ABSTRACT
Rheumatoid arthritis (RA) is a chronic inflammatory disease of unknown etiology characterized clinically by morning stiffness associated with swelling and pain of involved joints. In its worse stages, cartilage and boney erosions occur with marked destruction and disability (1). The proposed immunological mechanisms include abnormal cellular immune function, primarily involving T helper cells, humoral immune mechanisms, with involvement of rheumatoid factor; and other cellular mechanisms, including macrophage and synovial fibroblast release of cytokines and growth factors associated with the release of neutral proteases and other destructive enzymes.
