Rheumatoid arthritis is a chronic autoimmune systemic inflammatory disease of connective tissue that mainly damages joints in an erosive-destructive progressive type of polyarthritis. On the basis of the pathogenesis of rheumatoid arthritis, genetically determined autoimmune processes lie, the origin of which is predisposed to the deficit of the T-suppressor function of lymphocytes. Changes in the structure of the joint occurring at the base of this disease – ankylosis, deformity and contracture formation-are associated to a large extent with early-onset treatment. Clinical-pathogenetic properties of rheumatoid arthritis in the articlelit.
Norbo'toyev et al. (Sun,) studied this question.