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MILLIONS WITH ARTHRITIS MAY BENEFIT FROM BONE LOSS DRUG

Johns Hopkins Medicine
Media Relations and Public Affairs
Media contact: Jeff Ventura
410 955 7832; jventur4@jhmi.edu
November 21, 2006

MILLIONS WITH ARTHRITIS MAY BENEFIT FROM BONE LOSS DRUG
Popular osteoporosis pills may also slow joint deterioration

People taking a widely used medication to strengthen fragile, aging bones may also be protecting their joints, according to a recent study led by Johns Hopkins rheumatologist Clifton Bingham, M.D.

Researchers began to wonder if risedronate might be used to treat osteoarthritis after noticing that the drug, and other compounds in the same class of drugs, not only slowed joint damage in animals, but also reduced cartilage-irritating bone lesions in humans.

For two years, an international team of investigators studied 2,483 arthritic men and women, from both the United States and Europe. All of those enrolled in the study had a loss in the cartilage that cushions the knee joint, a hallmark symptom of osteoarthritis.

Reporting in the most recent issue of the medical journal Arthritis & Rheumatism, Bingham and his team said study participants were given either a placebo or risedronate at a range of doses, including the standard doses normally prescribed to treat bone loss. The amount of cartilage detected in their knees was measured by X-ray analysis at the one- and two-year marks. Blood tests were also used to check for a marker of cartilage breakdown known as CTX-II.

CTX-II is released in the bloodstreams of people with osteoarthritis when cartilage begins to fray.  How fast and to what degree cartilage breaks down can be approximated by levels of CTX-II.

“The blood tests revealed not only that risedronate stabilized bone loss, but also that it was most likely slowing the breakdown of cartilage, too” says Bingham.

Bingham emphasizes that X-rays failed to show any dramatic visible changes in the structure of the joints with risedronate compared to a placeb however, the numbers of patients exhibiting significant progression of the disease were few in all treatment groups. A great challenge now is identifying the risk factors for joint deterioration in osteoarthritis, adds Bingham.

The investigators also did not see a significant reduction in joint pain with risedronate compared with the placebo.

In the United States, where an estimated 25 million people have osteoarthritis and 44 million have osteoporosis, participants in the study group taking risedronate experienced a noticeable drop in their CTX-II levels: 17.9 percent. The Europeans fared even better, with a 19.6 percent decrease. Patients taking the drug at normal levels and at higher than usual doses given for comparison experienced similar slowdowns in cartilage decline, without significant adverse side effects.

Those in the placebo group, however, experienced increases in CTX-II levels (26.3 percent for the Americans and 10.1 percent for the Europeans), suggesting that their cartilage was deteriorating faster than that in those taking the drug.

“We are not recommending that everyone with arthritis run out and get a prescription for these kinds of drugs, nor are we suggesting at this time that doctors use risedronate as an  arthritis treatment,” cautions Bingham. “But what we can say now is that drugs affecting bone turnover need to be further evaluated for their potential effects as arthritis therapies.”

The blood test changes seen in the study would suggest that people already taking bone strengthening drugs may be simultaneously helping their joints, concludes Bingham.


NOTE: Dr. Bingham has received consulting fees from Proctor & Gamble Pharmaceuticals, the makers of Actonel, the brand name for risedronate. Additionally, several other members of his research team have received consulting fees from other pharmaceutical companies.

 

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