associated with poor clinical outcome, with a high rate of recurrent glenoid loosening for the TSAs.
In our retrospective study, we reported no intra- or postoperative complications. Flury and colleagues22 reported a complication rate of 38% in 21 patients after conversion from a TSA to a RSA with a mean follow-up of 46 months. They removed all the components of the prosthesis with a crack or fracture of the humerus and/or the glenoid. Ortmaier and colleagues23 reported a rate of complication of 22.7% during the conversion of TSA to RSA. They did an osteotomy of the humeral diaphysis to extract the stem in 40% of cases and had to remove the glenoid cement in 86% of cases with severe damage of the glenoid bone in 10% of cases. Fewer complications were found in our study, as we did not need any procedure such as humeral osteotomy, cerclage, bone grafting, and/or reconstruction of the glenoid. The short operative time and the absence of extensive soft-tissue dissection, thanks to a standard deltopectoral approach, could explain the absence of infection in our series.
Other authors shared our strategy of a universal convertible system and reported their results in the literature. Castagna and colleagues24 in 2013 reported the clinical and radiological results of conversions of HA or TSA to RSA using a modular, convertible system (SMR Shoulder System, Lima Corporate). In their series, only 8 cases of TSAs were converted to RSA. They preserved, in each case, the humeral stem and the glenoid baseplate. There were no intra- or postoperative complications. The mean VAS score decreased from 8 to 2. Weber-Spickschen and colleague25 reported recently in 2015 the same experience with the same system (SMR Shoulder System). They reviewed 15 conversions of TSAs to RSAs without any removal of the implants at a mean 43-month follow-up. They reported excellent pain relief (VAS decreased from 8 to 1) and improvement in shoulder function with a low rate of complications.
Kany and colleagues26 in 2015 had already reported the advantages of a shoulder platform system for revisions. In their series, the authors included cases of failure of HAs and TSAs with loose cemented glenoids and metal-backed glenoids. The clinical and radiological results were similar, with a final Constant score of 60 (range, 42-85) and a similar rate of humeral stems which had to be changed (24%). These stems were replaced either because they were too proud or because there was not enough space to add an onlay polyethylene socket.
Continue to: Despite the encouraging results...
Despite the encouraging results reported in this study, there are some limitations. Firstly, no control group was used. Attempting to address this issue, we compared our results with the literature. Secondly, the number of patients in our study was small. Finally, the follow-up duration (mean 22 months) did not provide long-term outcomes.
CONCLUSION
This retrospective study shows that a complete convertible system facilitates conversion of TSAs to RSAs with excellent pain relief and a significant improvement in shoulder function. A platform system on both the humeral and the glenoid side reduces the operative time of the conversion with a low risk of complications.
ABSTRACT
Removal of a cemented glenoid component often leads to massive glenoid bone loss, which makes it difficult to implant a new glenoid baseplate. The purpose of this study was to demonstrate the feasibility of revisions with a completely convertible system and to report clinical and radiographic results of a retrospective review of 13 cases.
Between 2003 and 2011, 104 primary total shoulder arthroplasties (TSAs) were performed with an uncemented glenoid component in our group. Of these patients, 13 (average age, 64 years) were revised to reverse shoulder arthroplasty (RSA) using a modular convertible platform system and were included in this study. Average follow-up after revision was 22 months. Outcome measures included pain, range of motion, Constant-Murley scores, Simple Shoulder Tests, and subjective shoulder values. Active flexion increased significantly from a mean of 93° (range, 30°-120°) to 138° (range, 95°-170°) (P = 0.021), and active external rotation increased significantly from 8° (range, −20°-15°) to 25° (range, −10°-60°). Mean pain scores significantly improved from 4.2 to 13.3 points. The mean Constant Scores improved from 21 (range, 18-32) to 63 (range, 43-90). Subjectively, 12 patients rated their shoulder as better or much better than preoperatively. This retrospective study shows that a complete convertible system facilitates conversion of TSAs to RSAs with excellent pain relief and a significant improvement in shoulder function.
Continue to: Polyethylene glenoid components...
Polyethylene glenoid components are the gold standard in anatomic total shoulder arthroplasty (TSA). However, even though TSA survivorship exceeds 95% at 10-year follow-up,1 glenoid component loosening remains the main complication and the weak link in these implants. This complication accounts for 25% of all complications related to TSA in the literature.2 In most cases, glenoid component loosening is not isolated but combined with a rotator cuff tear, glenohumeral instability, or component malposition.
We hypothesized that a completely convertible platform system on both the humeral and the glenoid side could facilitate the revision of a failed TSA to a RSA. This would enable the surgeon to leave the humeral stem and the glenoid baseplate in place, avoiding the difficulty of stem removal and the reimplantation of a glenoid component, especially in osteoporotic glenoid bone and elderly patients. The revision procedure would then only consist of replacing the humeral head by a metallic tray and polyethylene bearing on the humeral side and by impacting a glenosphere on the glenoid baseplate (Figures 2A, 2B).
The purpose of this study was to demonstrate the feasibility of revisions with this completely convertible system and to report clinical and radiographic results of a retrospective review of 13 cases.
MATERIALS AND METHODS
PATIENT SELECTION
Between 2003 and 2011, 104 primary TSAs were performed with an uncemented glenoid component in our group. Of these patients, 18 underwent revision (17.3%). Among these 18 patients, 13 were revised to RSA using a modular convertible platform system and were included in this study, while 5 patients were revised to another TSA (2 dissociations of the polyethylene glenoid implant, 2 excessively low implantations of the glenoid baseplate, and 1 glenoid loosening). The mean age of the 13 patients (9 women, 4 men) included in this retrospective study at the time of revision was 64 years (range, 50-75 years). The reasons for revision surgery were rotator cuff tear (5, among which 2 were posterosuperior tears, and 3 were tears of the subscapularis), dislocations (5 posterior and 1 anterior, among which 4 had a B2 or C glenoid), suprascapular nerve paralysis (1), and dissociation of the polyethylene (1). The initial TSA was indicated for primary osteoarthritis with a normal cuff (9), primary osteoarthritis with a reparable cuff tear (2), posttraumatic osteoarthritis (1), and chronic dislocation (1). The right dominant shoulder was involved in 10 cases. The mean time interval between the primary TSA and the revision was 15 months (range, 1-61 months).
OPERATIVE TECHNIQUE
PREOPERATIVE PLANNING
Revision of a failed TSA is always a difficult challenge, and evaluation of bone loss on both the humeral and the glenoid sides, as well as the status of the cuff, is mandatory, even with a completely convertible arthroplasty system. The surgeon must be prepared to remove the humeral stem in case reduction of the joint is impossible. We systematically performed standard radiographs (anteroposterior, axillary, and outlet views) and computed tomography (CT) scans in order to assess both the version and positioning, as well as potential signs of loosening of the implants and the status of the cuff (continuity, degree of muscle trophicity, and fatty infiltration). A preoperative leucocyte count, sedimentation rate, and C-reactive protein rates were requested in every revision case, even if a mechanical etiology was strongly suspected.
Continue to: REVISION PROCEDURE
REVISION PROCEDURE
All the implants that had been used in the primary TSAs were Arrow Universal Shoulder Prostheses (FH Orthopedics). All revisions were performed through the previous deltopectoral approach in the beach chair position under general anesthesia with an interscalene block. Adhesions of the deep part of the deltoid were carefully released. The conjoint tendon was released, and the location of the musculocutaneous and axillary nerves was identified before any retractor was placed. In the 10 cases where the subscapularis was intact, it was peeled off the medial border of the bicipital groove to obtain sufficient length for a tension-free reinsertion.
The anatomical head of the humeral implant was disconnected from the stem and removed. All stems were found to be well fixed; there were no cases of loosening or evidence of infection. A circumferential capsular release was systematically carried out. The polyethylene glenoid onlay was then unlocked from the baseplate.
The quality of the fixation of the glenoid baseplate was systematically evaluated; no screw was found to be loose, and the fixation of all baseplates was stable. Therefore, there was no need to revise the glenoid baseplate, even when its position was considered excessively retroverted (Glenoid B2) or high. A glenosphere was impacted on the baseplate, and a polyethylene humeral bearing was then implanted on the humeral stem. The thinnest polyethylene bearing available (number 0) was chosen in all cases, and a size 36 glenosphere was chosen in 12 out of 13 cases. Intraoperative stability of the implant was satisfactory, and no impingement was found posteriorly, anteriorly, or inferiorly.
In one case, the humeral stem was a first-generation humeral implant which was not compatible with the new-generation humeral bearing, and the humeral stem had to be replaced.
In 2 cases, reduction of the RSA was either impossible or felt to be too tight, even after extensive soft-tissue release and resection of the remaining supraspinatus. The main reason for this was an excessively proud humeral stem because of an onlay polyethylene humeral bearing instead of an inlay design. However, removal of the uncemented humeral stem was always possible with no osteotomy or cortical window of the humeral shaft as the humeral stem has been designed with a bone ingrowth surface only on the metaphyseal part with a smooth surface on diaphyseal part. After removal of the stem, a small amount of humeral metaphysis was cut, and a new humeral stem was press-fit in a lower position. This allowed restoration of an appropriate tension of the soft tissue and, therefore, an easier reduction. The subscapularis was medialized and reinserted transosseously when possible with a double-row repair. In 3 cases, the subscapularis was torn and retracted at the level of the glenoid, or impossible to identify to allow its reinsertion.
Continue to: According to our infectious disease department...
According to our infectious disease department, we made a minimum of 5 cultures for each revision case looking for a possible low-grade infection. All cultures in our group are held for 14 days to assess for Propionibacterium acnes.
POSTOPERATIVE MANAGEMENT
A shoulder splint in neutral rotation was used for the first 4 weeks. Passive range of motion (ROM) was started immediately with pendulum exercises and passive anterior elevation. Active assisted and active ROM were allowed after 4 weeks, and physiotherapy was continued for 6 months. Elderly patients were referred to a center of rehabilitation. We found only 1 or 2 positive cultures (Propionibacterium acnes) for 4 patients, and we decided to consider them as a contamination. None of the patients were treated with antibiotics.
CLINICAL AND RADIOLOGICAL ASSESSMENT
Clinical evaluation included pre- and postoperative pain scores (visual analog scale [VAS]), ROM, the Constant-Murley13 score, the Simple Shoulder Test (SST),14 and the subjective shoulder value.15 Subjective satisfaction was assessed by asking the patients at follow-up how they felt compared with before surgery and was graded using a 4-point scale: 1, much better; 2, better; 3, the same; and 4, worse. Radiographic evaluation was performed on pre- and postoperative standard anteroposterior, outlet, and axillary views. Radiographs were reviewed to determine the presence of glenohumeral subluxation, periprosthetic lucency, component shift in position, and scapular notching.
STATISTICAL ANALYSIS
Descriptive statistics are reported as mean (range) for continuous measures and number (percentage) for discrete variables. The Wilcoxon signed-rank test was used for preoperative vs postoperative changes. The alpha level for all tests was set at 0.05 for statistical significance.
RESULTS
CLINICAL OUTCOME
At a mean of 22 months (range, 7-38 months) follow-up after revision, active ROM was significantly improved. Active flexion increased significantly from a mean of 93° (range, 30°-120°) to 138° (range, 95°-170°) (P = 0.021). Active external rotation with the elbow on the side increased significantly from 8° (range, −20°-15°) to 25° (range, −10°-60°) (P = 0.034), and increased with the arm held at 90° abduction from 13° (range, 0°-20°) to 49° (range, 0°-80°) (P = 0.025). Mean pain scores improved from 4.2 to 13.3 points (P < 0.001). VAS improved significantly from 9 to 1 (P < 0.0001). The mean Constant Scores improved from 21 (range, 18-32) to 63 (range, 43-90) (P = 0.006). The final SST was 7 per 12. Subjectively, 4 patients rated their shoulder as much better, 8 as better, and 1 as the same as preoperatively. No intra- or postoperative complications, including infections, were observed. The mean duration of the procedure was 60 minutes (range, 30-75 minutes).
Continue to: RADIOLOGICAL OUTCOME
RADIOLOGICAL OUTCOME
No periprosthetic lucency or shift in component was observed at the last follow-up. There was no scapular notching. No resorption of the tuberosities, and no fractures of the acromion or the scapular spine were observed.
DISCUSSION
In this retrospective study, failure of TSA with a metal-backed glenoid implant was successfully revised to RSA. In 10 patients, the use of a universal platform system allowed an easier conversion without removal of the humeral stem or the glenoid component (Figures 3A-3D). Twelve of the 13 patients were satisfied or very satisfied at the last follow-up. None of the patients were in pain, and the mean Constant score was 63. In all the cases, the glenoid baseplate was not changed. In 3 cases the humeral stem was changed without any fracture of the tuberosities of need for an osteotomy. This greatly simplified the revision procedure, as glenoid revisions can be very challenging. Indeed, it is often difficult to assess precisely preoperatively the remaining glenoid bone stock after removal of the glenoid component and the cement. Many therapeutic options to deal with glenoid loosening have been reported in the literature: glenoid bone reconstruction after glenoid component removal and revision to a hemiarthroplasty (HA),10,16-18 glenoid bone reconstruction after glenoid component removal and revision to a new TSA with a cemented glenoid implant,16,17,19,20 and glenoid reconstruction after glenoid component removal and revision to a RSA.12,21 These authors reported that glenoid reconstruction frequently necessitates an iliac bone graft associated with a special design of the baseplate with a long post fixed into the native glenoid bone. However, sometimes implantation of an uncemented glenoid component can be unstable with a high risk of early mobilization of the implant, and 2 steps may be necessary. Conversion to a HA,10,16-18 or a TSA16,17,19,20 with a new cemented implant have both been associated with poor clinical outcome, with a high rate of recurrent glenoid loosening for the TSAs.
In our retrospective study, we reported no intra- or postoperative complications. Flury and colleagues22 reported a complication rate of 38% in 21 patients after conversion from a TSA to a RSA with a mean follow-up of 46 months. They removed all the components of the prosthesis with a crack or fracture of the humerus and/or the glenoid. Ortmaier and colleagues23 reported a rate of complication of 22.7% during the conversion of TSA to RSA. They did an osteotomy of the humeral diaphysis to extract the stem in 40% of cases and had to remove the glenoid cement in 86% of cases with severe damage of the glenoid bone in 10% of cases. Fewer complications were found in our study, as we did not need any procedure such as humeral osteotomy, cerclage, bone grafting, and/or reconstruction of the glenoid. The short operative time and the absence of extensive soft-tissue dissection, thanks to a standard deltopectoral approach, could explain the absence of infection in our series.
Other authors shared our strategy of a universal convertible system and reported their results in the literature. Castagna and colleagues24 in 2013 reported the clinical and radiological results of conversions of HA or TSA to RSA using a modular, convertible system (SMR Shoulder System, Lima Corporate). In their series, only 8 cases of TSAs were converted to RSA. They preserved, in each case, the humeral stem and the glenoid baseplate. There were no intra- or postoperative complications. The mean VAS score decreased from 8 to 2. Weber-Spickschen and colleague25 reported recently in 2015 the same experience with the same system (SMR Shoulder System). They reviewed 15 conversions of TSAs to RSAs without any removal of the implants at a mean 43-month follow-up. They reported excellent pain relief (VAS decreased from 8 to 1) and improvement in shoulder function with a low rate of complications.
Kany and colleagues26 in 2015 had already reported the advantages of a shoulder platform system for revisions. In their series, the authors included cases of failure of HAs and TSAs with loose cemented glenoids and metal-backed glenoids. The clinical and radiological results were similar, with a final Constant score of 60 (range, 42-85) and a similar rate of humeral stems which had to be changed (24%). These stems were replaced either because they were too proud or because there was not enough space to add an onlay polyethylene socket.
Continue to: Despite the encouraging results...
Despite the encouraging results reported in this study, there are some limitations. Firstly, no control group was used. Attempting to address this issue, we compared our results with the literature. Secondly, the number of patients in our study was small. Finally, the follow-up duration (mean 22 months) did not provide long-term outcomes.
CONCLUSION
This retrospective study shows that a complete convertible system facilitates conversion of TSAs to RSAs with excellent pain relief and a significant improvement in shoulder function. A platform system on both the humeral and the glenoid side reduces the operative time of the conversion with a low risk of complications.
1. Brenner BC, Ferlic DC, Clayton ML, Dennis DA. Survivorship of unconstrained total shoulder arthroplasty. J Bone Joint Surg Am. 1989;71(9):1289-1296.
2. Budge MD, Nolan EM, Heisey MH, Baker K, Wiater JM. Results of total shoulder arthroplasty with a monoblock porous tantalum glenoid component: a prospective minimum 2-year follow-up study. J Shoulder Elbow Surg. 2013;22(4):535-541. doi:10.1016/j.jse.2012.06.001.
3. Chin PY, Sperling JW, Cofield RH, Schleck C. Complications of total shoulder arthroplasty: are they fewer or different? J Shoulder Elbow Surg. 2006;15(1):19-22. doi:10.1016/j.jse.2005.05.005.
4. Torchia ME, Cofield RH, Settergren CR. Total shoulder arthroplasty with the Neer prosthesis: long-term results. J Shoulder Elbow Surg. 1997;6(6):495-505.
5. Wirth MA, Rockwood CA Jr. Complications of total shoulder-replacement surgery. J Bone Joint Surg Am. 1996;78(4):603-616.
6. Gohlke F, Rolf O. Revision of failed fracture hemiarthroplasties to reverse total shoulder prosthesis through the transhumeral approach: method incorporating a pectoralis-major-pedicled bone window. Oper Orthop Traumatol. 2007;19(2):185-208. doi:10.1007/s00064-007-1202-x.
7. Goldberg SH, Cohen MS, Young M, Bradnock B. Thermal tissue damage caused by ultrasonic cement removal from the humerus. J Bone Joint Surg Am. 2005;87(3):583-591. doi:10.2106/JBJS.D.01966.
8. Sperling JW, Cofield RH. Humeral windows in revision shoulder arthroplasty. J Shoulder Elbow Surg. 2005;14(3):258-263. doi:10.1016/j.jse.2004.09.004.
9. Chacon A, Virani N, Shannon R, Levy JC, Pupello D, Frankle M. Revision arthroplasty with use of a reverse shoulder prosthesis-allograft composite. J Bone Joint Surg Am. 2009;91(1):119-127. doi:10.2106/JBJS.H.00094.
10. Iannotti JP, Frangiamore SJ. Fate of large structural allograft for treatment of severe uncontained glenoid bone deficiency. J Shoulder Elbow Surg. 2012;21(6):765-771. doi:10.1016/j.jse.2011.08.069.
11. Kelly JD 2nd, Zhao JX, Hobgood ER, Norris TR. Clinical results of revision shoulder arthroplasty using the reverse prosthesis. J Shoulder Elbow Surg. 2012;21(11):1516-1525. doi:10.1016/j.jse.2011.11.021.
12. Melis B, Bonnevialle N, Neyton L, et al. Glenoid loosening and failure in anatomical total shoulder arthroplasty: is revision with a reverse shoulder arthroplasty a reliable option? J Shoulder Elbow Surg. 2012;21(3):342-349. doi:10.1016/j.jse.2011.05.021.
13. Constant CR, Murley AH. A clinical method of functional assessment of the shoulder. Clin Orthop Relat Res. 1987;(214):160-164.
14. Matsen FA 3rd, Ziegler DW, DeBartolo SE. Patient self-assessment of health status and function in glenohumeral degenerative joint disease. J Shoulder Elbow Surg. 1995;4(5):345-351.
15. Gilbart MK, Gerber C. Comparison of the subjective shoulder value and the Constant score. J Shoulder Elbow Surg. 2007;16(6):717-721. doi:10.1016/j.jse.2007.02.123.
16. Antuna SA, Sperling JW, Cofield RH, Rowland CM. Glenoid revision surgery after total shoulder arthroplasty. J Shoulder Elbow Surg. 2001;10(3):217-224. doi:10.1067/mse.2001.113961.
17. Cofield RH, Edgerton BC. Total shoulder arthroplasty: complications and revision surgery. Instr Course Lect. 1990;39:449-462.
18. Neyton L, Walch G, Nove-Josserand L, Edwards TB. Glenoid corticocancellous bone grafting after glenoid component removal in the treatment of glenoid loosening. J Shoulder Elbow Surg. 2006;15(2):173-179. doi:10.1016/j.jse.2005.07.010.
19. Bonnevialle N, Melis B, Neyton L, et al. Aseptic glenoid loosening or failure in total shoulder arthroplasty: revision with glenoid reimplantation. J Shoulder Elbow Surg. 2013;22(6):745-751. doi:10.1016/j.jse.2012.08.009.
20. Rodosky MW, Bigliani LU. Indications for glenoid resurfacing in shoulder arthroplasty. J Shoulder Elbow Surg. 1996;5(3):231-248.
21. Bateman E, Donald SM. Reconstruction of massive uncontained glenoid defects using a combined autograft-allograft construct with reverse shoulder arthroplasty: preliminary results. J Shoulder Elbow Surg. 2012;21(7):925-934. doi:10.1016/j.jse.2011.07.009.
22. Flury MP, Frey P, Goldhahn J, Schwyzer HK, Simmen BR. Reverse shoulder arthroplasty as a salvage procedure for failed conventional shoulder replacement due to cuff failure--midterm results. Int Orthop. 2011;35(1):53-60. doi:10.1007/s00264-010-0990-z.
23. Ortmaier R, Resch H, Hitzl W, et al. Reverse shoulder arthroplasty combined with latissimus dorsi transfer using the bone-chip technique. Int Orthop. 2013;38(3):1-7. doi:10.1007/s00264-013-2139-3.
24. Castagna A, Delcogliano M, de Caro F, et al. Conversion of shoulder arthroplasty to reverse implants: clinical and radiological results using a modular system. Int Orthop. 2013;37(7):1297-1305. doi:10.1007/s00264-013-1907-4.
25. Weber-Spickschen TS, Alfke D, Agneskirchner JD. The use of a modular system to convert an anatomical total shoulder arthroplasty to a reverse shoulder arthroplasty: Clinical and radiological results. Bone Joint J. 2015;97-B(12):1662-1667. doi:10.1302/0301-620X.97B12.35176.
26. Kany J, Amouyel T, Flamand O, Katz D, Valenti P. A convertible shoulder system: is it useful in total shoulder arthroplasty revisions? Int Orthop. 2015;39(2):299-304. doi:10.1007/s00264-014-2563-z.
1. Brenner BC, Ferlic DC, Clayton ML, Dennis DA. Survivorship of unconstrained total shoulder arthroplasty. J Bone Joint Surg Am. 1989;71(9):1289-1296.
2. Budge MD, Nolan EM, Heisey MH, Baker K, Wiater JM. Results of total shoulder arthroplasty with a monoblock porous tantalum glenoid component: a prospective minimum 2-year follow-up study. J Shoulder Elbow Surg. 2013;22(4):535-541. doi:10.1016/j.jse.2012.06.001.
3. Chin PY, Sperling JW, Cofield RH, Schleck C. Complications of total shoulder arthroplasty: are they fewer or different? J Shoulder Elbow Surg. 2006;15(1):19-22. doi:10.1016/j.jse.2005.05.005.
4. Torchia ME, Cofield RH, Settergren CR. Total shoulder arthroplasty with the Neer prosthesis: long-term results. J Shoulder Elbow Surg. 1997;6(6):495-505.
5. Wirth MA, Rockwood CA Jr. Complications of total shoulder-replacement surgery. J Bone Joint Surg Am. 1996;78(4):603-616.
6. Gohlke F, Rolf O. Revision of failed fracture hemiarthroplasties to reverse total shoulder prosthesis through the transhumeral approach: method incorporating a pectoralis-major-pedicled bone window. Oper Orthop Traumatol. 2007;19(2):185-208. doi:10.1007/s00064-007-1202-x.
7. Goldberg SH, Cohen MS, Young M, Bradnock B. Thermal tissue damage caused by ultrasonic cement removal from the humerus. J Bone Joint Surg Am. 2005;87(3):583-591. doi:10.2106/JBJS.D.01966.
8. Sperling JW, Cofield RH. Humeral windows in revision shoulder arthroplasty. J Shoulder Elbow Surg. 2005;14(3):258-263. doi:10.1016/j.jse.2004.09.004.
9. Chacon A, Virani N, Shannon R, Levy JC, Pupello D, Frankle M. Revision arthroplasty with use of a reverse shoulder prosthesis-allograft composite. J Bone Joint Surg Am. 2009;91(1):119-127. doi:10.2106/JBJS.H.00094.
10. Iannotti JP, Frangiamore SJ. Fate of large structural allograft for treatment of severe uncontained glenoid bone deficiency. J Shoulder Elbow Surg. 2012;21(6):765-771. doi:10.1016/j.jse.2011.08.069.
11. Kelly JD 2nd, Zhao JX, Hobgood ER, Norris TR. Clinical results of revision shoulder arthroplasty using the reverse prosthesis. J Shoulder Elbow Surg. 2012;21(11):1516-1525. doi:10.1016/j.jse.2011.11.021.
12. Melis B, Bonnevialle N, Neyton L, et al. Glenoid loosening and failure in anatomical total shoulder arthroplasty: is revision with a reverse shoulder arthroplasty a reliable option? J Shoulder Elbow Surg. 2012;21(3):342-349. doi:10.1016/j.jse.2011.05.021.
13. Constant CR, Murley AH. A clinical method of functional assessment of the shoulder. Clin Orthop Relat Res. 1987;(214):160-164.
14. Matsen FA 3rd, Ziegler DW, DeBartolo SE. Patient self-assessment of health status and function in glenohumeral degenerative joint disease. J Shoulder Elbow Surg. 1995;4(5):345-351.
15. Gilbart MK, Gerber C. Comparison of the subjective shoulder value and the Constant score. J Shoulder Elbow Surg. 2007;16(6):717-721. doi:10.1016/j.jse.2007.02.123.
16. Antuna SA, Sperling JW, Cofield RH, Rowland CM. Glenoid revision surgery after total shoulder arthroplasty. J Shoulder Elbow Surg. 2001;10(3):217-224. doi:10.1067/mse.2001.113961.
17. Cofield RH, Edgerton BC. Total shoulder arthroplasty: complications and revision surgery. Instr Course Lect. 1990;39:449-462.
18. Neyton L, Walch G, Nove-Josserand L, Edwards TB. Glenoid corticocancellous bone grafting after glenoid component removal in the treatment of glenoid loosening. J Shoulder Elbow Surg. 2006;15(2):173-179. doi:10.1016/j.jse.2005.07.010.
19. Bonnevialle N, Melis B, Neyton L, et al. Aseptic glenoid loosening or failure in total shoulder arthroplasty: revision with glenoid reimplantation. J Shoulder Elbow Surg. 2013;22(6):745-751. doi:10.1016/j.jse.2012.08.009.
20. Rodosky MW, Bigliani LU. Indications for glenoid resurfacing in shoulder arthroplasty. J Shoulder Elbow Surg. 1996;5(3):231-248.
21. Bateman E, Donald SM. Reconstruction of massive uncontained glenoid defects using a combined autograft-allograft construct with reverse shoulder arthroplasty: preliminary results. J Shoulder Elbow Surg. 2012;21(7):925-934. doi:10.1016/j.jse.2011.07.009.
22. Flury MP, Frey P, Goldhahn J, Schwyzer HK, Simmen BR. Reverse shoulder arthroplasty as a salvage procedure for failed conventional shoulder replacement due to cuff failure--midterm results. Int Orthop. 2011;35(1):53-60. doi:10.1007/s00264-010-0990-z.
23. Ortmaier R, Resch H, Hitzl W, et al. Reverse shoulder arthroplasty combined with latissimus dorsi transfer using the bone-chip technique. Int Orthop. 2013;38(3):1-7. doi:10.1007/s00264-013-2139-3.
24. Castagna A, Delcogliano M, de Caro F, et al. Conversion of shoulder arthroplasty to reverse implants: clinical and radiological results using a modular system. Int Orthop. 2013;37(7):1297-1305. doi:10.1007/s00264-013-1907-4.
25. Weber-Spickschen TS, Alfke D, Agneskirchner JD. The use of a modular system to convert an anatomical total shoulder arthroplasty to a reverse shoulder arthroplasty: Clinical and radiological results. Bone Joint J. 2015;97-B(12):1662-1667. doi:10.1302/0301-620X.97B12.35176.
26. Kany J, Amouyel T, Flamand O, Katz D, Valenti P. A convertible shoulder system: is it useful in total shoulder arthroplasty revisions? Int Orthop. 2015;39(2):299-304. doi:10.1007/s00264-014-2563-z.
TAKE-HOME POINTS
- Full polyethylene is the gold standard, but the revision of glenoid loosening leads a difficult reconstruction of a glenoid bone.
- A complete convertible system facilitates the revision and decreases the rate of complications.
- The functional and subjective results of the revision are good.
- During the revision, the metalback was well fixed without any sign of loosening.
- In 3 cases the humeral stem was changed; in 2 cases there was no space to reduce (onlay system) and in 1 case it was an older design, nonadapted.
