Inflammation May Affect Osteoarthritis

Findings Could Lead to New Drugs, Research Strategies

From the WebMD Archives

Aug. 1, 2003 -- New research is challenging the long-held notion that inflammation is not a cause of osteoarthritis, the most common type of arthritis.

If confirmed, the early findings could have implications for the development of drugs that slow the progression of a joint disease that affects roughly half of Americans over the age of 50.

Genetics and joint wear-and-tear are known to be factors in the development of osteoarthritis, but other causes remain unidentified. Unlike rheumatoid arthritis, a joint disease that is more common in young adults, inflammation has not been thought to drive osteoarthritis. Instead, it is characterized by degeneration of joint cartilage and is considered a degenerative rather than an inflammatory joint disease.

Which Came First? Inflammation or Osteoarthritis

"There has been increasing evidence in recent years of an inflammatory component to osteoarthritis, but inflammation is widely believed to be a consequence of joint damage and not the other way around," researcher David A. Walsh, PhD, of the U.K.'s University of Nottingham tells WebMD.

Walsh and colleagues looked for evidence of joint inflammation among patients with osteoarthritis of the knee and hip. Specifically, the researchers examined the tissue lining the joints, known as synovial tissue. Synovial inflammation plays a major role in rheumatoid arthritis.

Tissue samples from roughly one in three patients showed evidence of severe inflammation. These samples also showed new blood vessel formation, which has been linked to inflammatory joint disease. The findings are published in the August issue of the journal Arthritis and Rheumatism.

Walsh says a much larger percentage of tissue samples showed evidence of less severe inflammation, and he adds that the synovial inflammation was not confined to patients with extensive joint damage or even the most advanced cases of osteoarthritis.

Reduce Inflammation, Slow the Disease?

He calls for further studies to examine the role of inflammation and blood vessel formation in the progression of osteoarthritis, with one aim being the development of drugs to slow disease progression.

Medications known as disease-modifying antirheumatic drugs (DMARDS) are already being used to prevent joint damage from rheumatoid arthritis, in which inflammation plays a major role, but no such preventive treatments exist for osteoarthritis.


"Inflammation is very complex, and the type of inflammation we saw in these patients with osteoarthritis is probably different from the inflammation seen in patients with rheumatoid arthritis," Walsh says.

"The hope is that when we know more about the mechanisms that drive this disease we may be able to develop treatments to slow its progression. This is one avenue, but obviously there are others that equally well may lead to new drugs."

Chicago rheumatologist Eric Ruderman, MD, says earlier efforts to develop drugs that stop or slow the progression of osteoarthritis have been disappointing. A recently published review of studies evaluating the nutritional supplements glucosamine and chondroitin found that glucosamine may slow osteoarthritis progression, although the effects appear modest.

Ruderman says the U.K. research, while preliminary, could lead to therapeutic trials exploring osteoarthritis drugs that target inflammation and blood vessel formation.

"Most of the research into the prevention of disease progression has been aimed at preventing cartilage degradation," Ruderman tells WebMD. "But this would suggest that other routes which tackle tissue inflammation might be worth pursuing, along the lines of the therapies that already exist for rheumatoid arthritis."

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SOURCES: Arthritis and Rheumatism, August 2003. David A. Walsh, PhD, University of Nottingham, Nottingham, Nottingham, U.K. Eric Ruderman, MD, clinical rheumatologist, Northwestern Medical Faculty Foundation; assistant professor of medicine, Northwestern University Medical School, Chicago, Ill.
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