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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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Helicobacter pylori is found in the stomach, which is its optimal habitat, and is considered an important factor in various serious diseases, including stomach cancer. The World Health Organization has identified H. pylori as a causative agent of gastric cancer, as confirmed by animal experiments in rodents. The fact that H. pylori can live in the harsh environment of stomach acid was the greatest hindrance to the discovery of H. pylori. It was not so long ago, in 1983, that it was successfully isolated and cultured. Subsequently, H. pylori eradication therapy was established, and it became possible to control gastric cancer to some extent. However, the mechanism, route, and mode of H. pylori infection still remain unclear. Furthermore, currently, the prevention of first‐episode gastric cancer and control of recurrent gastric cancer are not perfect. One of the reasons for this may be that the status of H. pylori in the oral cavity, which is the entry point for the organism (the beginning of the digestive system: the first route of infection), is still unknown. Therefore, we reviewed the current status of H. pylori infection in the stomach and oral cavity, focusing on (1) the mechanism of infection, (2) pathogenic factors, (3) the actual status of eradication therapy, and (4) control strategies. [ABSTRACT FROM AUTHOR]

In Japan, gastric Helicobacter pylori infection prevalence has markedly decreased with socioeconomic development. We aimed to investigate the prevalence of oral H. pylori in Japanese adults in 2020 by sex, age, sampling site, and medical history. Unstimulated saliva, supragingival biofilm, and tongue coating were obtained from 88 subjects–with no complaints of upper digestive symptoms–attending a dentist's office for dental check-up or disorders. Supragingival biofilm was collected from the upper incisors, lower incisors, upper right molars and lower left molars to analyze the characteristic distribution. Oral H. pylori was detected using nested polymerase chain reaction. Oral H. pylori prevalence did not statistically differ by sex or age. Supragingival biofilm (30.7%) was the most common oral H. pylori niche; it was also detected in 4.5% of saliva and 2.3% of tongue samples. The lower incisor was the most common site among the supragingival biofilm samples, followed by the upper incisors, lower left molars, and upper right molars. Oral H. pylori DNA was frequently detected in patients with a history of gastric H. pylori infection. Oral H. pylori has a characteristic distribution independent of sex and age, suggesting that it is part of the normal microflora in the adult oral cavity. [ABSTRACT FROM AUTHOR]

To evaluate the genetic susceptibility to metabolic disorders induced by high fructose diet, we investigated the metabolic characteristics in 10 strains of inbred mice and found that they were separated into CBA and DBA groups according to the response to high fructose diet. The hepatic mRNA expression of the sterol regulatory element-binding protein-1 (SREBP-1) in CBA/JN was remarkably enhanced by high fructose diet but not in DBA/2N. Similar results were observed in primary hepatocytes after exposure to fructose. The nucleotide sequence at -468 bp from the putative starting point of the SREBP-1c gene was adenine in the DBA group while it was guanine in the CBA group. In hepatocytes from CBA/JN, the activity of CBA-SREBP-1c promoter was significantly increased by 2.4- and 2.2-fold, in response to 30 mm fructose or 10 nm insulin, respectively, whereas the activity of DBA-SREBP-1c promoter responded to insulin but not to fructose. In hepatocytes from DBA/2N, both types of SREBP-1c promoter activities in response to insulin were attenuated. Furthermore, electrophoretic mobility shift assay revealed an unidentified nuclear protein bound to the oligonucleotides made from the region between -453 to -480 bp of the SREBP-1c promoter of CBA/JN but not to the probe from DBA/2N. Thus, in DBA/2N, the reduced mRNA expression of SREBP-1 after fructose refeeding appeared to associate with two independent mechanisms, 1). loss of binding of unidentified proteins to the region between -453 to -480 bp of the SREBP-1c promoter and 2). impaired insulin stimulation of SREBP-1c promoter activity.