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Objective To explore the anti-caries efficacy of three fluoride compounds at increasing maturation of a microcosm biofilm. Design Microcosm biofilm, obtained from saliva collected from three donors (IRB #1406440799), was grown on enamel samples (n = 18/group) for 24-h (Brain Heart Infusion; 0.2 % sucrose). Then, pH cycling model started. Three maturations were explored (4d, 8d, and 12d). The pH cycling consisted of daily 2 × 5 min treatments (NaF, SnF2, AmF: 287.5 ppm F, and de-ionized water [DIW]), 4 × 10 min remineralization (BHI, no sucrose, pH 7.0), and 3 × 2:15 h demineralization (BHI, 1% sucrose, pH 4.5). We analyzed the enamel (surface microhardness [VHNchange], integrated mineral loss [ΔZ], lesion depth [L]), and the biofilm (viability [log10 CFU/mL], lactic acid production [LDH], and exopolysaccharide [EPS] amount). Data were analyzed using two-way ANOVA (p = 0.05). Results The interaction between tested variables was significant for VHNchange, viability, LDH, EPS (p = 0.0354, p = 0.0001, p Conclusions Biofilm’s maturation may influence the selection of fluoride compounds to achieve an optimum cariostatic effect.

Objective We investigated the residual antibiofilm effects of different concentrations of double antibiotic paste (DAP) applied on radicular dentin for 1 or 4 weeks. Design Dentin samples were prepared (n = 120), sterilized and pretreated for 1 or 4 weeks with the clinically used concentration of DAP (500 mg/mL), low concentrations of DAP (1, 5 or 50 mg/mL) loaded into a methylcellulose system, calcium hydroxide (Ca(OH)2), or placebo paste. After the assigned treatment time, treatment pastes were rinsed off and the samples were kept independently in phosphate buffered saline for 3 weeks. Pretreated dentin samples were then inoculated with Enterococcus faecalis and bacterial biofilms were allowed to grow for an additional 3 weeks. Biofilms were then retrieved from dentin using biofilm disruption assays, diluted, spiral plated, and quantified. Fisher’s Exact and Wilcoxon rank sum tests were used for statistical comparisons (α=0.05). Results Dentin pretreatment for 4 weeks with 5, 50 or 500 mg/mL of DAP demonstrated significantly higher residual antibiofilm effects and complete eradication of E. faecalis biofilms in comparison to a 1 week pretreatment with similar concentrations. However, dentin pretreated with 1 mg/mL of DAP or Ca(OH)2 did not provide a substantial residual antibiofilm effect regardless of the application time. Conclusions Dentin pretreatment with 5 mg/mL of DAP or higher for 4 weeks induced significantly higher residual antibiofilm effects in comparison to a 1 week pretreatment with the same concentrations.

Several epidemiology studies have reported a positive relationship between smoking and dental caries. Nicotine, an alkaloid component of tobacco, has been demonstrated to stimulate biofilm formation and metabolic activity of Streptococcus mutans, one of the most important pathogens of dental caries. The first aim of the present study was to explore the possible mechanisms leading to increased biofilm by nicotine treatment from three aspects, extracellular polysaccharides (EPS) synthesis, glucosyltransferase (Gtf) synthesis and glucan-binding protein (Gbp) synthesis at the mRNA and protein levels. The second aim was to investigate how nicotine affects S. mutans virulence, particular in lactate dehydrogenase (LDH) activity. Confocal laser scanning microscopy results demonstrated that both biofilm bacterial cell numbers and EPS were increased by nicotine. Gtf and GbpA protein expression of S. mutans planktonic cells were upregulated while GbpB protein expression of biofilm cells were downregulated by nicotine. The mRNA expression trends of those genes were mostly consistent with results on protein level but not statistically significant, and gtfD and gbpD of biofilm cells were inhibited. Nicotine was not directly involved in S. mutans LDH activity. However, since it increases the total number of bacterial cells in biofilm, the overall LDH activity of S. mutans biofilm is increased. In conclusion, nicotine stimulates S. mutans planktonic cell Gtf and Gbp expression. This leads to more planktonic cells attaching to the dental biofilm. Increased cell numbers within biofilm results in higher overall LDH activity. This contributes to caries development in smokers.

To assess the effects of smokeless tobacco on the secretory immune system and dental caries, we examined users of smokeless tobacco and non-tobacco users. There were no significant differences in the prevalence of DMFS between users and non-users. There was significantly more salivary IgA, IgA2 and J-chain in users. Levels of salivary lysozyme and lactoferrin were significantly lower in users than controls. Because there was no difference in levels of secretory component in relation to the increased IgA levels of smokeless tobacco users, this suggests an effect of smokeless tobacco on secretory epithelial cells responsible for synthesis of secretory component, lysozyme and lactoferrin, and for the packaging of secretory component on IgA. There were only slight differences in salivary or serum antibody levels to Streptococcus mutans. These findings indicate that although smokeless tobacco has a significant influence on the synthesis of secretory IgA, the numbers of DMFS were similar between smokeless tobacco users and controls.

The use of a mouthrinse of bovine milk containing antibodies to Streptoccus mutans resulted in an initial reduction in the numbers of recoverable Strep. mutans in a group of 9 individuals. Ten volunteers who used control bovine milk that contained no antibody activity to Strep. mutans had variable levels of plaque Strep. mutans . In addition, after culture on Mitis Salivarius and Gold's agar, the plaque Strep. mutans from subjects who used the immune bovine milk rinse formed smaller colonies than those from pre-treatment plaque and from all plaque samples of subjects who used the control rinse.