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Study Sheds New Light on Caries Development

New research is pinpointing just how dental caries works.

Even though it’s preventable, early childhood caries (ECC) affects nearly 600 million kids under the age of 6 across the globe. It is reportedly the most common disease affecting the world’s children.1 Diet plays a significant role in caries development due to interactions between sugars and oral bacteria. But the precise process that brings about cavitation is less clear.


It’s long been understood that sugar, metabolized by oral bacteria, lowers pH in the oral cavity. This produces acid that eats away at tooth structure, resulting in demineralization. Streptococcus mutans, seen as the major player in tooth decay, lives with other pathogens in oral biofilm. But the exact nature of how these microbes interact and which of them, aside from S. mutans, contribute to tooth decay has been more ambiguous.


A recent community-based pediatric oral health study conducted by researchers at the University of North Carolina at Chapel Hill and the University of Pennsylvania used a multidisciplinary approach to show that dental caries in childhood is characterized by an imbalance in the oral microbiome. Their work uncovered the complex ways in which certain bacterial community members interact.2

The researchers employed a “multi-omic” strategy in analyzing supragingival biofilm from 416 preschool children. This approach integrates data from multiple “omes,” such as genomes, microbiomes, proteomes, and metabolomes, to gain a more holistic perspective into organism interactions. In this case, they sought to discover whether microorganisms are active contributors to caries or merely interact with pathogens.

They were able to identify three other microbes of interest: Selenomonas sputigena, Prevotella salivae, and Leptotrichia wadei. All of these species can metabolize sugar, produce acid, and are acid tolerant, especially in the presence of S. mutans. Each was examined individually or with S. mutans. Notably, however, it was the mixed culture of S. sputigena and S. mutans that achieved the lowest final pH of 3.9.


The research revealed the previously unrecognized ability of S. sputigena to colonize supragingival tooth surfaces. But while S. sputigena can’t itself cause caries, when co-infected with S. mutans, it can inflict extensive damage.

S. sputigena cells, which have appendages called flagella that allow movement, become immobilized by a sticky matrix exuded by S. mutans. Trapped in place, they create a honeycomb-like structure, encapsulating S. mutans cell clusters. This provides the scaffolding for biofilm growth and acid production on a scale much larger than S. mutans could produce on its own.

The research suggests that this new understanding of the cooperative interaction between S. mutans and S. sputigena may pave the way to better prevention of carious lesions. As researcher Hyun (Michel) Koo, DDS, MS, PhD, a professor in the Department of Orthodontics and divisions of Community Oral Health and Pediatric Dentistry at the University of Pennsylvania School of Dental Medicine puts it, “Disrupting these protective S. sputigena superstructures using specific enzymes or more precise and effective methods of tooth-brushing could be one approach.”3


  1. Uribe SE, Innes N, Maldupa I. The global prevalence of early childhood caries: a systematic review with meta-analysis using the WHO diagnostic criteria. Int J Paediatr Dent. 2021;31:817–830.
  2. University of North Carolina, Chapel Hill, Adams School of Dentistry. Two Schools, Eight Years and 16 Investigators: Community-Based Study Offers Dental Disease Insights.
  3. Reynolds S. Identifying a new contributor to tooth decay.
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