Osteonecrosis, also known as avascular necrosis, is a pathological process that has been associated with numerous conditions and therapeutic interventions. The male to female ratio of this disorder is 8 to 1 with an average age at diagnosis of less than 40 years.

The pathogenesis of osteonecrosis is controversial. Most believe that it is the result of the combined effects of metabolic and local factors affecting blood supply such as vascular damage, increased intraosseous pressure, and mechanical stresses. It likely begins by interruption of the blood supply to the bone. Subsequently, the adjacent area becomes hyperemic, resulting in demineralization, trabecular thinning, and if stressed, collapse.

A variety of traumatic and nontraumatic factors contribute to the etiology of osteonecrosis. These include long-term corticosteroid use, excessive alcohol intake, SLE, trauma, sickle cell disease, Guacher’s disease, renal transplant, and dysbarism. A definitive etiologic role has been established for some of these factors, but the majority are probable relationships. Corticosteroid use and excessive alcohol intake are reported to account for more than 90 percent of cases.

Early diagnosis of osteonecrosis may provide the opportunity to prevent collapse and ultimately the need for joint replacement. However, most patients present late in the course of the disease. Thus, a high index of suspicion is necessary for those with known or probable risk factors, particularly high dose steroid use. The most common presenting symptom of osteonecrosis is pain. A small proportion of patients are asymptomatic; in these cases the diagnosis is usually incidental.

Osteonecrosis usually occurs in the anterolateral femoral head, although it may also affect the humeral head, femoral condyles, proximal tibia, vertebrae, and small bones of the hand and foot. Many patients have bilateral involvement at the time of diagnosis, including disease of the hips, knees, and shoulders.
   
The plain radiograph can remain normal for months after symptoms of osteonecrosis begin; the earliest findings are mild density changes, followed by sclerosis and cysts as the disease progresses. The pathognomonic crescent sign (subchondral radiolucency) is evidence of subchondral collapse. Later stages reveal loss of normal shape or collapse of the bone. Ultimately, joint-space narrowing and degenerative changes in the acetabulum are visible.

Magnetic resonance imaging (MRI) is far more sensitive than plain radiographs or bone scintigraphy, with an overall reported sensitivity of 91 percent. Changes can be seen early in the course of disease when other studies are negative. Focal lesions are well demarcated and inhomogeneous on T-1 weighted images. The earliest finding is a single density line (low intensity signal) that represents the separation of normal and ischemic bone. A second high intensity line appears on T-2 weighted images, representing hypervascular granulation tissue; this is the pathognomonic double-line sign.

The treatment of osteonecrosis remains one of the most controversial subjects in the orthopedic literature. The goal of therapy is to preserve the native joint for as long as possible. There are four main therapeutic options: Conservative management (bed rest, partial weightbearing with crutches, and weightbearing as tolerated, in addition to nonsteroidal agents or other analgesics), joint (eg, total hip) replacement, core decompression with or without bone-grafting, osteotomy.