Multifactorial Pathogenesis and Epidemiological Patterns of Rheumatoid Arthritis

Abstract

Rheumatoid arthritis (RA) is a common chronic autoimmune inflammatory disease with a global prevalence of approximately 0.5%–1%, primarily manifesting as synovial inflammation, joint bone destruction, and systemic damage. This review, based on a systematic literature search covering 2000–2024, summarises epidemiological trends, pathogenic mechanisms, and risk factors for RA. Research indicates that RA onset is closely associated with genetic susceptibility (such as HLA-DRB1 shared epitopes), immune dysregulation, and environmental factors including smoking and chemical exposure. Health conditions such as obesity and periodontitis may also increase risk. Complex interactions between immune cells and cytokines lead to synovial hyperplasia, formation of erosive ‘synovial overgrowth’, and autoantibody production. Existing non-steroidal anti-inflammatory drugs, glucocorticoids, and disease-modifying antirheumatic drugs (DMARDs) can alleviate symptoms, yet early recognition and precise intervention remain essential. This paper aims to provide reference for RA aetiological research, early prediction model development, and personalised treatment strategies, highlighting the need for integrative multi-omics approaches and translational studies to improve patient outcomes.