4 New UB Studies Suggest Ways Gum Disease Contributes to Development of Heart Disease

By Lois Baker

Release Date: July 23, 1998

BUFFALO, N.Y. -- New studies by researchers in the University at Buffalo School of Dental Medicine have identified several possible pathways gum disease may contribute to the development of heart disease.

Scientists have uncovered evidence of a link between the two conditions: The question remaining is how the relationship develops.

o Components of periodontal bacteria are present along blood-vessel walls in and around vascular plaques and may contribute to formation of the blockages.

o The body's immune and inflammatory responses to proteins produced by these bacteria may be a factor in cardiovascular disease.

o Persons with periodontal disease have increased blood levels of oxygen free radical, molecules known to damage blood-vessel walls and set the stage for arterial plaque formation.

Results of the studies were presented recently at the International Association of Dental Research meeting held in Nice, France.

Medical and dental researchers suspected early on that periodontal bacteria played a role in the development of heart disease by contributing to arterial plaque formation or hardening of the arteries, via several possible pathways.

In one study to investigate the role of these bacteria in the formation of arterial plaque, or atheroma, UB researchers in oral biology collected atheroma samples from patients who had undergone endarterectomy, a procedure that removes blockages from the carotid artery. The researchers extracted bacterial DNA from the samples, amplified it and identified the specific microorganisms present.

Forty percent of the 50 samples contained bacteria of periodontal origin, results showed. In addition, organisms associated with pneumonia and gastric ulcers, two other infections thought to be associated with hardening of the arteries and heart disease, also were found.

Robert Genco, D.D.S., Ph.D., SUNY Distinguished Professor and chair of the UB Department of Oral Biology, said the findings suggest periodontal bacteria contribute to formation of plaques that block arteries, and may be one way periodontal disease and heart disease are linked.

Violet Haraszthy, D.D.S., a post-doctoral associate in the UB Department of Oral Biology, was lead researcher on the study.

Two other studies examined how the body's immune and inflammatory response to periodontal infection may contribute to the development of vessel blockages.

"The body's immune response to periodontal bacteria may result in the production of antibodies, proteins that 'tag' material for removal from the body," said Ingrid Glurich, Ph.D, lead researcher on the studies and a post-doctoral associate in the UB Department of Oral Biology.

"In addition to tagging bacteria, however, these antibodies may also tag cells that actually are part of the vessel wall. This leads to tissue destruction and an effort by the body to replace the lost cells and 'wall off' toxic material, resulting in a thickening of the blood-vessel walls."

Glurich and colleagues found that more than half of their periodontal patients had antibodies to heat shock protein, a molecule shared by periodontal bacteria and human heart tissue. None of the healthy subjects had detectable antibody to this protein. The researchers are investigating the possibility that periodontal infections result in antibodies to heat shock protein and that these antibodies "tag" cells in the heart arteries, contributing to plaque formation and heart disease.

The body also produces substances in response to bacterial infections known as acute phase proteins, Glurich said. "Acute phase proteins are known to play a role in lipid and cholesterol transport and metabolism, which have long been thought to be a major factor in the development of arterial blockages. Some of these proteins can be found deposited along the carotid blood vessels, where they appear to increase inflammation and tissue destruction."

The research group collected blood samples and assessed the levels of these proteins in four sets of subjects: those with periodontal disease and no cardiovascular disease; those with cardiovascular disease and no periodontal disease; those with both diseases, and those with neither.

Results showed a three-fold increase of C-reactive protein, a type of acute phase protein, in patients with either periodontal or heart disease, and an eight-fold increase when both diseases were present, Glurich said. Levels of two other acute phase proteins also were elevated in patients with both diseases.

moderate-to-severe periodontal disease was four-times greater than in persons with slight or no disease. Free radicals are known to damage vessel walls and promote formation of plaque and blockages.

Sultan Al-Mubarak, D.D.S., clinical assistant professor in the UB Department of Periodontology, was lead researcher on the study.