Written By: Team Pharmacally
Medically Reviewed By: Dr. Rahul Gaikwad, MBBS, MD (General Medicine)
When we think about heart disease, we usually blame cholesterol buildup, high blood pressure, diabetes, obesity, or smoking. These are well-established risk factors that damage arteries over time and increase the chance of heart attack or stroke.
But scientists are now uncovering another, less noticeable players in this space like bacteria from our mouths. New research shows that oral microbes may travel from the mouth to the bloodstream, where they can stay inside blood vessels and influence the health of the heart.
A team of researchers from Finland and the UK recently studied this link and focused on a group of bacteria called viridans streptococci. These bacteria are extremely common they are part of the normal flora of the mouth and are among the first microbes to colonize teeth, contributing to form dental plaque. For most people, they cause no harm. Under certain conditions, especially when gum disease or dental procedures allow them to enter the blood. This study, suggests their role may go even further. Instead of only affecting the heart valves, viridans streptococci appear capable of settling inside fatty deposits (plaques) in the coronary arteries, where they can hide, survive, and eventually contribute to plaque rupture the final step that causes a heart attack.
The findings of the study, published in the Journal of the American Heart Association suggest that oral health and cardiovascular health are deeply connected, and that the bacteria we carry in our mouths could be far more important for heart disease than previously recognized.
How Bacteria Travel to the Heart
Viridans streptococci are bacteria that naturally live in the mouth. They help form dental plaque, the sticky film on teeth. Most of the time, they don’t cause any problems.
However, when the gums are inflamed or infected, or during activities like tooth brushing, flossing, or chewing in people with gum disease, tiny cuts can open in the gums. Through these small openings, bacteria can enter the bloodstream.
Once in the blood, these bacteria can sometimes stick to the inner lining of blood vessels, especially in areas already weakened by atherosclerosis. Inside these plaques, the bacteria may survive for a long time, forming communities (biofilms) that the body’s immune system unable to detect them.
In this way, bacteria from the mouth can end up contributing to artery disease and even heart attacks.
Biofilms: Bacteria’s Shield inside Arteries
Once the bacteria from the mouth reach the arteries, they do not simply float around as single cells. Instead, they gather and form biofilms, which are dense, sticky communities of bacteria that can attach firmly to surfaces like the fatty deposits inside artery walls. A biofilm acts like a protective shield for the bacteria. Inside this shield, they become almost invisible to the body’s immune system and are extremely difficult to eliminate with antibiotics. This allows them to survive silently for long periods, sometimes even years, without causing obvious infection. However, biofilms are not completely harmless. Under certain conditions such as changes in blood flow, inflammation, or nutrient availability some of the bacteria can break free from the biofilm. Once released, they adopt a more aggressive form. These free-floating bacteria are quickly recognized by the immune system, which reacts strongly by sending in immune cells and triggering inflammation. Inside an artery plaque, this sudden burst of inflammation can weaken the thin covering (the fibrous cap) of the plaque, causing it to rupture. When a plaque ruptures, blood clots form, which can completely block the artery and result in a heart attack.
Linking Mouth Bacteria to Heart Attacks
To test the idea that oral bacteria might contribute to heart disease, researchers carried out one of the most detailed investigations to date. They examined two sets of patients:
121 people who had died suddenly (through medicolegal autopsies).
96 patients who underwent surgery for advanced atherosclerosis in their neck, leg, or abdominal arteries.
From these individuals, the researchers collected samples of atherosclerotic plaques the fatty buildups inside arteries that are known to cause heart disease. Using modern techniques like DNA testing and immunohistochemistry (a staining method to visualize bacteria in tissues), they searched for signs of bacteria.
The results were striking. In both the autopsy group and the surgical group, the most common bacterial DNA found was from viridans streptococci, the same group of bacteria that normally live in the mouth. About four in every ten plaques tested positive for these bacteria. This was not a random finding the presence of viridans streptococci strongly correlated with the severity of atherosclerosis. The worse the artery disease, the more likely it was to contain these bacteria.
Even more importantly, in cases of fatal heart attack, the researchers found streptococci right at the critical weak spot: the ruptured area of the plaque. These bacteria were not just sitting quietly; they were actively involved in triggering inflammation. The study showed that when bacteria escaped from their hidden biofilm form, they were recognized by immune sensors in the artery wall, known as toll-like receptors (TLRs). This recognition switched on powerful inflammatory pathways, including the NF-κB pathway, which controls the release of inflammatory molecules.
This chain reaction of immune activity weakened the protective fibrous cap of the plaque. Once the cap tore open, blood clotted rapidly at the site, blocking the artery. This blockage cut off blood supply to the heart muscle exactly what happens in a myocardial infarction (heart attack).
In simple terms, the bacteria acted like a hidden match inside the plaque. Most of the time, they lay low, unnoticed within biofilms. But when they were released, they set off an inflammatory “explosion” that destabilized the plaque and led directly to a heart attack.
Why Antibiotics Fail
A natural question arises: if bacteria are part of the problem, wouldn’t antibiotics help? In fact, this idea has been tested before. In the 1990s and early 2000s, several large clinical trials gave antibiotics to patients with heart disease. The focus at the time was mostly on Chlamydia pneumoniae and other suspected infectious agents. But the results were disappointing antibiotics did not reduce the risk of future heart attacks or strokes.
The new study on viridans streptococci helps explain why these trials failed. The bacteria found inside artery plaques are not free-floating, where antibiotics could easily reach them. Instead, they are locked away inside biofilms. A biofilm is like a fortress: it’s a slimy, sticky layer of bacteria and protective substances that prevents antibiotics from getting in. It also keeps the bacteria hidden from the body’s immune system.
Because of this protective environment, standard antibiotic courses like the pills we take for chest or dental infections are simply not strong enough or long enough to clear bacteria living deep inside an artery plaque. By the time a biofilm has formed in the artery wall, antibiotics can do very little.
This is why the researchers stress that the key may not be traditional antibiotics, but rather new strategies aimed at preventing biofilm formation, breaking down biofilms once they exist, or detecting them early before they cause damage.
Practical takeaways
Maintain good oral hygiene: Regular brushing, flossing, and dental check-ups help reduce the risk of bacteria entering the bloodstream.
Treat gum disease early: Periodontal infections may increase the chances of harmful bacteria spreading.
Future treatments: Scientists are exploring whether new drugs or imaging tools could target bacterial biofilms in arteries.
Rethinking Heart Disease
For a long time, doctors have explained heart disease mainly through the lens of cholesterol and fat buildup in the arteries. While this remains true, the new research highlights that the story is more complex. Heart disease is not only about blocked arteries but also about inflammation the body’s immune response that, when triggered in the wrong place, can do more harm than good.
The study on viridans streptococci shows that some of this inflammation may come from a surprising source: bacteria that begin their life in the mouth. When these bacteria travel into the bloodstream and settle inside artery plaques, they can remain hidden for years. At some point, they can awaken and set off a storm of inflammation that ruptures the plaque and causes a heart attack.
This changes how we think about prevention. It means that protecting the heart is not just about lowering cholesterol, exercising, or controlling blood pressure although those remain vital. It also means taking oral health seriously. Brushing, flossing, treating gum disease, and seeing a dentist regularly may have benefits that go beyond preventing cavities. They may also reduce the chances of harmful bacteria entering the bloodstream and ultimately protect the heart.
In short, your mouth and heart are connected in ways that scientists are only beginning to fully understand. A healthy smile might, quite literally, be a step toward a healthier heart.
Reference
Karhunen PJ, Pessi T, Hörkkö S, et al, Viridans streptococcal biofilm evades immune detection and contributes to inflammation and rupture of atherosclerotic plaques. J Am Heart Assoc. 2025;14(17):e041521. doi:10.1161/JAHA.125.041521.