Rheumatoid arthritis (RA) is a chronic autoimmune disease. Persistent inflammation, joint degradation, and extra-articular symptoms are the hallmarks of RA. Environmental triggers like smoking and microbial exposures, as well as genetic predispositions, particularly HLA-DRB1 alleles, interact intricately in the pathophysiology of RA. The breakdown of immunological tolerance brought on by pro-inflammatory cytokines including TNF-α, IL-1, and IL-6 results in the production of autoantibodies, especially anti-citrullinated protein antibodies (ACPAs). Progressive joint deterioration results from the hyperplasia of the synovial membrane, which creates pannus tissue that erodes the adjacent bone and cartilage. The goal of managing RA is to achieve remission or low disease activity through early and robust treatments. Disease-modifying antirheumatic drugs (DMARDs) like methotrexate and biologics that target specific immune pathways are the foundation of pharmacologic therapy. For patients who are not responding to traditional therapy, Janus kinase (JAK) inhibitors provide an oral option. In order to preserve function and enhance quality of life, non-pharmacological approaches like physical therapy, occupational support, and anti-inflammatory foods are essential. Nonsteroidal anti-inflammatory drugs and corticosteroids can be used to relieve symptoms, but long-term use is limited by adverse effects. Individualized treatment plans, regular monitoring, and patient education are essential for best outcomes.