Microbial Risk Markers for Childhood Caries in Pediatricians’ Offices

Kanasi, Eleni; Johansson, Ingegerd; Lu, Shulin C.; Kressin, Nancy R.; Nunn, Martha E.; Kent, Ralph; Tanner, A. C. R.

doi:10.1177/0022034509360010

Cited by 95 publications

(96 citation statements)

References 32 publications

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“…A number of factors precluded direct comparisons between the two studies. First, childhood caries and adult caries might differ in etiology (Becker et al, 2002;Li et al, 2005;Kanasi et al, 2010;Soncini et al, 2010). Second, the previous study targeted V3 variable region with an average read length of 145 bp and the average number of reads per sample at 1914; in contrast, results in our study were based on 400-bp-long reads on V4-V5 region and on average 9458 reads per sample.…”

Section: Saliva Microbiomes Distinguish Caries-active Hosts F Yang Et Almentioning

confidence: 75%

“…First, the depth and breadth of sampling for oral microbiota have been insufficient. It was limited to a few dozen sequences using clone-based methods or only a partial, biased and a prior determined list of microorganisms in DNA chip (Corby et al, 2005;Aas et al, 2008;Kanasi et al, 2010). Second, most high-throughput sequencing-based surveys are on normal individuals (Keijser et al, 2008;Lazarevic et al, 2009;Zaura et al, 2009), and few studies have interrogated the oral microbiota associated with caries (Ling et al, 2010).…”

Section: Saliva Microbiomes Distinguish Caries-active Hosts F Yang Et Almentioning

confidence: 99%

“…More recently, 'Ecological Plaque Hypothesis' (Marsh, 1994(Marsh, , 2003(Marsh, , 2006a emerged and proposed that caries resulted from a populational balance shift of the resident microbiota, driven by environmental changes in oral conditions. Culture-independent methods for bacterial identification and enumeration such as array-based DNA hybridization (Corby et al, 2005;Aas et al, 2008;Kanasi et al, 2010) or Sanger sequencing of 16S rRNA gene clones have revealed a wide array of bacteria correlated with caries progression.…”

Section: Introductionmentioning

confidence: 99%

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Saliva microbiomes distinguish caries-active from healthy human populations

et al. 2011

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The etiology of dental caries remains elusive because of our limited understanding of the complex oral microbiomes. The current methodologies have been limited by insufficient depth and breadth of microbial sampling, paucity of data for diseased hosts particularly at the population level, inconsistency of sampled sites and the inability to distinguish the underlying microbial factors. By cross-validating 16S rRNA gene amplicon-based and whole-genome-based deep-sequencing technologies, we report the most in-depth, comprehensive and collaborated view to date of the adult saliva microbiomes in pilot populations of 19 caries-active and 26 healthy human hosts. We found that: first, saliva microbiomes in human population were featured by a vast phylogenetic diversity yet a minimal organismal core; second, caries microbiomes were significantly more variable in community structure whereas the healthy ones were relatively conserved; third, abundance changes of certain taxa such as overabundance of Prevotella Genus distinguished caries microbiota from healthy ones, and furthermore, caries-active and normal individuals carried different arrays of Prevotella species; and finally, no 'caries-specific' operational taxonomic units (OTUs) were detected, yet 147 OTUs were 'caries associated', that is, differentially distributed yet present in both healthy and caries-active populations. These findings underscored the necessity of species-and strain-level resolution for caries prognosis, and were consistent with the ecological hypothesis where the shifts in community structure, instead of the presence or absence of particular groups of microbes, underlie the cariogenesis.

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Section: Saliva Microbiomes Distinguish Caries-active Hosts F Yang Et Almentioning

confidence: 75%

Section: Saliva Microbiomes Distinguish Caries-active Hosts F Yang Et Almentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Saliva microbiomes distinguish caries-active from healthy human populations

et al. 2011

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“…Children in this study had not used antibiotics within the last 3 months, and the parent or guardian consented to the child’s clinical examination and microbial sampling. The children’s primary caregivers completed a survey that incorporated caries risk factors including: demographics, socioeconomic status, dental history and dietary habits [18,19]. The study was performed in full accordance with ethical principles including the World Medical Association Declaration of Helsinki and the study design, protocol, and informed consent were approved by the Institutional Review Board at the Forsyth Institute.…”

Section: Methodsmentioning

confidence: 99%

Functional profiles of coronal and dentin caries in children

Kressirer

Chen

Harriman³

et al. 2018

Journal of Oral Microbiology

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Background: Dental caries results from a dysbiosis of tooth-associated biofilms and frequently extends through enamel into dentin which has a different structure and composition.Objective: To evaluate the metatranscriptome of caries to determine the metabolic potential of caries communities compared with health.Design: Samples from children, caries-free (CF: n = 4) or with coronal (CC: n = 5) or dentin (DC: n = 5) caries were examined for gene expression potential. Functional profiling was performed using HUMAnN2 (HMP Unified Metabolic Analysis Network).Results: There was increased gene expression diversity in DC compared with CC and CF. Genes in CF included alcohol dehydrogenase from Neisseria sicca, methylenetetrahydrofolate reductase from Streptococcus sanguinis and choline kinase from streptococci. Genes in CC mapped mainly to Streptococcus mutans. Arginine deiminase in DC mapped to S. sanguinis and Actinomyces naeslundii. Glycerol kinase genes mapped to S. sanguinis in all groups whereas glycerol kinase in DC were from Rothia, Prevotella and streptococci. Uracil-DNA glycosylase in DC mapped to Prevotella denticola and Actinomyces. Repressor LexA in DC mapped to Scardovia wiggsiae, Dialister invisus and Veillonella parvula.Conclusions: Functional profiling revealed enzyme activities in both caries and caries-free communities and clarified marked differences between coronal and dentin caries in bacterial composition and potential gene expression.

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“…(2)(3)(4). These bacterial species are characterized by common virulence factors, including the adhesion and colonization ability of teeth surfaces by sucroseindependent and sucrose-dependent mechanisms (6)(7)(8).…”

mentioning

confidence: 99%

Streptococcus Mutans and Streptococcus Sobrinus are Able to Adhere and Invade Human Gingival Fibroblast Cell Line

Berlutti

Catizone

Ricci

et al. 2010

Int J Immunopathol Pharmacol

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Streptococcus mutans and Streptococcus sobrinus, the principal etiologic agents of caries decay of teeth, are generally acquired in oral cavity at the moment of tooth eruption. However, as S. mutans has been detected in oral cavity of predentate children, the eruption of teeth seems not to be a necessary prerequisite, suggesting that this species may be not confined to dental plaque. Here, we evaluate the ability of S. mutans and S. sobrinus in planktonic and biofilm lifestyle to adhere, invade and survive within human gingival fibroblast (HGF-l) cells. Planktonic and biofilm streptococci adhered and invaded host cells to different extents, showing higher efficiencies of biofilm than planktonic counterparts. Moreover, planktonic and biofilm streptococci showed the same percentage of survival within host cells. Transmission electron and confocal microscopy observations confirmed intracellular localization of planktonic and biofilm bacteria. The adhesion, invasion and survival abilities within human oral cells may be considered S. mutans and S. sobrinus virulence mechanisms to colonize and persist in the oral cavity in the absence of tooth surface.Streptococcus mutans and S. sobrinus belonging to the phylogenetic mutans group (1) are considered the principal etiologic agents of caries decay of teeth . (2-4). These bacterial species are characterized by common virulence factors, including the adhesion and colonization ability of teeth surfaces by sucroseindependent and sucrose-dependent mechanisms (6-8). Sucrose availability induces the up-expression of biofilm-associated genes thus promoting biofilm development on tooth surfaces (9-10). The biofilm lifestyle increases streptococcal resistance against antimicrobial substances allowing the survival and persistence in oral cavity (11)(12).Studies on timing of acquisition have shown that S. mutans and S. sobrinus can be acquired at any time from 6 months to over 3 years of age, corresponding to the eruption of teeth as they require a nonshedding surface to adhere, colonize and multiply (4-5, 13). However, tooth eruption seems not to be a necessary prerequisite for mutans streptococci

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Microbial Risk Markers for Childhood Caries in Pediatricians’ Offices

Cited by 95 publications

References 32 publications

Saliva microbiomes distinguish caries-active from healthy human populations

Saliva microbiomes distinguish caries-active from healthy human populations

Functional profiles of coronal and dentin caries in children

Streptococcus Mutans and Streptococcus Sobrinus are Able to Adhere and Invade Human Gingival Fibroblast Cell Line

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