Who is likely to develop Rheumatoid
Arthritis?
Causes of Rheumatoid Arthritis
Rheumatoid arthritis is an autoimmune disease, i.e., one in which the body’s immune system attacks the body’s own tissue. It is a chronic inflammatory condition affecting the whole body, particularly the synovial membranes of the joints. The joints typically affected are the hands and feet, wrists, ankles and knees. These will be warm, tender and swollen, and the skin over the joint will take on a ruddy purplish hue. Joint deformities occur in the hands and feet, as the disease progresses.
Between 1% and 3% of the population is affected by rheumatoid arthritis, female sufferers outnumbering males by almost three to one. The onset of the disease is usually between 20 and 40 years, although it may begin at any age.
Anaemia; enlargement of the spleen; inflammation of the blood vessels (vasculitis); inflammation of the heart and lungs; low white blood cell count; muscle wasting; skin nodules.
Diagnosis of early rheumatoid arthritis is difficult, the disease being more easily recognised in its most advanced and characteristic form. Anyone who suspects that they may have rheumatic arthritis should consult their medical practitioner for a definitive diagnosis.
Evidence suggests that rheumatoid arthritis is an autoimmune reaction, in which antibodies develop against components of joint tissues, although the cause of this autoimmune reaction is largely unknown. Speculation and investigation has focussed on genetic susceptibility, abnormal bowel permeability, and microorganisms, in addition to dietary factors. Rheumatoid arthritis is a classic example of a multifactorial disease in which a combination of genetic and environmental factors contributes to the disease process.
A specific genetic marker is found in 70% of rheumatoid arthritis sufferers compared with 28% of the general population. This indicates the likelihood that the development of the disease is influenced by genetic factors governing immune response. Severe rheumatoid arthritis occurs at four times the average rate in children of parents with rheumatoid arthritis.
However strong the genetic association, environmental factors must be present in order for the disease to develop. Studies of identical twins show that it is quite rare for both twins to develop rheumatoid arthritis.
A link between rheumatoid arthritis and abnormal bowel function may provide a unified theory as to the cause of rheumatoid arthritis. Sufferers of rheumatoid arthritis have increased intestinal permeability (‘leakiness’ of the gut). Food allergies are considered to contribute greatly to increased intestinal permeability in rheumatoid arthritis.
A leaky gut results in an increased absorption of large dietary and bacterial molecules. These molecules are normally prevented from being absorbed because they are too large, but in rheumatoid arthritis, they are absorbed into the body, and, as a response, the body forms antibodies to bind them. Antibodies are released by white blood cells to bind to foreign molecules such as those seen on bacteria, viruses, and cancer cells. This results in the formation of an immune complex.
In rheumatoid arthritis, food and bacterial molecules act as antigens that are being bound by the antibodies. The resulting immune complex triggers the immune system to release compounds to destroy it. These compounds, when deposited in joint tissues, destroy not only the immune complex, but surrounding joint tissue also.
The presence of immune complexes in joint tissues is one of the major contributory factors in the development of rheumatoid arthritis, and results in much inflammation and joint destruction. As the joint tissues are destroyed, large molecules that are normally protected from the immune system by cell membranes and connective tissue are exposed. The body can then develop antibodies to the exposed antigens.
The body may also develop antibodies to its own tissue by developing ‘cross-reacting’ antibodies. The increased intestinal permeability and altered bacterial flora result in the absorption of antigens similar to those in joint tissues. Antibodies formed to these antigens would ‘cross-react’ with the antigens in the joint tissues.
Physicians use the presence of immune complexes to monitor rheumatoid arthritis patients, as the serum and joint fluid of almost all sufferers contain the ‘rheumatoid factor’ (RF). The RF represents the formation of multiple immune complexes, and is mostly formed locally in the affected joints by white blood cells. The level of RF can be measured in the blood, and usually corresponds to the severity of arthritis symptoms.
A variety of microorganisms (e.g., Epstein-Bar virus, rubella virus, amoebic organism, and mycoplasma) have been suggested as causative factors in the development of rheumatoid arthritis, but no microbial agent has been consistently isolated in sufferers of the disease. However, the role of microbial factors in increasing the level of circulating immune complexes does contribute to the disease process of rheumatoid arthritis.
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