Rheumatoid arthritis (RA) is a chronic disease affecting up to 3% of the po
pulation in most countries. The causes of Re have not been completely eluci
dated. This paper aims to review the role of reactive oxygen and nitrogen s
pecies in the etiopathogenesis of RA. Reactive oxygen species (ROS), such a
s superoxide radical, hydrogen peroxide, hydroxyl radical and hypochlorous
acid, as well as reactive nitrogen species (RNS), such as nitric oxide and
peroxynitrite, contribute significantly to tissue injury in RA. Several mec
hanisms are involved in the generation and action of ROS and RNS. Superoxid
e radical, hydrogen peroxide and nitric oxide do not directly damage the ma
jority of biological molecules. They are however converted into the highly
reactive hydroxyl radical, which reacts with almost all molecules in living
cells. The resulting chronic inflammation process can be reduced with anti
oxidant therapy. To date, scavenging, preventive, and enzyme antioxidants a
re available. The most important mode is scavenging of the hydroxyl radical
and of hypochlorous acid. Another important way is to inhibit production o
f RNS and ROS by neutrophils, monocytes, and macrophages. The control of in
flammation in arthritic patients by natural as well as synthetic antioxidan
ts could become a relevant component of antirheumatic prevention and therap
y.