Objectives: In the present in situ/ex vivo study the impact of tannic acid on the erosion-protective properties of the enamel pellicle was tested. Additionally, the antiadherent and antibacterial effects of tannic acid were evaluated. Methods: The pellicle was formed in situ on bovine enamel samples fixed on individual splints worn by 6 subjects. Following 1 min of pellicle formation the volunteers rinsed for 10 min with tannic acid. After further oral exposure for 19 min, 109 min, and 8 h overnight, respectively, slabs were incubated in HCl ex vivo (pH 2.0, 2.3, 3.0) over 120 s. Subsequently, kinetics of calcium and phosphate release were measured photometrically. Samples after a 1-min fluoride mouth rinse as well as enamel samples with and without a 30-min in situ pellicle served as controls. Antiadherent effects were evaluated after a 1-min rinse with tannic acid and oral exposure of the slabs overnight. DAPI (4 ′ ,6-diamidino2-phenylindole) combined with concanavalin A staining and live/dead staining was used for fluorescence microscopic visualization and quantification of adherent bacteria and glucans. Modification of the pellicle’s ultrastructure by tannic acid was evaluated by transmission electron microscopy (TEM). Results: Tannic acid significantly improved the erosion-protective properties of the pellicle in a pH-dependent manner. Bacterial adherence and glucan formation on enamel were significantly reduced after rinses with tannic acid as investigated by fluorescence microscopy. TEM imaging indicated that rinsing with tannic acid yielded a sustainable modification of the pellicle; it was distinctly more electron dense. Conclusion: Tannic acid offers an effective and sustainable approach for the prevention of caries and erosion.

Aim: The study aimed to investigate the effect of a customary fluoride solution, containing sodium fluoride and amine fluoride, on initial biofilm formation on enamel and dentin in situ compared directly to chlorhexidine. Methods: Bovine enamel and dentin specimens were mounted on maxillary splints carried by 9 subjects. After 1 min of pellicle formation, rinses with tap water (control), chlorhexidine (meridol med CHX 0.2%, GABA) and a fluoride mouthrinse (elmex, GABA) were performed for 1 min. Subsequently, the slabs were carried for another 8 h. The adherent bacteria were determined by DAPI staining, live-dead staining and determination of colony-forming units after desorption; glucan formation was visualized with concanavalin A. Additionally, energy-dispersive X-ray spectroscopy (EDX) analysis of the in situ biofilm layers was conducted, and contact angle measurements were performed. Statistical evaluation was performed by means of the Kruskal-Wallis test followed by the Mann-Whitney U test (p < 0.05). Results: In the control group, significantly higher amounts of adherent bacteria were detected on dentin (4.8 x 10⁶ ± 5.4 x 10⁶ bacteria/cm²) than on enamel (1.2 x 10⁶ ± 1.5 x 10⁶ bacteria/cm² , DAPI). Chlorhexidine significantly reduced the amount of adherent bacteria (dentin: 2.8 x 10⁵ ± 3.4 x 10⁵ bacteria/cm² ; enamel: 4.2 x 10⁵ ± 8.7 x 10⁵ bacteria/cm²). Rinses with the fluoride solution also significantly reduced bacterial adherence to dentin (8.1 x 10⁵ ± 1.5 x 10⁶ bacteria/cm²). Fluoride could not be detected by EDX analysis of the biofilms. Fluoride mouthrinsing did not influence the wettability of the pellicle-covered enamel surface. Conclusion: In addition to the reduction of demineralization and antibacterial effects, fluorides inhibit initial biofilm formation on dental hard tissues considerably, especially on dentin.

Objective: The aim of this study was to investigate the direct and indirect influence of fluoridated toothpastes and fluoride-free toothpaste with hydroxyapatite (HAP) as active ingredient on initial bacterial colonization on enamel in situ. Methods: For this clinical-experimental pilot study, eight subjects were instructed to brush their teeth with three different toothpastes (Elmex®: 1400 ppm AmF, Meridol®: 1400 ppm AmF +SnF2, Karex®: HAP), using each for two consecutive days. As a control, brushing without toothpaste was performed. To evaluate bacterial colonization, subject wore splints with buccally placed bovine enamel platelets overnight. Two modes were tested. In a first pass (regimen A), the splints were inserted after toothbrushing to examine the indirect effects of the dentifrices. In order to investigate the direct effects, the specimens were brushed in situ in a second pass (regimen B). Biofilm formation was visualized and quantified using fluorescence microscopy (DAPI and BacLight) and transmission electron microscopy (TEM). Results: For brushing regimen A (indirect effect of dentifrices), no statistical differences were detected between any of the tested dentifrices or the control. Likewise, no statistically significant differences were recorded for brushing regimen B (direct effect of dentifrices). Furthermore, no differences between the different brushing techniques were determined with regard to the ultrastructure of the overnight biofilm. Conclusion: Within the limitations of the present pilot study, it can be concluded that in patients with good oral hygiene, dentifrices and their chemical composition have no statistically significant effect on the initial bacterial colonization of enamel platelets in situ, irrespectively of the mode of application.