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Pathophysiology of Rheumatoid Arthritis
Rheumatoid arthritis (RA) is a chronic and progressive inflammatory disorder, characterised by synovitis and severe joint destruction.1,2
The pathogenesis of RA is a complex process, involving synovial cell proliferation and fibrosis, pannus formation, and cartilage and bone erosion. This process is mediated by an interdependent network of cytokines, prostanoids and proteolytic enzymes.3,4 Proinflammatory cytokines, such as interleukin-1 (IL-1) and tumour necrosis factor-alpha (TNF-α), are central mediators in RA.5,6 This is illustrated in patients with RA, who experience an initial cell-mediated response that leads to the presence of elevated levels of IL-1 in the synovial fluid.7-9 Furthermore, IL-1 concentrations in the plasma have been reported to correlate with disease activity.8,9 It has also been demonstrated that patients with erosive RA have higher synovial and circulating levels of IL-1 than patients without erosions.7
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RA patients with erosive disease have higher synovial and circulating levels of IL-1 than patients without erosions
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IL-1 has a broad range of activities within the rheumatoid joint (see figure) that are believed to contribute towards the painful inflammatory signs and symptoms of RA. IL-1 is a key mediator of synovial inflammation and pannus formation,10-12 and is thought to contribute to the impairment of tissue repair processes and the destruction of bone and cartilage in RA.6,9,13-18
For more information on the role of IL-1 in RA, click here.
Figure IL-1 has a broad range of pathological mechanisms within the rheumatoid joint11
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References
(Click below to visualise the complete reference)
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Dayer JM, et al. 2002 |
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