Background. When silver diamine fluoride (SDF) is used in conjunction with conservative caries removal in deep carious lesions, the distribution depth of silver is critical for safety and effectiveness. Objective. The purpose of this study is to determine the effect of selected caries removal on silver penetration when 38% SDF is applied to deep carious lesions in permanent teeth. Methods. Extracted permanent teeth with caries extending to the inner third of the dentin were used (N = 18). The periphery of the carious lesion was completely removed to the dentinoenamel junction (DEJ). In group A (n = 9), no further removal of carious tissue was performed, leaving necrotic dentin inner to the DEJ, whereas in group B (n = 9) superficial necrotic dentin was completely removed until leathery, slightly moist, reasonably soft dentin remained. SDF was applied for 3 minutes in both groups. Microcomputer tomography (micro-CT) and field emission scanning electron microscopy coupled with energy-dispersive X-ray spectroscopy (FESEM-EDS) were used to measure mineral density and silver distribution. The silver penetration depth/lesion depth (PD/LD) ratio was calculated for each sample. The Mann–Whitney U test was used to compare differences between the two groups. Results. The micro-CT analysis showed that the PD/LD ratios of group B (1.07–2.29) were marginally greater than those of group A (1.00–1.31). However, a statistically significant difference was not observed (value = 0.5078). When stratified by remaining dentin thickness (RDT), the PD/LD ratios of group B were still greater than those of group A only when RDT was >500 µm. The FESEM-EDS analysis indicated that silver particles precipitated throughout the entire thickness of the carious lesions. Conclusion. Applying SDF on a deep carious lesion and leaving the necrotic dentin pulpally did not affect silver penetration. However, the extent to which silver penetrates the remaining dentin beneath the lesions is dependent on the amount and characteristics of that dentin.

This study aimed to investigate the effects of dental coating materials on Streptococcus mutans biofilm formation. The test materials were PRG Barrier Coat (PRG), BioCoat Ca (BioC), and FluorDental Jelly (FluorJ). Bovine enamel specimens were demineralized to mimic early enamel lesions. The biofilm was developed on a specimen treated with one of the materials by using a modified Robbins device flow-cell system. Scanning electron and fluorescence confocal laser scanning microscopy, viable and total cell counts, and gene expression assessments of the antibiofilm were performed. Ion incorporation was analyzed using a wavelength-dispersive X-ray spectroscopy electron probe microanalyzer. All materials allowed biofilm formation but reduced its volume. FluorJ was the only material that inhibited biofilm accumulation and had a bactericidal effect, revealing 0.66 log CFU in viable cells and 1.23 log copy reduction in total cells compared with the untreated group after 24 h of incubation. The ions released from PRG varied depending on the element. BioC contributed to enamel remineralization by supplying calcium ions while blocking the acid produced from the biofilm. In summary, the dental coating materials physically prevented acid attacks from the biofilm while providing ions to the enamel to improve its mechanical properties.

Applying a saturated potassium iodide (KI) solution immediately after silver diamine fluoride (SDF) application may affect the inhibitory effects of SDF on biofilm formation. This study compared the efficacy of 38% SDF with and without KI on preventing mixed-species biofilm formation on human root dentin surfaces and assessed ion incorporation into root dentin. The biofilms, composed of Streptococcus mutans, Lactobacillus rhamnosus, and Actinomyces naeslundii, were grown on specimen surfaces treated with either SDF or SDF + KI. After 24 h, the biofilms were evaluated using scanning electron microscopy, live/dead staining, adenosine triphosphate (ATP) assays, colony-forming unit (CFU) counts, and quantitative polymerase chain reaction. A Mann–Whitney U test was used to compare the results between the groups. Ion incorporation was assessed using an electron probe microanalyzer. The relative ATP content in the SDF + KI group was significantly higher than that in the SDF group (p < 0.05). However, biofilm morphology and the logarithmic reduction in CFUs and bacterial DNA were comparable across the groups. The SDF + KI treatment resulted in less silver and fluoride ion incorporation than that yielded by SDF alone. The inhibitory effects of SDF and SDF + KI on mixed-species biofilm formation were almost equivalent, although KI application affected the ion incorporation.

This study aimed to assess the antibiofilm effects of dentin desensitizers using a modified Robbins device flow cell system. The test desensitizers were Saforide, Caredyne Shield, and Clinpro White Varnish. Standardized dentin specimens were prepared from human single-rooted premolars, treated with one of the materials, and mounted on the modified Robbins device flow cell system. Streptococcus mutans biofilms were developed for 24 h at 37 °C under anaerobic conditions. Scanning electron microscopy, fluorescence confocal laser scanning microscopy, viable and total cell counts, acid production, and gene expression analyses were performed. A wavelength-dispersive X-ray spectroscopy electron probe microanalyzer was used to analyze the ion incorporations. Clinpro White Varnish showed the greatest inhibition, suggesting its suppression of bacterial adherence and transcription of genes related to biofilm formation. Saforide reduced only the number of viable bacteria, but other results showed no significant difference. The antibiofilm effects of Caredyne Shield were limited. The uptake of ions released from a material into dentin varies depending on the element. Clinpro White Varnish is effective for the short-term treatment of tooth sensitivity due to dentin demineralization. It prioritizes remineralization by supplying calcium and fluoride ions while resisting biofilm formation.