This study explored the association between tooth extraction, dental visit frequency, and blood glucose levels over a 3-year period in middle-aged and older adults using a large health insurance claims database (DeSC, Tokyo, Japan). Data from 31,373 individuals aged 45–70 years who participated in Specified Medical Checkups and Health Guidance between April 2018 and March 2022 were analyzed. Participants were categorized based on the frequency of their annual dental visits and tooth extractions. The primary outcome was high blood glucose level, defined as HbA1c≥6.5%, or fasting plasma glucose level, at ≥126 mg/dl. Individuals who underwent tooth extractions at baseline had lower odds of high blood glucose levels after 3 years, regardless of their baseline glycemic status. Participants with three or more yearly dental visits had lower odds of a high blood glucose level, particularly those with a high baseline blood glucose level and a body mass index ≥25.0 kg/m². These findings suggest an association between regular dental care and improved glycemic control, particularly in individuals with obesity. However, causal relationships cannot be inferred from this study, and further research is required to examine the impact of periodontal treatment and other dental interventions on diabetes management.

More than 700 types of bacteria coexist in the human oral cavity, including motile and non-motile taxa. Fusobacterium nucleatum plays an important role in this environment as a bridge between early- and late-colonizing bacteria. We hypothesized that Treponema denticola, a motile bacterium, receives a non-contact benefit from coexisting F. nucleatum. To evaluate this hypothesis, the growth and gene expression of T. denticola were investigated in an environment where F. nucleatum was present but not in contact with it. The results showed that proliferation of T. denticola increased in this environment, and that this was attenuated by autoinducer-2 (AI-2) inhibitor _D-ribose. The results of RNA-seq and qRT-PCR showed that the presence of F. nucleatum increased the gene expression levels of TDE_0039 and TDE_0040. These findings revealed that proliferation of T. denticola increased via a substance produced by F. nucleatum. Importantly, this phenomenon occurs even without direct contact between the two species. In other words, T. denticola may gain a survival advantage by moving through the oral environment, and F. nucleatum may play a crucial role in facilitating this.

Porphyromonas gingivalis, a key periodontal pathogen, employs extra-cytoplasmic function (ECF) sigma factors to adapt to the dynamic oral environment and establish chronic infection. Among these, PGN_1740 (SigH) has been implicated in oxidative stress response and iron acquisition, yet its transcriptional regulatory mechanisms remain poorly understood. The aim of this study was to elucidate the functional role of SigH using sigH-deficient mutants. Quantitative reverse transcription-polymerase chain reaction was performed to assess the transcriptional profiles of sigH and its putative target genes, sod and ltp1, throughout the growth of P. gingivalis. Electrophoretic mobility shift assay (EMSA) was conducted to evaluate the direct binding of recombinant SigH to the sod and ltp1 promoter regions. Oxygen sensitivity was also assessed using hydrogen peroxide susceptibility and cell invasion assays. The results of these experiments revealed that sigH transcription peaked during the mid-log and early stationary phases, followed by a significant decline in the late stationary phase. The EMSA analysis demonstrated that rSigH directly binds to the ltp1 promoter, but not to the sod promoter. Notably, the sigH-deficient mutant exhibited increased oxidative stress sensitivity in the hydrogen peroxide susceptibility assay. Furthermore, unlike the wild type, the sigH-deficient mutant was unable to invade telomerase-immortalized gingival keratinocytes. These findings suggest that the ECF sigma factor SigH regulates oxidative stress tolerance via sod, and iron metabolism via ltp1, in P. gingivalis.