Glucosamine And Chondroitin - Do They Work For Joint Pain?

Glucosamine is derived from the shells of crabs and oysters, and is widely promoted as a natural substance for the treatment of arthritis and joint pain. Glucosamine is felt to be a precursor of proteoglycans. Proteoglycans are thought to be instrumental in helping cartilage retain water and in promoting formation of an elastic layer, which may improve the functional characteristics of cartilage.

Chondroitin is a product derived from the cartilage of sharks and cows that is promoted for the prevention of arthritis and the treatment of joint pain. Chondroitin is often combined with glucosamine where it is sold in health food stores. Chondroitin stimulates the production of proteoglycans and hyaluronic acid and inhibits proteolytic enzymes, which destroy cartilage. Chondroitin and glucosamine are often given in combination for osteoarthritis.

Most of the earlier studies of glucosamine and chondroitin were performed by manufacturers and were not well controlled (1). A meta-analysis performed in 2000 of studies of glucosamine and chondroitin found that studies funded by supplement manufacturers resulted in more favorable results for the supplement combo than independent studies; few of the manufacturers' studies were properly controlled. Overall there was a moderate effect for both, and the authors concluded that some degree of efficacy was probable (1).

Only one of the studies reviewed in 2000 reported that patients definitely did not know whether they were being given a supplement or a placebo. In that study, 252 patients with osteoarthritis of the knee were randomly assigned to receive four weeks of glucosamine or placebo. Glucosamine was associated with a drop in pain ratings from 10.6 to 7.5 versus 10.6 to 8.4 in placebo; fifty two percent of glucosamine patients had a clinically significant change as measure by a three-point drop on an index of arthritis severity compared to 37% on placebo. These differences were statistically significant.

More recently several randomized placebo controlled trials have been performed.

In one study 212 patients with osteoarthritis of the knee were assigned to placebo or glucosamine for three years of treatment. Patients on placebo had a greater narrowing of the disk space in the knee compared to glucosamine as measured on X-ray (-.31 mm v -.06 mm). Glucosamine patients had a significant improvement in pain ratings compared to placebo. Glucosamine showed no increase in side effects compared to placebo (2).

In another study 98 males with osteoarthritis of the knee were assigned to glucosamine or placebo for two months of treatment. There was no difference in pain ratings between patients treated with glucosamine (3.3) and placebo (3.5) (3). Glucosamine was also associated with more side effects, including loose stools, nausea, heartburn, and headache.

Another study randomized 202 patients with osteoarthritis of the knee to three years of treatment with glucosamine or placebo. Placebo treated patients had a greater degree of joint space narrowing as measured by X-ray than glucosamine (-.19 mm v +.04 mm). There were statistically significantly greater reductions in glucosamine for measures of pain self ratings (-2 v -1.3) as well as measures of stiffness and function. One randomized placebo controlled study showed efficacy with a glucosamine-chondroitin combination compared to placebo (4).

In 2006 a large well-controlled study assigned 1583 patients with osteoarthritis of the knee to glucosamine, chondroitin, a glucosamine/chondroitin combination, Celecoxib, or placebo for six months of treatment. A positive treatment outcome was defined as a 20% change in knee pain severity. Sixty percent of placebo patients responded to treatment compared to 67% of glucosamine/chondroitin patients, a difference that was not statistically significant. Celecoxib had a 70% response that was statistically significantly better than placebo. A subgroup of patients with moderate to severe pain at baseline did significantly better with glucosamine/chondroitin than placebo (79% response v 54%) (5). In summary the glucosamine and chondroitin combination shows some efficacy for treatment of osteoarthritis.

1. McAlindon, T.E., LaValley, M.P., Gulin, J.P., Felson, D.T. Glucosamine and chondroitin for treatment of osteoarthritis: A systematic quality assessment and meta-analysis. Journal of the American Medical Association. 2000;283(11):1469-1475.

2. Reginster, J.-Y., Deroisy, R., Rovati, L.C., Lee, R.L., Lejeune, E., Bruyere, O., Giacovelli, G., Henrotin, Y., Dacre, J.E., Gossett, C. Long-term effects of glucosamine sulphate on osteoarthritis progression: a randomised, placebo-controlled clinical trial. Lancet. 2001;357:251-256.

3. Rindone, J.P., Hiller, D., Collacott, E., Nordhaugen, N. Randomized, controlled trial of glucosamine for treating osteoarthritis of the knee. Western Journal of Medicine. 2000;172(2):91-94.

4. Lefler, C.T., Philippi, A.F., Leffler, S.G. Glucosamine, chondroitin, and manganese ascorbate for degenerative joint disease of the knee or low back: a randomized, double-blind, placebo-controlled pilot study. Military Medicine. 1999;164:85-91.

5. Clegg, D.O., Reda, D.J., Harris, C.L., Klein, M.A., O'Dell, J.R., Hooper, M.M., Bradley, J.D., Bingham, C.O., 3rd, Weisman, M.H., Jackson, C.G., Lane, N.E., Cush, J.J., Moreland, L.W., Schumacher, H.R., Jr., Oddis, C.V., Wolfe, F., Molitor, J.A., Yocum, D.E., Schnitzer, T.J., Furst, D.E., Sawitzke, A.D., Shi, H., Brandt, K.D., Moskowitz, R.W., Williams, H.J. Glucosamine, chondroitin sulfate, and the two in combination for painful knee osteoarthritis. New England Journal of Medicine. Feb 23 2006;354(8):795-808.

Learn more about vitamins and supplements as well as the hidden risks of prescription medications in 'Before You Take That Pill: Why the Drug Industry May be Bad for Your Health: Risks and Side Effects You Won't Find on the Label of Commonly Prescribed Drugs, Vitamins and Supplements', by researcher and physician J. Douglas Bremner, MD.

Stevens-Johnson Syndrome

Stevens-Johnson syndrome is a very serious medical condition that causes inflammation of the skin and mucous membranes. Stevens-Johnson syndrome is caused by a reaction to drugs. Some types of drugs that are known to cause Stevens-Johnson syndrome are antibiotics (penicillin and sulfa), anti-convulsants, and pain relievers.

Prescription pain relievers like Bextra (valdecoxib), Celebrex (Celecoxib) and Daypro, as well as over-the-counter pain relievers like ibuprofen (Motrin, Children's Motrin, and Advil), have been reported to have caused Stevens-Johnson syndrome. Cocaine has recently been added to this list of drugs. Stevens-Johnson syndrome can also be caused by illness or infections. Between 25% and 50% of cases are from undetermined causes.

Stevens-Johnson syndrome affects the mucus membranes. Since mucus membranes are present in many parts of the body, such as the eyes, digestive system, lungs, and respiratory system, Stevens-Johnson syndrome can have a profound impact on the human body.

Technically, Stevens-Johnson syndrome is an immune-complex-mediated hypersensitivity (allergic) condition. The first line of defense is the removal of the allergen that has caused Stevens-Johnson syndrome. Identifying the culprit can be difficult, but basically all drugs that could possibly have caused Stevens-Johnson syndrome should be stopped. The patient should then be treated much like a burn victim. Those who suffer with Stevens-Johnson syndrome often have severe loss of fluid so immediate treatment should include fluid replacement and

electrolyte correction.

Unfortunately, at this time there is no known cure or treatment to prevent the progression of Stevens-Johnson syndrome and there are many cases in litigation against drug companies at this time.

Dante Rambaldi is an guru in the field of Skin Care and has helped thousands of acne sufferers cure their condition. He runs a highly popular and comprehensive Skin Care web site. For more articles and resources on Skin Care related topics, Acne Treatments, Natural Skin Care, Oily Skin Care, Skin Beauty Mineral and much more visit his site at: http://skincare.explore-me.com/.

Common Medications for Dental Pain (Part 1)

The pathophysiology of dental pain is a complex central and peripheral nervous system process, and the use of combination analgesics that act at multiple pain sites can improve dental pain relief. In general, for the treatment of mild to moderate dental pain, the most appropriate options are:

- Acetaminophen (Tylenol), 650mg every 4-6 hour as needed for dental pain;

- Non-steroidal anti-inflammatory drugs, or NSAIDs (Advil, Motrin, Aleve), 400mg every 4-6 hours as needed for dental pain; and

- COX-2-selective inhibitors, Celecoxib (Celebrex) and rofecoxib (Vioxx), 25-50mg per day as needed for dental pain.

Acetaminophen: Acetic acid and p-aminophenol, or APAP-commonly known as Acetaminophen-is classified as a nonnarcotic pain reliever. Dentists generally use it for mild to moderate dental pain. It acts as both anti-pain and anti-fever. It has rapid painkiller action. Acetaminophen, unlike nonsteroidal anti-inflammatory drugs, or NSAIDs, has little anti-inflammatory action. It generally is safe for acute dental pain. At very high single doses it causes liver damages.

Acetaminophen's dose of 500-650 milligrams is good dental pain-reliever. However, such relief is brief, peaking one hour after administration. Significantly more dental pain relief can be provided by Acetaminophen's dose of 1,000 mg. At this dosage, the maximal efficacy of Acetaminophen is achieved and last up to four hours after administration. There is no more oral pain relief in dose higher than 1000 mg. Because of this "ceiling-dose" effect, Acetaminophen is good shot-term reliever for mild dental pain.

NSAIDs: NSAIDs have been the traditional treatment for moderate dental pain and inflammation. NSAIDs such as ibuprofen, ketorolac, flurbiprofen, ketoprofen, diclofenac, aspirin and aspirin derivatives diminish local dental pain. Long-term use of NSAIDs, however, can gastrointestinal distress, bleeding, kidney damages, and cardiovascular problems. Also, NSAIDs have been shown to interact with several high blood pressure drugs, which may compromise blood pressure control. The most common short-term side effects of NSAID usage are upset stomach, diarrhea and abdominal pain.

NSAIDs generally require a higher dose to achieve maximum anti-inflammatory and anti-pain effect. Dosage of 800 mg three times per day may be needed for dental pain. The FDA-recommended daily dose is 2,400 mg. Studies has indicated that no more dental pain reliever is achieved with higher-than-the-recommended dosage. Comparing to Acetaminophen, NSAID's are better pain killer, but they act slower and last about the same time (about 4 hours).

COX-2 NSAIDs: COX-2 NSAIDs were developed to limit NSAID's adverse effects. The two COX-2-selective inhibitors, Celecoxib (Celebrex) and rofecoxib (Vioxx) are characterized by the following:

- less risk of GI ulceration than nonselective NSAIDs;

- similar types of other GI side effects, such as abdominal pain, dyspepsia, diarrhea and nausea;

- lack of effect on platelet function, unlike nonselective NSAIDs;

- renal toxicity similar to that of other NSAIDS;

- generally long duration of action, with once-daily administration for rofecoxib and once- or twice-daily administration for Celecoxib.

However, while COX-2 therapy may reduce the risk of GI ulcerations, recent evidence indicates that COX-2 therapy may not reduce the risk of cardiovascular complications (heart attacks). This is the reason why Vioxx is currently taken off the US market.

For information, contact Dr. Nguyen at drnguyen@softdental.com. SoftDental (http://www.softdental.com) is Houston's Premier Laser, Family and Cosmetic Dentistry.