Superoxide Dismutase (SOD) is an endogenous enzyme with potent antioxidant properties, catalyzing the dismutation of superoxide radicals into oxygen and hydrogen peroxide. In the context of rheumatoid arthritis (RA), oxidative stress is implicated in joint inflammation and tissue damage, providing a rationale for investigating antioxidants such as SOD. Several preclinical studies have demonstrated that SOD administration can reduce inflammation and tissue injury in animal models of RA, suggesting a potential therapeutic effect. However, clinical data in humans are limited and mixed.

Some small-scale clinical trials have explored oral or injectable SOD preparations in RA patients. Results from these studies are inconsistent, with a few reporting modest improvements in inflammatory markers or symptoms, while others show little to no benefit. Major limitations include poor bioavailability of orally administered SOD due to degradation in the digestive tract, and the small size or methodological weaknesses of available studies. Reviews and meta-analyses conclude that while there is a theoretical basis and some preliminary evidence for SOD's role in RA, robust, large-scale clinical trials are lacking.

In summary, the use of SOD for RA is supported by mechanistic and animal evidence, and limited human data. The current scientific evidence is weak to moderate (rating: 2), and further research is needed to establish efficacy and safety in RA patients.