GAINESVILLE, Fla. — Gum disease has been linked to hardening of the arteries for nearly a decade, and scientists have long fingered a gang of oral bacteria as the obvious suspects behind many cases of the vessel-clogging killer.
Now University of Florida researchers have cornered the bacterial ringleaders of gum disease inside human artery-clogging plaque — the first concrete evidence to place the pathogens at the heart of the circulatory crime scene. Their report appears in the current issue of Atherosclerosis, Thrombosis and Vascular Biology.
“Our finding is important because it has proved there are live periodontal bacteria in human atherosclerotic tissue,” said study investigator Ann Progulske-Fox, Ph.D., a professor of oral biology at the UF College of Dentistry. “Now we can begin to understand how these bacteria contribute to the disease process.”
The oral bacteria UF researchers found in the plaque, Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans, are two of the most aggressive offenders in periodontal disease, the leading cause of adult tooth loss. Because of the strong association between periodontal and cardiovascular diseases, scientists have postulated for years that oral pathogens contribute to arterial damage that leads to heart attack or stroke, which kill nearly a million Americans a year. In fact, a recent study conducted elsewhere found a direct correlation between the amount of periodontal bacteria in the mouth and the formation of blockages in the carotid artery in the neck.
To reach the circulatory system, the bacteria have to breech the barrier between tissues in the mouth and the bloodstream, Progulske-Fox said. For patients with periodontal disease, whose gums are inflamed and bleed easily, bristles from even the softest toothbrush can tear tiny blood vessels in the compromised gum tissues, leaving the door wide open for bacteria to enter.
But could the bacteria elude the body’s protective immune response once within the bloodstream?
Researchers worldwide have sought to empirically nab oral bacteria — dead or alive — in atherosclerotic tissues. They have found remnants of bacterial DNA in arteries, signaling that bacteria had entered the bloodstream. Yet scientists have never been able to grow periodontal bacteria isolated from arterial plaque in Petri dishes, even though the same species of bacteria swabbed from oral plaque can be cultured that way. Therefore, researchers could not be sure the DNA was from bacterial trespassers destroyed by the immune system in the bloodstream, or if live bacteria were actually directly involved in plaque formation within the vessel walls.
“It makes sense that those periodontal bacteria most invasive in the mouth could be able to adapt to the vascular situation,” said study project leader Emil Kozarov, Ph.D., an adjunct associate professor of oral biology at UF and a faculty member at Nova Southeastern University.
Probably only a handful of periodontal bacteria have been successful in making the jump of being infectious to both the oral and vascular tissues. Identifying these bacteria would give researchers the inside scoop on how the