The resulting decay can become so severe that treatment frequently requires surgery.
New research by the University of Pennsylvania School of Dental Medicine’s Hyun (Michel) Koo and colleagues suggests that this condition may result from an unhealthy partnership between a bacterium and a fungus.
“Our data will certainly open the way to test agents to prevent this disease and, even more intriguing, the possibility of preventing children from acquiring this infection,” Koo said.
The research was published ahead of print in the journal Infection and Immunity.
Koo is a professor in Penn Dental Medicine’s Department of Orthodontics. His collaborators on the study included the University of Rochester Medical Center’s Megan L. Falsetta, Damian J. Krysan and William H. Bowen, among others.
Koo has spent 15 years studying how microbes construct the biofilms, also known as dental plaque, that have plagued teeth since humans invented agriculture, bringing large quantities of sugar and starch into the diet. Caries are common in Neolithic skeletons but virtually absent from our Paleolithic ancestors.
The bacterium Streptococcus mutans has long been assumed to be the main microbial culprit, but Koo and collaborators, as well as other investigators, noticed that a fungus, Candida albicans, was almost always present in plaque from cases of early childhood caries. S. mutans sticks to the surfaces of teeth by converting sugars to a sticky glue-like material called extracellular polysaccharide. In the mouth, Candida adheres mainly to cheek and tongue but had rarely been seen in dental plaque.
“However, we and others noticed that Candida was very frequently observed in plaque from patients who have early childhood caries,” Koo said. “We were puzzled. Candida usually does not associate with S. mutans, nor does it colonize teeth very effectively.”
The investigators discovered that the “exoenzyme” that S. mutans uses to produce extracellular polysaccharides from sugar also enables Candida to produce a glue-like polymer in the presence of sugar. This polymer, which is formed by the bacterial exoenzyme on the surface of Candida, allows the fungus to adhere to teeth and to bind S. mutans, two abilities it otherwise lacks. Under these circumstances, the fungus contributes the bulk of the plaque.
“The combination of the two organisms led to a greatly enhanced production of the glue-like polymer,” Koo said, “drastically boosting the ability of the bacterium and the fungus to colonize the teeth, increasing the bulk of the biofilms and the density of the infection.”
Because the biofilm has pockets of low pH, this accumulation led to greater levels of acid next to the teeth, dissolving enamel and leading to cavity formation.
The investigators showed that infection by S. mutans and C. albicans together doubled the number of cavities and boosted their severity several fold in rats.
“This represents a truly unique physical interaction where a bacterially-produced product attaches to and functions on the surface of an organism from another kingdom, converting this relatively innocuous fungus, with respect to teeth, into a fierce stimulator of cariogenic biofilm formation,” Koo said.
That observation, Koo noted, supports his hypothesis that early childhood caries in toddlers results from infection by both organisms, along with frequent exposure to sucrose.
A copy of the manuscript is at http://bit.ly/asmtip0314b. The final version of the article is scheduled for the May issue of Infection and Immunity.
The research was supported by the National Science Foundation and the National Institute for Dental and Craniofacial Research.
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