ABSTRACT Background Chronic intestinal inflammation is a hallmark of inflammatory bowel disease (IBD). Studies suggest that salivary bacteria associated with periodontitis may exacerbate colitis, but the specific contributory microbes and mechanisms remain unclear. Patients and methods We analyzed stool samples from 28 IBD patients and 21 controls. Bacterial DNA was extracted and quantified using qPCR targeting Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans). In a murine model, C57BL/6 mice received DSS followed by daily oral gavage with A. actinomycetemcomitans. Disease activity, histopathology and the gut microbiota were evaluated. Results Oral administration of A. actinomycetemcomitans exacerbated inflammatory symptoms in DSS-induced colitis. The bacterium was detectable in intestinal tissue transiently following high-dose oral administration during the inflammatory phase. Following high-dose gavage, bacterial DNA was transiently detectable in intestinal tissue during inflammation. This treatment was associated with reduced expression of the tight junction protein ZO-1 and mucin MUC-2, elevated inflammatory mediators, and altered gut microbial community structure, including an expansion of taxa associated with dysbiosis. Conclusion In a murine colitis model, A. actinomycetemcomitans exposure was associated with worsened disease severity, coinciding with impaired barrier integrity, heightened inflammation and gut microbiota alterations. These exploratory findings highlight the potential role for specific periodontal microbes in modulating intestinal inflammation and warrant further investigation.

ABSTRACT Background/Objective Gastric cancer (GC) is a major cause of cancer mortality worldwide. We evaluated whether oral microbiota could be sensitive, specific, and non-invasive markers for early GC detection. Materials and methods Saliva samples were analyzed using 16S rRNA sequencing, and oral microbial markers were validated using an internal validation dataset. Machine learning was used to identify key genera, and functional associations were inferred using Kyoto Encyclopedia of Genes and Genomes pathway and ortholog analyses. Blood samples were also collected, and plasma cytokines were quantified by enzyme-linked immunosorbent assay (ELISA) for pathway-level interpretations. Results Eight genera—Lautropia, Megasphaera, Ralstonia, Pseudomonas, Peptostreptococcus, Anaerovorax, Fusobacterium, and Neisseria—were validated as diagnostic microbial markers (area under the receiver operating characteristic curve [AUC] = 0.91). Megasphaera and Ralstonia were enriched in GC, whereas Lautropia was depleted and associated with reduced risk. These genera may be functionally linked to pathways involved in GC progression, including NF-κB, IL-6, STAT3, TGF-β1, and Smad2/3. The proposed classification method effectively identified early-stage and tumor-marker–negative GCs, underscoring its clinical translation potential. Conclusions Oral microbial markers, including Ralstonia, Megasphaera, and Lautropia, may serve as non-invasive diagnostic markers for GC and may be related to carcinogenic signaling activity.

Dental caries is a biofilm-mediated disease that arises from polymicrobial dysbiosis in dental plaque. Among these microorganisms, Streptococcus mutans plays a prominent role because of its strong capacity to metabolize fermentable carbohydrates into organic acids that drive enamel demineralization. Central to this process is pyruvate, a key metabolic intermediate that connects glycolysis, energy production, biosynthesis, and stress adaptation. Pyruvate metabolism in S. mutans directs carbon flow into various pathways that contribute to its cariogenic potential, including acidogenesis, biofilm formation, and oxidative stress tolerance. This review explores the multifaceted roles of pyruvate in S. mutans, emphasizing its involvement in the production of lactate, acetate, formate, and branched-chain amino acids. We also discuss the regulatory mechanisms that control pyruvate metabolism, such as the Pta-Ack pathway, LrgAB-mediated pyruvate transport, and transcriptional regulation by CcpA/CodY. Furthermore, we highlight promising strategies for caries prevention, including the targeting of pyruvate metabolism using natural compounds and metabolic inhibitors. Future research should focus on elucidating the regulatory networks governing pyruvate metabolism, the metabolic byproducts, and the impact of disrupting pyruvate-based metabolic crosstalk in polymicrobial biofilms. Understanding how pyruvate functions as a carrier or precursor metabolite in central carbon metabolism of S. mutans and its regulation of survival and metabolic processes will have significant implications for caries prevention.

Background Peri-implantitis, driven by microbial‒host immune interactions, is the leading reason that dental implants fail. Implant surface design plays a crucial role in microbial colonization. Objective To investigate how surface characteristics of implant materials impact periodontal disease biofilm formation and host immune response. Design Biofilms, cultured on Ti-6Al-4V and CoCr disks, had biomass quantified by crystal violet and microbial populations by agar enumeration. We assessed the influence of Ti-6Al-4V post-processing treatments on surface chemistry (energy dispersive spectroscopy), topography (optical profilometry) and microbial dynamics (through complex oral biofilm culture and 16S rRNA sequencing). To evaluate immune responses, biofilms were co-cultured with dysplastic oral keratinocytes, and IL-6, IL-8, IL-1β, TNFα and GRO-α ELISAs were performed. Results Sandblasting markedly increased surface roughness (3.9 vs 0.2–0.6 Ra), biomass (0.72–0.99 vs 0.13–0.62 AU) and total viable counts (TVC). Ti-6Al-4V demonstrated significant enrichment of firmicutes compared to CoCr, together with increased proportions of sulphate-reducing and periodontal disease-associated taxa. Rougher surfaces provoked stronger immune activation under microbial challenge, highlighting the link between topography and host response. Conclusions Surface roughness influenced biofilm formation and inflammation. Assessment of implant materials should integrate microbial and cellular responses for deeper insights. Smoother surfaces, combined with antimicrobial coatings may help reduce peri-implant disease.

ABSTRACT Background This study evaluated the antimicrobial effect of cannabidiol (CBD) on a multi-species subgingival biofilm model. Materials and methods Biofilms were formed using 33 bacterial species on a Calgary device. Two protocols were tested: (A) biofilm in contact with CBD (125, 250 and 500 µg/mL) and chlorhexidine 0.12% (CHX) for the entire period; (B) treatments with CBD (500 and 1000 µg/mL) and CHX started on day 3, twice a day, for 1 minute. The total biofilm counts, the proportion of complexes, and the counts of each species were evaluated by DNA-DNA hybridization (Checkerboard). Results In Experiment A, CBD at concentrations of 250 and 500 µg/mL, as well as CHX, significantly reduced the total biofilm count. At 500 µg/mL, CBD also decreased the proportion of the red complex and reduced the counts of 10 bacterial species, whereas CHX affected 20 species. In Protocol B, both CBD at 1000 µg/mL and CHX reduced the total biofilm count and the proportion of the red complex, while increasing the proportion of the green complex. Both protocols led to a reduction in Porphyromonas gingivalis and Tannerella forsythia. Conclusion CBD reduced the total bacterial count and the red complex, inhibiting known periodontal pathogens. Within the limitations, the results provide exploratory evidence that CBD may reduce the total bacterial count in the proposed polymicrobial biofilm model, including the red complex bacteria, and may thus be postulated as an inhibitor of known periodontal pathogens. However, future in vivo studies with robust sample sizes and standardized CFU-based quantification are required to confirm these findings.

ABSTRACT Background Patients hospitalized with severe odontogenic infections (SOI) receive empiric intravenous antibiotics. Microbiological cultivation and antibiotic susceptibility testing are commonly performed, although the clinical value is debated. Objective To assess the value of routine microbiological cultivation and susceptibility testing in patients hospitalized with SOI. Design This retrospective cohort study included patients hospitalized with SOI, at the University Hospital of Copenhagen, Denmark, from November 2012 to 2019. Data on microbiological cultivation, bacterial identification and antibiotic susceptibility testing were obtained from hospital records. Statistical analysis included χ² test, Fisher's exact test, analysis of variance and logistic regression. Results A total of 384 patients were included, with microbiological data available for 243 patients. Antibiotic treatment was modified in 47 patients and in seven cases, the modification was based on cultivation and antibiotic susceptibility testing. Higher age was associated with the need for cultivation and susceptibility testing (p = 0.006). The infections were polymicrobial, predominantly involving resident oral microbiota. Streptococcus was the most frequent genus (34% of isolates). Penicillin resistance was observed in 30% of all isolates. Conclusion Testing rarely influences antibiotic management in SOI. Higher age showed limited predictive value. The high prevalence of penicillin resistance among patients with SOI warrants further investigation.

ABSTRACT Background Periodontal pathogens disrupt the gingival epithelial barrier, but the molecular links among junctional damage, ferroptosis, and inflammation remain unclear. Objective To investigate whether Bifidobacterium longum (BL) counteracts Aggregatibacter actinomycetemcomitans (Aa)-induced junctional injury via regulation of ferroptosis in human gingival epithelial cells (HGECs). Design Oral microbiota differences between periodontitis patients and healthy controls were analyzed using 16S rRNA sequencing, combined with GSE16134 bioinformatics analysis. HGECs were exposed to Aa (1 × 10⁴ CFU/ml) and treated with BL (1 × 10⁸ CFU/ml) or ferrostatin-1 (Fer-1, 2 μM). Cell viability, mitochondrial morphology, ROS, junction proteins (CDH1, CLDN1), ferroptosis markers (SLC7A11, GPX4, NFE2L2), and inflammatory cytokines (IL-6, IL-10, TNF) were assessed. Results Bioinformatics revealed enrichment of junction-related pathways associated with ferroptosis. Aa induced mitochondrial damage, ROS accumulation, suppression of ferroptosis-protective signaling and junction proteins, and pro-inflammatory cytokine imbalance. BL significantly restored mitochondrial integrity, ferroptosis-related signaling, epithelial junctions, and inflammatory homeostasis, with effects comparable to or exceeding Fer-1. Conclusion Aa disrupts gingival epithelial integrity through ferroptosis-mediated oxidative and inflammatory damage. BL effectively suppresses this cascade and protects epithelial junctions, highlighting its therapeutic potential for periodontitis.

Background Fat taste impairment has been implicated in visceral lipid accumulation and insulin resistance, with emerging evidence linking it to the oral microbiota. However, the role and mechanisms of the oral microbiota in this process remain unclear. Objective We aimed to explore the manifestations of Prevotella in fat taste, visceral lipid accumulation and insulin sensitivity, as well as to elucidate the mechanism involved. Design We characterized the oral microbiota in humans with fat taste impairment, visceral lipid accumulation and insulin resistance, as well as in catch-up fat rats. Fat taste sensitivity, serum biochemistry and tissue morphology were assessed in rats colonized orally with Prevotella to explore potential mechanisms. Results Reduced fat taste sensitivity correlated with visceral lipid accumulation and insulin resistance in both individuals and rats. Prevotella was enriched in individuals and rats with low fat taste sensitivity. Additionally, rats with visceral lipid accumulation and insulin resistance were associated with lower proliferation in taste buds and inhibition in Hedgehog (Hh) signaling. Prevotella colonization downregulated the Hh signaling, fat taste impairment, visceral lipid accumulation and insulin resistance, whereas Hh pathway agonist supplementation mitigated these effects. Conclusions Oral microbiota and fat taste impairment are associated with visceral lipid accumulation and insulin resistance, and Prevotella may play a vital role in fat taste impairment, visceral lipid accumulation and insulin resistance by downregulating the Hh signaling in taste buds.

ABSTRACT Background Candida albicans has been implicated in oral carcinogenesis, but its role in the progression of oral potentially malignant disorders (OPMDs) remains unclear. We investigated whether high Candida burden in OPMD lesions predicts malignant transformation (MT) and whether this association varied by OPMD subtype. Patients and methods In a multicenter prospective cohort study across seven hospitals in Taiwan, 734 OPMD patients were followed for a mean of 2.4 years. Oral lesion swabs were cultured on chromogenic agar to quantify Candida albicans level. Cox models were used to estimate hazard ratios (HRs) for MT to oral cancer. Results MT occurred in 6.8% of patients. High Candida burden was independently associated with increased MT risk (aHR = 2.84; 95% CI: 1.40–5.75). Patients with oral submucous fibrosis (OSF) or verrucous hyperplasia (VH) also had elevated risk (aHR = 4.99; 95% CI: 1.54–10.38). Interaction analysis revealed strong individual risks for high Candida burden (aHR = 13.83) and OSF/VH (aHR = 13.67), with an attenuating interaction term (aHR = 0.11), yielding a substantial combined risk (HR ≈ 20.8). Stratified analysis showed the strongest effect in leukoplakia (HR = 12.19). Conclusions High Candida albicans burden is a significant, subtype-dependent risk factor for malignant progression in OPMDs. These findings underline the role of fungal–host interactions in oral carcinogenesis and support the integration of fungal profiling into routine surveillance of OPMDs.