Abstract

BackgroundThe etiology of dental caries is multifactorial, but frequent consumption of free sugars, notably sucrose, appears to be a major factor driving the supragingival microbiota in the direction of dysbiosis. Recent 16S rRNA-based studies indicated that caries-associated communities were less diverse than healthy supragingival plaque but still displayed considerable taxonomic diversity between individuals. Metagenomic studies likewise have found that healthy oral sites from different people were broadly similar with respect to gene function, even though there was an extensive individual variation in their taxonomic profiles. That pattern may also extend to dysbiotic communities. In that case, shifts in community-wide protein relative abundance might provide better biomarkers of dysbiosis that can be achieved through taxonomy alone.ResultsIn this study, we used a paired oral microcosm biofilm model of dental caries to investigate differences in community composition and protein relative abundance in the presence and absence of sucrose. This approach provided large quantities of protein, which facilitated deep metaproteomic analysis. Community composition was evaluated using 16S rRNA sequencing and metaproteomic approaches. Although taxonomic diversity was reduced by sucrose pulsing, considerable inter-subject variation in community composition remained. By contrast, functional analysis using the SEED ontology found that sucrose induced changes in protein relative abundance patterns for pathways involving glycolysis, lactate production, aciduricity, and ammonia/glutamate metabolism that were conserved across taxonomically diverse dysbiotic oral microcosm biofilm communities.ConclusionsOur findings support the concept of using function-based changes in protein relative abundance as indicators of dysbiosis. Our microcosm model cannot replicate all aspects of the oral environment, but the deep level of metaproteomic analysis it allows makes it suitable for discovering which proteins are most consistently abundant during dysbiosis. It then may be possible to define biomarkers that could be used to detect at-risk tooth surfaces before the development of overt carious lesions.Electronic supplementary materialThe online version of this article (doi:10.1186/s40168-015-0136-z) contains supplementary material, which is available to authorized users.

Highlights

  • The etiology of dental caries is multifactorial, but frequent consumption of free sugars, notably sucrose, appears to be a major factor driving the supragingival microbiota in the direction of dysbiosis

  • Taxonomic diversity was reduced by sucrose pulsing, considerable inter-subject variation in community composition remained

  • Functional analysis using the SEED ontology found that sucrose induced changes in protein relative abundance patterns for pathways involving glycolysis, lactate production, aciduricity, and ammonia/glutamate metabolism that were conserved across taxonomically diverse dysbiotic oral microcosm biofilm communities

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Summary

Introduction

The etiology of dental caries is multifactorial, but frequent consumption of free sugars, notably sucrose, appears to be a major factor driving the supragingival microbiota in the direction of dysbiosis. The etiology of caries is multifactorial, frequent consumption of foods rich in free sugars, notably sucrose, appears to be one of the major factors driving the microbiota in the direction of dysbiosis, in the case of otherwise healthy children with normal salivary flow [3,4,5]. It is very tolerant of low pH and produces an insoluble extracellular polysaccharide that may sequester acid at tooth surfaces [6] The mechanisms behind those putative virulence factors have been intensively studied in monoculture [7, 8] and recently in simple multi-species consortia [9]. Some strains of oral “non-mutans streptococci” produce and tolerate acid at levels comparable to S. mutans [11, 12], while others show increased arginolytic capabilities, which may act to raise pH within the biofilm matrix [13]

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