The effects of glucocorticoid on bone architecture and strength

Abstract

Glucocorticoid-induced osteoporosis is the leading cause of osteoporosis in young adults and the most common cause of secondary osteoporosis. Glucocorticoid use results in rapid bone loss and elevated risk of fracture. However, glucocorticoid- induced osteoporosis is characterized by relative dissociation between the bone mineral density values and the fracture risk, which is higher than expected based on the bone mineral density values. The excess bone fragility from glucocorticoid treatment is multifactorial. Recently, many published studies have focused on the cellular and molecular mechanisms of bone metabolism, the pathophysiology of glucocorticoid-induced osteoporosis, and the imaging assessment of bone fragility in glucocorticoid-induced osteoporosis. In this review, recent advances in glucocorticoid-induced osteoporosis are summarized, particularly recent progress in our understanding of the effects of glucocorticoid on bone architecture and strength resulting in improved insight that might result in the development of new treatment options in the near future.