The Role of Reactive Oxygen Species in Immunopathogenesis of Rheumatoid Arthritis

Rheumatoid arthritis is a disease associated with painful joints that affects approximately1% of the population worldwide, and for which no effective cure is available. it is characterizedby chronic joint inflammation and variable degrees of bone and cartilage erosion. oxygenmetabolism has an important role in the pathogenesis of rheumatoid arthritis. reactiveoxygen species (ros) are produced in many normal and abnormal processes in humans, includingatheroma, asthma, joint diseases, aging, and cancer. tnf-alpha overproduction isthought to be the main contributor to increased ros release in patients with ra. increasedros production leads to tissue damage associated with inflammation. the prevailing hypothesisthat ros promote inflammation was recently challenged when polymorphisms inneutrophil cytosolic factor 1(ncf1), that decrease oxidative burst, were shown to increasedisease severity in mouse and rat arthritis models. it has been shown that oxygen radicalsmight also be important in controlling disease severity and reducing joint inflammation andconnective tissue damage. in this review article, our aim is to clarify the role of ros in immunopathogenesisof rheumatoid arthritis.