Effect of high levels of corticosteroids on the lipids of the long bones of the mature rabbit.
Corticosteroid administration is associated with the development of nontraumatic osteonecrosis in man. However, the pathogenesis of steroid-induced osteonecrosis is unknown. Osteopenia, occurring as a result of corticosteroid treatment is thought to be one factor contributing to the compromise of vascular space. We have treated rabbits daily with hydrocortisone-acetate (15 mg per 4 kg rabbit for 4 and 9 weeks, respectively). These animals progressively developed osteoporosis. Cholesterol accumulated in both the unwashed cancellous bone and the marrow-free compact bones of the treated rabbits when contrasted with age-matched controls. Elevations in marrow lipid content were also observed in the treated animals. Although none of the treated rabbits developed osteonecrosis during the short time of the study, the findings of elevated cholesterol suggest that alterations in bone cell membranes may lead to cell dysfunction and osteopenia. This osteopenia may eventually cause osteonecrosis by occlusion of subchondral vessels. The elevated marrow lipids may also contribute to the development of osteonecrosis by increasing intramedullary pressure and causing venous stasis.
D000818:Animals; D001853:Bone Marrow / Q000378:metabolism; D001842:Bone and Bones / Q000378:metabolism*; D002784:Cholesterol / Q000378:metabolism; D006854:Hydrocortisone / Q000031:analogs & derivatives* / Q000494:pharmacology; D050356:Lipid Metabolism; D008297:Male; D010024:Osteoporosis / Q000139:chemically induced; D010743:Phospholipids / Q000378:metabolism; D011817:Rabbits; D014280:Triglycerides / Q000378:metabolism
D010743:Phospholipids; D014280:Triglycerides; C021650:hydrocortisone acetate; D002784:Cholesterol; D006854:Hydrocortisone