Author: Brandon Eden
Arthritis is a very common condition characterized by joint pain, stiffness, swelling, and decreased range of motion. Osteoarthritis is the most common form of arthritis and what most people think of when they hear arthritis, and rheumatoid arthritis is the second most common form. Osteoarthritis comes with age, and occurs when wear and tear of the joints causes cartilage (the tissue on the ends of bones) to break down, resulting in bone on bone rubbing. On the other hand, rheumatoid arthritis is an autoimmune disorder, which results when the body’s immune system does not function properly and attacks its own tissues. It currently affects one percent of the population worldwide. In rheumatoid arthritis, the body perceives cells of the joint as foreign invaders and attacks them, resulting in inflammation and the breakdown of cartilage.
Rheumatoid arthritis is three times more common in women than men, and usually sets in between 40 and 60 years of age. The onset of rheumatoid arthritis usually occurs gradually, and begins in small joints of the hands and feet. Immune cells and chemicals that promote inflammation called cytokines can invade the lining of the joint, causing it to become inflamed and penetrate nearby cartilage and bone resulting in the joint to lose its shape and alignment. Joint cells that are promoting inflammation can enter the bloodstream and travel to other locations in the body. This is why rheumatoid arthritis can spread and affect not only joints, but also the skin, eyes, heart, lungs, and the digestive system.
The immune response is carried out by antibodies, which are proteins that attack foreign invaders. When antibodies mistakenly attack the body’s own cells, they are then called autoantibodies. Two common autoantibodies that spearhead rheumatoid arthritis are rheumatoid factor (RF) and anti-cyclic citrullinated peptide (ACCP) autoantibodies. Doctors will often take blood tests of patients and check for the presence of these autoantibodies when diagnosing rheumatoid arthritis.
Many research studies have been done to find out what went wrong with the immune system and why certain immune cells attack joints. There are many factors that can cause the autoimmune response of rheumatoid arthritis including genetic and environmental influences. Studies have shown that healthy cells in the joint can undergo chemical modifications that make them more susceptible to the immune response. Researchers have shown that smoking and certain infections can result in a specific type of chemical modification called citrullination. This process entails the chemical alteration of protein found in the joint, and the altered protein activates ACCP antibodies resulting in an autoimmune response. The detection of ACCP antibodies is a very conclusive way of diagnosing rheumatoid arthritis since other forms of autoantibodies can be found in other autoimmune disorders whereas ACCP antibodies are mostly only found in rheumatoid arthritis patients.
Some rheumatoid arthritis patients have been shown to have a slightly different T-cell structure. T-cells are crucial cells of the immune system which interact with foreign invaders and stimulate as well as tailor the immune response for that specific invader. The alteration of some T-cells found in rheumatoid arthritis patients enables the T-cell to more efficiently interact with the foreign invader, making an immune response more likely to occur. A larger immune response corresponds with a more aggressive case of rheumatoid arthritis.
Several genetic factors increase rheumatoid arthritis susceptibility, but the disease itself is not passed down through a gene. The combination of several genetic and environmental factors such as smoking is what can stimulate the onset of rheumatoid arthritis. The largest genetic risk factor for rheumatoid arthritis is a gene called HLA-DR. This gene stimulates the immune response by allowing T-cells to become more efficiently activated by the joint cells that have been modified by environmental risk factors.
The goal of rheumatoid arthritis treatment is to reduce pain, swelling, deformities, and maintain quality of life. This is possible to accomplish with disease-modifying antirheumatic drugs (DMARDS). These drugs inhibit cytokines from stimulating inflammation. Nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids can also reduce inflammation, but DMARDs are more specific for rheumatoid arthritis and yield better results. In very severe cases, joint replacement surgery may be an option if joint damage and symptoms cannot be controlled with medication and physical therapy.
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