RESUMO
The relation between obesity and osteoarthritis (OA) development has been traditionally explained as consequence of the excessive joint effort derived of overweight. However, in the last two decades a metabolic OA has been suggested through diverse molecular mechanism implying metabolic syndrome, although more investigation must be conducted to elucidate it. Metabolic syndrome is responsible of the release of diverse inflammatory cytokines, specially the increased adipokine in obesity, causing a chronic low-grade inflammatory status that alters the joint homeostasis. In this scenario, the microbiota dysbiosis contribute by worsening the low-grade chronic inflammation or causing metabolic disorders mediated by endotoxemia generated by an increased lipopolysaccharides intake. This results in joint inflammation and cartilage degradation, which contributes to the development of OA. Also, the insulin resistance provoked by type 2 Diabetes contributes to the OA development. When intake patterns are considered, some coincidences can be pointed between the food patterns associated to the metabolic syndrome and the food patterns associated to OA development. Therefore, these coincidences support the idea of a molecular mechanism of the OA development caused by the molecular mechanism generated under the metabolic syndrome status. This review points the relation between metabolic syndrome and OA, showing the connected molecular mechanisms between both pathologies as well as the shared dietary patterns that promote or prevent both pathologies.
