Glucocorticoid-induced osteoporosis

Endogenous cortisol excess and glucocorticoid (GC) treatment have a profound effect on bone metabolism, acting at many sites. The mechanism of GC action on bone turnover is complex and has not been elucidated completely. GCs increase bone resorption, inhibit bone formation and have an indirect action on bone by decreasing intestinal Ca2+ absorption, modifying vitamin D metabolism, and sustaining a marked hypercalciuria, with variable changes in plasma PTH levels; finally, GCs inhibit the gonadotropic and somatotropic axis. GC-induced osteoperosis is preventable, treatable and potentially reversible. 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 antiresorptive agents. Recent trials suggest that bisphosphates are an effective therapeutic tool in the treatment of GC-induced bone damage. Recent data on GC receptor-selective modulators indicate that these new molecules might induce only minimal bone loss while maintaining the typical anti-inflammatory properties of GC. Another new line of study for the prevention of GC-induced osteoperosis is the characterization of the individual's susceptability to GC-induced bone damage.