Comparison of modified bass, rolling, and current toothbrushing techniques for the efficacy of plaque control - A randomized trial.

OBJECTS: This study aimed to compare the effectiveness of the modified Bass technique (MBT), the Rolling technique and the current brushing technique(CBT) for plaque removal and to assess the acceptability of the first two brushing techniques. METHODS: 180 participants were randomly assigned to PowerPoint-based training with a demonstration of either the MBT plus basic toothbrushing, the Rolling technique plus basic toothbrushing, or the basics of tooth brushing alone (CBT group). The participants were asked to brush their teeth based on what they had learned. The Turesky modification of the plaque index of Quigley & Hein (TQHI) and marginal plaque index (MPI) were assessed at the baseline examination and after 1, 2, and 4 weeks. Brushing sequence, brushing technique, and brushing duration were measured immediately after training and at each subsequent interview. RESULTS: After instruction (0 weeks), all groups showed a significant decrease in TQHI and MPI (p<0.001), followed by a gradual increase. There was no difference in the overall effect of plaque removal between the groups(p>0.05). MBT had a better effect on cervical plaque removal than the Rolling technique after 4 weeks (p<0.05). More participants in the Rolling group were able to fully master the brushing technique during the whole four weeks. CONCLUSIONS: There was no difference in the overall plaque removal effect among the three groups. The MBT was most effective in removing plaque at the cervical margin but more difficult to master. CLINICAL SIGNIFICANCE STATEMENT: This study was conducted to compare the teaching and plaque removal effects of two brushing techniques and to understand which method is better for plaque removal as well as adoption. This study provides a reference and basis for future clinical work and oral hygiene education.

Streptococcus mutans membrane vesicles inhibit the biofilm formation of Streptococcus gordonii and Streptococcus sanguinis.

Streptococcus mutans, whose main virulence factor is glucosyltransferase (Gtf), has a substantial impact on the development of dental caries. S. mutans membrane vesicles (MVs), which are rich in Gtfs, have been shown to affect biofilm formation of other microorganisms. Streptococcus gordonii and Streptococcus sanguinis are initial colonizers of tooth surfaces, which provide attachment sites for subsequent microorganisms and are crucial in the development of oral biofilms. S. mutans and S. gordonii, as well as S. mutans and S. sanguinis, have a complex competitive and cooperative relationship, but it is unclear whether S. mutans MVs play a role in these interspecific interactions. Therefore, we co-cultured S. mutans MVs, having or lacking Gtfs, with S. gordonii and S. sanguinis. Our results showed that S. mutans MVs inhibited biofilm formation of S. gordonii and S. sanguinis but did not affect their planktonic growth; contrastingly, S. mutans ΔgtfBC mutant MVs had little effect on both their growth and biofilm formation. Additionally, there were fewer and more dispersed bacteria in the biofilms of the S. mutans MV-treated group than that in the control group. Furthermore, the expression levels of the biofilm-related virulence factors GtfG, GtfP, and SpxB in S. gordonii and S. sanguinis were significantly downregulated in response to S. mutans MVs. In conclusion, the results of our study showed that S. mutans MVs inhibited biofilm formation of S. gordonii and S. sanguinis, revealing an important role for MVs in interspecific interactions.

Streptococcus Mutans Membrane Vesicles Enhance Candida albicans Pathogenicity and Carbohydrate Metabolism.

Streptococcus mutans and Candida albicans, as the most common bacterium and fungus in the oral cavity respectively, are considered microbiological risk markers of early childhood caries. S. mutans membrane vesicles (MVs) contain virulence proteins, which play roles in biofilm formation and disease progression. Our previous research found that S. mutans MVs harboring glucosyltransferases augment C. albicans biofilm formation by increasing exopolysaccharide production, but the specific impact of S. mutans MVs on C. albicans virulence and pathogenicity is still unknown. In the present study, we developed C. albicans biofilms on the surface of cover glass, hydroxyapatite discs and bovine dentin specimens. The results showed that C. albicans can better adhere to the tooth surface with the effect of S. mutans MVs. Meanwhile, we employed C. albicans biofilm-bovine dentin model to evaluate the influence of S. mutans MVs on C. albicans biofilm cariogenicity. In the S. mutans MV-treated group, the bovine dentin surface hardness loss was significantly increased and the surface morphology showed more dentin tubule exposure and broken dentin tubules. Subsequently, integrative proteomic and metabolomic approaches were used to identify the differentially expressed proteins and metabolites of C. albicans when cocultured with S. mutans MVs. The combination of proteomics and metabolomics analysis indicated that significantly regulated proteins and metabolites were involved in amino acid and carbohydrate metabolism. In summary, the results of the present study proved that S. mutans MVs increase bovine dentin demineralization provoked by C. albicans biofilms and enhance the protein and metabolite expression of C. albicans related to carbohydrate metabolism.

Small molecule targeting amyloid fibrils inhibits Streptococcus mutans biofilm formation.

Amyloid fibrils are important scaffold in bacterial biofilms. Streptococcus mutans is an established cariogenic bacteria dwelling within biofilms, and C123 segment of P1 protein is known to form amyloid fibrils in S. mutans biofilms, among which C3 segment could serve as a promising anti-amyloid target due to its critical role in C123-P1 interactions. Recently, small molecules have been found to successfully inhibit biofilms by targeting amyloid fibrils. Thus, our study aimed to screen small molecules targeting C3 segment with the capacity to influence amyloid fibrils and S. mutans biofilms. In silico screening was utilized to discover promising small molecules, which were evaluated for their effects on bacterial cells and amyloid fibrils. We selected 99 small molecules and enrolled 55 small molecules named D1-D55 for crystal violet staining. Notably, D25 selectively inhibit S. mutans biofilms but had no significant influence on biofilms formed by Streptococcus gordonii and Streptococcus sanguinis, and D25 showed no bactericidal effects and low cytotoxicity. In addition, amyloid fibrils in free-floating bacteria, biofilms and purified C123 were quantified with ThT assays, and the differences were not statistically significant in the presence or absence of D25. Morphological changes of amyloid fibrils were visualized with TEM images, where amorphous aggregates were obvious coupled with long and atypical amyloid fibrils. Moreover, amyloid-related genes were upregulated in response to D25. In conclusion, D25 is a promising antimicrobial agent with the capacity to influence amyloid fibrils and inhibit S. mutans biofilms.