Rheumatoid arthritis and osteoarthritis: disease pathogenesis

pathogenesis Rheumatoid arthritis (RA) is a chronic infl ammatory disease characterized by the activation of synovial tissue lining the joint capsule, which results in the invasion of the cartilage and bone leading to the progressive joint dysfunction [1]. Severe morbidity and structural damage of joints caused by chronic infl ammation often lead to major personal, family, and fi nancial consequences, as well as increased mortality. Recent understanding of the RA pathogenesis has clarifi ed the role of cytokines and other infl ammatory mediators in this process and has provided a scientifi c rationale in the process of developing targeted therapies [2]. Osteoarthritis (OA) is a common disorder of synovial joints characterized pathologically by focal areas of damage to the articular cartilage, centered on load-bearing areas, which is associated with new bone formation at the joint margins (osteophytosis), changes in the subchondral bone, variable degrees of mild synovitis, and thickening of the joint capsule [3]. Th e severity of OA diff ers from patient to patient, but the very common clinical symptoms include pain, reduced range of motion, infl ammation, and deformity [4]. Th is condition is strongly age related, being less common before the age of 40 but showing a marked increase in frequency with age [3]. Although OA is considered the disease of the destruc tion of articular cartilage, recent evidence suggests that it may also damage bone and synovium in the arthritic joints [3,4]. Despite existing evidence of the crosstalk between tissues at the cellular and molecular levels, however, intertwined pathophysiological processes causing OA have reduced the focus in choosing from one of these three tissues – articular cartilage, bone, or synovium – to serve as the key therapeutic target [3].