Fig. 1

Role of oxidative stress in cartilage damage during OA. OA is hypothesised as a chronic inflammation disease that occurs with gradual changes in the immune system (see Pathophysiology of knee OA). IL-1β and TNF-α and other inflammatory factors increase in OA. This pathway leads to induction of NO synthase, production of larger amounts of NO and a deficiency in SOD and catalase (see Role of ROS in OA). The deficiency in SOD leads to higher levels of superoxide which combines with NO to produce peroxynitrite which can cause telomere erosion by targeting guanine repeats in their DNA telomeres. The net result is a decrease in the synthesis of collagen II. The decrease in catalase results in accumulation of peroxide to increase lipid peroxidation which produces 4-hydroxynonenal. The 4-hydroxynonenal increases factors which breakdown collagen II and also inhibits the expression of collagen II. The net result is the cartilage damage that occurs in OA. Note that the scheme shown here is only a summary