New breakthroughs on how cavities form—and how to prevent them
Until recent research that originated at the University of Minnesota, most scientists concluded that dental decay was caused by acids from bacteria that broke down sugars on teeth. But, in 2018, an interdisciplinary team of University researchers published a study concluding that oral bacteria also removed phosphate from the mouth, altering the chemistry of saliva and making it a friendly environment for decay-causing bacteria.
Over the next eight years, the team continued to research and publish about possible ways that oral bacteria can be managed over time to improve clinical outcomes. Now it’s published a major paper in the Journal of Medical Microbiology. Studying the bacterium Rothia dentocariosa, they found that it accumulates phosphate when a tooth is demineralizing.
Led by School of Dentistry professor of pediatric dentistry Rob Jones, DDS, PhD, and including University professors Jake Bailey and Beverly Flood, the team has demonstrated that the bacterium can not only liberate inorganic free phosphate after acid generation, but can also internalize the free phosphate from the tooth mineral and store the it as the chemical compound polyphosphate, which helps the bacteria survive, manage nutrient limitation stress and continue to colonize. The study found that attenuating polyphosphate synthesis and storage stopped external phosphate uptake from the demineralized tooth.
A promising element that has therapeutic potential is gallein, an enzymatic inhibitor of the bacterial phosphate-accumulating process. “If bacteria are exposed to gallein, then they can’t uptake the demineralized phosphate that helps them survive, and humans do not possess the enzyme that gallein targets,” Jones said, but added this caution: “Before we proceed any further, we must consider the safety of human gallein exposure, which is currently considered to be low toxicity.”
The study has shown that there is more to the formation of tooth decay than had previously been thought. “Our work points out that the story of tooth decay isn’t just about sugar, acid, fluoride and sticky plaque,” Jones said. “We have to recognize that our diet also may affect how bacteria uptake phosphate from the tooth.” The CDC's National Center for Health Statistics states that dental caries is the most common chronic disease among youth aged six to 19 years old. Tooth decay, however, is preventable and treatable, which is why this research is so important.
Jones foresees that the wealth of findings from this area of study might eventually lead to two distinct paths for future research—with one path seeking a better understanding of the role of polyphosphate in calculus build up and periodontal inflammation, and the other being a creation of more comprehensive models and clinical investigations into the role of phosphate-accumulating bacteria in dental caries. For now, Jones suggests that interested readers can view the data that supports findings of the 2026 study in the searchable Data Repository for University of Minnesota (DRUM).
The Journal of Medical Microbiology is a publication of The Microbiology Society, a not-for-profit publisher and membership charity for scientists interested in microbes, their effects and their practical uses. It has a worldwide membership based in universities, industry, hospitals, research institutes, schools, and other organisations. Find out more at microbiologysociety.org, or email contact [email protected].