Glucocorticoid-induced osteonecrosis.pdf

REVIEW Glucocorticoid-induced osteonecrosis Robert S. Weinstein Received: 19 November 2011 / Accepted: 22 November 2011 / Published online: 15 December 2011  Springer Science+Business Media, LLC 2011 Abstract Awareness of the need for prevention of glu- cocorticoid-induced fractures is growing, but glucocorti- coid administration is often overlooked as the most common cause of nontraumatic osteonecrosis. Glucocorti- coid-induced osteonecrosis develops in 9–40% of patients receiving long-term therapy although it may also occur with short-term exposure to high doses, after intra-articular injection, and without glucocorticoid-induced osteoporosis. The name, osteonecrosis, is misleading because the pri- mary histopathological lesion is osteocyte apoptosis. Apoptotic osteocytes persist because they are anatomically unavailable for phagocytosis and, with glucocorticoid excess, decreased bone remodeling retards their replace- ment. Glucocorticoid-induced osteocyte apoptosis, a cumulative and unrepairable defect, uniquely disrupts the mechanosensory function of the osteocyte–lacunar–cana- licular system and thus starts the inexorable sequence of events leading to collapse of the femoral head. Current evidence indicates that bisphosphonates may rapidly reduce pain, increase ambulation, and delay joint collapse in patients with osteonecrosis. Keywords Glucocorticoids  Osteonecrosis  Avascular necrosis  Apoptosis  Osteoblasts  Osteocytes  Bisphosphonates Introduction Less than 1 year after the introduction of cortisone for the treatment of rheumatoid arthritis in 1950, investigators became aware of injurious effects that were considered uncommon in Cushing’s syndrome [1]. These effects included insomnia, gastrointestinal bleeding, a post-corti- sone-withdrawal syndrome, and hip fracture [2, 3]. As vertebral fractures and radiographic osteoporosis had not been observed, the investigators were uncertain whether the hip fractures were the result of falls due to steroid my