Accumulated knowledge of the inflammatory process in rheumatoid arthritis has been effectively summarized in recent years (1-4). Although the data are only circumstantial, the favored hypothesis is that an immune response to an as yet unknown antigen leads to the development of acute inflammation in synovial tissue and synovial fluid and to the establishment of chronic, active inflammation below the lining cells.
Associated with (and probably caused by) the inflammation is the proliferative lesion of rheumatoid arthritis. This term refers to the enormous excess of connective tissue, small blood vessels, mesenchymal cells with both phagocytic and synthetic function, and macrophages that comprise the bulky synovial tissue in rheumatoid arthritis. This proliferative response becomes polarized and organized into an invasive front with the capacity to destroy cartilage, subchondral bone, and tendons. It is ultimately responsible for irreversible destruction of joints.
This paper reviews both the mechanisms by which joints are destroyed and the growing body of