Cam-Type FAI
Cam-type impingement results from femoral-sided deformities. The mechanism was described as inclusion-type impingement in which “jamming of an abnormal femoral head with increasing radius into the acetabulum during forceful motion, especially flexion.”1 This results in outside-in abrasion of the acetabular cartilage of the anterosuperior rim with detachment of the “principally uninvolved labrum”1 and potentially delamination of the adjacent cartilage from the subchondral bone. Ganz and colleagues1 recognized in their initial descriptions of FAI that cam-type FAI could involve decreased femoral version, femoral head–neck junction asphericity, and decreased head–neck offset. The complexity and variability in the topography and geography of the cam morphology have been increasingly recognized. Accurate understanding and characterization of the proximal femoral deformity are important in guiding surgical correction of the cam deformity.
Advances in understanding the prevalence of the cam morphology and the association with OA have been important to our understanding of the pathophysiology of FAI. Several studies12 have established that a cam morphology of the proximal femur (defined by a variety of different metrics) is common among asymptomatic individuals. In light of this fact, a description of the femoral anatomy as a “cam morphology” rather than a cam deformity is now favored. Similarly, FAI is better used to refer to symptomatic individuals and is not equivalent to a cam morphology. The cam morphology seems significantly more common among athletes. Siebenrock and colleagues13 demonstrated the correlation of high-level athletics during late stages of skeletal immaturity and development of a cam morphology. A recent systematic review of 9 studies found that elite male athletes in late skeletal immaturity were 2 to 8 times more likely to develop a cam morphology before skeletal maturity.14Several population-based studies15,16 have quantified the apparent association of the cam morphology with hip OA. However, the studies were limited in their ability to adequately define the presence of cam morphology based on anteroposterior (AP) pelvis radiographs.
In a prospective study, Agricola and colleagues15 found the risk of OA was increased 2.4 times in the setting of moderate cam morphology (α angle, >60°) over a 5-year period. Thomas and colleagues16 found increased risk in a female cohort when the α angle was >65°.
Treatment of cam-type FAI is focused on adequate correction of the abnormal bone morphology. Inadequate or inappropriate bony correction of FAI is a common cause of treatment failure and is more common with arthroscopic techniques.9,10,17 Inadequate bony resection may be the result of surgical inexperience, poor visualization, or lack of understanding of the underlying bony deformity. Modern osteoplasty techniques also focus on gradual bony contour correction that restores the normal concavity–convexity transition of the head–neck junction. Overresection of the cam deformity not only may increase the risk of femoral neck fracture but may result in early disruption of the hip fluid seal from loss of contact between the femoral head and the acetabular labrum earlier in the arc of motion. In addition, high range-of-motion impingement can be seen in various athletic populations (dance, gymnastics, martial arts, hockey goalies), and the regions of impingement tend to be farther away from classically described impingement. Impingement in these situations occurs at the distal femoral neck and subspine regions, adding a level of complexity and unpredictability from a surgical standpoint.
FAI can also occur in the setting of more complex deformities than the typical cam morphology. Complex cases of FAI caused by slipped capital femoral epiphysis (SCFE) and residual Legg-Calvé-Perthes disease are relatively common. Complex deformities may also result in extra-articular impingement of the proximal femur (greater/lesser trochanter, distal femoral neck) on the pelvis (ilium, ischium) in addition to typical FAI. Mild to moderate cases of residual SCFE may be adequately treated with osteoplasty by arthroscopic techniques. In the setting of more severe residual SCFE, presence of underlying femoral retroversion and retrotilt of the femoral epiphysis may prevent adequate deformity correction and motion improvement by arthroscopy. Surgical hip dislocation (with or without relative femoral neck lengthening) and/or proximal femoral flexion derotational osteotomy may be the best means of treatment in these more severe deformities but may be dependent on the chronicity of the deformity and associated compensatory changes occurring on the acetabular side. Similarly, in moderate to severe residual Legg-Calvé-Perthes disease, presence of coxa vara, high greater trochanter, short femoral neck, and ovoid femoral head may be better treated in open techniques to allow comprehensive deformity correction, including correction of acetabular dysplasia in some cases.
Pincer-Type FAI
Pincer-type FAI results from acetabular-sided deformities in which acetabular deformity leads to impaction-type impingement with “linear contact between the acetabular rim and the femoral head–neck junction.”1 Pincer FAI causes primarily labral damage with progressive degeneration and, in some cases, ossification of the acetabular labrum that further worsens the acetabular overcoverage and premature rim impaction. Chondral damage in pincer-type FAI is generally less significant and limited to the peripheral acetabular rim.