CDA Essentials 2018 • Volume 5 • Issue 2

18 | 2018 | Issue 2 N ews and E vents Severe early childhood caries (S-ECC) is an aggressive form of early childhood caries (ECC) that disproportionately affects Indigenous children in North America. Although the causes of ECC are varied and complex (such as socioeconomic status, nutrition and education), it is not clear why ECC sometimes progresses to its more severe form. A new study examines whether some of the answers can be found in studying the microbial communities that live in the plaque (or biofilms) of Indigenous children, specifically Canadian First Nations and Métis. According to Dr. Robert Schroth, associate professor in the college of dentistry at the University of Manitoba and one of the study’s authors, ECC presents early and progresses rapidly in these populations. “We thought that by looking at the microbial characteristics of children with S-ECC and comparing it to a similar but caries-free group of children, we might be able to account for the aggressive presentation of ECC,” he says. Plaque samples were collected by swabbing available tooth surfaces of children between age 2–4; 30 children with S-ECC and 20 caries-free children. DNA extracted from the plaque samples was sequenced at the 16S rRNA gene, revealing 10 phyla, 95 genera and 280 species. The results showed that the two groups didn’t really differ in terms of the number of species found in the plaque microbial communities, or in terms of species diversity (a measure that accounts for the number of species and their abundance). But researchers found a major difference in the oral microbiomes of children from the S-ECC group compared to their caries-free counterparts: microbes associated with caries were detected in all samples, but many caries-associated species were found in much higher levels in the S-ECC group compared to the caries-free group. Notably, Streptococcus mutans , a well-known significant contributor to dental caries, was three times more abundant in the S-ECC group compared to the caries- free group. “It’s quite shocking to see the marked difference between the two groups and realize how abundant S. mutans can be in some children,” says Dr. Schroth. “In one child, S. mutans accounted for 24% of the oral microbiome.” Distinct microbial communities were also found in caries-free children, where microbes associated with health were found in greater numbers. For example, there was a 5-fold higher abundance of Streptococcus gordonii and 2-fold higher abundance of Streptococcus sanguinis . In theory, Dr. Schroth maintains that the pathogenic and protective species co-exist in a delicate balance within a dynamic microbial community. When changes in the environment favour the more pathogenic species, the population shift leads to caries. “For instance, S. mutans —although it’s not the only driver for caries—can dominate and take over when kids consume too much sugar. The whole ecology of the microbiome changes and shifts to an imbalance where kids are at a higher risk for decay.” He hopes that future research can replicate the study on a larger scale. Other research teams are already looking at this study, and others like it, to develop technologies that potentially change the microbiome by eradicating or suppressing the harmful bacteria to allow less harmful microbes to dominate. “There’s a lot more to learn about the shifting ecology of the mouth,” he says. “This is where the science is starting to lead us.” a To listen to an interview with Dr. Schroth, visit oasisdiscussions.ca/2018/01/22/msc ALL PLAQUES ARE NOTCREATEDEQUAL