Glucocorticoid-induced osteoporosis

Endogenous cortisol excess and glucocorticoid (GC) treatment have a profoun d effect on bone metabolism, acting at many sites. The mechanism of GC acti on on bone turnover is complex and has not been elucidated completely. GCs increase bone resorption, inhibit bone formation and have an indirect actio n on bone by decreasing intestinal Ca2+ absorption, modifying vitamin D met abolism, and sustaining a marked hypercalciuria, with variable changes in p lasma PTH levels; finally, GCs inhibit the gonadotropic and somatotropic ax is. GC-induced osteoperosis is preventable, treatable and potentially rever sible. The prevention and treatment of GC-induced osteoperosis include some general measures (as well as the use of the minimal effective dose of GC), Ca2+ and vitamin D suplementation and treatment with bone anabolic and ant iresorptive agents. Recent trials suggest that bisphosphates are an effecti ve therapeutic tool in the treatment of GC-induced bone damage. Recent data on GC receptor-selective modulators indicate that these new molecules migh t induce only minimal bone loss while maintaining the typical anti-inflamma tory properties of GC. Another new line of study for the prevention of GC-i nduced osteoperosis is the characterization of the individual's susceptabil ity to GC-induced bone damage.