چكيده لاتين :
Rheumatoid arthritis is a disease associated with painful joints that affects approximately
1% of the population worldwide, and for which no effective cure is available. It is characterized
by chronic joint inflammation and variable degrees of bone and cartilage erosion. Oxygen
metabolism has an important role in the pathogenesis of rheumatoid arthritis. Reactive
oxygen species (ROS) are produced in many normal and abnormal processes in humans, including
atheroma, asthma, joint diseases, aging, and cancer. TNF-alpha overproduction is
thought to be the main contributor to increased ROS release in patients with RA. Increased
ROS production leads to tissue damage associated with inflammation. The prevailing hypothesis
that ROS promote inflammation was recently challenged when polymorphisms in
Neutrophil cytosolic factor 1(Ncf1), that decrease oxidative burst, were shown to increase
disease severity in mouse and rat arthritis models. It has been shown that oxygen radicals
might also be important in controlling disease severity and reducing joint inflammation and
connective tissue damage. In this review article, our aim is to clarify the role of ROS in immunopathogenesis
of Rheumatoid arthritis.
