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.
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 in 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," said Bingham, an
assistant professor in the School of Medicine.
Bingham emphasizes that X-rays failed to show any
dramatic visible changes in the structure of the joints
with risedronate compared to a placebo; however, the number
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, Bingham said.
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 of 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," Bingham cautioned.
"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, Bingham concluded.
Before joining the Johns Hopkins faculty in January
2005, Bingham 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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