<unk>  arthritis is mediated by the combination of a predisposing genotype along with which genetic factors, environmental factors, and microorganisms contribute, resulting in the inflammation and destruction of the synovial membrane. These factors lead to citrullination or post-translational modifications, resulting in the production of altered peptides. The altered peptides bind to MHC protein with shared epitopes which further leads to antigen presentation to T-cells.
T-cells further stimulate B-cells and cytokines which results in cartilage damage. Mutation of human leukocyte antigen (HLA) genes on chromosome 6 is involved in pathogenesis of<unk>  arthritis. Various conditions associated with RA include vasculitis, uveitis, scleritis, peripheral ulcerative keratitis, 
interstitial fibrosis, pulmonary nodules, bronchiolitis obliterans, organizing pneumonia, venous thromboembolism, pericarditis, myocarditis, congestive heart failure, atrial fibrillation, sjogren's syndrome, and felty's syndrome.
Rheumatoid arthritis pathophysiology
Septic arthritis pathophysiology
Ankylosing spondylitis pathophysiology
Bursitis pathophysiology
Psoriatic arthritis pathophysiology
Osteoarthritis pathophysiology
Osteomyelitis pathophysiology
Polymyalgia rheumatica pathophysiology