Fusobacterium nucleatum: How a Gum Bacterium May Accelerate Heart Disease

Adapted from research by Jieyu Zhou, Lin Liu, Peiyao Wu, Lei Zhao, and Yafei Wu.

Introduction

Periodontitis, a chronic gum infection, is increasingly linked to serious systemic diseases — including atherosclerosis, the hardening and narrowing of arteries that drives heart attacks and strokes. One oral bacterium, Fusobacterium nucleatum (F. nucleatum), commonly found in periodontal disease, has shown a surprising ability to invade the bloodstream and influence cardiovascular health.

This blog breaks down new research showing how F. nucleatum disrupts the body’s immune response, worsens cholesterol balance, and may contribute to unstable artery plaque.

From the Mouth to the Heart

In healthy gums, bacteria remain localized. But in periodontitis, inflamed tissue allows harmful bacteria like F. nucleatum to enter the bloodstream. Once there, they can attach to the inner lining of blood vessels, cause inflammation, and alter how immune cells behave — key steps in the formation of atherosclerotic plaque.

Researchers have discovered that F. nucleatum can:

• Invade vascular tissues — DNA from the bacterium has been found in the arteries of infected animals.

• Trigger systemic inflammation — raising blood levels of TNF-α, IL-1β, IL-6, C-reactive protein (CRP), and MCP-1, all known drivers of heart disease.

• Alter lipid metabolism — decreasing protective HDL cholesterol and increasing harmful oxidized LDL (ox-LDL).

  
  

Macrophages: The Immune Cells That Go Rogue

A key part of the study focused on macrophages, the immune cells responsible for cleaning up debris in blood vessels. When exposed to F. nucleatum:

• Macrophages shifted into a pro-inflammatory “M1” state rather than the protective “M2” type.

• They engulfed large amounts of cholesterol, turning into foam cells — the hallmark of early atherosclerosis.

• They underwent apoptosis (cell death), which destabilizes plaque and makes it more prone to rupture.

This activity makes artery plaques more vulnerable, raising the risk of acute cardiovascular events like heart attacks.

Disrupting the Arterial Environment

Beyond inflammation, F. nucleatum affects the structural stability of plaques:

• It degrades collagen and fibronectin, key proteins that keep plaque caps strong and less likely to rupture.

• It triggers enzymes called matrix metalloproteinases (MMP-2, MMP-8, MMP-9), which break down the protective extracellular matrix.

• It worsens the lipid environment, tipping the balance toward dangerous cholesterol build-up.

  
  

The Role of MicroRNAs — Emerging Biomarkers

The study also found changes in microRNAs (miRNAs) — small molecules that regulate gene activity and can serve as biomarkers of disease:

• miR-146a and miR-23b levels rose significantly in both blood and arterial tissues after F. nucleatum infection.

• These miRNAs correlated strongly with plaque size and inflammatory burden.

This suggests that miRNAs could one day help detect cardiovascular risk in patients with periodontal disease.

Why This Matters for Patients

These findings highlight the mouth–body connection and reinforce that oral health is directly linked to cardiovascular well-being. For patients:

• Treat gum disease early — routine cleanings, home care, and advanced periodontal therapy reduce bacterial load.

• Ask about salivary or pathogen testing if you’re at risk for cardiovascular disease.

• Control systemic risk factors — diabetes, smoking, and high cholesterol make oral bacteria more dangerous.

For clinicians, this research suggests that periodontal pathogens like F. nucleatum are more than just local irritants; they can act as systemic inflammatory triggers.

Key Takeaways

• F. nucleatum, a common periodontal bacterium, can travel from the mouth to blood vessels and worsen atherosclerosis.

• It promotes chronic inflammation, disrupts cholesterol balance, and destabilizes arterial plaques.

• Oral health screening and periodontal care are vital components of heart disease prevention.