The microbiota-metabolic syndrome axis as a promoter of metabolic osteoarthritis

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.

Automated summary

The relationship between obesity and osteoarthritis (OA) development has traditionally been explained as a result of excessive joint effort due to overweight. However, in the past two decades, a metabolic OA has been suggested, which involves metabolic syndrome and various molecular mechanisms. Metabolic syndrome leads to the release of inflammatory cytokines, particularly increased adipokines in obesity, causing chronic low-grade inflammation that disrupts joint homeostasis. Microbiota dysbiosis exacerbates chronic inflammation or mediates metabolic disorders through endotoxemia, leading to joint inflammation and cartilage degradation, ultimately contributing to the development of OA. Insulin resistance associated with type 2 diabetes also contributes to OA development. Notably, there are similarities between the food patterns associated with metabolic syndrome and those associated with OA development, further supporting the idea of a molecular mechanism linking metabolic syndrome and OA. This review highlights the relationship between metabolic syndrome and OA, exploring the shared molecular mechanisms and dietary patterns that promote or prevent both pathologies.