5th June 2025

Pathophysiology

Central to the pathogenesis is the formation of inflamed synovium in joints. Increased inflammation in the synovium causes the synovial lining to become hyperplastic with immune cell infiltration in the sublining. Increased cytokines are seen, with tumour necrosis factor (TNF), interleukin-1 (IL-1) and interleukin-6 (IL-6) most abundantly seen. Angiogenesis serves the hypertrophic synovium. The inflammatory setting, along with increased levels of metalloproteinase activity is thought to drive the joint destruction.