- Usually presents with pain upon weight-bearing and motion of the affected joint.
- The most common site is the femoral head, but the distal femur, ankles, shoulders, wrists and elbows may also be affected.
- There are many predisposing conditions but glucocorticoid therapy, alcohol abuse, and trauma account for the great majority of cases.
- MRI has sensitivity for early disease and can detect characteristic abnormalities before radiographic changes are apparent.
Osteonecrosis results from impaired delivery of adequate oxygen to underlying bone. It typically affects the poorly vascularized fatty marrow and is characterized by areas of dead marrow and trabecular bone extending to the subchondral plate. Other terms frequently used for this condition are “ischemic necrosis,” “avascular necrosis” and “aseptic necrosis.” Osteochondritis dessicans and Kienböck disease are forms of osteonecrosis.
The femoral head is particularly susceptible to osteonecrosis. Typically, osteonecrosis of the femoral head develops in the anterolateral aspect just below the weight-bearing articular surface; this is the site of greatest mechanical stress. Once radiographic abnormalities are apparent, collapse of the femoral head is usually inevitable, at intervals ranging from weeks to years.
Osteonecrosis is not a discrete disease but represents the final common pathway of multiple conditions, most of which result in impaired blood supply to bone. Proposed mechanisms include occlusion of smaller arteries of the femoral head by lipid droplets, sickled red blood cells, or nitrogen bubbles from caisson disease. Alternatively, structural damage to the arterial or venous walls from trauma, vasculitis, radiation, or release of vasoactive substances may lead to ischemia. In some conditions, increased intraosseous pressure from enlargement of intramedullary fat cells or osteocytes may play a role. Through one or more of these pathways, osteonecrosis begins with interruption of the blood supply to bone; subsequently, the adjacent area becomes hyperemic, leading to demineralization, trabecular thinning and, if stressed, bony collapse. The process is usually progressive, resulting in joint destruction within 3–5 years if left untreated.
Elderly persons seem to be at decreased risk for developing osteonecrosis. In this age group, fat cells become smaller. The space between fat cells fills with a loose reticulum and mucoid fluid, resistant to ischemic necrosis. This is termed “gelatinous marrow,” and even in the presence of increased intramedullary pressure, interstitial fluid is able to escape into the blood vessels, leaving the spaces free to absorb additional fluid.
The true prevalence of osteonecrosis is unknown, but it is estimated that there are approximately 10,000 to 20,000 new cases annually in the United States. Osteonecrosis is the underlying diagnosis in approximately 10% of all total hip replacements. For the most part, osteonecrosis affects the epiphyses of the long bones, such as the femoral and humeral heads, but other bones (eg, carpal and tarsal) can also be affected. The disease occurs more frequently in men than women, with the overall male to female ratio in the range of 8:1. The age distribution is wide, but most patients ...