Adverse effects of corticosteroids on bone metabolism: a review

Glucocorticoid (GC) exposure is the most common etiology of drug-induced (secondary) osteoporosis. Twenty percent of all cases of osteoporosis have been attributed to GC exposure. Significant risk factors for the development of fractures after GC exposure include age older than 65 years, prolonged GC exposure (>3 months), positive family history of osteoporosis, and low calcium intake. GCs are known to inhibit bone remodeling and to increase fracture risk. GC exposure alters the fragile balance between osteoclast and osteoblast activity in bone metabolism. GC stimulates osteoclast-mediated bone resorption and reduces osteoblast-mediated bone formation, which results in increased overall net bone resorption. Specifically, the 2 main effects of GCs on bone metabolism are (1) inducing apoptosis in osteoblasts and osteocytes, thereby decreasing bone formation, and (2) prolonging the lifespan of osteoclasts and increasing bone resorption. The risk of fracture decreases 3 months after cessation of GC therapy; thus, a 3-month period may be ideal between GC exposures in patients at high risk for the development of osteoporosis. Patients managed with GCs who are at high risk for the development of secondary osteoporosis should have appropriate diagnostic testing; pre-GC exposure medication management (ie, use of bisphosphonates, human parathyroid hormone); and a limitation of GC therapy, with a wait period of 3 months between GC exposures if possible.