Rheumatoid arthritis (RA) is a chronic, progressive and inflammatory disease often leading to irreversible destruction of articular structures and consequent disability. The key steps of RA pathogenetic mechanisms are the break of immune tolerance and the production of autoantibodies, followed by systemic and local inflammation resulting in damage of both subchondral bone (erosion) and cartilage (joint space narrowing (JSN)). Evidences from clinical trials suggest that erosions and JSN are the result of inter-related but partly independent pathogenetic pathways, in both cases mediated by pro-inflammatory cytokines, even if a direct effect of cyclic citrullinated peptides (anticitrullinated protein antibodies, ACPAs) on bone damage had been postulated. As a consequence, the suppression of inflammation provided by synthetic and biological disease-modifying antirheumatic drugs results in a decreased progression of bone and cartilage damage, supporting the effectiveness of the treat-to-target strategy. Nevertheless, radiographic progression may also be detected in patients achieving a sustained clinical remission. Two main reasons for this apparent uncoupling between clinical synovitis and damage progression should be considered. First, in some cases, the use of composite indices to define remission may not be completely adequate to identify residual disease activity, requiring the concomitant introduction of more sensible tools such as imaging. Second, the direct effect of biological drugs on bone destruction inducers, such as pro-inflammatory cytokines, may explain the suppression of radiographic progression despite the persistence of clinical synovitis. In this review, we discuss the link between autoimmunity, inflammation, joint damage and disability, focusing on how radiographic progression may predict functional disability.
- Rheumatoid Arthritis
- Disease Activity
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