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Review
. 2021 Jan 14:11:609614.
doi: 10.3389/fphys.2020.609614. eCollection 2020.

Inflammation in Periodontal Disease: Possible Link to Vascular Disease

Oindrila Paul  1 , Payal Arora  2 , Michael Mayer  3 , Shampa Chatterjee  1
Affiliations
Review

Inflammation in Periodontal Disease: Possible Link to Vascular Disease

Oindrila Paul et al. Front Physiol. .

Abstract

Inflammation is a well-organized protective response to pathogens and consists of immune cell recruitment into areas of infection. Inflammation either clears pathogens and gets resolved leading to tissue healing or remains predominantly unresolved triggering pathological processes in organs. Periodontal disease (PD) that is initiated by specific bacteria also triggers production of inflammatory mediators. These processes lead to loss of tissue structure and function. Reactive oxygen species and oxidative stress play a role in susceptibility to periodontal pathogenic bacterial infections. Periodontal inflammation is a risk factor for systemic inflammation and eventually cardiovascular disease (CVD). This review discusses the role of inflammation in PD and its two way association with other health conditions such as diabetes and CVD. Some of the mechanisms underpinning the links between inflammation, diabetes, CVD and PD are also discussed. Finally, we review available epidemiological data and other reports to assess possible links between oral health and CVD.

Keywords: NLRP3 inflammasome; antioxidants; cardiovascular disease; dental plaque; oxidative stress; periodontal disease (PD); risk factors; vascular inflammation.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
An illustration of the inflammatory immune response with PD. (A) PAMPs (like LPS) are recognized by TLRs. The PAMP-TLR interaction triggers a proinflammatory signaling cascade that drives a chemokine and cytokine rich environment into which multiple immune cells [macrophages (MΦ), T and B lymphocytes, dendritic cells (DC)] are recruited. (B) Multiple immune cells produce ROS. (C) T cells produce the cytokine RANKL that participates in bone resorption.
FIGURE 2
FIGURE 2
The feed forward mechanism of the “Infection-ROS-Inflammation” triad that seems to accelerate susceptibility to infection, inflammation and oxidative stress.
FIGURE 3
FIGURE 3
Possible mechanisms by which PD contributes to inflammation at distal sites and thus drives an atherosclerotic phenotype. (1) Direct: vascular infection by periodontal bacterial pathogens and (2) Indirect: facilitating the passage of inflammatory modulators into the systemic circulation.
See this image and copyright information in PMC

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