Streptococcus mutans and Candida albicans are often isolated from plaques associated with early childhood caries. However, there are limited studies examining how these microorganisms interact with one another and how best to manage them. Recent studies have shown that curcumin (CUR), a natural compound, has the potential to independently control both of these microorganisms. The purpose of this study was to investigate how S. mutans and C. albicans respond in mono‐ and dual‐species biofilms challenged with CUR. Quantitative biofilm biomass and viability were first evaluated and supported by live–dead PCR to assess biofilm composition. Confocal laser scanning microscopy (CLSM) was used to evaluate the exopolysaccharide (EPS) content and thickness of the biofilms, and the structure of the biofilms and morphology of the cells were observed by scanning electron microscopy (SEM). Quantitative real‐time PCR (qRT‐PCR) was applied to assess relative gene expression. The 50% minimum biofilm eradication concentration (MBEC50) of CUR against S. mutans and C. albicans was 0.5 mM. The biomass and viability decreased after treatment with CUR both in dual‐species biofilms and in mono‐species biofilm. CUR inhibited S. mutans and C. albicans in both mono‐ and dual‐species biofilms. Streptococcus mutans was more sensitive to CUR in dual‐species biofilm than in mono‐species biofilms, whereas C. albicans was less sensitive in dual‐species biofilms. EPS production was decreased by CUR in both mono‐ and dual‐species biofilms, which coincided with the downregulation of glucosyltransferase and quorum sensing‐related gene expression of S. mutans. In C. albicans, the agglutinin‐like sequence family of C. albicans was also downregulated in dual‐species biofilms. Collectively, these data show the potential benefit of using a natural antimicrobial, CUR, to control caries‐related dual‐species plaque biofilms.

Evidence suggests that small noncoding RNAs (sRNAs) are involved in the complex regulatory networks governing biofilm formation. Few studies have investigated the role of sRNAs in Streptococcus mutans (S. mutans). In the present study, the association between sRNA and biofilm formation in S. mutans was explored. sRNAs that are differentially expressed in the biofilm and planktonic states of this bacterium were identified by quantitative real‐time PCR (qRT‐PCR). Confocal laser scanning microscopy was used to investigate the characteristics of biofilm formation in a standard strain of S. mutans (UA159, ATCC 700610) and ten clinical strains. Bioinformatics analyses were employed to predict and examine potential sRNA regulatory pathways. The results showed that sRNA0426 has a strong positive relationship with dynamic biofilm formation. Moreover, sRNA0426 expression was positively correlated with exopolysaccharide (EPS) production. Bioinformatics analyses showed that sRNA0426 is involved in biofilm formation such as metabolic pathways, especially carbon metabolism. Five target mRNAs (GtfB, GtfC, GtfD, ComE, and CcpA) involved in the synthesis of EPS were selected for further evaluation; the expression levels of three of these mRNAs (GtfB, GtfC, and CcpA) were positively correlated with sRNA0426 expression levels, and the expression level of one (ComE) was negatively correlated. In conclusion, the results suggested that sRNA0426 may play an important and positive role in the biofilm formation of S. mutans and provide novel insight into the S. mutans biofilm regulatory network.

The aim of this study was to identify genetic factors under additive and dominance models that contribute to caries susceptibility, and to investigate into the interactions between these genes. A cross-sectional study was conducted among 1055 adolescents in Foshan, South China. The International Caries Detection and Assessment System (ICDAS) was used to identify caries. Demographic and environmental variables were analyzed. Twenty-three single nucleotide polymorphisms (SNPs) in 14 genes were identified from saliva samples. Regression analysis was used for the evaluation of direct and epistasis of genes under the hypothesis of an additive model and using the minor allele as the reference allele. After the adjustment by environmental factors, the G allele in AMBN (rs13115627) was a protective factor for caries under both additive model (P=0.007; OR=0.728; 95% CI, 0.579-0.916) and dominance model (P=0.021; OR=0.728; 95% CI, 0.556-0.953). No interactions between selected genes met the Bonferroni correction significance cutoff for multiple testing. Our results suggests that gender, one-child family, Cariostat score and Plaque Index have independent protective effects on dental caries. The polymorphisms in AMBN (rs13115627), under both additive and dominance models alters caries susceptibility of Adolescents in South China. No epistatic effect has been found between selected genes.