Current trends in epigenetic, cellular and molecular pathways in management of rheumatoid arthritis

Rheumatoid arthritis is a systemic chronic polyarticular autoimmune disorder of joints and joint membrane mainly affecting feet and hands. The pathological manifestation of the disease includes infiltration of immune cells, hyperplasia of the lining of synovium, formation of pannus and bone and cartilage destruction. If left untreated, the appearance of small focal necrosis, adhesion of granulation, and formation of fibrous tissue on the surface of articular cartilage is noted. The disease primarily affects nearly 1% of the population globally, women being more affected than men with a ratio 2:1 and can initiate regardless of any age. The synovial fibroblast in rheumatoid arthritis individuals exhibits an aggressive phenotype which upregulates the manifestation of protooncogenes, adhesive compounds, inflammatory cytokines and matrix-deteriorating enzymes. Apart from the inflammatory effects of cytokines, chemokines are also noted to induce swelling and pain in arthritic individuals by residing in synovial membrane and forming pannus. The current treatment of rheumatoid arthritis includes treatment with non-steroidal anti-inflammatory drugs, disease-modifying antirheumatic drugs, treatment with biologics such as inhibitors of TNF-a, interleukins, platelet activating factor, etc. which provides significant relief from symptoms and aids in management of the disease. The current review highlights the pathogenesis involved in the onset of rheumatoid arthritis and also covers epigenetic, cellular and molecular parameters associated with it to aid better and advanced therapeutic approaches for management of the debilitating disease.

Automated summary

Rheumatoid arthritis is a chronic autoimmune disorder that mainly affects the joints and joint membrane, resulting in immune cell infiltration, synovium lining hyperplasia, pannus formation, and bone and cartilage destruction. It affects approximately 1% of the global population, with a higher prevalence in women. The aggressive phenotype of synovial fibroblasts in rheumatoid arthritis individuals leads to the upregulation of proto-oncogenes, adhesive compounds, inflammatory cytokines, and matrix-deteriorating enzymes. Current treatment options include non-steroidal anti-inflammatory drugs, disease-modifying antirheumatic drugs, and biologics targeting specific molecules. Understanding the pathogenesis and associated parameters would facilitate the development of advanced therapeutic approaches for managing this debilitating disease.