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Tooth decay is the single most common chronic childhood disease, surpassing asthma, obesity and diabetes. However, little research on Early Childhood Caries exists, and current practices may not be effective enough. A new study from researchers at UPenn hopes to change that and reduce the prevalence of this preventable oral health epidemic. Continue below to learn about the latest research.
Koo and his fellow researchers conducted a two-part study to get to the bottom of childhood tooth decay.
Early Childhood Caries (ECC), a form of severe primary tooth decay in children between birth and 71 months, effects 23 percent of toddlers in the U.S. alone. But current preventative measures, such as fluoride rinse, operate on the outdated belief that the bacteria S. mutans acts alone in creating a biofilm over the teeth.
Dr. Hyun (Michel) Koo and his team at University of Pennsylvania School of Dental Medicine have discovered that ECC are caused by more than just bacteria. In fact, ECC come from a co-infection of bacteria and the fungus C. albicans, according to the new research.
Koo and his team have taken the first steps in developing an effective therapy to target both fungal and bacterial components of ECC. The new study, published in PLOS Pathogens, reveals specific molecular interactions which form the biofilm.
The two-part study determines if biofilm is created by binding between mannoproteins on the fungal surface and glue-like bacterial exoenzyme secretions. Mannoproteins, which are glycoproteins, protrude from many fungal surfaces and have mannose sugar components.
Performing the first stage using an in-vitro model, the team created multiple groups of biofilms using different types of mutated fungal strains. They then tested the mechanical strength of the biofilm using a custom atomic force microscopy system.
Results from the examination revealed a stark decrease in the mechanical strength of biofilms, which were created using fungal strains with inhibited mannoprotein production in comparison to biofilms created with the unaltered fungus. The mutation was so successful that it caused a three-fold reduction mechanical strength of the biofilm.
Inspired by these promising findings, the team took to phase two of the study to examine the mutation’s effect in-vivo. Studying rats that were infected with ECC-causing bacteria and the same groups of mutated fungi used in phase one, they fed the rats a high sugar diet to create the best environment for biofilms growth. Teeth from each of the rat groups were examined over the course of 30 days using a scanning electron microscope.
The in-vivo model proved to be even more effective in preventing biofilm formation than the in-vitro test. Rats infected with the mutated fungus had drastically less biofilm formation than those infected with the unaltered fungus. Biofilm production was so inhibited by the mutation that the team saw a complete absence of fungus when they performed microbiological analysis.
Koo said there was approximately five times less bacteria in the mutated biofilms than in the normal biofilms. This new research is essential to understanding of cross-kingdom biofilm formation between bacteria and fungi.
“[We hope our research will] provide new perspectives for devising effective therapies to disrupt this cross-kingdom relationship associated with an important childhood oral disease,” the team said in the study.
Going forward, the researchers will build on their recent findings by beginning the search for a topical formulation that targets ECC-causing bacteria and fungi. This research has the potential to considerably preserve the health and integrity of primary teeth in toddlers.