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Dietary Omega-3 Fatty Acids Moderate Severity of Osteoarthritis in a Mouse Model

By LabMedica International staff writers
Posted on 22 Jul 2014
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Image: Microcomputed tomography images (top) and histology images (bottom) of the knees of mice fed a very high fat diet containing omega-3 fatty acid supplement (left) or only omega-6 fatty acids (right) after a knee injury. The omega-6 diet showed abnormal bone remodeling and calcified tissue formation in the joint (white arrow). The omega-6 diet also showed significant loss of cartilage (red staining, yellow arrowhead) and increased joint inflammation (Photo courtesy of Duke University).
Image: Microcomputed tomography images (top) and histology images (bottom) of the knees of mice fed a very high fat diet containing omega-3 fatty acid supplement (left) or only omega-6 fatty acids (right) after a knee injury. The omega-6 diet showed abnormal bone remodeling and calcified tissue formation in the joint (white arrow). The omega-6 diet also showed significant loss of cartilage (red staining, yellow arrowhead) and increased joint inflammation (Photo courtesy of Duke University).
Researchers working with an osteoarthritis (OA) obese mouse model found that the fat content of the animals' diet contributed more to the development or arrest of OA than did body weight.

Investigators at Duke University (Durham, NC, USA) fed different groups of mice either a diet rich in saturated fatty acids (SFAs), omega-6 polyunsaturated FAs (PUFAs), or omega-6 PUFAs supplemented with omega-3 PUFAs. OA was induced by destabilizing the medial meniscus. Wound healing was evaluated using an ear punch. OA, synovitis, and wound healing were determined histologically, while bone changes were measured using microCT (computerized tomography).

Results published in the July 10, 2014, online edition of the journal Annals of the Rheumatic Diseases revealed that OA was significantly associated with dietary fatty acid content and serum adipokine levels, but not with body weight. Furthermore, spontaneous activity of the mice was independent of OA development. Small amounts of omega-3 PUFAs (8% by kilocalorie) in a high-fat diet were sufficient to mitigate injury-induced OA. Omega-3 PUFAs significantly enhanced wound repair, while SFAs or omega-6 PUFAs independently increased OA severity, ossification, and scar tissue formation.

“Our results suggest that dietary factors play a more significant role than mechanical factors in the link between obesity and osteoarthritis,” said senior author Dr. Farshid Guilak, professor of orthopedic surgery at Duke University. “While omega-3 fatty acids are not reversing the injury, they appear to slow the progression of arthritis in this group of mice. In fact, omega-3 fatty acids eliminated the detrimental effects of obesity in obese mice. A great next step would be to do a clinical study to look at effect of omega-3 fatty acids post-injury.”


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