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Related Experiment Video

Updated: Oct 27, 2025

Inducing Apical Periodontitis in Mice

Inducing Apical Periodontitis in Mice

Published on: August 6, 2019

Periodontitis induces endothelial dysfunction in mice.

Maria Parvaneh¹, Paul K Witting², Jaqueline Ku³

¹Charles Perkins Centre, University of Sydney School of Dentistry, Faculty of Medicine and Health, The University of Sydney, Sydney, NSW, Australia.

Scientific Reports

|July 23, 2021

Summary

This summary is machine-generated.

This study shows that periodontitis in mice leads to endothelial dysfunction, a key factor in cardiovascular disease. Early prevention of gum disease may help reduce early-stage vascular problems.

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Last Updated: Oct 27, 2025

Inducing Apical Periodontitis in Mice

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Published on: August 6, 2019

A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites

A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites

Published on: August 8, 2014

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils

Published on: January 21, 2020

Area of Science:

Cardiovascular Research
Oral Health
Metabolic Disease

Background:

Periodontitis treatment benefits chronic conditions like cardiovascular disease and diabetes.
Ethical constraints limit human trials on periodontitis's role in early chronic disease development.

Purpose of the Study:

To investigate if periodontitis induces endothelial dysfunction in hyperlipidemic apolipoprotein E gene-deficient (ApoE-/-) mice.
To explore systemic effects of periodontitis in a mouse model.

Main Methods:

Oral gavage with Porphyromonas gingivalis and Streptococcus gordonii in ApoE-/- mice to induce periodontitis.
Assessment of endothelial function, inflammatory markers, energy expenditure, and gut microbiota.
X-ray imaging for alveolar bone loss and aortic ring vasorelaxation assays.

Main Results:

Periodontitis was successfully induced in ApoE-/- mice, mirroring human conditions.
Significant increases in liver pro-inflammatory mediators (serum amyloid A1, tumor necrosis factor) were observed.
Impaired endothelial-dependent vasorelaxation and increased energy expenditure were noted in periodontitis mice.

Conclusions:

Periodontitis induces endothelial dysfunction in mice, providing a model for studying early chronic disease stages.
Systemic responses linked to periodontitis warrant further investigation.
Early periodontitis prevention may mitigate early endothelial dysfunction associated with atherogenesis.