Disrupting the chemical messages that oral bacteria use to coordinate growth may help prevent disease by keeping plaque communities in a healthier state.
Like all living things, bacteria adapt in order to survive. Over time, many have become resistant to widely used antibiotics and disinfectants, creating growing challenges for healthcare and sanitation. At the same time, a large portion of bacteria are helpful and play essential roles in human health.
This raises an important question: could shifting the behavior of bacteria inside the body help prevent disease and improve health outcomes?
The hidden language of oral microbes
Bacteria communicate constantly. Hundreds of species in the human mouth send and receive chemical messages in a process called quorum sensing. Many rely on signaling molecules known as N-acyl homoserine lactones (AHLs) to exchange information.
Researchers in the College of Biological Sciences and the School of Dentistry at the University of Minnesota set out to explore how oral bacteria use these signals and whether this communication could be altered to stop plaque from forming and support a healthier oral microbiome. Their findings, published in the journal npj Biofilms and Microbiomes, point to possibilities that could reshape future medical treatments.
What the researchers discovered about AHL signals
The team found:
- In dental plaque, bacteria release AHLs in oxygen-rich areas (such as above the gumline), and these chemical messages can still be detected by bacteria living in low-oxygen zones (beneath the gumline).
- When researchers used specialized enzymes called lactonases to remove AHL signals, the shift favored bacterial species that are linked to better oral health.
- These findings indicate that certain enzymes could be used to reshape the plaque community and help maintain a stable, health-supporting microbiome.
How oxygen changes the battle between good and bad bacteria
“Dental plaque develops in a sequence, much like a forest ecosystem,” said Mikael Elias, associate professor in the College of Biological Sciences and senior author of the study. “Pioneer species like Streptococcus and Actinomyces are the initial settlers in simple communities — they’re generally harmless and associated with good oral health. Increasingly diverse late colonizers include the ‘red complex’ bacteria like Porphyromonas gingivalis, which are strongly linked to periodontal disease. By disrupting the chemical signals bacteria use to communicate, one could manipulate the plaque community to remain or return to its health-associated stage.”
“What’s particularly striking is how oxygen availability changes everything,” said lead author Rakesh Sikdar. “When we blocked AHL signaling in aerobic conditions, we saw more health-associated bacteria. But when we added AHLs under anaerobic conditions, we promoted the growth of disease-associated late colonizers. Quorum sensing may play very different roles above and below the gumline, which has major implications for how we approach treatment of periodontal diseases.”
Toward new therapies that guide, not destroy, the microbiome
The next step for researchers is to study how bacterial messaging occurs in different parts of the mouth, and in patients with varying stages of periodontal disease.
“Understanding how bacterial communities communicate and organize themselves may ultimately give us new tools to prevent periodontal disease—not by waging war on all oral bacteria, but by strategically maintaining a healthy microbial balance,” said Elias.
The team hopes this method can be the foundation for therapeutics that can be used throughout the body, where microbiome dysbiosis causes health problems, and is linked to certain types of cancer.
Reference: “N-acyl homoserine lactone signaling modulates bacterial community associated with human dental plaque” by Rakesh Sikdar, Mai V. Beauclaire, Mark C. Herzberg, Bruno P. Lima and Mikael H. Elias, 17 November 2025, npj Biofilms and Microbiomes.
DOI: 10.1038/s41522-025-00846-z
Funding was provided by the National Institutes of Health.
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