Published Paper Details:

Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disorder characterized by progressive inflammation of synovial joints, leading to pain, stiffness, swelling, and ultimately irreversible joint destruction if not managed appropriately. Over the past decades, RA has been recognized not only as a joint-specific disease but also as a systemic condition that affects various organs, including the cardiovascular, pulmonary, and hematological systems. The pathogenesis of RA is exceptionally complex, involving a multifactorial interaction of genetic predisposition, environmental triggers, immune dysregulation, and aberrant cellular signaling pathways. The immune system, which normally protects the body from pathogens, mistakenly identifies components of the synovial membrane as foreign, triggering a cascade of inflammatory reactions. This autoimmune attack is mediated by a combination of T cells, B cells, macrophages, and fibroblast-like synoviocytes (FLS), all of which participate in driving chronic inflammation. Cytokines such as tumor necrosis factor-alpha (TNF-?), interleukin-1 (IL-1), and interleukin-6 (IL-6) are central mediators of RA pathogenesis. These cytokines amplify inflammatory responses, recruit additional immune cells to the synovial tissue, and stimulate enzymes that degrade cartilage and bone. The synovium, which is normally a thin, delicate membrane, becomes thickened and hyperplastic, forming an invasive tissue known as pannus. This pannus aggressively expands across joint surfaces, eroding cartilage and bone through the activation of osteoclasts and matrix metalloproteinases. Over time, this destruction leads to joint deformity, functional impairment, and significant disability.