[Action of glucocorticoid on bone-forming and bone-resorbing cells].
During the early phase of glucocorticoid (GC)-induced osteoporosis (GIO), GC increases the expression of receptor activator of NF-kappaB ligand (RANKL) in bone-forming cells and suppresses the production of interferon-beta in osteoclast progenitors, resulting in stimulation of bone resorption. On the other hand, GC represses the proliferation, differentiation and functional activities of bone forming cells, and finally induces their apoptosis throughout GIO, consequently causing the decrease in bone formation. In addition, as the number of bone-forming cells decrease, the osteoblast-dependent osteoclast formation also declines.
Hakeda
Yoshiyuki
Y
Meikai University School of Dentistry, Division of Oral Anatomy.
D017209:Apoptosis / Q000187:drug effects; D002454:Cell Differentiation; D002455:Cell Division; D005938:Glucocorticoids / Q000009:adverse effects* / Q000494:pharmacology*; D006801:Humans; D016899:Interferon-beta / Q000378:metabolism; D010006:Osteoblasts / Q000166:cytology / Q000378:metabolism*; D010010:Osteoclasts / Q000166:cytology / Q000378:metabolism*; D010012:Osteogenesis / Q000187:drug effects*; D010024:Osteoporosis / Q000139:chemically induced* / Q000378:metabolism; D053245:RANK Ligand / Q000378:metabolism
D005938:Glucocorticoids; D053245:RANK Ligand; C505688:TNFSF11 protein, human; D016899:Interferon-beta