Scientists uncover bacterial mechanism that links gum disease to heart disease

A new study clarifies the microbiology underlying the well-established link between

gum disease and heart disease by identifying the effect of a bacterium common to both

conditions.

Researchers found that a bacterium involved in gum disease alters the expression of genes that boost inflammation and atherosclerosis in the arteries that supply blood to the heart.

The study, from Orebro University in Sweden, is published in the journal Infection and

Immunity.

It surrounds the activity of a bacterium called Porphyromonas gingivalis, a

well-known culprit in the development of periodontitis – a serious gum infection that damages

the soft tissue that surrounds the teeth and attacks the bone that supports them.

The team found that P. gingivalis alters the expression of genes that

code for proteins that boost inflammation and atherosclerosis in the coronary arteries – the

vessels that supply blood to the heart.

Atherosclerosis, or hardening of the arteries, is caused by artery walls becoming clogged

up with fats, cholesterol and other substances. The build-up forms plaques that can burst and

trigger a blood clot.

Previous studies have already shown that P. gingivalis is present in coronary

artery plaques of heart attack patients, and animal studies have also shown that it triggers

and hastens atherosclerosis in the aorta – the main artery from the heart to the rest of the

body – and coronary arteries.

The new study, led by Torbjörn Bengtsson, a professor in the department of clinical

medicine, reveals the underlying molecular mechanisms behind such findings.

P. gingivalis enzymes boost inflammation in aortic smooth muscle cells

Prof. Bengtsson and colleagues began by culturing human aortic smooth muscle cells and

infecting them with P. gingivalis.

Human aortic smooth muscle cells offer an ideal model for studying cardiovascular function

and diseases like atherosclerosis at the cell level. When the heart pumps, it stretches the

aorta, and the smooth muscle cells in the wall of this main artery contract it again. Changes

in the wall of the aorta – such as those caused by atherosclerosis and high blood pressure –

strongly influence this process.

When they injected P. gingivalis into the smooth muscle cells, the

researchers found it secretes enzymes called gingipains that alter the ratio between two

angiopoietins – proteins involved in inflammation – in a direction that boosts inflammation,

which is thought to play an important role in atherosclerosis.

Specifically, the team found that the gingipains boosted the expression of the pro-inflammatory protein angiopoietin 2 (Angpt2) and dampened the expression of the anti-inflammatory protein angiopoietin 1 (Angpt1).

The cell-signaling protein tumor necrosis factor (TNF) – which is produced in the human

body – is also a cardiovascular risk factor that promotes atherosclerosis via Angpt1 and

Angpt2. However, Prof. Bengtsson points out that their study shows the ginginpains from

P. gingivalis influence the two proteins independently from TNF.

First author Boxi Zhang, a PhD student in Prof. Bengtsson’s lab, concludes:

“Our research clarifies the mechanism behind the association of periodontitis

and cardiovascular disease. Our aim is to find biomarkers that can help us diagnose and treat

both diseases.”

In severe cases of periodontitis, dentists may prescribe antibiotics to fight the

infection. However, Medical News Today recently learned of a study that suggests wild blueberry extract may prevent the dental plaque that

leads to gum disease. The researchers say the dual antibacterial and anti-inflammatory

action of lowbush blueberry polyphenols make them strong candidates for such a treatment.

Written by Catharine Paddock PhD

Copyright: Medical News Today