[Joint destruction and its repair in rheumatoid arthritis].
It is supposed that autoaggressive T cell activation, triggered by unknown microorganisms, initiates inflammation in rheumatoid arthritis. It leads to activation of macrophages and synovial fibroblasts in the synovial tissues, which form a granulomatous pannus tissue. It becomes a platform of joint destruction activating osteoclastogenesis and release of cartilage-degrading enzymes. Biological reagents recently brought into the clinics are potently anti-rheumatic, and, in some cases, stop progression of the joint destruction and even repair the joint. It is now a realistic goal for next-generation anti-rheumatic treatments to inhibit joint destruction completely.
Kohsaka
Hitoshi
H
Department of Medicine and Rheumatology, Graduate School, Tokyo Medical and Dental University.
D018501:Antirheumatic Agents; D001172:Arthritis, Rheumatoid / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology* / Q000628:therapy; D015195:Drug Design; D006801:Humans; D007596:Joints / Q000473:pathology* / Q000503:physiopathology*; D008262:Macrophage Activation; D013601:T-Lymphocytes / Q000276:immunology
D018501:Antirheumatic Agents