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Atherosclerosis, Periodontal Disease, and Treatment with Resolvins

  • Vascular Biology (J. Hamilton, Section Editor)
  • Published:
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Abstract

Purpose of Review

This review aims to discuss the existing evidence on the link between atherosclerosis and periodontitis by particularly presenting new findings that link the pathology and therapy of these diseases. Acute vascular ischemic events that can lead to stroke or myocardial infarction are initiated by inflammatory processes leading to rupture or erosion of plaques susceptible to thrombosis (“high risk” or “vulnerable”). These are highly inflamed plaques residing in the media and adventitia that may not be detected by angiography measurments of luminal narrowing. Statistically significant excess risk for atherosclerotic cardiovascular disease has been reported in persons with periodontitis independent of established risk factors. We hypothesized that the systemic pathologic links also represent potential therapeutic links.

Recent Findings

We recently demonstrated that periodontal inflammation promotes atherosclerotic plaque inflammation and destabilization. As discrete pathological regions, these plaques with a high susceptibility to rupture can be imaged and differentiated from lower risk plaques. In cholesterol-fed rabbits with periodontal disease, circulating inflammatory mediators were also significantly elevated thereby contributing to “vulnerable blood,” a systemic characteristic of high risk for cardiovascular events. New studies show that certain lipid mediators, including lipoxins and resolvins, are potent in preventing and possibly treating a number of inflammation-associated diseases, including periodontitis and vascular inflammation.

Summary

The concept of the vulnerable patient and the pro-resolving approach open new terrain for discovery of paradigm-changing therapies for the prevention and treatment of two of the most common diseases of man. Importantly, lipoxins and resolvins are natural receptor agonists that do not exhibit the same pro-atherogenic side effects attributed to anti-inflammatory medications (e.g., NSAIDs) but rather coordinate resolution of inflammation and a return to homeostasis.

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Acknowledgements

We thank Grace Yee for help in preparing the manuscript. The authors also thank Daniel Nguyen, Olivia Nguyen, and Konstantinia Almpani for their assistance in periodontitis and the CVD model in rabbits and histopathology. The preliminary studies were supported by the Forsyth Institute Pilot Grant Program.

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Authors and Affiliations

  1. Department of Physiology and Biophysics, Boston University School of Medicine, 700 Albany Street, W302, Boston, MA, 02118-2526, USA

    James A. Hamilton

  2. Department of Applied Oral Sciences, The Forsyth Institute, 245 First Street, Cambridge, MA, 02142, USA

    Hatice Hasturk, Alpdogan Kantarci & Thomas Van Dyke

  3. Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, 02115, USA

    Charles N. Serhan

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  1. James A. Hamilton
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Correspondence to James A. Hamilton.

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James A. Hamilton, Hatice Hasturk, Alpdogan Kantarci, Charles Serhan, and Thomas Van Dyke declare no conflict of interest.

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This article is part of the Topical Collection on Vascular Biology

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Hamilton, J.A., Hasturk, H., Kantarci, A. et al. Atherosclerosis, Periodontal Disease, and Treatment with Resolvins. Curr Atheroscler Rep 19, 57 (2017). https://doi.org/10.1007/s11883-017-0696-4

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