[Mechanisms and therapeutics of glucocorticoid-induced osteoporosis]

Abstract

Mechanisms of glucocorticoid-induced osteoporosis (GIOP) are categorized into local and systemic effects. In the local mechanisms, direct inhibitory effect of glucocorticoid on bone formation is thought to be one of the important mechanisms of GIOP. In contrast, secondary hyperparathyroidism induced by negative balance of calcium due to inhibition of absorption and increase of excretion is an important systemic mechanism of GIOP. Other mechanisms of GIOP are also shown in this review. From clinical points of view, serum markers for evaluation of GIOP have been discussed. Osteocalcin, procollagen type I N-terminal peptide, and bone-specific alkaline phosphatase as markers of bone formation are decreased in GIOP. Collagen I N-terminal telopeptide and tartrate resistent acid phosphatase isoform 5b as markers of bone resorption are increased in GIOP. Clinical guidelines have recommended that bisphosphonate is the first choice for the treatment of GIOP. Teriparatide is recombinant human parathyroid hormone 1-34, which should be considered as a therapeutic option for those at high risk of bone fracture. Denosumab, an anti receptor activator of nuclear factor-β ligand approved as a drug for postmenopausal osteoporosis was also effective for GIOP in clinical trials.