Abstract
High doses of glucocorticoid have adverse effects on bone, resulting in decreased bone mass and increased risk of fracture. There is substantial intraindividual variation in susceptibility to these effects and the condition is difficult to treat effectively. The mechanisms underlying the adverse effects of glucocorticoids are complex but actions on the bone-forming cell, the osteoblast, appear to be critical. Recent studies have clarified the epidemiology of fracture risk and have improved the understanding of the pathophysiology underlying glucocorticoid-induced osteoporosis. Agents that inhibit bone resorption have proven to be useful treatments and advances have been made toward the development of anabolic therapies. Future areas of research include the continued search for safe, effective anabolic agents and the development of predictive tests to allow more effective targeting of treatments to individuals most at risk of fracture.
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