by Marlowe HoodWed Sep 10, 7:16 PM ET

Here’s another reason to brush your teeth: poor dental hygiene boosts the risk of heart attacks and strokes, a pair of studies reported this week.

Heart disease is the number one killer worldwide, claiming upward of 17 million lives every year, according to the World Health Organization.

Smoking, obesity and high cholesterol are the most common culprits, but the new research shows that neglected gums can be added to the list.

“We now recognize that bacterial infections are an independent risk factor for heart diseases,” said Howard Jenkins of the University of Bristol in Britain, at a meeting of the Society for General Microbiology in Dublin.

“In other words, it doesn’t matter how fit, slim or healthy you are, you’re adding to your chances of getting heart disease by having bad teeth,” the professor said.

There are up to 700 different bacteria in the human mouth, and failing to scrub one’s pearly whites helps those germs to flourish.

Most are benign, and some are essential to good health. But a few can trigger a biological cascade leading to diseases of the arteries linked to heart attacks and stroke, according to the new research.

“The mouth is probably the dirtiest place in the human body,” Steve Kerrigan of the Royal College of Surgeons in Dublin said.

“If you have an open blood vessel from bleeding gums, bacteria will gain entry to your bloodstream.”

Once inside the blood, certain bacteria stick onto cells called platelets, causing them to clot inside the vessel and thus decreasing blood flow to the heart.

“We mimicked the pressure inside the blood vessels and in the heart, and demonstrated that bacteria use different mechanisms to cause platelets to clump together, allowing them to completely encase the bacteria,” he said.

This not only created conditions that can provoke heart attacks and strokes, it also shielded the bacteria from both, immune system cells and antibiotics.

“These findings suggest why antibiotics do not always work in the treatment of infectious heart disease,” Jenkins said.

In separate research, a team led by Greg Seymour of the University of Otago Dunedin in New Zealand showed how other bacteria from the mouth can provoke atherosclerosis, a disease that causes hardening of the arteries.

All organisms — including humans and bacteria — produce “stress proteins,” molecules produced by conditions such as inflammation, toxins, starvation, or oxygen deprivation.

One function of stress proteins is to guide other proteins across cell membranes.

But they can also can latch onto foreign objects, called antigens, and deliver then to immune cells, provoking an immune reactions in the body.

Normally, the body does not attack its own stress proteins.

But bacterial stress proteins — which are similar — do trigger a response, and once that has happened the immune system can no longer differentiate between the two, said Seymour.

“White blood cells can build up in the tissue of arteries, causing atherosclerosis,” he explained in a phone interview.

Copyright © 2008 Agence France Presse

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A Healthy Smile May Promote a Healthy Heart

Research continues to suggest the importance of periodontal health as related to cardiovascular health.CHICAGO—January 08, 2008—Each year, cardiovascular disease kills more Americans than cancer. And while most people are aware that lifestyle choices such as eating right, getting enough exercise and quitting smoking can help prevent cardiovascular disease, they may not know that by just brushing and flossing their teeth each day, they might also be avoiding this potentially lethal condition.

An article published in the December issue of the Journal of Periodontology (JOP), the official publication of the American Academy of Periodontology (AAP), suggests that periodontal patients whose bodies show evidence of a reaction to the bacteria associated with periodontitis may have an increased risk of developing cardiovascular disease. Study Abstract

“Although there have been many studies associating gum disease with heart disease, what we have not known is exactly why this happens and under what circumstances,” said JOP editor Kenneth Kornman, DDS, PhD. “The findings of this new analysis of previously published studies suggest that the long-term effect of chronic periodontitis, such as extended bacterial exposure, may be what ultimately leads to cardiovascular disease.”

Researchers at Howard University identified 11 studies that had previously examined clinically-diagnosed periodontal disease and cardiovascular disease. The team then analyzed the participants’ level of systemic bacterial exposure, specifically looking for the presence of the bacteria associated with periodontal disease, as well as measuring various biological indicators of bacterial exposure. They found that individuals with periodontal disease whose biomarkers showed increased bacterial exposure were more likely to develop coronary heart diseaseor atherogenesis (plaque formation in the arteries).

“While more research is needed to better understand the connection between periodontal disease and cardiovascular disease, this study suggests the importance of taking of your teeth and gums and how that can help you take care of your heart,” said Susan Karabin, DDS, President of the AAP. “With the number of people with heart disease continuing to increase, it is important to understand that simple activities like brushing and flossing twice a day, and regular visits to your dental professional can help lower your risk of other health conditions.”

from http://www.perio.org/consumer/healthy-heart.htm

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Bacteria Shown To Cause Blood Clots 04 Nov 2008 Bacteria can directly cause human blood and plasma to clot – a process that was previously thought to have been lost during the course of vertebrate evolution, according to new research at the University of Chicago, National Institute of Allergy and Infectious Diseases, and Institut Pasteur in Paris. Their findings were published online Nov. 2 in Nature Chemical Biology. The discovery will improve scientists’ understanding of coagulation during bacterial infections and may lead to new clinical methods for treating serious medical conditions such as sepsis and anthrax. It has long been known that blood often coagulates during sepsis or bacterial infections, but this has generally been regarded as a host’s immune and inflammatory response. It also has been known that bacteria can activate factors that precede coagulation, but it had not previously been known that bacteria can pass the coagulation threshold and cause blood clots to form. Once they form, the clots can grow and propagate. Although this may help prevent the dissemination of the bacteria through the host, it often leads to serious vascular damage due to blocked and injured blood vessels. The key to clot formation is the location of the bacteria, rather than the total number of bacteria or their level of concentration. In other words, for those bacteria that can activate coagulation factors, coagulation occurs only when a cluster of bacteria forms. “Our research demonstrates that coagulation can be controlled by changing the spatial distribution, or clustering, of bacteria,” said study co-author Christian Kastrup, Post-Doctoral Assistant at the Koch Institute for Integrative Cancer Research at the Massachusetts Institute of Technology. “Therefore, considering the location of bacterial cells, instead of just their presence or absence and their total numbers, could significantly change our understanding of coagulation.” Kastrup, who worked on this research as a graduate student in the Ismagilov Lab at the University of Chicago’s Department of Chemistry, is the first author of the Nature paper. Rustem Ismagilov, Professor of Chemistry at the University of Chicago, is the corresponding author. Researchers at the National Institute of Allergy and Infectious Diseases, Institut Pasteur in Paris, and Ben-May Department for Cancer Research at the University of Chicago co-authored the paper. Coagulation can occur if enough proteases that activate coagulation accumulate near the bacteria, rather than diffuse away. This research used Bacillus anthracis, the anthrax-causing pathogen (using a safe strain that does not infect humans). It found that in the case of human blood, coagulation required the secretion of zinc metalloprotease InhA1, which activated prothrombin and factor X directly – not via factor XII or tissue-factor pathways. “We refer to this mechanism as ‘quorum acting’ to distinguish it from quorum sensing, in which bacteria coordinate certain actions based, in part, on their density,” said Wei-Jen Tang, Professor at the Ben-May Department for Cancer Research. This work opens up a new field of st udy, he added. “We will now explore the commonality of quorum acting, and how quorum acting can affect evolutionary dynamics.” The results of this research have broad implications, according to Ismagilov. “The work emphasizes the importance of bacteria’s spatial distribution, rather than just its average concentration in the functioning of nonlinear biochemical networks,” he said.