[Pathophysiology of rheumatoid arthritis]

Rheumatoid arthritis (RA) is a systemic inflammatory disease mainly characterized by synovitis and joint destruction. Etiology of RA is unknown. Although the impact of genetic factors is obvious, the genetic basis is not sufficient to explain the triggering of the immune insult. The dominant feature is inflammation, primary in synovium. The synovial membrane in RA becomes hyperplastic. There is an increased number of both type synoviocytes and is infiltrated with immune and inflammatory cells: particularly macrophages, B- and T-lymphocytes, plasma cells and dendritic cells. Increased levels of cytokines are present. Cytokines play a central role in the perpetuation of synovial inflammation. The persistence of the chronic inflammatory response in conjunction with ongoing joint destruction (is finding in many patients with RA despite the use of effective anti-inflammatory agents and disease-modifying drugs) probably appears as a direct result of the sustained recruitment, inappropriate retention and impaired apoptosis.