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Decades of dancing // multiple marathons // instead, a 
complex collection of factors // from lesions to leptin.

Osteoarthritis: Why Joints Fail

By Tim Gower // Photographs by Peter Hapak // Spring 2010
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Peter Hapak for Proto

Most dogs love to run, and many develop joint problems late in life. The same thing often happens to their human companions, with or without pavement pounding. But arthritis researchers in Finland decided to speed up the process. In a yearlong study, they placed 10 female beagles on treadmills and made them run. By the time the study was coming to an end, the dogs were trotting at a brisk pace for 25 miles a day.

Tissue samples from the dogs’ knees indicated that some regions of their joints had lost as much as 35% of their glycosaminoglycan, or GAG, an essential carbohydrate that strengthens and stiffens cartilage. This led the investigators to conclude that long-distance running had the potential to damage cartilage and eventually cause osteoarthritis, the most common form of joint disease. When their paper appeared in Arthritis & Rheumatism, in 1993, it cast a shadow over the presumably healthy habit of jogging. But the beagle trials also reinforced conventional medical wisdom, which at the time held that osteoarthritis, or OA, was a disease of failing cartilage brought on by wear and tear.

Since then, though, research has shown OA to be much more complicated. Not only has running been largely exonerated as a cause but studies also show that exercise normally strengthens cartilage. And while cartilage loss may indeed lead to OA, new evidence suggests that metabolic imbalances also play a vital role. Moreover, it has become clear that other parts of the joint, including bone and synovial tissue, also are crucial in the genesis of OA, says Steven B. Abramson, director of rheumatology at New York University’s Langone Medical Center.

But while OA affects some 27 million Americans (who receive 1 million artificial knees and hips each year), it’s often not considered a research priority. So earlier this year, the Arthritis Foundation began a campaign to raise awareness about the disease. Could a renewed focus and fresh ideas about OA lead to better treatments and preventive therapies? If so, the timing couldn’t be better. With an aging population and rising rates of obesity—a chief risk factor for OA—the number of Americans with this disease is projected to nearly double by 2020.

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1. “Developments in the Scientific Understanding of Osteoarthritis,” by Steven B. Abramson and Mukundan Attur, Arthritis Research & Therapy, May 2009. An excellent review of current osteoarthritis research, covering genetics, epidemiology, biomechanics and molecular biology.

2. “The Futility of Current Approaches to Chondroprotection,” by David T. Felson and Young-jo Kim, Arthritis & Rheumatism, May 2007. Most drugs in development to treat osteoarthritis are designed to protect cartilage—an approach, the authors argue, that is likely to fail because it doesn’t address other major causes of pathology.

3. “Extreme Obesity Due to Impaired Leptin Signaling in Mice Does Not Cause Knee Osteoarthritis,” by Timothy M. Griffin, Janet L. Huebner, Virginia B. Kraus and Farshid Guilak, Arthritis & Rheumatism, October 2009. The authors offer powerful evidence that body fat raises the risk for osteoarthritis not only by crushing cartilage but also by producing systemic inflammation that destroys joint tissue.

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