What if brushing and flossing one day became unnecessary—not because oral hygiene was unimportant, but because our mouths could take care of themselves?
That’s the vision Wenjun Zhang, a chemical and biomolecular engineering professor at UC Berkeley, is working toward.
Her research focuses on turning the bacteria already living in our mouths into allies against tooth decay.
Our mouths contain hundreds of species of bacteria, together forming what’s known as the oral microbiome. These bacteria build communities on our teeth, known as plaque.
For decades, scientists have studied which species contribute to cavities, pointing the finger at acid-producing microbes like Streptococcus mutans.
But Zhang and her team emphasize that not all bacteria—or even all strains of the same species—behave the same way. Some strains are harmful, while others can be neutral or even beneficial.
Instead of focusing only on bacterial species, Zhang studies the metagenome—the combined DNA of all bacteria in the mouth. By scanning DNA sequences, her team looks for clusters of genes tied to cavity development.
In a recent paper published in the Proceedings of the National Academy of Sciences, Zhang’s group identified one such gene cluster that produces sticky molecules, helping bacteria form strong biofilms on teeth.
This gene cluster wasn’t found in every strain of harmful bacteria but appeared in some strains of S. mutans and other cavity-causing microbes. Interestingly, Zhang sees an opportunity: what if this sticky gene cluster could be added to “good” bacteria?
By boosting their ability to cling to teeth, the beneficial bacteria could outcompete their harmful counterparts, reshaping the balance of the oral microbiome.
“Particular strains belonging to the same species can be a pathogen, a neutral neighbor, or even a probiotic,” Zhang explained. “If we can give the good bacteria the tools to form stronger biofilms, they might push out the bad ones.”
The sticky molecules identified, which Zhang’s group has nicknamed mutanoclumpins, are part of a specialized metabolic system.
These systems are like extra toolkits bacteria carry—collections of genes that aren’t required for survival but can give them a competitive edge. In soil bacteria, such systems have led to the discovery of powerful antibiotics. In the mouth, Zhang argues, these specialized pathways may be just as important for health and disease.
Her team has already identified other gene clusters in oral bacteria that produce antibiotics or different sticky molecules. The discovery of mutanoclumpins adds to a growing picture of how specialized metabolites shape the oral microbiome.
One candidate for probiotic development is Streptococcus salivarius, a species known to support oral health and already marketed in probiotic lozenges. But it struggles to form biofilms on teeth, limiting its benefits. Zhang proposes equipping S. salivarius with biofilm-enhancing molecules to see if it could work more effectively as a cavity-preventing probiotic.
The long-term goal, Zhang says, is to build a comprehensive map of specialized metabolites in the oral microbiome. Such a map could guide strategies to block harmful molecules and enhance helpful ones, ultimately reducing cavities and promoting oral health.
For now, the best defense remains the toothbrush. “The best way to remove biofilm is still brushing,” said Berkeley graduate student McKenna Yao, a co-first author on the study. “But we’re just beginning to understand the complexity of the oral microbiome, and one day there may be better ways to manage it.”
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