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3.5 Rheumatoid Arthritis
3.5.1 De
nition and Occurrence
Rheumatoid arthritis (RA) is the most common type of in
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ammatory arthritis in
adults, affecting 0.5
1 % of the population. RA typically begins in middle-age or
old-age, and women are three times more likely to have RA than men. The cause of
RA is unknown. There are a number of gene variations that are associated with an
increased risk of RA, but RA is not strictly hereditary. Current theory holds that RA
develops as a consequence of exposure to an environmental trigger in a genetically-
susceptible person [
67
]. Whether the trigger is the same for all patients is unknown.
Smoking has been identi
-
ed as a risk factor for RA, and smokers who have par-
ticular variants of the HLA-DR gene are at greatly increased risk. For most patients,
RA is a life-long disease. While there is currently no cure for RA, medications can
improve and control symptoms, and remission is possible with treatment. A small
proportion of patients may have their RA spontaneously go into remission.
RA is an autoimmune disease. Autoimmune diseases are a category of diseases
characterized by immune reactions against the body
s own tissues. While the pri-
mary roles of the immune system are to provide protection from infections and to
seek and destroy cells that may progress to tumors, these immune responses
become subverted in autoimmune diseases. In autoimmune diseases, the immune
system senses certain normal proteins or cells as foreign or abnormal. In RA, the
immune system generates in
'
ammatory cells that target the lining tissue of the joint
(synovium), the cartilage that caps the end of bones and forms the gliding surface of
joints, and components of the immune system itself [
68
]. The immune system also
begins to make antibodies against normal proteins, which can inactivate them. In
RA, two of these so-called autoantibodies are commonly made. Rheumatoid factor
is an antibody to immunoglobulins, which are proteins that provide immune
protection against viruses and bacteria. Antibodies to citrullinated proteins bind
specific proteins found in the connective tissue between cells. Both of these anti-
bodies can be measured in clinical laboratories, and are used to aid in the diagnosis
of RA. About 80 % of patients with RA have either rheumatoid factor or antibodies
to citrullinated proteins detectable in their blood.
In
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ammation develops as a consequence of these autoimmune reactions. In the
joints, this in
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ammation causes joint swelling due to
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fluid accumulation in the joint
space, in
ltration of the synovium by white blood cells and expansion of blood
vessels, and over time, proliferation of the synovial cells. Persistent in
ammation
can, over weeks to months, lead to loss of mineralization of the surrounding bone,
wearing away of the joint cartilage, and eventually erosion of the bone surfaces at
the margins of the joints. Persistent joint swelling can also stretch and weaken
surrounding ligaments and tendons, resulting in shifting of the joints out of normal
alignment. RA is therefore known as a deforming arthritis. This shifting places the
joints at mechanical disadvantage, and which along with swelling, can cause
weakness.
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