Pathogenesis of rheumatoid arthritis.

Many types of cells are activated and transformed in rheumatoid synovium, thereby contributing to amplification of the disease process. The immune response in rheumatoid arthritis is probably initiated by an antigen, although there is some evidence that anticollagen antibodies develop in response to tissue destruction, after rheumatoid arthritis has evolved clinically. Early inflammation in the synovium is characterized by a striking vascular proliferation, occurring in response to angiogenesis factors released by activated macrophages. Generalized activation of macrophages and lymphocytes typical of the immune reaction in the synovium generates antibody production, including production of rheumatoid factor. Data suggest that immune complexes deposited within cartilage attract polymorphonuclear leukocytes, which then release enzymes onto the cartilage surface. Many products of inflammation act as mediators, driving proliferation of synovial cells. Stellate cells, macrophages, and fibroblasts have been found along the pannus/cartilage junction; by various interactions, these contribute to destruction of cartilage and bone.