Biomarkers of Oxidative Stress in Rheumatoid Arthritis: Clinical Relevance and Therapeutic Targets

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent synovial inflammation, joint destruction, and systemic complications. Among the diverse pathological mechanisms involved in RA, oxidative stress plays a critical role in disease initiation and progression. Oxidative stress results from an imbalance between the production of reactive oxygen species (ROS) and the body's antioxidant defense systems, leading to cellular and tissue damage. Several biomarkers have been identified to assess oxidative stress levels in RA patients, including malondialdehyde (MDA), 8-hydroxy-2'-deoxyguanosine (8-OHdG), advanced oxidation protein products (AOPP), and decreased levels of antioxidants such as glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT). These biomarkers not only reflect the oxidative burden but also correlate with disease activity, joint damage, and systemic manifestations. Measuring these markers can aid in early diagnosis, monitoring of disease progression, and evaluation of treatment efficacy. Furthermore, oxidative stress represents a promising therapeutic target. Antioxidant therapies, either as adjuncts to conventional treatments or as stand-alone interventions, have shown potential in reducing inflammation, improving clinical symptoms, and modulating immune responses. This review highlights the clinical significance of oxidative stress biomarkers in RA and discusses their potential role in guiding personalized treatment approaches. Understanding the interplay between oxidative stress and RA pathogenesis may open new avenues for targeted therapies, ultimately improving patient outcomes and quality of life.