Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disease characterized primarily by symmetric polyarthritis, progressive joint destruction, and systemic manifestations. The pathogenesis of RA involves a complex interplay of genetic predisposition, environmental triggers, and immune dysregulation leading to persistent synovitis, autoantibody production (notably rheumatoid factor and anti-cyclic citrullinated peptide antibodies), and subsequent joint destruction. Clinically, RA presents with joint pain, morning stiffness, swelling, and can involve extra-articular features such as interstitial lung disease, vasculitis, and cardiovascular complications. Recent advances in diagnostic criteria, including the 2010 ACR/EULAR classification, have facilitated early identification of RA. Biomarkers such as anti-CCP antibodies and imaging techniques like musculoskeletal ultrasound and MRI have improved disease assessment. Treatment strategies have evolved from conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) to biologic agents (bDMARDs) targeting specific immune pathways, and targeted synthetic DMARDs (tsDMARDs) such as Janus kinase (JAK) inhibitors. The treat-to-target approach, aiming for remission or low disease activity, is now standard in RA management. Despite these advances, challenges remain in early diagnosis, management of refractory disease, and addressing comorbidities and long-term complications.