![]() |
Do You Have Arthritis?
|
![]() |
Can Cracking Your Knuckles Cause Arthritis?
|
Rheumatoid arthritis (RA) is a chronic inflammatory disease affecting the joints, most often in the hands and feet. It results in swelling, stiffness, pain, and sometimes joint, bone, and cartilage destruction.
Although the exact cause of RA is unknown, the disease belongs to a group of diseases called autoimmune disorders. In these disorders, the immune system, the function of which is to protect the body, produces antibodies that attack the soft tissues lining the joints and may also attack connective tissue in many other parts of the body, including the blood vessels and lungs. Eventually, the cartilage, bone, and ligaments of the joint deteriorate, causing deformity, instability, and scarring within the joint. The rate at which the joints deteriorate varies with the individual. A number of risk factors, including genetic predisposition, gender, and unspecified environmental factors, may put a person at risk for developing the disease as well as influence the pattern of the disease.
As with other forms of arthritis, RA involves inflammation of the joints. A membrane called the synovium lines each of the body's movable joints. In RA, white blood cells, which usually attack foreign invaders such as bacteria and viruses, move from the bloodstream into the synovium. There, these blood cells appear to play an important role in causing inflammation to the synovial membrane, a condition called synovitis. This inflammation results in the release of proteins that, over months or years, causes thickening of the synovium. These proteins
can also damage cartilage, bone, tendons, and ligaments. Gradually, the joint loses its shape and alignment, and eventually may be destroyed.
Rheumatoid arthritis is a genetically complex disease. Studies in monozygotic (identical) and dizygotic (fraternal) twins indicate that genetic factors are involved in acquiring the susceptibility or tendency to RA rather than the disease itself. People with certain human leukocyte antigen (HLA) genes—specifically, the genetic marker called HLA-DR4 (the DR4 refers to the specific antigen)—are more likely to develop the disease than those without the genes. However, people without this antigen can develop the disease as well.
The HLA-DR4 marker is found in white blood cells and plays a role in helping the body distinguish between its own cells and foreign invaders. In addition, these genes also help predict the severity of the disease and how effectively the disease responds to treatment. The mechanism by which HLA alleles (HLA genetic variations) affect disease risk is still under investigation.
In one study, French scientists found 63 genes that appeared to be linked to the development of rheumatoid arthritis. The group studied and compared the expression of 5,200 genes in the synovial (joint) fluid of a group of patients with RA and another group with osteoarthritis. The researchers found 48 known and 15 unknown genes that were either overexpressed or underexpressed in RA patients compared with osteoarthritis patients. Two of the novel genes were located on chromosome 6, at the p21 region, which is an area already linked to inflammatory disease. Four other genes were located on the X chromosome. The French
However, not all the genes associated with RA have been discovered, and more research is needed.
Rheumatoid arthritis affects approximately 1% of the United States population. Although some people have a mild form of RA, 70% eventually develop chronic problems, and 15% have a severe crippling form of the disease.
The disease occurs in all races and countries. Although RA affects women two to three times more often than men, men tend to be affected more severely by it. The onset of RA most commonly occurs between the ages of 25 and 50, but children and adolescents as well as the elderly may be affected as well. When the disease occurs in children, it is referred to as juvenile RA.
|
|
Author Info: Genevieve T. Slomski PhD, Thomson Gale, Gale, Detroit, Gale Encyclopedia of Genetic Disorders Part II, 2005 |