Osteonecrosis: current perspectives on pathogenesis and treatment

Abstract

Nontraumatic osteonecrosis results from impairment of circulation to the affected bone. The femoral head is affected most frequently. The underlying cause for the circulatory defect in osteonecrosis varies and may involve both local and systemic changes. Steroid use, alcohol consumption, pancreatitis, and lipid disorders appear to lead to bone death either by development of fat emboli in the microcirculature surrounding the affected bone or by fatty infiltration of the marrow. Decompression syndrome results from the presence of gaseous emboli in the microcirculature. In Legg-Calvé-Perthes disease other associated features are present such as short stature, suboptimal growth velocity, and/or hormonal imbalances, and it is likely that osteonecrosis may be secondary to systemic abnormalities, although specific factors have not been identified. Other frequently suggested pathogenic factors that play a role in the development of osteonecrosis include increased intraosseous pressures, the presence of cytotoxic cellular factors, intravascular coagulation, venous stasis, and the hyperviscosity syndrome. Some investigators have attempted, without success, to find a common etiology for all cases of osteonecrosis. In addition, patients have developed osteonecrosis without any known risk factors; this syndrome has been coined idiopathic avascular necrosis. In advanced stages of femoral head osteonecrosis, total hip arthroplasty appears to be the best therapeutic modality, particularly in older individuals.