Does lipopolysaccharide-mediated inflammation have a role in OA?

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Abstract
Lipopolysaccharide derived from gastrointestinal microbiota contributes to systemic inflammation and obesity. Huang and Kraus propose that lipopolysaccharide is a major risk factor for osteoarthritis (OA), and suggest that therapeutic strategies for the reduction of systemic levels of lipopolysaccharide should be considered for prevention and treatment of OA. The nature of the gastrointestinal microbiome determines the reservoir of lipopolysaccharide, which can migrate from the gut into the circulation, where it contributes to low-grade inflammation. Osteoarthritis (OA) is a low-grade inflammatory condition, and the elevation of levels of lipopolysaccharide in association with obesity and metabolic syndrome could contribute to OA. A 'two- hit' model of OA susceptibility and potentiation suggests that lipopolysaccharide primes the proinflammatory innate immune response via Toll-like receptor 4 and that progression to a full-blown inflammatory response and structural damage of the joint results from coexisting complementary mechanisms, such as inflammasome activation or assembly by damage-associated molecular patterns in the form of fragmented cartilage-matrix molecules. Lipopolysaccharide could be considered a major hidden risk factor that provides a unifying mechanism to explain the association between obesity, metabolic syndrome and OA.

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