Derek Burnett
Derek Burnett is a Contributing Writer at Bottom Line Personal, where he writes frequently on health and wellness. He is also a contributing editor with Reader’s Digest magazine.
When all is functioning as it should, our immune system does an incredible job recognizing and neutralizing threats. Each time it encounters a new enemy, it takes a kind of imprint of the invader and distributes it to the components of the immune system that act like sentries. As soon as that particular enemy dares show itself again, the immune system recognizes it and leaps into action, releasing inflammatory substances that destroy the invader. Unfortunately, this complex process sometimes goes amiss. Rather than taking the imprint of an actual external threat, the immune system mistakenly memorizes the body’s own tissue as a menace that must be dealt with, and it releases antibodies and T cells that wreak havoc on what were once healthy cells.
That’s what happens with rheumatoid arthritis (RA), which is one of more than 100 autoimmune diseases affecting humans (other examples include multiple sclerosis, psoriasis, and lupus). It afflicts about 1.3 million Americans, making it the most common autoimmune inflammatory disease affecting the joints.
There is no known cause of rheumatoid arthritis. Certainly genetics plays a role, but most scientists think that a genetic predisposition is not a sufficient cause for someone developing the disease. Instead, some external trigger must occur. That could be an infection in which the joint tissue gets caught up as collateral damage in the body’s immune response, or it could be an environmental factor such as smoking. It could also be the case that a pathogen manages to mimic the body’s own proteins so that the immune system imprints the protein as a foreign threat and attacks it.
Rheumatoid arthritis can be tricky to diagnose, since its symptoms resemble those of other diseases. Rather than relying on one definitive blood test, doctors diagnose RA by doing a complete physical exam and then testing the blood for biomarkers or features consistent with the disease such as high levels of C-reactive protein, rheumatoid factor, and antibodies. The blood is also tested for its erythrocyte sedimentation rate (ESR), a measure of how quickly the red blood cells settle to the bottom of a test tube (inflammation causes them to clump together and sink abnormally slowly).
RA begins when the body generates inflammatory cells called cytokines within the synovium, a lining tissue that surrounds a joint. The synovium responds to the inflammation by proliferating. When that happens, the synovium produces a substance called pannus, a thick tissue that grows between bones, causing pain and immobility. Making things worse, those pannus cells in turn release substances that eat away at the joint’s cartilage and bone. They also cause the tendons and ligaments to become inflamed, and the entire capsule containing the joint may swell. When tendons are inflamed, they sometimes shrink, causing the joint to stop functioning. Or the tendons may rupture, rendering the joint loose and floppy. Left untreated, RA can cause permanent damage to joints.
The process in which RA develops appears to begin long before any symptoms are felt. Researchers have found autoantibodies and cytokines in the bloodstreams of people five years before any evidence of inflammation in the joints.
Unlike some types of arthritis, RA attacks multiple joints simultaneously, on both sides of the body at once. It typically appears in fingers, wrists, toes, ankles, elbows, knees, and feet. People with RA experience pain, weakness, immobility, instability, and sometimes bodily deformity as the joints and bones lose alignment and become enlarged or misshapen. Unfortunately, while RA is primarily a joint disease, it is progressive and spreads throughout the body. It can also affect organs such as blood vessels, lungs, eyes, and skin. Complications of RA can include carpal tunnel syndrome, pulmonary fibrosis (scarring of the lung tissue), pericarditis (inflammation of the lining of the heart), and neurologic disorders.
The B cells and T cells that are activated in rheumatoid arthritis can become malignant. People with rheumatoid arthritis are twice as likely to develop non-Hodgkins lymphoma than people without the disease, and this effect is strongest among RA patients whose disease is poorly controlled.
RA currently has no cure. It is critical to diagnose and treat the disease as early as possible so that the damage to joints does not become permanent. Medications used in the management of RA include:
Many RA patients also undergo surgeries to repair damaged joints. In a procedure called synovectomy, a surgeon can remove a patient’s synovium (joint lining) that has become inflamed. This can restore mobility and diminish pain in the joint. Surgeons can also repair tendons that have been loosened or ruptured by inflammatory processes. If the entire joint is damaged beyond repair, it may be replaced with a synthetic joint in a procedure called a total joint replacement. When a joint replacement is not possible, doctors sometimes surgically fuse the joint to stabilize it and reduce pain.
