Periodontal Pathogen Impacts on Atherosclerotic Disease

Periodontal pathogens, notably Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans and Fusobacterium nucleatum, contribute to the initiation and progression of atherosclerotic disease through multiple intersecting pathways. These bacteria invade oral tissues, form resilient biofilms and release virulence factors such as lipopolysaccharides and proteolytic enzymes. From the gingival sulcus, they can translocate into the circulation, localise to arterial walls and disrupt endothelial integrity. Systemic dissemination provokes chronic inflammation, characterised by elevated pro-inflammatory cytokines, acute-phase reactants and oxidative stress, which in turn accelerates lipid deposition, foam cell formation and plaque destabilisation. Polymicrobial interactions further amplify pathogenicity, while host factors such as hyperlipidaemia, genetic predisposition and comorbid conditions modulate individual susceptibility. Collectively, these processes establish periodontitis not merely as a comorbidity but as a potential modifiable risk factor for atherosclerotic cardiovascular disease on a global scale, underscoring the importance of integrated oral and vascular health strategies.

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Periodontal Pathogen Impacts on Atherosclerotic Disease publication trend

The graph below shows the total number of articles in periodontal pathogen impacts on atherosclerotic disease across all publications each year (not limited to Nature Index journals).

Technical terms

Biofilm: A structured community of microorganisms adhering to a surface, embedded in a self‐produced extracellular matrix.

Endothelial dysfunction: Impairment of the inner lining of blood vessels, leading to reduced vasodilation, inflammation and increased permeability.

Foam cell: A lipid‐laden macrophage found within atherosclerotic plaques, formed by uptake of modified low-density lipoproteins.

Lipopolysaccharide (LPS): A pro-inflammatory component of the outer membrane of Gram-negative bacteria that triggers host immune responses.

Virulence factor: A molecule produced by a pathogen that enhances its ability to colonise, invade or damage the host.

References

1. Cardiovascular disease therapeutics via engineered oral microbiota: Applications and perspective. iMeta (2024).
2. Porphyromonas gingivalis regulates atherosclerosis through an immune pathway. Frontiers in Immunology (2023).
3. Periodontitis and atherosclerotic cardiovascular disease. Molecules and Cells (2024).
4. The Roles of Periodontal Bacteria in Atherosclerosis. International Journal of Molecular Sciences (2023).
5. Polymicrobial Oral Infection with Four Periodontal Bacteria Orchestrates a Distinct Inflammatory Response and Atherosclerosis in ApoEnull Mice. PLOS ONE (2015).
6. Mechanisms of vascular damage by systemic dissemination of the oral pathogen Porphyromonas gingivalis. The FEBS Journal (2020).