Recent Advances in the Management of Steroid Induced Osteoporosis

Correspondence to: Lai-Wa Kwok Abstract: Glucocorticoid-induced osteoporosis is the most common cause of drug-induced osteoporosis, leading to fragility fractures, decrease in mobility and quality of life. Patients who receive equivalent dose of prednisolone 5 mg for more than six months are at risk of glucocorticoid-induced osteoporosis, but there is no conclusive evidence for a safe cutoff for either dose or duration of steroid exposure and bone loss. The general view is 'dual action'. Both increased bone resorption and decreased bone formation contribute to the pathogenesis of glucocorticoid-induced osteoporosis. Glucocorticoids increase the expression of receptor activator of nuclear factor kB ligand (RANKL) and decrease the expression of its soluble receptor osteoprotegerin (OPG) in stromal and osteoblastic cells, leading to increased differentiation of pre-osteoclast to osteoclast. Fracture risk is related not only to bone mineral density, bone structural and mechanical properties, but also other clinical risk factors such as smoking, excessive alcohol, lack of exercises. Treatment threshold in glucocorticoid-induced osteoporosis is much lower than that in postmenopausal osteoporosis since fractures in glucocorticoid-induced osteoporosis occur at a higher bone mineral density than in postmenopausal osteoporosis. Bisphosphonates, being the first line therapy, have been shown to be effective in the prevention of vertebral fractures and they should be given together with adequate vitamin D and calcium supplement. The anabolic therapy parathyroid hormone, which targets on bone formation, has shown to be effective in increasing bone mineral density and reducing fractures and it may act as an alternative therapy.