Medication

Medication is the first line of treatment for pain relief in many joint disorders. Non-steroidal anti-inflammatory (NSAIDs) are effective for treating a number of mildly painful conditions such as minor sprains, strains, and early-stage osteoarthritis. Most people are familiar with a variety of over the counter NSAIDs such as aspirin, naproxen (Aleve), and ibuprofen (Advil, Motrin). Prescription versions of these drugs are also available.

NSAIDs prevent some of the enzymes involved in the inflammatory response from doing their jobs. The enzyme involved is called cyclooxygenase, or COX, and has two forms. COX-1 helps protect the stomach from acids and digestive enzymes and maintains kidney function. COX-2 is the version produced by joint inflammation. Traditional NSAIDs inhibit both COX-1 and COX-2, which can cause stomach upset and bleeding. Newer NSAIDs are specific COX-2 inhibitors. These target only the COX-2 enzyme in the inflammatory response. These medications generally do not cause stomach upset or bleeding like traditional NSAIDs do. Several of these exist and are sold as Vioxx, Celebrex, and Bextra.

On September 30, 2004, Merck, a large pharmaceutical company, withdrew Vioxx from the market after studies demonstrated a significantly increased risk of cardiovascular disease (heart attack and stroke) in patients taking the drug.

Steroids (also called corticosteroids) compose the second tier of medications used for inflammatory pain release. These are synthetic compounds similar to the body’s naturally occurring hormone, cortisone, which is produced by the adrenal gland. They may be either injected at the site of pain or taken orally. Steroid mechanisms of action include limiting the small blood vessel dilatation and permeability (reducing swelling). They also restrict the accumulation of white blood cells that release tissue destroying enzymes. Additionally, new research suggests that corticosteroids inhibit the formation of prostaglandins, which contribute to the inflammatory process.

Steroids can produce dramatic anti-inflammatory results, but they have little lasting benefit and become less effective overtime. Additionally, the injections, themselves, may damage the joint. Other side effects exist as well, including weight gain, facial rounding, high blood pressure, acne, easy bruising, cataracts, thinning of skin and bone, and increased risk of developing diabetes and infection. When taken along with NSAIDs, there is a markedly increased risk of stomach ulcers.

Because the side effect profile is bad, steroids are generally prescribed in short “bursts” to relieve acute symptoms. The dosage is then slowly tapered. As side effects are more common if steroids are taken over prolonged periods at high doses, these drugs are prescribed at the lowest possible effective.

If anti-inflammatories fail, or the arthritis appears to be autoimmune in origin, disease-modifying antirheumatic drugs are often used. These medications were first used to treat diseases like cancer and malaria, but have proven effective in rheumatoid disorders. These agents suppress inflammation, presumably through action on the immune system, which means there is an associated risk of serious side effects.

Disease-modifying antirheumatic drugs have a variety of side effects. Drugs of this sort may cause diarrhea, rashes, anemia (lack of red blood cells), leucopenia (lack of white blood cells), and increased risk of infection. Greater risk of infection is a side effect shared by all immunosuppressants. Some of these drugs can also damage the liver and eyes, so it is important to have them monitored.

Arthritis Medications

Another group of disease-modifying antirheumatic drugs, gold salts, has been used for more than half a century. However, goldês mechanism of action is not well understood. However, it is now rare for physicians to prescribe gold due to the lack of an understood mechanism and the development of new therapies. New arthritis therapies include drugs that suppress the action of tumor necrosis factor (TNF). These TNF-suppressing drugs appear to slow the destruction of joints by disrupting activity of TNF, which is involved in the body's immune response. Other new medications include drugs that reduce the action of immune cells by impairing a protein required for DNA synthesis, slowing the activity of white blood cells. Still other new agents inhibit interleukin-1 (IL-1) another chemical mediator of inflammation.