Glucocorticoids remain a key component in the management of many inflammatory disorders but the adverse consequences, especially on bone, can be devastating. The incidence of glucocorticoid-induced osteoporosis (GIO) may be as high as 50% after 6 months' treatment with steroids. This manifests itself as a 30 to 400% increase in the incidence of low trauma fractures. The incidence rates can be even greater in specific clinical settings such as following organ transplantation. The pathogenesis of glucocorticoid-induced osteoporosis remains complex and perplexing.
The concomitant prescription of bone-active drugs for the prevention and treatment of GIO in the United Kingdom population remains low, despite the availability of effective therapies. In addition, there remain many unanswered questions about the pathogenesis of GIO and clinical management. These include identification of the optimum bone mineral density threshold at which to intervene with bone-active drugs, the dose or duration of exposure to steroid therapy that warrants intervention, and the demonstration of the efficacy of fracture prevention for different bone-active drugs or for a combination of these drugs.