Rheumatoid Arthritis


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Rheumatoid Arthritis (RA) is a complex, systemic autoimmune disorder likely triggered by an infectious organism that initiates the interplay of genetic factors and inflammatory mediators . Chronic inflammation, the hallmark of RA, is thought to be the result of the body’s long term exposure to an antigen. The body’s initial attack is unsuccessful and over time development of autoantibodies occurs. The autoantibodies attack the body’s own tissues resulting in painful, chronic inflammation . The exact cause of the disorder has yet to be identified despite extensive research.

The disease process of RA is related to an immune complex-mediated hypersensitivity reaction, commonly referred to as Type III hypersensitivity (Rote, 2007).  According to Rote (2007, 127), an antibody binds to a soluble antigen that is released into blood or body fluids. It is then transported through the circulatory system and eventually deposited into the body’s tissues. These deposits are called antigen-antibody complexes; in patients with RA, they are referred to as rheumatoid factors (RF). In RA, these antigen-antibody complexes are deposited in the synovial membrane which lines the joint cavity . Once the antigen-antibody complex is in the synovial membrane, it triggers a reaction called the complement cascade. The end result of the cascade is the release of chemotactic factors that attract neutrophils and other lymphocytes to the area to attack the antigen . Neutrophils mount a defense by attempting to ingest the immune complex using lysosomal enzymes. In addition, cytokines are attracted to the area stimulating the synthesis of proinflammatory compounds which in turn prompt chondrocytes to attack the cartilage. The synovium digests the cartilage, stimulating a release of inflammatory molecules.

The body’s immune system is designed to recognize any sign of cellular injury and act promptly to mitigate the damage. In the case of RA, the immune response perpetuates the damage with the activation of B and T lymphocytes.  The B lymphocytes develop additional RF which again deposit into the synovial membrane. The T lymphocytes stimulate the production of enzymes that amplify and reinitiate the inflammation process . A vicious cycle of deposition of antigen-antibody complexes and resultant inflammation is created.

The chronic inflammation impacts the joint by causing the synovial membrane to thicken and the cells to mutate and proliferate. The mutated cells occlude the blood supply leading to hypoxia and metabolic acidosis. Further erosion of the joint and surrounding tissues occurs eventually leading to the development of granulation tissue called pannus.  Pannus leads to scar tissue formation and eventually immobilizes the joint

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