Abstract
The authors review the current literature data on the pathogenesis, clinical manifestations and treatment of glucocorticoid induced osteoporosis in patients with endogenous hypercortisolism. High levels of glucocorticoids lead to bone loss, bone quality deterioration and low traumatic fractures as a consequence of reduced bone formation. In addition to this, muscle weakness and sex steroids hormone abnormalities increase the risk of falls and fractures. The new available data on possible mechanisms of these changes including the involvement of RANKL/RANK/OPG, Wnt-betacatenin signaling pathway and pathogenesis of myopathy are discussed. This review also outlines the practical recommendation and new questions that should be evaluated in future research.
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