Journal of Oral Microbiology最新文献

Background: Hepatitis B virus-related chronic liver disease (HBV-CLD), chronic hepatitis B (CHB), liver cirrhosis (LC), and hepatocellular carcinoma (HCC) patients' tongue coating microbiota dysbiosis has not yet been clearly defined.

Objectives: We aimed to reveal shifts in the bacterial composition of tongue coating microbiota during the progression of HBV-CLD in three different phases.

Design: We examined tongue coating microbiota of 16 healthy individuals and 81 patients with HBV-CLD, including 25 with CHB, 27 with LC, and 29 with HCC, using 16S rRNA gene sequencing technique.

Results: The bacterial richness in tongue coating was higher in patients with HBV-CLD (all P < 0.05) than in healthy controls. A clear clustering pattern between patients with HBV-CLD and healthy controls is shown using beta diversity analysis (all p < 0.05). Linear discriminant analysis revealed multiple taxa that varied significantly in abundance between healthy controls and patients with HBV-CLD; Firmicutes were higher in patients with LC and HCC, whereas CHB patients had higher levels of Bacteroidetes. PICRUSt2 analysis of the sequencing data revealed changes in microbial activity with disease development.

Conclusions: Our investigation revealed tongue coating microbiota dysbiosis in patients with HBV-CLD, which may offer unique diagnostic possibilities and provide microbial biomarkers for monitoring disease progression.

Objective: The oral-gut axis, the pathway by which oral bacteria reach the intestine, has recently attracted attention. However, no recent studies have isolated live Streptococcus mutans, a major pathogen of dental caries, in the gastrointestinal tract. In the present study, we isolated S. mutans from the gastrointestinal tract of corpses.

Methods: Fifty corpses from forensic autopsies (ages 0-94 years, median age 49) were used. Samples were taken from the oral cavity and gastrointestinal tract (esophagus, stomach, duodenum, small intestine, and large intestine) using sterile swabs. S. mutans isolates was cultured from the swabs, and DNA and RNA of the bacteria were extracted for genetic analysis.

Results: S. mutans was isolated from each organ with the following frequency: oral cavity, 14 cases (28%); esophagus, 3 cases (6%); stomach, 1 case (2%); duodenum, 0 cases (0%); small intestine, 1 case (2%); and large intestine, 4 cases (8%). When S. mutans strains isolated from the oral cavity and gastrointestinal tract of the same corpses were compared, the serotypes and genotypes were completely consistent. Bioinformatic analysis showed that gene expression and predicted functions differed between S. mutans strains isolated from the oral cavity and the gastrointestinal tract, even though these S. mutans strains were the same genotype.

Conclusion: These results suggest that S. mutans strains existing in the gastrointestinal tract may undergo changes in gene expression to adapt to the environment of each organ.

Background: Implementing local adjunctive therapy during scaling and root planing has become increasingly crucial for optimizing the therapeutic efficacy of periodontitis and reshaping the periodontal microecological environment.

Objective: This study aimed to reveal the additional clearance effect of local adjunctive therapy on the microbiota of periodontitis.

Design: An autologous randomized controlled trial included 25 periodontitis patients. After scaling and root planing, one oral side randomly received laser or minocycline, the other as control. Three hundred and seventy-six subgingival samples were collected at nine time points within 1 month for integrated analysis of microbiota and clinical indicators.

Results: Compared with laser adjunctive therapy, minocycline hydrochloride adjunctive therapy showed no difference in pathogen clearance rate within 6 h, but significant differences emerged in days 1, 3 and 7 (χ² test, P < 0.05). Meanwhile, within the 7-day period, the number of core bacteria of periodontitis with significant intergroup differences increased progressively over time (LDA > 2.0, P < 0.05). After 4 weeks, minocycline hydrochloride adjunctive therapy eliminated 12 more core bacteria of periodontitis than scaling and root planing alone, while significantly reduced the bleeding on probing (Wilcoxon test, p = 0.0085) and clinical attachment loss indicators (Wilcoxon test, p = 0.0456). In the long term, minocycline hydrochloride adjunctive therapy weakened microbial network connectivity, strongly influencing bacterial interactions involving Leptotrichia, Dialister and Atopobium.

Conclusions: Minocycline hydrochloride local adjunctive therapy outperforms semiconductor laser local adjunctive therapy in terms of eliminating periodontitis core bacteria, improving the microbial community structure, and enhancing clinical indicators.

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 R_a), 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.

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.

Background: Dental caries prevention can be approached through ecological modulation of the oral biofilm. Among oral probiotics, Streptococcus dentisani stands out for its arginine deiminase (ADI) pathway, producing ammonia with an alkalinizing effect, and for bacteriocins active against cariogenic organisms, suggesting restoration of acid-base homeostasis and displacement of dysbiosis-associated taxa.

Objective: To systematically review clinical evidence on S. dentisani and other probiotics regarding their effects on pH modulation and oral microbiota shifts.

Methods: A PRISMA-guided systematic review of PubMed, Scopus, and Web of Science was conducted, including randomized controlled trials (RCTs) and observational studies reporting at least one prespecified outcome (pH or microbiota).

Results: Two clinical studies specifically assessed S. dentisani, reporting transient oral colonization, increased salivary alkalinity, and reductions in S. mutans, with one trial documenting a favorable community shift by 16S sequencing. Across the remaining studies, which mainly involved Lactobacillus and Bifidobacterium strains, nine reported reductions in cariogenic markers and five reported increases in pH/buffering capacity; these findings do not pertain to S. dentisani but to other probiotic strains. Caries incidence was evaluated only in lactic probiotic trials with mixed findings; no caries-incidence data were available for S. dentisani.

Conclusions: S. dentisani demonstrates consistent mechanistic benefits-pH increase and modulation of the oral microbiota-supporting its candidacy as an oral probiotic. Evidence on caries prevention remains insufficient, underscoring the need for longer, standardized trials incorporating clinical endpoints and microbiological profiling.

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.

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.

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: 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.