Inflammatory, genetic and endothelial axis between periodontitis and cardiovascular disease: shared mechanisms and clinical perspectives
DOI:
https://doi.org/10.16921/pfr.v10i3.393Keywords:
periodontitis; cardiovascular diseases; systemic inflammation; endothelial dysfunction; biomarkers; microRNA; atherosclerosis; oral-systemic healthAbstract
Cardiovascular diseases are the leading cause of death worldwide, and their development is closely linked to chronic inflammatory processes. Periodontitis, a multifactorial inflammatory disease affecting the supporting dental tissues, has been recognized as a potential contributor to cardiovascular risk. This article reviews recent evidence on the inflammatory, molecular, and genetic mechanisms connecting both pathologies, as well as the effects of periodontal therapy on systemic biomarkers.
Evidence suggests that periodontal bacteria and their endotoxins can enter the bloodstream, activate Toll-like receptors 2 and 4, and trigger the nuclear factor kappa B pathway, leading to the release of pro-inflammatory cytokines. This cascade promotes endothelial dysfunction and the formation of atherosclerotic plaque. Shared biomarkers include C-reactive protein, matrix metalloproteinase-9, and asymmetric dimethylarginine; small non-coding regulatory RNA molecules and genetic variants in innate immune response genes are also implicated. Clinical trials indicate that periodontal treatment reduces systemic inflammation and improves vascular parameters, although direct causality has not yet been fully demonstrated.
Overall, periodontitis should be considered a modifiable cardiovascular risk cofactor, and its integrated management may strengthen strategies to prevent chronic non-communicable diseases.
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