Rheumatoid Arthritis
A Review of The Literature

Mechanisms of Human Pathology
Charles Childers

Rheumatoid Arthritis Rheumatoid Arthritis (RA) is a chronic, autoimmune systemic inflammatory process that primarily attacks synovial joints as well as other tissues and organs of the body. This disorder is characterized by hyperplasia of synovial cells leading to an inflammatory response of the synovium that may ultimately cause destruction of articular cartilage. In cases of severe comprehensive damage joints can become ankylosed. RA is usually known to affect the wrist and hands bilaterally and symmetrically, but may be seen in any of the other synovial joints. The destruction can be progressive leading to joint deformations and disabilities.1 RA can also bring inflammation of the lungs, pleura, sclera of the eye, and pericardium. Nodules have been seen in the extensor tendons subcutaneously especially over the olecranon process. As has been reported,1 mechanistic paths to synovitis leading to this articular damage have shown tumor necrosis factor alpha (TNF-α) to take a significant part in joint inflammation responsible for the destruction. Therapies have developed to target TNF-α bringing a substantial impact on patient care. The exact etiology remains unclear in this autoimmune progressive disorder, but much is being looked at in search of an autoantigen or another triggering agent. According to Robinson,2 the importance of early diagnosis and subsequent treatment of RA is becoming more accepted. He goes on to say that accurate triaging is needed of primary care physicians to accomplish this, along with the expedition of rheumatologist’s assessments. Patients will typically complain of swollen joints, which upon assessment and confirmation by a general practitioner (GP) would be seen as urgent along with a raised C-reactive protein.