Rheumatic disease Risk factors, pathophysiology and management

Abstract

Rheumatic diseases, because of their systemic inflammatory component, are associated with several shared comorbidities. The high affinity of shared epitope for citrullinated peptides could accelerate the amount of human leukocyte antigen peptide complexes on the surface of antigen-presenting cells, thus leading to a (possible joint-specific) T- cell response. Molecules such as receptor activator of nuclear factor κB ligand, prostaglandins, and matrix metalloproteinases are induced by pro-inflammatory cytokines, involving tumor necrosis factor and interleukin 6, and mediate signs and symptoms of the disease, involving pain and swelling, and degradation of cartilage and bone. Steroids at dosages equivalent to less than 10 mg of prednisone daily are highly effective for relieving symptoms of rheumatoid arthritis and can slow joint injury.