[Secondary osteoporosis UPDATE. Rheumatoid arthritis and bone damage: trends in treatment].
Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic synovitis and bone damage. The bone manifestation in RA consists of joint destruction and systemic osteoporosis, which are brought about by different mechanisms. During the pathological processes, inflammatory cytokines such as TNF are largely produced from inflamed synovium and cause activation of osteoclasts deviated from bone remodelling cycle, resulting in joint destruction. But by the combinational use of methotrexate and TNF-inhibitors, clinical remission, structural remission and functional remission have become possible for the treatment of RA. Especially TNF-inhibitors remarkably suppress the progression of joint destruction in the vast majority of the patients. On the other side, systemic osteoporosis, mainly caused by menopause and glucocorticoid (GC), is often complicated in RA. However, bisphosphonate is well known to be effective for not only treatment but also prevention of GC-induced osteoporosis. Furthermore, anti-RANKL antibody denosumab possesses a potential to inhibit joint destruction as well as systemic and GC-mediated osteoporosis.
Tanaka
Yoshiya
Y
The First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health.
D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D001172:Arthritis, Rheumatoid / Q000150:complications* / Q000188:drug therapy; D050071:Bone Density Conservation Agents / Q000627:therapeutic use; D016723:Bone Remodeling; D000069448:Denosumab; D004164:Diphosphonates / Q000627:therapeutic use; D005938:Glucocorticoids / Q000009:adverse effects; D006801:Humans; D008727:Methotrexate / Q000627:therapeutic use; D010010:Osteoclasts / Q000502:physiology; D010024:Osteoporosis / Q000188:drug therapy / Q000209:etiology* / Q000517:prevention & control; D053245:RANK Ligand / Q000627:therapeutic use; D013583:Synovial Membrane; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000502:physiology
D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D050071:Bone Density Conservation Agents; D004164:Diphosphonates; D005938:Glucocorticoids; D053245:RANK Ligand; D014409:Tumor Necrosis Factor-alpha; D000069448:Denosumab; D008727:Methotrexate