Journal Article | Cardio-Metabolic, Others

September 21, 2020



Chhibber-Goel, J. et al

Introduction:

 

The oral cavity is a complex human system. It facilitates speech, pronunciation, mastication, and aids in taste and olfaction. It houses over 700 bacterial species that populate and establish a microenvironment and maintain harmony via biofilm formation and polymicrobial communities.

 

Infections can alter the healthy condition of the oral microbiome. These can result to a highly prevalent gum disease called periodontitis, an autoimmune dental disease that damages the periodontal ligament and bone.

 

Cardiovascular disease is the leading cause of mortality worldwide. One of its causes is coronary artery disease (CAD), the narrowing of coronary artery due to plaque formation. This may be due to an atherosclerotic plaque that blocks the coronaries and reduces oxygen-rich blood supply to the heart.

 

A link has been established between dental disease and CAD. As early as 1993, De Stefano et al. found that atherosclerotic plaque is 25% higher among patients with periodontitis. The study by Chhibber-Goel et al in 2016 identifies oral bacteria present in atherosclerotic plaques and the role they play in CAD. This article summarizes the findings of the study.

 

Relevance:

 

Poor oral health, infections, and dental procedures such as periodontal scaling, probing, and tooth extractions provide a way for bacterial components and toxins to be translocated into the bloodstream. Bacteria and their components, along with the inflammatory mediators that they trigger, become part of the atherosclerotic plaque in the coronaries that drive CAD.

 

Oral bacteria contribute in the development of CAD. This makes good dental health and hygiene more necessary than ever.

 

Objectives:

 

The study aims to analyze the link between plaque-associated bacteria in CAD patients. Further, it determines the non-cardiac distribution of oral bacteria in the human body. It also dissects probable entry routes of bacteria into coronary vasculature and analyzes the bacterial communities within the plaques.

 

Highlights:

 

This is a meta-analysis of 63 studies which involved 1791 patients who underwent carotid endarterectomy, catheter-based atherectomy, and similar procedures. Bacteria were identified based on their morphological characteristics, culture studies, immunohistochemistry, real time polymerase chain reaction, and gene sequencing. These methods confirm the presence of 23 bacteria in atherosclerotic plaques.

 

With the exception of Streptococcus spp., these bacteria are Gram-negative. The bacteria are anaerobes either facultative or obligate except for Pseudomonas luteola.

 

Five of these bacteria, namely Campylobacter rectus, Porphyromonas spp. (gingivalis and endodontalis) and Prevotella spp.(intermedia and nigrescens), are exclusively found in the coronary plaques while the remaining 18 are found in both cardiac and non-cardiac organs. Notable examples of bacteria present in cardiac and non-cardiac organs include Chlamydia pneumonia, Helicobacter pylori, and Pseudomonas aeruginosa.

 

Proteins secreted by atherosclerotic plaque-associated bacteria act as virulence factors and as regulators of the host’s immune response. They degrade oral mucous membranes and periodontal pockets enabling entry of the bacteria to the bloodstream. Bacteria then invade the endothelial layer of blood vessels and their proteins stimulate inflammatory cytokine production.

 

There are various survival strategies employed by the polymicrobial community in the mouth. Biofilm formation is one and initially, it entails the binding of the cell wall of Streptococcus with the type II fimbriae of Actinomycetes. Aggregation of these early bacterial colonizers is followed by adhesion of other colonizers.

 

Fusobacterium nucleatum secretes lecithin-carbohydrate-specific adhesins and Treponema denticola secretes chymotrypsin-like proteinases for the late bacterial colonizers to form the polymicrobial community. This is followed by invasion of the healthy gingival crevice by Porphyromonas gingivalis, detaching and distorting the existing oral biofilm. Together with Prevotella intermedia, they result to periodontitis.

 

These processes result to damages to the epithelium and provide an access to the bloodstream. Upon entry to the coronary vasculature, bacteria can form biofilm structures within atherosclerotic plaques.

 

Conclusion:

 

The oral cavity is a significant source of bacteria. Once bacteria abnormally proliferate, they can destroy the periodontal ligament, bone, and connective tissue. Patients with gum disease such as periodontitis pose an increased risk of atherosclerotic plaque formation.

 

It is important to understand that oral health is a reflection of overall health. Good oral hygiene practices, a visit to the dentist for consultation, and oral prophylaxis every 6 months can prevent gum diseases and the buildup of atherosclerotic plaque-associated bacteria in the coronaries.

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