A wide range of evidence supports the contribution of reactive oxygen species (ROS) and reactive nitrogen species (RNS) to osteoarticular disorders. An imbalance between the production of ROS and/or RNS and the activity of the antioxidant defense systems result in oxidative stress, which contributes to rheumatoid arthritis (RA) pathology. The functioning of immune cells is influenced by alterations in the intracellular redox balance. Synovial hyperplasia and chronic inflammation are associated with a lack of apoptosis of immune cells and synovial fibroblasts, which depends on the activation of nuclear factor-kappa B (NF-KB) and other signaling pathways inducing the expression of antiapoptotic molecules. Degradation of joint components in osteoarthritis (OA) is thought to be largely elicited by mechanical stress and proinflammatory cytokines inducing ROS production and inducible nitric oxide synthase (iNOS) expression. Accumulated evidence in recent years indicates that oxidative stress is a pivotal pathogenetic culprit in aging and other osteoporosis-related conditions.