Physicians have long held that being overweight significantly increases the risk of developing osteoarthritis (OA). A recent study, however, suggests that obesity by itself does not predictably lead to OA.
Some researchers believe that extra weight exerts mechanical force on joints that they weren’t designed to handle, eventually destroying cartilage, while others blame the breakdown on inflammatory chemicals, including the appetite controlling hormone leptin.
A research team from the Duke University Medical Center, in Durham, N.C., studied mice that did not produce leptin. The mice were given unlimited food and water, and without the leptin they quickly gained weight, eventually becoming three times the weight of normal mice and with 10 times as much body fat.
The knee bones of the leptin-free, obese mice did change, but without forming osteoarthritis. The inflammation levels which are used to measure arthritis were essentially unchanged in these mice. The results suggested that leptin may have a dual role in the development of osteoarthritis by regulating both the skeletal and immune systems.
“To our surprise, they didn’t get arthritis. That tells us that obesity in and of itself may not be the cause of osteoarthritis.” – Farshid Guilak, PhD, director of Duke’s Orthopaedic Bioengineering Laboratory.
Researchers also note that the joints from the obese mice looked better than those of the normal control mice.
On the other hand, another study found that mice that processed leptin normally gained only half as much weight when put on a high-fat diet but showed significant knee osteoarthritis.
The researchers state that the study has several limitations. The obese, leptin-deficient mice didn’t develop osteoarthritis but they didn’t move around as much as the normal mice. This may have prevented their joints from being excessively stressed by their body weight, as human bodies are.
The results of the study are published in the October 2009 issue of the journal Arthritis & Rheumatism
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