Genes encoding fluoride transporters have been identified in bacterial and archaeal species. The genome sequence of the cariogenic Streptococcus mutans bacteria suggests the presence of a putative fluoride transporter, which is referred to as a chloride channel permease. Two homologues of this gene (GenBank locus tags SMU\_1290c and SMU\_1289c) reside in tandem in the genome of S. mutans . The aim of this study was to determine whether the chloride channel permeases contribute to fluoride resistance. We constructed SMU\_1290c- and SMU\_1289c-knockout S. mutans UA159 strains. We also constructed a double-knockout strain lacking both genes. SMU\_1290c or SMU\_1289c was transformed into a fluoride transporter- disrupted Escherichia coli strain. All bacterial strains were cultured under appropriate conditions with or without sodium fluoride, and fluoride resistance was evaluated. All three gene-knockout S. mutans strains showed lower resistance to sodium fluoride than did the wild-type strain. No significant changes in resistance to other sodium halides were recognized between the wild-type and double-knockout strains. Both SMU\_1290c and SMU\_1289c transformation rescued fluoride transporter-disrupted E. coli cell from fluoride toxicity. We conclude that the chloride channel permeases contribute to fluoride resistance in S. mutans .

Although a significant association between periodontal disease and atherosclerotic cardiovascular disease has been reported, their cause-to-effect relationship remains controversial. This randomized controlled clinical trial aimed to investigate the effect of advanced self-care on atherosclerotic cardiovascular disease-related vascular function markers flow-mediated brachial artery dilatation (FMD) and serum asymmetric dimethylarginine (ADMA) level in patients with early-stage periodontal disease. The study was designed as a parallel group, 3-month follow-up, open-label, randomized controlled trial. The control group received standard care for periodontal diseases, whereas the test group additionally applied disinfectant using a custom-fabricated prescription tray for advanced self-care twice a day. Overall, 110 patients provided data for FMD and serum ADMA level. No significant improvements in FMD were observed in the control (mean increase, −0.1%; 95% confidence interval [CI], −1.0–0.8; P = 0.805) or test (mean increase, −0.3%; 95% CI, −1.1–0.4; P = 0.398) group. No significant changes in serum ADMA levels were observed (mean reduction, 0.01 μmol/L; 95% CI, −0.00–0.02; P = 0.366 and mean reduction, 0.00 μmol/L; 95% CI, −0.01–0.01; P = 0.349, respectively). No significant between-group differences were found in FMD (mean difference, −0.2%; 95% CI, −1.4–0.9; p = 0.708) or serum ADMA levels (mean difference, 0.01 nmol/L; 95% CI, −0.00–0.03; p = 0.122). Significant improvements in the average probing pocket depth were observed in the control and test groups. The bleeding on probing score in the test group was significantly reduced, while that in the control group was reduced, although not significantly. Periodontal care for a 3-month duration did not provide better endothelial function although improvements of periodontal status in patients with early-stage periodontal diseases. This trial is registered in UMIN Clinical Trials Registry (www.umin.ac.jp/ctr/; ID: UMIN000023395).

Candida albicans (C. albicans) and Streptococcus mutans (S. mutans) are frequently detected in the plaque biofilms of children with early childhood caries. This study investigated the effects of sucrose and farnesol on biofilm formation by the oral pathogens S. mutans and C. albicans, including their synergistic interactions. Biofilm formation dynamics were monitored using the Cell Index (CI). The CI for S. mutans increased in the brain–heart infusion medium, peaking at 10 h; however, the addition of sucrose reduced the CI. For C. albicans yeast cells, the CI increased at sucrose concentrations > 0.5%, peaking at 2 h. Mixed cultures of S. mutans and C. albicans yeast cells showed significantly higher CI values in the presence of sucrose, suggesting a synergistic effect on biofilm formation. Farnesol consistently suppressed biofilm formation by C. albicans yeast cells, even in the presence of sucrose, and higher farnesol concentrations resulted in greater inhibition. Regarding C. albicans hyphal cells, sucrose did not enhance biofilm formation, whereas farnesol significantly reduced biofilm formation at all concentrations tested. These findings elucidate the complex roles of sucrose and farnesol in biofilm formation by S. mutans and C. albicans and emphasize the potential of farnesol as an effective oral biofilm inhibitor.