Journal of Oral Microbiology最新文献

Background: Molecular identification of dental caries microbes is advancing rapidly, yet sampling methods remain outdated and imprecise.

Objective: To refine microbe sample harvesting and preserve taxa pre-harvest spatial positions relative to lesion pulpal depth.

Methods: Refinements included a sterile zone surrounding the dissection site and emphasize asepsis, surgical microscope magnification and lighting, and micro-surgical techniques. Retention of taxa pre-harvest spatial positions relative to lesion pulpal depth used shallow-layered dissection (mean 6 mg/layer, SD 2.65 mg), where each layer became a separate sample for molecular identification before sequential reassembly in a layered lesion diagram. To evaluate the method's robustness, 14 lesions varying in severity and type from private dental practices were dissected using the method (7 pit and fissure and 7 facial lesions; 4 untreated, 3 treated).

Results: Pre-harvest taxa detail, not possible previously, showed taxa location, abundance and diversity relative to lesion pulpal depth, as well as absolute abundance per milligram and taxa transitions and fluctuations from superficial through the deepest dissected layers. The method provides these data regardless of lesion type, stage, or complexity, whether untreated or treated.

Conclusions: This method provides new details and perspectives on dental caries taxa that could help develop diagnostic instruments and treatments to halt dental caries progression.

Background: Tonsillar hypertrophy (TH) and adenotonsillar hypertrophy (ATH) are primary risk factors for paediatric obstructive sleep apnoea (OSA), but their salivary microbiota differ.

Objective: This study aimed to investigate whether the tonsillar surface and core microbiota resemble the salivary microbiota, and whether these microbial profiles are influenced by adenoid hypertrophy and related clinical factors.

Design: Forty-nine children undergoing tonsillectomy were enrolled, including 21 children with TH and 28 with ATH. Saliva and tonsillar surface swabs were collected preoperatively, and core tissues were obtained intraoperatively. Microbiota were profiled via 16S rRNA sequencing, compared across sites and groups, and correlated with preoperative clinical indicators.

Results: The tonsillar core microbiota was relatively stable across all children, whereas the surface and salivary microbiota shifted with adenoid hypertrophy. Prevotella, Neisseria, Veillonella, Alloprevotella, Lancefieldella and Haemophilus were consistently more abundant on the tonsillar surface compared to the core. Gemella was uniquely enriched on the surface and positively correlated with the obstructive apnoea-hypopnoea index and red cell distribution width in the TH group.

Conclusions: This study reveals distinct microbial profiles between the tonsillar surface and core. In TH, surface microbiota was associated with OSA severity and haematological indicators, suggesting potential relevance that warrants further investigation.

Background: Smoking increases mortality risk and alters the oral microbiome, but its mediating role in the smoking-survival relationship remains unclear. This study examined whether oral microbiome diversity mediates the association between smoking and all-cause mortality.

Methods: We included 8,223 participants from the National Health and Nutrition Examination Survey with linked mortality data through 2019. Oral microbiome diversity was assessed using alpha and beta diversity metrics. Associations between smoking, diversity, and mortality were assessed using Weibull Accelerated Failure Time models. Multivariable linear regression evaluated the relationship between smoking and oral microbiome diversity. Mediation analysis estimated the Natural Direct Effect (NDE) and Natural Indirect Effect (NIE). Sensitivity analyses assessed effect heterogeneity.

Results: Among participants, 429 were deceased. Current smoking was associated with a 42.3% shorter survival time (TR = 0.577). Greater ln-transformed observed Operational Taxonomic Units (OTU) richness was associated with 33.2% longer survival time (TR = 1.332). Smoking was associated with survival time through NIE = 1.013 (95% CI: 1.003, 1.033) and NDE = 0.577 (95% CI: 0.474, 0.697). Sensitivity analyses supported the findings.

Discussion: Oral microbiome diversity partially mediated the association between smoking and mortality. Although smoking shortened survival, its effect on increasing OTU richness modestly suppressed this risk. These results highlight a complex microbial pathway and support further investigation into species-level mechanisms and potential microbiome-targeted interventions.

Background: Porphyromonas gingivalis, a key pathogen in chronic periodontitis, produces heterogeneous lipopolysaccharides (LPS) that are weakly recognized by Toll-like receptor 4 (TLR4). Human cells detect cytosolic LPS via caspase-4 (CASP4); however, whether P. gingivalis LPS (PgLPS) can directly activate CASP4 remains unclear. This study aimed to investigate the CASP4-activating properties of purified PgLPS.

Methods: Standard-grade (ST) and ultrapure-grade (UP) purified PgLPS were tested for CASP4 activation using recombinant CASP4 in fluorogenic and IL-18 assays. PgLPS-CASP4 interactions were examined by pull-down. In HSC-2 cells, IL-18 maturation, gasdermin D cleavage, pyroptosis, and dependence on CASP4 or TLR4 were assessed after cytosolic LPS delivery. Guanylate-binding protein-1 (GBP1) involvement was evaluated by siRNA knockdown. Effects of outer membrane vesicles (OMVs) were also tested.

Results: ST-PgLPS directly activated recombinant CASP4, while UP-PgLPS did not. Intracellular delivery of ST-PgLPS induced weak pyroptosis, while UP-PgLPS had no effect. Responses were abrogated by CASP4 inhibition but not by TLR4 inhibition. IFN-γ priming enhanced responses: ST-PgLPS induced moderate activation, whereas UP-PgLPS triggered robust, GBP1-dependent activation. OMVs activated CASP4 in IFN-γ-primed cells.

Conclusion: CASP4 activation depends on PgLPS purity and host cell priming. GBP1 contributes to PgLPS sensing, and OMVs serve as vehicles for PgLPS delivery to the cytosol.

Background: Aging is characterized by progressive physiological decline and increased susceptibility to age-related diseases. The oral microbiome, a complex community of microorganisms, has been increasingly recognized as a potential key player in the aging process.

Objective: This review aims to explore and summarize the relationship between the oral microbiome and aging, with a specific focus on contrasting microbial changes in healthy and unhealthy aging populations.

Design: We conducted a comprehensive review of the current literature to synthesize evidence on oral microbiome shifts during aging, the influencing factors, associations with age-related conditions, and potential interventions.

Results: Evidence indicates that the composition of the oral microbiome changes with age, although findings on diversity are inconsistent, with reports of both increases and decreases in older adults. These shifts are influenced by factors such as diet, oral hygiene, and immune function. Unhealthy aging, including conditions like frailty, neurodegenerative diseases, and sarcopenia, is associated with distinct oral dysbiosis. Potential mechanisms linking the oral microbiome to aging include chronic inflammation and immunosenescence. Interventions targeting the oral microbiome, such as probiotics and dietary modifications, show promise in promoting healthspan.

Conclusions: The oral microbiome is significantly altered during aging and is implicated in age-related health status. It represents a promising target for strategies aimed at promoting healthy aging. Future research should prioritize elucidating the functional mechanisms of oral microbiota and developing targeted microbiome-based interventions.

Objective: This longitudinal study aimed to characterize the spatial and temporal dynamics of oral microbiome colonization on removable partial dentures (RPDs) and corresponding dental surfaces at species-level resolution, to elucidate ecological succession patterns and identify potential pathogenic colonizers.

Methods: We conducted a longitudinal study of 10 participants requiring RPDs. Plaque samples were collected from four sites at five time points. The microbial communities were profiled using PacBio full-length 16S rRNA sequencing, enabling high accuracy taxonomic assignment to the species level. Bioinformatic analyses included alpha/beta diversity, LEfSe, and PICRUSt2 functional prediction.

Results: Significant differences in microbial composition were observed between RPD and dental plaques, despite similar alpha diversity. Temporal analysis revealed a progressive decrease in RPD plaque diversity. Notably, the potential respiratory pathogen Klebsiella pneumoniae was detected in early RPD biofilms. A three-stage ecological succession model for RPD biofilm was proposed, initiating with acidogenic pioneers, followed by functional amplification of taxa involved in extracellular polysaccharide production, and culminating in a stable, acid-tolerant community.

Conclusion: This study provides a species-level understanding of microbiome changes associated with RPDs, confirms differences between RPD plaque and dental plaque, proposes a succession model for RPD-associated bacteria, and determines key turning points and potential pathogens.

Background: The host microbiome is increasingly recognized as a key modulator of brain function and disease progression, yet the role of the oral microbiome in patients with prolonged disorders of consciousness remains underexplored.

Methods: This study characterized oral microbiota differences among pDoC patients (n = 89) in the vegetative state (VS), the minimally conscious state (MCS), and emerging from the MCS (EMCS), with a particular focus on the impact of antibiotic use. We used 16S ribosomal RNA sequencing to profile oral microbiota in patients with different levels of consciousness.

Results: β-diversity was significantly reduced in the VS group compared to the EMCS group. Differential abundance analysis identified five taxa (i.e., species Streptococcus danieliae, species Corynebacterium durum, family Lachnospiraceae, species Phocaeicola abscessus, and species Campylobacter showae) that exhibited significant differences between VS and EMCS, suggesting they were potentially involved in regulating oral microbial dysbiosis and brain-microbiome interactions. Antibiotic treatment induced pronounced microbial shifts in the VS group, while no such effect was observed in the MCS or EMCS groups. Prognostic models built using differential and dominant microbiota panels demonstrated strong predictive performance, achieving areas under the curve of 0.820 and 0.920, respectively.

Conclusions: These findings highlight oral microbiome alterations in pDoC and their potential relevance to disease progression, emphasizing the importance of microbiome-informed clinical strategies.

Background: The targeted manipulation of the microbiome using bacteriophages represents a novel approach for addressing antibiotic resistance and polymicrobial diseases.

Objective: To isolate and characterise bacteriophages for key bacteria associated with pathogenic periodontal biofilms.

Design: Using standard microbiological and bioinformatics techniques, this study isolated and characterized lytic (FNU2 and FNU3) and temperate (FNU4) bacteriophages specific to Fusobacterium nucleatum, a key bacterium in oral biofilms linked to periodontitis and a range of cancers.

Results: Morphological and genomic analyses revealed distinct features, with FNU2 and FNU3 classified as Latrobevirus and FNU4 as an unclassified Caudoviricetes. Comparative bioinformatic analysis revealed various defence and anti-defence systems in bacterial hosts and bacteriophages, highlighting complex interactions. Functional assays demonstrated the efficacy of these bacteriophages in disrupting single-species F. nucleatum biofilms and dual-species biofilms of F. nucleatum and Porphyromonas gingivalis.

Conclusion: These findings highlight the potential of F. nucleatum-specific bacteriophages as precise tools for microbiome modulation in chronic diseases such as periodontitis and cancer.

Proper tooth alignment is important for oral and periodontal health, allowing better hygiene and reducing plaque build-up. While traditional braces are effective, clear aligners offer an aesthetic advantage and are also thought to promote better oral hygiene. However, their specific impact on the oral microbiome is not yet fully understood. This longitudinal study used 16S amplicon sequencing to study the oral microbiome (from saliva, subgingival, and supragingival samples) of 11 patients undergoing clear aligner treatment. Samples were collected at three time points: before treatment and at 3 and 6 months during therapy. Our results revealed large differences between the microbiomes of different oral sites but no significant overall changes in the oral microbiome composition due to orthodontic treatment. While some species-specific changes were observed, their effect sizes were very small. Although these results should be confirmed in a larger and more diverse cohort, they suggest that the treatment had a small or negligible impact. Given the observed stability of the oral microbiome in all three studied niches throughout the treatment and the known benefits to oral hygiene, clear aligners may present a favorable therapeutic alternative compared to fixed appliances.

Background: Porphyromonas gingivalis (P. gingivalis) is one of the few bacteria that can produce sphingolipids (SLs). Bacterial SLs have been shown to modulate the host immune response.

Objective: Since neutrophil activation is critical for the pathogenesis of periodontal disease, we hypothesized that SL synthesis by P. gingivalis is important for neutrophil function.

Design: We treated primary human neutrophils with P. gingivalis strains W83 that either produce SL (W83) or lack expression (W83 ΔSPT). We compared the phagocytosis capacity and toll-like receptor 2 (TLR2), TLR4, the adhesion molecule CD62L, and sphingosine 1 phosphate receptor 1 (S1PR1) expressions of the neutrophils. We evaluated the migration speed of neutrophils using microfluidic and transwell systems. We quantified their superoxide formation, measured neutrophil extracellular trap (NET), and inflammatory mediator release.

Results: When P. gingivalis cannot synthesize SLs, this promotes early neutrophil recruitment, higher levels of phagocytosis, and a decrease in bacterial survival. P. gingivalis can stimulate TLR2 expression, prevent S1PR1 expression, and suppress the production of inflammatory mediators in the presence of SL expression.

Conclusions: Our data suggest that SL synthesis is an efficient immune evasion mechanism of P. gingivalis, which dampens the inflammatory response of neutrophils to this endogenous pathogen.