Rheumatoid inflammation and joint destruction: cause and effect or parallel phenomena?
Joint damage is a characteristic and important consequence of rheumatoid arthritis; it is usually considered to be a direct result of the inflammatory synovitis. This view implies that by treating actively the synovial inflammation subsequent joint damage will be reduced and the long-term outlook of patients with rheumatoid arthritis thus improved. However, there is relatively little clinical evidence that suppressing inflammation reduces rheumatoid joint damage. An alternative view is that the mechanisms causing inflammation and those leading to joint destruction are parallel processes related only indirectly. Considerable evidence supports such a concept. Clinical studies show radiological progression of the disease occurs despite improvements in measures of joint inflammation and a reduction in the levels of acute phase proteins. Damage can progress in either actively inflamed hot joints or cool swollen joints. Histopathologically the features of rheumatoid synovitis are non-specific, while the radiological pattern of joint damage is very characteristic. There is evidence that lymphocytic infiltration is not a poor prognostic finding, despite it being a typical feature of inflamed joints. Experimental studies also fail to show a close correlation between inflammation and cartilage damage: this is seen in experimental arthritis, coculture in vitro systems, and the air pouch model of cartilage damage. We suggest that attempts to improve the outcome of rheumatoid arthritis should not merely concentrate on controlling inflammation but should also seek to modify the associated connective tissue changes of the disease.
D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D007249:Inflammation; D007596:Joints / Q000473:pathology / Q000503:physiopathology*
D000893:Anti-Inflammatory Agents