Avascular necrosis (AVN) of the femoral head is a clinical entity in which bone death occurs as a result of interruption of blood at the level of the microcirculation. The etiology and pathogenesis of nontraumatic AVN have not been fully elucidated. The understanding of this disease progression is important for several reasons. First, AVN is a devastating musculoskeletal condition that strongly impacts those affected. Second, it tends to occur in young people. Third, current treatments are suboptimal since they are, for the most part, palliative rather than curative. Finally, we are currently unable to identify individuals who will develop AVN, even in the group considered at high risk; consequently, practitioners are not able to stop the progression of the disease or reverse the process once AVN has developed.

Although the actual prevalence of the disease is unknown, an estimated 10,000 to 20,000 new patients with AVN are diagnosed each year in the United States (1). AVN is the underlying diagnosis in 5% to 18% of the more than 500,000 total hip arthroplasties performed yearly in the United States and Western Europe (1).

AVN has been associated with a variety of risk factors, and classified as either secondary or idiopathic. Environmental risk factors include hyperlipidemia, steroid use, alcohol, various blood dyscrasias (e.g., hemoglobinopathies, coagulopathies), pregnancy, hyperbaric exposure, use of chemotherapeutic agents, systemic lupus erythematosus, inflammatory bowel disease, lipid storage diseases (Gaucher disease), and familial thrombophilias (1).

The condition may occur in up to 30% of patients with lupus erythematosus. In a large U.S. study of 2,590 patients with sickle cell disease, Milner and associates reported a prevalence of 9.8% (1). There is also a high incidence of AVN among organ transplant recipients.