Fragility fractures are caused by falls from standing height or repetitive physiological loads.1 With the growing aging population in the United States, it is estimated that 3 million people will be affected by fragility fractures yearly.2 In the setting of osseous insufficiency, fractures that are typically associated with high-energy trauma are encountered in patients who simply trip over a parking lot curb or fall off their bike. After surgery, the severe disruption of patients’ lives continues with a prolonged rehabilitation period.
Fragility fractures are not only traumatizing for patients; they are also associated with significantly increased mortality. A study by Gosch and colleagues found that 70.6% of patients died during the normal follow-up period, and 29.4% of patients died within the first year of suffering a fracture.3 Also, the mean life expectancy post-fragility fracture was only 527 days.3 Diagnosis and treatment of osteoporosis is imperative to prevent fragility fractures before they occur.
RISK FACTORS AND CAUSES
The incidence of fragility fractures increases in patients with comorbidities such as thyroid disease, diabetes, hypertension, and heart disease.4 Hyperthyroidism and treated hypothyroidism cause an imbalance between osteoblast and osteoclast activity, resulting in osteoporosis.5 A thyroid-stimulating hormone level < 0.1 increases the risk of vertebral and non-vertebral fractures by a factor of 4.5 and 3.2 mIU/L respectively.4 Patients with diabetes also have an increased risk of fragility fractures, which is due to impaired healing capabilities, especially that of bone healing. Approximately 2 million people are affected by type 1 diabetes in the United States, and 20% of those patients will develop osteoporosis.6
Hypertension and osteoporosis are 2 diseases that occur often in the elderly. Common etiological factors believed to cause both hypertension and osteoporosis are low calcium intake, high consumption of salt, and vitamin D and vitamin K deficiency. Also, hypertension treated with loop diuretics has been found to cause negative effects on bone and increase the risk of osteoporosis.7 The only antihypertensive medications that preserve bone mineral density (BMD) and reduce fracture risk are thiazide diuretics.7 Lastly, an association between coronary artery disease and osteoporosis has been hypothesized. The link is not completely understood, but it is believed that oxidative stress and inflammation are the culprits in both diseases.8 In contrast to previous hypotheses, Sosa and colleagues found an independent association between beta blockers and fragility fractures.9 The idea that beta blockers and fragility fractures are linked is still controversial and needs more study. Unlike beta blockers, statins provide a protective effect on bone. They increase BMD and reduce fracture risk by inhibiting osteoclastogenesis.10
In addition to loop diuretics and beta blockers, inhaled glucocorticoids, oral glucocorticoids, proton pump inhibitors (PPIs), H2 receptor antagonists, and anticonvulsants decrease bone density and increase the incidence of fragility fractures.11 Chronic glucocorticoid therapy is the most common cause of secondary osteoporosis. Osteoblasts and osteocytes undergo apoptosis in the presence of glucocorticoids.12 Patients on glucocorticoid therapy have an increased risk of fracture, even with higher BMD values.13 Bone changes that occur while a patient is taking glucocorticoids may not be detected during BMD testing. Therefore, a high level of suspicion of osteoporosis in patients on long-term glucocorticoids is imperative.
Proton pump inhibitors are among the most prescribed medications in the world; they reduce bone resorption, increasing the risk of fracture.14 Proton pump inhibitors and H2 receptor antagonists are hypothesized to cause malabsorption of calcium and indirectly cause osteoporosis. The risk of osteoporosis increases with the length of PPI treatment.15 However, exposure lasting <7 years does not increase the risk of fracture.16 It is recommended that patients on long-term PPIs be referred for BMD testing.
An association between anticonvulsants and osteoporosis has been found in observational studies. The mechanism of this association is not yet fully understood, but it is believed that exacerbation of vitamin D deficiency leads to increased bone metabolism.17 Gastrointestinal (GI) calcium absorption also decreases with anticonvulsant use. Prolonged antiepileptic therapy and high-dose therapy rapidly decrease BMD. Primidone, carbamazepine, phenobarbital, and phenytoin are the drugs most often associated with decreased BMD. Osteoporosis and fragility fracture in these patients can be prevented with calcium, vitamin D, and the bisphosphonate risedronate. These medications have been shown to improve BMD by 69%.18
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