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What is the Pathophysiology of Rheumatoid Arthritis?

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  • Written By: Toni Henthorn
  • Edited By: W. Everett
  • Last Modified Date: 11 November 2016
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Researchers have not fully brought to light the exact pathophysiology of rheumatoid arthritis (RA), but many discoveries are now expanding the scope of beneficial treatments for this immune system disorder that afflicts almost 2 million people in the United States. Rheumatoid arthritis is one of a group of diseases, called autoimmune diseases, in which the body's immune cells mistakenly attack the body's own tissues or organs. In the case of RA, the assault occurs in the joints of the body, producing inflammation, pain, and impaired movement. An antibody, called rheumatoid factor, causes the immune system to misidentify the body's healthy joint tissues as foreign tissue, targeting them for destruction. Although the precise cause of rheumatoid arthritis is unknown, several factors apparently are involved, including gender, infection, genetics, smoking, and a poorly regulated immune system.

Females develop rheumatoid arthritis three times more often than males, particularly during the first postpartum year. Women typically develop the first symptoms during the third through the fifth decades of life. Scientists hypothesize that female sex hormones, which tend to promote inflammation, play a role in the pathophysiology of rheumatoid arthritis. The increased incidence of RA in females mirrors the pattern seen with other autoimmune diseases.

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Scientists also believe that infection may serve as a triggering event in the pathophysiology of rheumatoid arthritis. In response to an infection, the body produces proteins, called antibodies, which attack foreign particles. If the antibodies are not sufficiently specific to the bacteria, they may attach to normal body cells that resemble the bacteria in some way, disabling the cells and marking them for elimination by the immune cells. Many physicians have suspected parvovirus, rubella, herpes, and mycoplasma, which causes "walking pneumonia," to be agents that potentially instigate RA. Studies, however, have been unable to confirm definitively the triggering infectious organisms.

While only present in 20 percent of the general population, the genetically coded cell marker, HLA-DR4, occurs in greater than two thirds of Caucasian RA patients. The genetic code for this antigen marker is located on the short arm of the sixth chromosome in humans. Patients who have the marker have an increased chance of developing rheumatoid arthritis relative to those who do not. The presence of the marker does not guarantee the onset of rheumatoid arthritis, however. Researchers believe that the marker indicates only a genetic predisposition.

Cigarette smoking doubles the risk for developing the pathophysiology of rheumatoid arthritis. Patients who smoke longer than 25 years have a three-fold increase in the probability of having rheumatoid arthritis with development of bone erosion. Tobacco use increases the white blood cell count and the circulating blood levels of the antibody, rheumatoid factor. The link between smoking and RA is stronger in men than women.

Without doubt, the immune cells and the cells lining the joints mediate the chronic joint inflammation characteristic of rheumatoid arthritis. White blood cells stream into the joints, causing pain, swelling, heat, and redness. The cells also release chemical mediators, including cytokines, antibodies, interleukins, and tumor necrosis factors (TNF), which promote scarring and destruction of the joint lining and cartilage. In the late stages, the bone erodes and the joint distorts. Cytokines also produce the whole body pathophysiology of rheumatoid arthritis, such as muscle aches, weight loss, and fever.

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