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Kristen Mott is the associate editor for Dental Products Report and Digital Esthetics.
Researchers from the University of Pennsylvania have discovered that a fungus may be contributing to tooth decay in children.
One-third of children have cavities by ages 3 to 5, according to an article in USA Today. Most of these cavities are due to bacteria, such as Streptococcus mutans; however, researchers have recently discovered that a fungus may also be contributing to tooth decay in toddlers.
In previous studies, researchers discovered that Candida albicans, a fungal pathogen, was frequently detected with high numbers of S. mutans in plaque-biolfilms formed on tooth surfaces of toddlers with early childhood caries. They determined that C. albicans took advantage of an enzyme produced by S. mutans. C. albicans does not colonize teeth effectively on its own nor does it co-adhere well with S. mutans unless in the presence of sucrose. C. albicans is also usually absent in plaque-biofilms of healthy children who are not exposed high levels of sugar.
In a new study, a team of researchers from the University of Pennsylvania School of Dental Medicine attempted to pinpoint the surface molecules on the fungus that interact with the enzyme produced by S. mutans and how to block that interaction. The team based its research off of the fact that an enzyme called GftB that is secreted by S. mutans uses sugar from a child’s diet to create glue-like polymers called glucans, which form the core of the extracellular matrix in biofilms. GtfB is capable of binding to the cell surface of C. albicans and produces large amounts of extracellular glucans on the fungal service, providing an enhanced bacterial binding site for S. mutans that promote co-adhesion and mixed-species biofilm formation.
The researchers tested whether mannans in the outer cell wall layer of C. albicans mediated the binding. To do this, they measured the binding strength between various mutant Candida strains and GtfB using biophysical methods. They found that the GtfB enzyme bound more weakly to mutant strains that lacked components of the manna layer than the wild-type Candida. Furthermore, the mutant strains that had impaired binding with GtfB were also mostly unable to form biofilms with S. mutans, resulting in reduced production of the glucan molecules.
To confirm the in vitro observations, the researchers then tested them in vivo using a rat biofilm model. When the rats were infected with both S. mutans and either the wild type or mutant strains of C. albicans, they found that biofilm formation was abundant in the wild type. The biofilm formation was reduced in the rats infected with the mutant strain.
“Using a rodent model of dental caries, we observed that this interaction synergistically enhances the carriage of S. mutants and C. albicans, and the virulence of plaque-biofilms, leading to rampant caries in vivo,” the study states. “The available data show a distinctive cross-kingdom association, which relies on a biochemical interaction mediated by a bacterial exoenzyme (and its product) attached to the fungal service.”
The researchers concluded that enhanced understanding of GtfB-Candida interactions may provide new perspectives for devising effective therapies to disrupt this cross-kingdom relationship and thus reduce the rate of childhood oral disease.
“The unveiled mechanism emphasizes the need to target C. albicans either by blocking the binding of GtfBs to the fungal cell wall or use of topical antifungal agents," the researchers state. "Enhanced understanding of GtfB-Candida interactions may accelerate progress toward devising new and effective therapies to disrupt this cross-kingdom biofilm association with an important childhood oral disease.”
Dr. Paul S. Casamassimo, D.D.S., M.S., director of the American Academy of Pediatric Dentistry’s Pediatric Oral Health Research and Policy Center, says the results of the study help expand dentists’ understanding of the complex interactions in the oral cavity that relate to early childhood caries; however, he notes that the translation of basic research into clinical care is often a slow process.
“It will probably be some time before these findings reach chairside, barring some more momentous revelations or research findings,” Dr. Casamassimo says. “Should this research translate into a useful therapeutic intervention, we might see a drug or other anti-fungal agent added to our anti-caries tools. Such an approach has value for both dentists and physicians who may have access to children earlier. What the public needs to recognize is the rigors of getting some new form of treatment into our care programs. Efficacy, safety, cost and other considerations have to be addressed before an approach that modifies oral organisms is allowed widespread application. Add to that a public skeptical about such approaches as we have seen with GMO foods, immunizations, and to some degree, fluoride. So, the potential impact would be reduction in caries, but I don’t believe we will see that soon, as a lot more clarity is needed followed by further animal and human studies.”
Dr. Casamassimo encourages parents to utilize preventive therapies currently available to reduce the risk of early childhood caries.
“First, a dental home under care of a dentist is critical to access to these therapies and ensuring oral health literacy of a child’s caregivers,” he says. “Preferably, every child should see a dentist by one year of age. Should this current research pan out with an effective therapy, imagine the effect of applying it before ECC begins, at the first dental visit! Second, we need to be sure that children have optimal access to fluoride therapies, beginning with drinking water and fluoride toothpaste, both of which are known to reduce dental caries. A diet low in sugar and sugar-sweetened beverages and regular oral hygiene associated with fluoride toothpaste are also known to have a positive effect on dental caries. These can be monitored and modified by regular dental care for the patient’s better health.”
The full study, “Candida albicans mannans mediate Streptococcus mutans exoenzyme GtfB binding to modulate cross-kingdom biofilm development in vivo,” appeared in the peer-reviewed medical journal PLOS Pathogens.