The first step toward taking control involves understanding what's happening inside your body.
RA is an autoimmune disease. This means that your immune system, which normally fights "invaders" such as bacteria and viruses, goes haywire and instead attacks your body's healthy tissue.
One site of this self-attack is the synovium, a delicate lining only a few cells thick that surrounds your joints and produces fluid that lubricates them. With RA, your synovium becomes swollen and inflamed. This puts pressure on your nerves, which, in turn, send pain signals to your brain. The swollen synovium also protrudes into the joints and releases chemicals that eat away at the bone. This process is what leads to the pain, stiffness and swelling associated with RA.
Although much progress has been made, doctors still don't understand everything about the way RA works. In part, that's because the disease progresses differently in different people. Your body's immune system can change over time—making your symptoms better or worse. It also can cause a treatment you're trying to suddenly stop working.
"Many factors are involved in the workings of the immune system," explains Allan Gibofsky, MD, professor of medicine and public health at Weill Cornell Medical College and attending physician at the Hospital for Special Surgery, both in New York City. "When these factors get out of balance, problems can result. Your doctor's challenge is to get them back into a reasonable balance."
Possible causes of RA include:
T cells. One theory about how RA develops involves T cells. T cells are a type of white blood cell that jump-start the disease process and make inflammation worse. Some medications are designed to halt the actions of these inflammatory T cells.
TNF and IL-1 cytokines. Another theory about RA focuses on the activities of cytokines. These small, immune-system proteins transmit signals between cells. An oversupply of cytokines known as tumor necrosis factor-a (TNF-a) and interleukin-1 (IL-1) are often found in joints affected by RA. Some medications are designed to "inhibit" the activity of TNF-a and IL-1 cells.
IL-6 cytokines. Interleukin-6 (IL-6) is yet another type of cytokine. In a healthy person, T cells secrete IL-6 to help the body recover from trauma. In a person with RA, however, IL-6 levels can be too high. This is why some treatments are designed to "block" the activity of IL-6 cells.
"Patients have to keep in mind that, no matter what treatment you're currently receiving, you may have to do something different at another time," says Dr. Gibofsky. That's because RA is a disease that can change in your body over time. "If your doctor is suppressing TNF in you now, he may need to suppress IL-6 in you later. It's all about achieving the right balance."
Bottom line? Working closely and continuously with your doctor to understand the right treatment options for you is critical to long-term treatment success.