title: [Secondary osteoporosis. Pathogenesis of glucocorticoid-induced osteoporosis].
abstract: Direct inhibitory effect of glucocorticoid (GC) on bone formation and promotion of apoptosis of bone cells are thought to be the major mechanism of glucocorticoid-induced osteoporosis (GIO). GC reduces not only bone mineral density (BMD) but also bone quality, therefore, patients with GIO have a higher risk of fracture than those with postmenopausal osteoporosis with the same level of BMD. Recently, GC has been shown to suppress a Wnt signal pathway which is essential for bone growth.
authors.affiliation: Kyushu University, Graduate School of Medical Sciences, Department of Medicine and Bioregulatory Science.
authors.forename: Ryoichi
authors.initials: R
authors.lastname: Takayanagi
mesh_terms: D017209:Apoptosis / Q000187:drug effects; D015519:Bone Density / Q000187:drug effects; D003864:Depression, Chemical; D005260:Female; D050723:Fractures, Bone / Q000209:etiology; D005938:Glucocorticoids / Q000009:adverse effects* / Q000494:pharmacology; D006801:Humans; D010012:Osteogenesis / Q000187:drug effects; D010024:Osteoporosis / Q000139:chemically induced*; D015663:Osteoporosis, Postmenopausal; D012306:Risk; D015398:Signal Transduction / Q000187:drug effects; D051153:Wnt Proteins / Q000502:physiology
chemical_list: D005938:Glucocorticoids; D051153:Wnt Proteins