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Study suggests osteoarthritis results from inflammatory processes, not just wear and tear

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Investigators from the Stanford University School of Medicine have shown the development of osteoarthritis is driven by low-grade inflammatory processes.

“It’s a paradigm change,” study author William Robinson, MD, PhD, stated in a news release. “Recent findings suggest that low-grade complement activation contributes to the development of degenerative diseases … our results suggest that osteoarthritis (OA) can be added to this list of diseases.”

The findings, published in Nature Medicine, noted increased numbers of certain specialized inflammatory proteins early in the progress of OA — before it becomes symptomatic. This suggests, according to the release, inflammation may be a driver, rather than a secondary consequence, of the disease.

The researchers reported that initial damage to the joint can set in motion a chain of molecular events that escalate into an attack upon the damaged joints by the body’s complement system. This process begins early in the development of OA, according to the release.

The initial hint that the complement system may play a role in OA came when Robinson and his colleagues compared the levels of large numbers of proteins present in the joint fluid of patients with OA with the levels present in fluid from healthy individuals. They noted more expression of genes encoding complement-activating and related inflammatory proteins in the fluid of patients with OA when compared to the fluid of those without.

To investigate further, researchers induced meniscal tears or removal in four groups of mice: one that contained normal mice and three separate groups that each missed a different protein component of the complement system. The normal mice developed OA as expected, but the two strains of mice lacking a complement-accelerating protein developed less severe arthritis while the mice that lacked complement-inhibiting proteins got worse at a faster rate. Thus, mice with impaired complement activation were protected against the development of OA.

Reference:

• Wang O, Rozelle AL, Lepus CM, et al. Identification of a central role for complement in osteoarthritis. Nat Med. 2011. doi: 10.1038/nm.2543

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