Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disease marked by inflammatory arthritis and extra-articular involvement. This disorder is primarily characterized by inflammation in the synovial joints and often starts in small peripheral joints, typically presenting in a symmetric pattern. The pathogenesis of RA is complex, involving multiple factors including genetic, environmental, immunologic, and others, which contribute to the disease’s development and expression.
Key elements in the pathogenesis include changes in the synovial lining or intimal layer, which in RA becomes greatly hypertrophied, increasing from 1-3 cells thick to 8-10 cells. This layer primarily comprises fibroblasts and macrophages. The subintimal area of the synovium, where the synovial blood vessels are located, normally has very few cells but is also affected in RA.
The disease’s progression can be dissected into specific stages: (i) triggering, (ii) maturation, (iii) targeting, and (iv) the fulminant stage, which is concurrent with hyperplastic synovium, cartilage damage, bone erosion, and systemic consequences. The role of the adaptive immune pathway is crucial in RA, highlighted by the presence of dendritic cells, a major class of antigen-presenting cells, and the expression of various cytokines and HLA class II molecules.
For a comprehensive understanding of RA’s pathogenesis, several resources can be explored. Vignesvararajah Lokeesan’s presentation on Rheumatoid Arthritis and Venkata Pradeep Babu Koyyala’s presentation on Rheumatoid Arthritis Pathogenesis offer valuable insights. Additional information can be obtained from the Johns Hopkins Arthritis Center, UpToDate, American Journal of Managed Care, and the NCBI Bookshelf.
Understanding the epidemiology, pathophysiology, and diagnosis of RA is crucial for medical professionals and researchers. This knowledge aids in the development of modern pharmacologic therapies and the management of the disease, improving the quality of life for individuals affected by RA.
