Apoptosis in glucocorticoid-induced bone disease

Abstract

Purpose of review Glucocorticoid-induced bone disease may be mediated by direct actions on bone cells, actions on extraskeletal tissues, or both. This review examines recent advances in the understanding of the pathogenesis of glucocorticoid-induced osteoporosis and osteonecrosis. Recent findings Current evidence indicates that glucocorticoid-induced bone disease is due to suppression of the birth of osteoblast and osteoclast precursors in the bone marrow, increased apoptosis of osteoblasts and osteocytes and prolongation of the lifespan of osteoclasts. In addition, glucocorticoid-induced fractures as well as osteonecrosis of the hip may be due to osteocyte apoptosis. Summary Excess glucocorticoids directly affect the lifespan of osteoblasts, osteocytes and osteoclasts. Furthermore, glucocorticoid-induced loss of bone strength results in part from increased death of osteocytes, independent of bone loss. Treatment of glucocorticoid-induced bone disease with bisphosphonates or intermittent injections of parathyroid hormone is effective, perhaps partly because it prevents osteoblast and osteocyte apoptosis.