ABSTRACT
Arthritis (either rheumatoid arthritis (RA) or osteoarthritis) is a chronic in–ammatory disease, characterized by in–ammation of the synovial tissues lining the joints [1-4]. In–ammation starts with the in—ltration of in–ammatory cells, including monocytes and activated leukocytes, into the joints [5-10]. These cells release enzymes and proin–ammatory and other factors that degrade and destroy synovial tissue [8-10]. In–ammation eventually leads to coagulation and —brin deposits on the synovial membrane and in the intracellular matrix of the joints. This —brin develops into granulation tissue called pannus, which is considered as a scar tissue in the healing process. Pannus tissue around the joint eventually immobilizes the joint. In addition to this process, synovial membrane cells abnormally proliferate and enlarge and eventually occlude small blood causing reduced blood –ow or ischemia. This causes hypoxia and metabolic acidosis. Acidosis stimulates the release of hydrolytic enzymes from synovial cells into the surrounding tissue, initiating erosion of the cartilage and bone and —nally joint deformity and functional disability [11-14].
