Abstract
Rheumatoid arthritis (RA) is an autoimmune disease characterized by the infiltration of various leukocyte subpopulations into both the developing pannus and synovial space. The chronic nature of this disease results in multiple joint inflammation with subsequent destruction of cartilage and joint. The etiologic cause of RA has not been clearly understood, but pro-inflammatory cytokine such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, and IL-6 mediated autoimmune responses are considered to play a crucial role in the pathogenesis of RA. The diagnosis of RA is primarily based on clinical grounds. However, not only clinical findings, but also serological and radiological examinations are required for the diagnosis, according to the classification criteria of RA established by American College of Rheumatology. Several clinical trials revealed the existence of "windows of opportunity" since radiological progression of RA is most prominent within the first two years of disease. Therefore, present treatment strategies for RA is use of disease-modifying anti-rheumatic drugs (DMARDs) singly or in combination as early as possible in the disease process, because suppression of disease activity correlates with reduction in radiological joint damage. However, many patients have persistent disease even when treated with DMARDs. There has been an increased understanding of the phenomenon of immune dysregulation in RA during the past several years and it is now possible to treat several autoimmune diseases based on this knowledge. An example is the successful treatment of clinical signs and symptoms and radiographic progression by blocking TNF, which is a key cytokine in the pathogenesis of RA. Therefore, the ultimate goals in managing RA are shifting from the prevention of joint damage, loss of function, and decrease pain to the complete remission clinically and radiologically.
