Journal of Oral Microbiology最新文献

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.

Aim: This study aimed to explore the composition of the tooth-surface plaque (subgingival with marginal supragingival) microbiome in dentate older adults residing in long-term care (LTC) facilities, stratified by clinically assessed oral disease burden (ODB). A total of 196 LTC residents aged ≥62 years underwent oral examinations and microbial sampling from each dentate quadrant. Microbial profiling was performed using 16S rRNA gene sequencing.

Results: Participants were more frequently categorized into Moderate (n = 95, 48%) than Low (n = 32, 16%) or High (n = 69, 35%) ODB groups. Those with High ODB were oldest and had lowest number of remaining teeth. Alpha diversity did not differ between the ODB groups, whereas beta diversity analysis revealed significant differences between groups (Bray-Curtis: P = 0.005; weighted Unifrac: P = 0.025). The Low and Moderate ODB groups were enriched with both commensals and disease-associated genera, such as Ottowia, Lactococcus, Pseudoramibacter, and Anaeroglobus. High ODB group exhibited an increased abundance of genera linked to both oral and systemic diseases, including Cardiobacterium, Leptotrichia, Stomatobaculum, and Pseudopropionibacterium. Among ODB groups, periodontitis was a stronger determinant of oral microbiome composition than caries, whereas caries had a stronger effect on bacterial diversity.

Conclusion: These findings indicate a progressive shift toward a dysbiotic oral microbiome with increasing ODB.

Background: Porphyromonas gingivalis is a Gram-negative bacterium that plays a central role in the development of periodontal disease. It uses a type IX secretion system (T9SS) to export virulence factors to the bacterial surface where they are attached to A-LPS, one of the two forms of lipopolysaccharide (LPS) produced in P. gingivalis, and then packaged into outer membrane vesicles (OMVs). We previously showed that 1-P dephosphorylation of the lipid A component of LPS is regulated by the T9SS outer membrane protein PorV, and this is linked to membrane destabilisation and OMV blebbing/formation. Objective: This study aimed to investigate whether other T9SS outer membrane proteins are required for correct OMV biogenesis. Design: We examined gingipain activity, gingipain secretion, A-LPS production, OMV morphology, and lipid A structure in P. gingivalis W50, T9SS mutant strains, and a lipid A 1-phosphatase (ΔlpxE) mutant strain. Results: A functional T9SS is required for LpxE activity and correct vesicle formation, and this is likely through the function of an exported type IX-cargo protein. Conclusion: This study provides insight into a new mechanism that links type IX cargo sorting with OMV blebbing, which may also be present in other Bacteroidota that colonise the gut and oral cavity.

Background: Streptococcus suis is a zoonotic pathogen, and its colonization of the host tonsil is believed to be a vital source causing infection, while its mechanism competing for a stable tonsil niche is unknown. Rearrangement hotspot (Rhs) proteins are characterized to facilitate interbacterial competition by their polymorphic C-terminal toxins (CTs) in diverse bacteria, while their distant homologues emerged in S. suis, referred to as wall-associated protein A (WapA), has not been identified.

Methods: Bioinformatics, western blot and interbacterial competition analyses were performed to identify Rhs/WapA toxins and their roles during S. suis infection.

Results: The 350 kDa WapA-CT1, linked with a SecF-like protein and a SrtB sortase, was verified to manipulate the tonsil microbiota for S. suis optimal colonization. The unfolded WapA-CT1 was translocated across the cell membrane via the canonical Sec pathway. Afterward, autocleavage generated four fragments: the N-terminal NCWB fragment, two middle Rhs domains (Rhs1&2) that may fold as a β-barrel structure, and a C-terminal PreT-CT toxin domain. SrtB interacts with the NCWB region, and plays vital roles for the interbacterial antagonism mediated by the toxic CT1.

Conclusion: This discovery underscores the diversity of mechanisms by which pathogens delivering Rhs/WapA polymorphic toxins, and their roles in competing with the host microbiota.