Idiopathic necrosis of the femoral head: pathogenesis and treatment

The classic features of idiopathic femoral head necrosis - increased roentgenologic density, the subchondral crescent-fracture and distortion of the femoral head - are now known to be late manifestations of the disease. The early changes have been studied prospectively in 34 patients receiving corticosteroids in high dosage and 11 patients with femoral head necrosis attributed to alcohol abuse. In five patients with unilateral femoral head necrosis, intraosseous pressure studies and core biopsy were carried out on the apparently unaffected side. The earliest pathologic changes were a relative increase in cancellous bone fat at the expense of myeloid tissue, swelling and necrosis of the fat cells, and variable areas of cell death in the trabeculae. All of these were fairly widespread throughout the proximal femur. Intraosseous pressures were raised, suggesting the presence of venous stasis. Fat cell size was measured in undistorted femoral heads with osteonecrosis and in a comparable series with osteoarthritis. There was a significant (P less than 0.001) increase in fat cell size and a virtual absence of sinusoids in histologic sections from those with osteonecrosis. It is posited that idiopathic osteonecrosis results from the following sequence: fatty accumulation and replacement of myeloid tissue, followed by compression of vascular sinusoids, venous stasis, ischemia, fat necrosis and then bone necrosis. The earliest stages in this chain of events are clinically asymptomatic and produce no radiologic abnormality. The results of treatment by core decompression in 22 hips are discussed. This is an effective prophylactic measure in all early cases and it has a place even in the management of more advanced cases, especially if the patient is considered too young for hip arthroplasty.