Background: Rheumatoid arthritis (RA) is a systemic, autoimmune disease characterized by chronic synovial inflammation, progressive joint destruction, and multiple systemic manifestations. Affecting approximately 1% of the global adult population, RA significantly contributes to disability, morbidity, and economic burden. Objective: This review outlines the current understanding of RA pathogenesis, diagnostic approaches, and therapeutic strategies, while highlighting emerging insights and treatment gaps. Methods: A comprehensive overview was conducted based on current literature detailing the immunological, genetic, and environmental factors contributing to RA, as well as established and emerging treatment modalities. Results: RA pathophysiology involves immune cell infiltration, synovial hyperplasia (pannus formation), neovascularization, and the production of inflammatory cytokines (TNF-α, IL-1, IL-6), matrix metalloproteinases, and autoantibodies such as rheumatoid factor and anti-citrullinated protein antibodies (ACPA). Genetic predisposition (notably HLA-DR4/DR1) interacts with environmental triggers (e.g., smoking, periodontitis, microbiome dysbiosis) to initiate autoimmunity. Diagnosis is supported by clinical evaluation, serological markers, and imaging modalities such as ultrasound and MRI. Early intervention using nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying antirheumatic drugs (DMARDs)—including methotrexate and biologics—is critical for improving outcomes. Surgical management is reserved for end-stage disease.
D et al. (Wed,) studied this question.
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