For this study, researchers analyzed coronary plaque samples from 121 people who had died from sudden cardiac death, and from 96 people who had undergone surgery to have the plaque from their arteries cleaned, a procedure known as an endarterectomy.

At the study’s conclusion, the scientists discovered that the bacteria viridans group Streptococci — an umbrella-term for types of Streptococcus bacteria commonly found in the mouth, in saliva and dental plaque — were the most common bacteria in the coronary plaque samples.

“Oral viridans group Streptococci are known to act as early colonizers in the buildup of the dental biofilm known as dental plaque,” Karhunen explained. “This signals that the streptococci may not be there alone — it is possible that there is a biofilm composed of many bacteria. In fact we have unpublished results confirming this.”

“In the bacterial biofilm, the bacteria are safe inside the jelly-like cover and they do not cause any harm to the individual,” he continued.

However, he noted, “the situation changes dramatically when the biofilm activates for [some] reason or other, and starts to produce new generation of bacteria that break out from the biofilm and infiltrate the atherosclerotic plaque, causing inflammation that can rupture the plaque ending up in the formation of a thrombus.”

“We aim to show that there is a biofilm consisting of many bacteria in the atherosclerotic plaques and we also study the possibility that calcification of the biofilm — which occurs in the surface of the teeth — might also be involved in the calcification of coronary arteries,” Karhunen added. “We also studied the possibility of developing a vaccine against the formation of a biofilm and bacterial-induced thrombosis.”

MNT spoke with Sergiu Darabant, MD, a cardiologist with Miami Cardiac & Vascular Institute, part of Baptist Health South Florida, about this study, who said he did not find the study surprising, but intriguing.

“We’ve long suspected that inflammation is a key driver of cholesterol plaque formation and plaque rupture leading to heart attacks,” Darabant, who was not involved in the research, said. “This study adds another piece to the puzzle — showing how bacteria from the mouth might play a hidden role in driving coronary inflammation.”

“Even though we’ve made significant progress over the years in the advancement of medical therapies aimed at cardiovascular risk reduction and secondary prevention of cardiovascular events, our prevention toolkit is still limited,” he continued.

“Pinpointing modifiable, time-varying triggers — e.g., transient bacteremia, respiratory infections — could enable targeted new therapies that complement commonly used medication for lipid, blood-pressure, and diabetes control,” added Darabant.

MNT also spoke with Yu-Ming Ni, MD, a board-certified cardiologist and lipidologist at MemorialCare Heart and Vascular Institute at Orange Coast Medical Center in Fountain Valley, CA, likewise not involved in the study, about these research findings.

“This bacteria, strep viridans, is a very common oral bacteria, and the fact that it seems to be implicated in atherosclerosis is interesting,” Ni commented.

However, he cautioned that “it’s important to recognize that these studies have some limitations because you’re taking a picture in the aftermath, so you don’t have a great timeline for what exactly is happening in someone’s plaque that leads them to have this vascular event.”

“So I would be cautious to just go and make the assumption that these bacteria are definitely the reason for plaque disruption. I think there’s maybe more to that than just that, but it does support the idea of inflammation as a key factor in the development of clinical heart disease.”

– Yu-Ming Ni, MD