Conventional Therapies: Many of the therapies for OA and RA have the inflammatory component as their target. Glucocorticoids (steroids) have long been employed to control inflammation. Their use over the long-term is discouraged because of potential severe toxicities to muscle and other organs. However, over the past 20 years, treatment regimens have indicated that the commonly employed steroid prednisone in low doses of 7.5 mg or less may be employed over long periods and are usually well tolerated and safe. Non-steroidal anti-inflammatory drugs (NSAIDs) are also commonly used in initial treatment of RA and OA.

NSAIDs (i.e., diclofenac, tenoxicam, indomethacin, tenidap, ibuprofen, to name just a few) are powerful anti-inflammatory drugs that act by inhibiting several components of the inflammatory pathways, including macrophage function and by the pharmacological inhibition of prostaglandin synthesis, in general. Long-term use of NSAIDs can produce gastrointestinal side effects, and the gastrointestinal mucosa can be injured so that bleeding occurs without warning. However, NSAIDs may be the most common drug therapy in the treatment of OA. The so-called Disease Modifying Anti-Rheumatic Drugs (DMARDs) are usually not the first line of treatment in RA because of associated toxicity with long-term use. However, x-rays and clinical evidence of aggressive joint damage with progression in patients treated only with steroids or NSAIDs usually requires DMARDs to be employed in RA therapy. DMARDs are less commonly used in OA treatment. The DMARDs commonly employed in RA include, sulfasalazine (Azulfidine), hydroxychloroquine (Plaquenil) and methotrexate (Rheumatrex). These DMARDs appear to be less toxic than previously commonly employed DMARDs such as gold, penicillamine and azathioprine (Imuran). Methotrexate appears to be particularly effective in RA and combination therapy where multiple DMARDs may be required to fully regulate clinical symptoms of RA at different disease stages. Thus, DMARDs appear to alter the activity of inflammatory and immune cells active in the progression of RA.

Status of Novel Therapies:

Cox-2 inhibitors. NSAIDs inhibit the activity of enzymes, termed cyclooxygenase, required for the synthesis of prostaglandins and other eicosanoids. Prostaglandins synthesized by macrophages and other inflammatory cells are, in part, responsible for significant inflammation in arthritis. The finding in 1991 that a least two forms of cyclooxygenases exist, called Cox-1 and Cox-2, resulted in numerous experimental and clinical studies that showed that Cox-1 was a normal enzyme involved in tissue homeostasis, whereas Cox-2 was induced in that it was synthesized only at sites of inflammation. Thus, according to Dr. David Gotlieb, a South African rheumatologist, “Inhibition of Cox-1 is therefore undesirable… while the inhibition of Cox-2 is desirable.” Cox-2 inhibitors, such as celecoxib (Celebrex) are about 375-fold more selective for Cox-2 than Cox-1. Celebrex is effective in controlling the inflammation of arthritis with no significant complications when compared to placebo.

Inhibitors of tumor necrosis factor-alpha. Inflammatory arthritis is characterized, in part, by an increase in the amount of soluble mediators of inflammation called cytokines. One of these cytokines is tumor necrosis factor-alpha (TNF-alpha). Some RA patients resistant to conventional therapies with steroids, NSAIDs and even DMARDs have been treated with an anti-TNF-alpha antibody called infliximab (Remicade), which is a genetically engineered hybrid molecule made by combining human and mouse cell proteins or with another genetically engineered, human-derived molecule, etanercept (Enbrel). According to Drs. Maini and Taylor (Kennedy Institute of Rheumatology, London, UK) randomized phase II and III clinical trials of anti-TNF reagents have shown an acceptable safety profile and significant clinical efficacy in cases of RA that have not responded to conventional therapy. Anti-TNF combined with methotrexate appears to be particularly effective in RA patients whose disease persists even after therapy with DMARDs. However, RA patients with co-morbid conditions, including serious infection or cancer, are not advised to use anti-TNF therapies.

Oral Collagen. “Ingesting low doses of Type II collagen (the collagen type found in articular cartilage of synovial joints) may help relieve the severe joint pain, swelling and stiffness of the disease. In a clinical trial to determine the efficacy of oral collagen, RA patients continued on NSAIDs or oral steroids, but prednisone use did not exceed 10 mg. daily. The mechanism of the action of oral collagen presumably involves a reduction in the severity of the immune response associated with RA. According to Dr. John Stuart, a rheumatologist at the University of Tennessee in Memphis, oral collagen, “has the tremendous advantage in that it has no side effects.” The use of oral collagen therapy as an adjunctive treatment in RA continues to be studied.

Prosorba column. At 1999, the first non-drug therapy to treat RA was approved by the FDA. While the mechanism of action is incompletely understood, the Prosorba column improves RA symptoms with moderate to severe disease. The column is manufactured of purified bacterial protein A covalently bonded to silica. In a trial to study the effectiveness of this treatment, RA patients for two hours weekly for 12 weeks had their blood passed through the Prosorba column. The protein A is thought to collect the circulating immune complexes and antibodies, which significantly contribute to RA pathology.

According to an article published on The Lancet Interactive, the device worked so well that a phase III trial was halted early. Almost 50 percent of the 109 RA patients on the study, who had RA for a mean of 15.5 years, have significant improvement in symptoms. Additional studies are needed to further ascertain the mechanism of action of the Prosorba column and whether or not it will be useful in treating other autoimmune disorders in addition to RA.

B Cell Depletion. RA is perpetuated by a chronic cycle in which “autoreactive B lymphocytes generate their own antigen, called IgG rheumatoid factor,” according to Dr. Jonathan C. Edwards (University College, London, UK). Studies were designed by his group to determine whether or not B lymphocyte depletion would lead to clinical remission in RA patients. A monoclonal antibody, called anti-CD20 was employed in combination with prednisolone and cyclophosphamide (Cytoxan) to treat 20 patients who had RA refractory to other therapies for about 20 years. The results of these studies were reported this month at the American College of Rheumatology annual meeting in Philadelphia. The majority of RA patients responded to B-lymphocyte depletion brought about by anti-CD20 and were able to discontinue DMARDs. Reappearance of RA symptoms in some patients correlated with increased levels of B lymphocytes. Side effects of this novel therapy were reported to be minimal. A formal controlled clinical trial is planned.

Both conventional and novel therapies for the medical treatment of OA and RA provide an increased armamentarium for use by physicians in the care of patients with these diseases. More recently, novel therapies are directed at altering specific pathways implicated in both the pathogenesis and progression of OA and RA. The discovery of new pathways in these diseases will offer additional targets for drug intervention and perhaps even gene therapy. A better understanding of the relevance of these pathways integral to the inhibition of immune system dysfunction and inflammation should provide us with important new treatments for OA and RA in the next few years.

It is especially important to pay attention to this disease, not only because it can be disabling, but also because probably the most important single lifestyle factor that prevents major fatal diseases is exercise. It is crucial that we keep our joints in as good condition as possible, so that we can be as active as we choose in order to maintain healthy cardiovascular systems and many other vital systems in our bodies.

Injuries, overuse, excessive weight or pressure on the joints, or biochemical changes in the joint cartilage can trigger the process that causes deterioration of the cartilage, the lubricated cushion that keeps the joints working smoothly and freely. If old cartilage is degraded faster than new cartilage is formed, the result is deterioration. In early stages, not enough proteoglycans, glucosaminoglycans and collagen are produced to rebuild cartilage. As the cartilage thins and loses its elasticity, it becomes more prone to damage due to excessive use and injury. Then inflammation can occur. Bone exposure from loss of cartilage causes minute fractures and over-growth of bone with sharp edges within the joint. This then leads to pain, stiffness, swelling and deformity.

Conventional medical therapy such as non-steroidal anti-inflammatory drugs (NSAIDS) can reduce pain and inflammation, but they do not slow the deterioration of the joints, and in fact they cause more degradation of the cartilage if they are used regularly for a long time.

As with other chronic disease, it would make the most sense to prevent these changes from happening, and after they begin to occur, to provide the best support for the cartilage to repair itself.

One important support is proper exercise. Since there is no blood circulation in the cartilage, the cells can only get nourishment by a sponge-like action that comes from squeezing and releasing the cartilage through weight-bearing or other force-producing exercise. The pressure on the joint also has to be not excessive or too repetitive; therefore, obesity and activities that are too repetitive can cause harm. For example, running on hard pavement without properly cushioned shoe soles more than 10 miles per week could cause repetitive injury. Other similar excessive wear on joints could do the same.

What are some of the biochemical factors that promote cartilage deterioration? Dr. Sutter points out that free radical damage is being implicated increasingly in this disease, and research has shown that antioxidant nutrients do protect against degradation of cartilage.

If this is so, then all the other preventive measures that prevent free radical generation, applicable in most other degenerative diseases, could be applied here. Avoiding excess chemical and radiation exposure, avoiding high-fat foods and fried foods, managing and decreasing stress, improving detoxification ability, reducing allergic reactions, preventing diabetes and insulin resistance, and minimizing the use of prescription and non-prescription drugs, all are things that can reduce free radical damage. Eating foods high in antioxidants, such as colored fruits and vegetables, and taking antioxidant supplements also helps quench free radicals.

Also, any nutrient that prevents inflammation could slow or reverse the inflammatory stage of this cartilage deterioration. Foods high in ogega-3 fatty acids such as fish and vegetables, certain nuts and flax oil, and foods low in saturated fat could reduce tendencies for inflammation.

Drs. Alan Gaby, M.D., and Jonathan V. Wright, M.D., have found in their experience that some people are sensitive to foods in the nightshade family such as potatoes, peppers, tomatoes, eggplant, etc., and that they improve in arthritis symptoms when avoiding them.

I have found in my practice that several people were sensitive to other foods that, when eliminated, made the arthritis symptoms disappeared, in this case often the food was orange juice. It can be useful to do an elimination diet to try to detect which specific foods may be causing flare-ups of pain and inflammation for that particular person.

Dr. Sutter lists many nutrient supplements that can decrease free radicals, reduce inflammation, and supply building blocks for the cartilage cells to use to make new cartilage.

Glucosamine sulfate and chondroitin sulfate supply material for making more glucosaminoglycans, proteogllycans and synovial fluid, for building new cartilage. Vitamins E and C are important antioxidants that prevent free radical damage. Niacinamide helps to reduce inflammation by slowing the synthesis of nitric oxide (NO), which is a potent trigger for the degradation of cartilage. N-acetylcysteine, a nutrient also produced by the body, helps to reduce inflammation and increase production of the body’s own antioxidant, glutathione. Selenium assists vitamin E in antioxidant activity. Zinc, copper and manganese are needed for production of the body’s own antioxidant, superoxide dismutase (SOD).

Human studies have shown effectiveness in reducing symptoms of osteoarthritis with these aforementioned supplements. Several herbs have also been found in human studies to reduce symptoms, probably by reducing inflammation. These are ginger and turmeric (common kitchen spices), and boswellia serrata, a traditional Ayurvedic anti-inflammatory herb related to frankincense.

The amounts of the supplements our recommends are as follows: (Note: Caution should be exercised if turmeric or ginger is used in combination with drugs that prevent blood clotting, and niacinamide in these doses recommended should be done under a physician’s supervision, possibly with blood tests for liver function.)

Glucosamine sulfate — 500 milligrams three times daily.
Chondroitin sulfate — 400 milligrams two to three times daily.
Vitamin E — 400 to 800 IU per day.
Vitamin E — 500 milligrams three times daily.
Niacinamide — 500 milligrams two to three times daily.
N-acetylcysteine — 200 milligrams two to three times daily.
Selenium — 200 to 400 micrograms per day.
Zinc — 5 milligrams three times daily.
Copper — 2 milligrams per day.
Manganese — 20 milligrams per day.
Boswellia standardized extract — equivalent to 150 milligrams boswellic acids three times daily
Turmeric standardized extract — equivalent to 150 milligrams curcuminoids three times daily
Ginger standardized extract — equivalent to 10 milligrams gingerols three times daily

There are several homeopathic remedies that also have been useful in osteoarthritis.

Physical therapy can be useful in designing the proper exercise and activities to do for a person suffering from arthritis.

There is much we can do by way of natural therapies that can prevent or reduce osteoarthritis and its pain and inflammation, a disease for which it was once thought there was nothing that could be done for it.