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Fat necrosis of osteocytes as a causative factor in idiopathic osteonecrosis in heritable hyperlipemic rabbits.

Since idiopathic osteonecrosis (IO) has been observed to occur in association with abnormalities of fat metabolism, eight inbred rabbits with heritable hyperlipidemia were examined for IO. Studies of circulating fatty elements and peripheral tissues were also done. Necrotic changes in 60% of the femoral heads were observed by light and electron microscopic examinations. The most characteristic changes included thickening of the subchondral bone trabeculae due to reactive new bone on dead bone, diminished marrow cavities filled with fatty tissue, haversian canals with fat, and loss or pyknosis of osteocyte nuclei with cytoplasmic "fatty" vacuolation. Sudan-IV-positive substances were frequently observed in the osteocytes of necrotic trabeculae. The appositional new bone lining dead trabeculae was also subject to necrotic change. Diseased vessels or emboli in the location of bone necrosis were not observed. Electrophoresis of serum lipoproteins showed a marked decrease in high density lipoprotein (HDL) associated with the accumulation of lipids in the peripheral tissues. These changes may represent a failure in lipid transport. Based on these aberrations, we propose that the decrease in HDL may play a role in the pathogenesis of IO in rabbits with heritable hyperlipemia.