title: [Rheumatoid arthritis and osteoporosis: trends in their treatments].
abstract: Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic synovitis and bone damages, which consist of joint destruction and systemic osteoporosis. During the pathological process, pro-inflammatory cytokines such as TNF-alpha are largely produced from inflamed synovium and cause activation of osteoclasts deviated from bone remodeling cycle, resulting in joint destruction. On the other side, systemic osteoporosis, mainly caused by glucocorticoid (GC) is often complicated in RA, in which GC decreases number of osteoblasts, reduces synthesis of bone matrix proteins from them and enhances bone resorption, resulting in impairment of bone remodeling. Thus, joint destruction and systemic osteoporosis are brought about by different mechanisms. However, recent treatment strategies have improved managements of RA-related joint destruction as well as GC-induced osteoporosis. Treatments using biologics including infliximab and etanercept, effective for treating RA disease activity, also reduce joint destruction. Also, bisphosphonate is well known to be effective for not only treatment but also prevention of GC-induced osteoporosis. Thus, it is a clinical trend that physicians treat joint destruction as an inflammatory disease and osteoporosis as a metabolic disease.
authors.affiliation: First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health.
authors.forename: Yoshiya
authors.initials: Y
authors.lastname: Tanaka
mesh_terms: D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000209:etiology; D050071:Bone Density Conservation Agents / Q000627:therapeutic use*; D001857:Bone Matrix / Q000378:metabolism; D016723:Bone Remodeling; D001862:Bone Resorption / Q000209:etiology; D002986:Clinical Trials as Topic; D004164:Diphosphonates / Q000627:therapeutic use*; D000068800:Etanercept; D005938:Glucocorticoids / Q000009:adverse effects; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use*; D000069285:Infliximab; D010006:Osteoblasts / Q000378:metabolism; D010010:Osteoclasts / Q000502:physiology; D010024:Osteoporosis / Q000188:drug therapy* / Q000209:etiology / Q000517:prevention & control; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use*; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
chemical_list: D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D050071:Bone Density Conservation Agents; D004164:Diphosphonates; D005938:Glucocorticoids; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068800:Etanercept