Glucocorticoid‐induced osteoporosis: lessons from Cushing's syndrome

Glucocorticoid-induced osteoporosis (GIO) is the most frequent form of secondary bone disorders. Most of our knowledge on its pathogenesis and treatment has been obtained by investigating patients treated with exogenous glucocorticoids. This review will focus on the bone disorder in endogenous Cushing's syndrome, updating recent advances in its pathophysiology, diagnostic aspects and the various predictors which are important in determining bone mineral density (BMD) and fracture risk. We now know strong evidence that beside BMD, bone microarchitecture, one of the most important elements of bone quality, is a key factor in determining fracture risk. Recently, two new methods (spinal deformity index and trabecular bone score) have been shown to be useful markers of bone microarchitecture in GIO. Investigations of GIO in endogenous Cushing's syndrome have also contributed to our understanding on its natural history and reversibility. Relying on recently published guidelines for management of exogenous GIO, a short list of suggestions is provided regarding the optimal diagnostic and therapeutic approach to patients with endogenous GIO.