The role of fat embolism in the etiology of corticosteroid-induced avascular necrosis: clinical and experimental results.

Case reports since 1957 implicate corticosteroids in excess of physiologic requirements as a cause of nontraumatic osteonecrosis. Both laboratory and clinical studies demonstrate marked alterations in lipid metabolism with hyperlipemia, fatty liver and systemic fat embolism. Intra-arterial infusion of fat produces embolic vascular obstruction, focal marrow necrosis and osteocytic death in the femoral head of the rabbit. Induced hypercortisonism in rabbits produces severe hyperlipemia, fatty liver, systemic fat emboli, terminal vascular obstruction in bone and associated areas of osteocytic death representing avascular necrosis. Osteoporosis develops without fracture. Histologic evidence of vasculitis, thrombosis, or microfracture is lacking. The specific biochemical pathway of corticosteroid lipid alterations is unknown.