Rheumatoid Arthritis

Disease / Phenomenon

Rheumatoid arthritis is a chronic systemic autoimmune disease in which the immune system attacks the synovial lining of joints. It characteristically affects small joints of the hands and feet symmetrically, producing pain, swelling, warmth, and prolonged morning stiffness that typically lasts more than an hour — a useful distinction from osteoarthritis. Left uncontrolled, the inflamed synovium invades and erodes cartilage and bone, causing the joint deformity historically associated with the disease. Rheumatoid arthritis is not confined to joints: fatigue, low-grade fever, anemia, rheumatoid nodules, interstitial lung disease, ocular inflammation, and elevated cardiovascular risk are all part of its systemic profile. It affects women more often than men and can begin at any age.

Disease typically begins with loss of tolerance to citrullinated self-proteins, generating anti-citrullinated protein antibodies and rheumatoid factor years before symptoms appear. Within the joint, activated T cells, B cells, macrophages, and fibroblast-like synoviocytes form an invasive pannus. TNF-alpha, IL-6, IL-1beta, and IL-17 drive NF-kB and JAK-STAT signaling, sustaining inflammation and angiogenesis. Matrix metalloproteinases degrade cartilage, while RANKL-mediated osteoclast activation erodes bone. Genetic risk concentrates in HLA-DRB1 shared epitope alleles and PTPN22. This page organizes these processes into their pathways and biomarkers.