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Updated: Oct 30, 2025

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils
Published on: January 21, 2020
Emerging Role of Epigenetics in Explaining Relationship of Periodontitis and Cardiovascular Diseases
Syed Ameer Hamza1, Saba Asif2, Zohaib Khurshid3
1Department of Oral Medicine, University Medical & Dental College, Faisalabad 38000, Pakistan.
Insights
Epigenetics, including DNA methylation and miRNA regulation, influences cardiovascular diseases (CVDs) and periodontal disease (PD). Understanding these epigenetic mechanisms offers new diagnostic and therapeutic strategies for inflammatory diseases.
Area of Science:
- Cardiovascular and Oral Health
- Epigenetics and Disease Pathophysiology
Background:
- Cardiovascular diseases (CVDs) are leading global causes of death, influenced by genetics, environment, and lifestyle.
- Periodontal disease (PD), a common oral inflammatory condition, is linked to increased CVD risk.
- Epigenetic modifications, such as DNA methylation and microRNA (miRNA) regulation, play a role in both PD and CVD development.
Purpose of the Study:
- To explore the role of epigenetic mechanisms in the interplay between periodontal disease and cardiovascular diseases.
- To highlight the potential of epigenetics in understanding disease predisposition and developing novel therapeutic approaches.
Main Methods:
- Review of existing evidence on genetic, environmental, and lifestyle factors in CVD and PD.
- Analysis of epigenetic mechanisms, including DNA methylation and miRNA regulation, in disease pathogenesis.
- Discussion of the implications of epigenetic profiling for patient diagnosis and stratification.
Main Results:
- Epigenetic factors, including chronic inflammation from PD, contribute to CVD risk through mechanisms like DNA methylation.
- Atherosclerosis development and vulnerability are influenced by epigenetic modifications.
- Epigenetic pathways are crucial in regulating inflammation, a common link between PD and CVD.
Conclusions:
- Epigenetics provides a novel framework for understanding and managing complex diseases like CVDs and PD.
- Further research into epigenetic regulatory mechanisms driving inflammation is essential for developing targeted treatments.
- Epigenetic profiling may enhance early diagnosis and personalized risk stratification for predisposed individuals.
Abstract:
Cardiovascular diseases such as ischemic heart diseases or stroke are among the leading cause of deaths globally, and evidence suggests that these diseases are modulated by a multifactorial and complex interplay of genetic, environmental, and lifestyle factors. Genetic predisposition and chronic exposure to modifiable risk factors have been explored to be involved in the pathophysiology of CVD. Environmental factors contribute to an individual's propensity to develop major cardiovascular risk factors through epigenetic modifications of DNA and histones via miRNA regulation of protein translation that are types of epigenetic mechanisms and participate in disease development. Periodontal disease (PD) is one of the most common oral diseases in humans that is characterized by low-grade inflammation and has been shown to increase the risk of CVDs. Risk factors involved in PD and CVD are determined both genetically and behaviorally. Periodontal diseases such as chronic inflammation promote DNA methylation. Epigenetic modifications involved in the initiation and progression of atherosclerosis play an essential role in plaque development and vulnerability. Epigenetics has opened a new world to understand and manage human diseases, including CVDs and periodontal diseases. Genetic medicine has started a new era of epigenetics to overcome human diseases with various new methodology. Epigenetic profiling may aid in better diagnosis and stratification of patients showing potential predisposed states for disease. A better understanding of the exact regulatory mechanisms of epigenetic pathways driving inflammation is slowly emerging and will aid in developing novel tools for the treatment of disease.
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