March 2016
Volume 12, Issue 3

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Oral Biofilms and the Systemic Connection

Tracking the health implications of inflammation due to periodontal disease

Gregori M. Kurtzman, DDS, MAGD, DICOI

Research has demonstrated a direct link between oral health and systemic disease that is becoming stronger as further evidence is produced. The American Dental Association highlighted 200 possible connections between systemic diseases and oral health.1 Poor oral hygiene habits and the resulting worsening periodontal conditions lead to a situation locally within periodontal pockets that can have negative repercussions throughout the entire body. Microbiology has demonstrated that specific, harmful microorganisms are always present in periodontal disease and that certain people are predisposed to harboring these oral organisms, increasing health risks. Evidence linking periodontal disease and chronic inflammation to certain major health conditions, including cardiovascular and renal issues, diabetes, osteoporosis, and pulmonary disorders, is presented here.

Formation and Effects of Biofilm

More than 700 different species of bacteria typically reside in the mouth. Most are considered innocuous, but some of these microorganisms have been identified as pathogenic. The mouth is the perfect incubator for bacteria, which can double in number in a few hours if left undisturbed. As bacteria increase in number, they quickly create an intricate network of protective layers (ie, matrix) and channels that develops into biofilm, previously referred to as “plaque.” Dental biofilm is the major cause of periodontal disease.

This aggregation of bacteria works together as a community, producing specific proteins and enzymes by way of quorum sensing, utilizing oral fluids as the vector for transmission.2 Quorum sensing is a cell-to-cell communication mechanism that synchronizes gene expression in biofilm in reaction to the density of population cells. Via quorum sensing, the bacteria in biofilm have the ability to regulate numerous processes. These can include secreting specific enzymes to activate or deactivate the genes of other bacteria.

The bacteria in biofilm and their byproducts provoke an immune response from the host, which sends white blood cells (WBC) to the site to kill the invading bacteria, resulting in localized inflammation in the surrounding gingiva. Using quorum sensing, the bacteria have the ability to confuse the defending WBC chemotactically by releasing chemicals into the environment, rendering the immune response ineffective. Because neutrophils, a type of WBC, have a 3-day life cycle,3 if they do not engulf a bacterium and destroy it within that timeframe, they lyse and die. The neutrophil elastase enzyme that was intended to kill the bacteria are now available to turn on the very tissue they were meant to protect.4 Dentally, this translates into periodontal bone loss and a deepening of the pockets and inflammation.

There is increasing evidence that indicates patients with periodontal disease also have a much higher risk of developing cardiovascular and other systemic issues than those individuals who take preventive measures to eliminate and control the biofilm in their mouths. Harmful strains of bacteria in biofilm can enter the bloodstream during the inflammatory response and can travel to other areas of the body, exerting a distant systemic effect that has been linked to numerous diseases.

Cardiovascular Disease (CVD)

CVD, an umbrella term for heart and blood vessel conditions (eg, atherosclerosis, coronary heart disease, stroke, myocardial infarction) is the result of a complex set of genetic and environmental factors.5 These genetic factors include age, lipid metabolism, obesity, hypertension, and diabetes. Environmental risk factors include socioeconomic status, exercise, stress, diet, smoking, and chronic infections. The classic risk factors such as hypertension, hypercholesterolemia, and cigarette smoking may only account for one half to two thirds of the incidence of CVD.6 Evidence linking chronic infection and inflammation to CVD has been increasing; the inflammation caused by biofilm may be a predisposing factor as well.7,8

The connection between oral bacteria and cardiac disease is not a recent development in the literature. Oral bacteria, specifically the cariogenic Streptococcus mutans and the periodontitis-inducing Porphyromonas gingivalis, induce platelet aggregation, which leads to thrombus formation.9 Studies have reported one or more periodontal pathogens found in 42% of the atheromas in patients with severe periodontal disease.10 Deshpande reported that P gingivalis actively can adhere to and invade fetal bovine heart endothelial cells and aortic endothelial cells.11 A 14-year study found patients with periodontitis had a 25% higher risk to develop CVD than their healthy counterparts.12 Men younger than 50 years with periodontal disease demonstrate 72% more risk to develop CVD. Additionally, periodontal disease increased risk for both fatal and non-fatal strokes two-fold.13,14 Despite strong evidence of an association between periodontal disease and CVD, it is unknown if it is a direct causal relationship.

Three biologic mechanisms explain the association between periodontal disease and CVD. First, periodontal diseases release bacteria that may enter the circulation, invading the heart and vascular tissue, causing harmful effects. People with higher levels of bacteria in their mouths tend to have thicker carotid arteries, an indicator of CVD.15 A systemic study reported that antibody response to periodontal bacteria was associated with coronary heart disease,16 and periodontal bacteria have been found in samples of plaque removed from arteries.17,18 Bacteria in the plaque near diseased gingiva appears to induce clumping of blood platelets, which can then cause the clotting and blockages that can lead to heart attacks or strokes. Second, the body’s response to the periodontal infection includes production of inflammatory mediators, which travel through the circulatory system and may cause harmful effects on the heart and blood vessels. Inflammatory mediators such as lipoprotein and triglycerides are significantly higher in patients with periodontitis than in control groups.19 Additionally, increased levels of C-reactive protein, which is considered a biomarker for inflammation, were associated with periodontitis. Clotting is increased as levels of C-reactive protein increase, which is associated with an elevated risk of heart disease.220Third, bacterial products, such as lipopolysaccharides, enter the blood stream, causing harmful effects on the blood vessels and heart.21

Periodontal disease’s emergence as a potential risk factor for CVD is leading to a convergence in oral and medical care. Proper management of oral health may very well be key to prevention of cardiac disease or worsening of existing heart conditions. In addition, more frequent prophylaxis, such as antibiotics before dental procedures, may be indicated in those patients who have gingival issues combined with a history of cardiac disease, including those with prosthetic cardiac valves, previous endocarditis history, some types of congenital heart disease, and previous cardiac transplant with valvular disease.

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