A new European study concludes that the popular food supplement chondroitin is no better than a placebo at preventing or reducing joint pain in people with osteoarthritis.

The findings are published in the journal Annals of Internal Medicine.

Scientists from universities in Bern in Switzerland, Bristol in the United Kingdom, and Göttingen in Germany, summarized data from 20 trials that compared the effect of chondroitin to either placebo or no treatment in patients with hip or knee osteoarthritis.

Many people with knee and hip pain use chondroitin as a dietary supplement, usually in combination with glucosamine. In the US the market is estimated to be worth 1 billion dollars a year. About 25 per cent of adults suffer from knee pain, and at least half of them have osteoarthritis.

In the body, chondroitin is a compound found in cartilage that helps to cushion joints from compression – it provides a stiffness that allows the cartilage to resume its shape after compression.

It is made of long chains of sugars and attaches itself to proteins to form matrices of filler tissue that provides structural support for cells, for example as in collagen.

The food supplement is extracted from animal cartilage, usually from cows and pigs (trachea, ear, nose) but also from shark, fish and birds.

The researchers, led by Dr Peter Jüni of the Department of Social and Preventive Medicine, University of Bern, conducted a meta-analysis of previous research.

This method uses statistical techniques to pool the results of a number of trials that test broadly the same hypotheses to see if there is a shared conclusion that is statistically robust.

For instance, to test for effect sizes, they calculated the differences in the means of the pain-related outcomes between treatment and control groups at the end of the trial and divided them by the pooled standard deviation of the samples.

The researchers found:

— 20 trials covering 3,846 patients met the first level of inclusion criteria for a meta-analysis: they were designed as randomized or quasi-randomized and compared chondroitin with placebo or with no treatment.
— There was a high degree of difference among the 20 trials (heterogeneity, I-squared was 92 per cent).
— Small trials and trials with “unclear concealment of allocation” and trials that did not follow the “intention to treat” principle were more likely to find in favour of chondroitin.
— Only 3 trials met the second level of inclusion criteria for a meta-analysis: they had a large sample size and followed an intention to treat principle. These covered 40 per cent of the patients in the meta-analysis.
— Based on the 3 larger trials that passed the second level of inclusion criteria, they found no significant effect of chondroitin on arthritis symptoms.
— The effect size was equivalent to a difference of 0.6 mm on a 10 cm visual analogue scale (effect size -0.03).
— They found no evidence that chondroitin does harm (12 trials showing a pooled relative risk of 0.99).

Dr Jüni and his team concluded that analysis of large-scale, methodologically sound trials shows the symptomatic benefit of chondroitin to be minimal or nonexistent, and its use in clinical practice should be discouraged.

Writing in an accompanying editorial, Dr David T. Felson, professor of medicine and epidemiology at Boston University, said that while chondroitin may not be doing anything, it is not dangerous either. He also said that he would not recommend that patients start taking glucosamine and chondroitin.

He reviews the methods that the researchers used, asking the question whether they were justified in isolating 3 trials to show that chondroitin had no effect, while leaving the other, mostly smaller trials to one side. He concludes that they did the right thing:

“I believe that, by identifying a subgroup of trials with high-quality, consistent evidence, they have provided a compelling estimate of the likely efficacy of chondroitin”, he writes.

In conclusion, Dr Felson said that what clinicians should take away from this study is that the “best current evidence is that chondroitin sulfate does not reduce joint pain in osteoarthritis.”

However, he says many patients are convinced that it helps, “If patients say that they benefit from chondroitin, I see no harm in encouraging them to continue taking it as long as they perceive a benefit”, he says.

Dr Felson also explains that while the notion that ingesting chondroitin as a supplement is appealing, given its function in the body, the logic of doing so is misleading, since it is unlikely that ingested chondroitin would be incorporated intact into cartilage. The body synthesizes it from other compounds.

“Meta-analysis: Chondroitin for Osteoarthritis of the Knee or Hip.”
Stephan Reichenbach, Rebekka Sterchi, Martin Scherer, Sven Trelle, Elizabeth Bürgi, Ulrich Bürgi, Paul A. Dieppe, and Peter Jüni.
Annals of Internal Medicine 17 April 2007, Volume 146 Issue 8, Pages 580-590.

Click here for Abstract.

Click here for Arthritis Foundation (US).

Written by: Catharine Paddock
Writer: Medical News Today