Journal of Oral Microbiology最新文献

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.

Background: Porphyromonas gingivalis, a keystone oral pathogen, secretes the enzyme peptidylarginine deiminase (PPAD), which catalyzes protein citrullination and is implicated in both dental biofilm formation and the pathogenesis of systemic inflammatory diseases.

Objective: This review aims to synthesize current knowledge on PPAD, with a specific focus on its mechanistic roles in oral biofilm dynamics and its potential contribution to the development of periodontitis and rheumatoid arthritis (RA).

Design: A comprehensive literature search was conducted using the PubMed database up to August 2025, employing keywords including 'PPAD', 'Porphyromonas gingivalis', 'citrullination', 'dental biofilm', 'periodontitis', and 'rheumatoid arthritis'.

Results: PPAD contributes critically to biofilm pathogenicity by modulating microbial pH, citrullinating virulence factors, and facilitating polymicrobial interactions. It promotes bacterial adhesion, disrupts host immunity, and sustains local inflammation. Systemically, PPAD-generated citrullinated antigens may trigger autoimmune responses, potentially linking periodontitis to RA.

Conclusion: PPAD represents a promising biomarker and therapeutic target for mitigating oral-systemic disease progression. Future research should prioritize elucidating its spatiotemporal regulation within biofilms and its immune-dysregulating effects to guide precision interventions.

Background: Periodontitisis a chronic inflammatory disease of the oral cavity, primarily driven by periodontopathogens such as Porphyromonas gingivalis (Pg)."

Objective: We investigated the therapeutic potential of BTK and SYK inhibitors on the pathological processes induced by two Pg strains, ATCC 33277 and W83, in human monocyte-derived macrophages (hMDMs) and human gingival fibroblasts (hGFs).

Design: hMDM and hGF were infected with Pg strains and assessed for viability, inflammatory activation, and phenotype, with or without the BTK inhibitor ibrutinib or SYK inhibitor R406, under acute and chronic infection conditions.

Results: Ibrutinib and R406 suppressed Pg infection-induced activation of the NLRP3-dependent pyroptosis pathway and IL-1β secretion in hMDMs. Both compounds also significantly reduced IL-6, IL-8, and TNFα release by hMDM in both infection models, regardless of differences between ATCC 33277 and W83 Pg strains. Ibrutinib and R406 potently suppressed inflammatory activation of hGFs, including IL-6 and IL-8 production, and NF-κB p65 phosphorylation triggered by the more immunostimulatory ATCC 33277 strain.

Conclusions: The pharmacological inhibition of BTK or SYK mitigates the pyroptotic pathway in hMDMs and exerts a broad anti-inflammatory effect in both hMDMs and hGFs. These results highlight the anti-inflammatory potential of BTK and SYK inhibitors for the treatment of periodontal disease.

Objectives: Polypharmacy has been linked to alterations in gut microbiota, but its effects on the oral microbiome remain underexplored. This study aimed to examine the association of polypharmacy and anticholinergic burden with oral microbiome diversity and composition.

Methods: We conducted a cross-sectional analysis using data from NHANES 2009-2012, including participants aged 55-69 years who reported at least one prescription medication. Polypharmacy was defined as the concurrent use of five or more medications. Anticholinergic burden was quantified by the Anticholinergic Cognitive Burden scale and the Anticholinergic Drug Scale. Oral microbiome profiling comprised alpha diversity, beta diversity, and taxonomic composition at multiple phylogenetic levels. Associations were analyzed via weighted multivariable linear regression, principal coordinate analysis (PCoA), and multivariate analysis of variance.

Results: Among 1,596 participants, 29.2% reported polypharmacy, which correlated with higher anticholinergic burden. Both polypharmacy and anticholinergic burden were inversely associated with alpha diversity across multiple measures. Taxonomic analyses showed heterogeneous associations, with Porphyromonadaceae negatively linked to both exposures. PCoA indicated significant differences in community structure by polypharmacy status (Bray-Curtis: R² = 0.35%, P < .001).

Conclusions: Among middle-aged and older U.S. adults, both polypharmacy and anticholinergic burden were inversely associated with oral microbiome diversity and linked to distinct microbiome composition.

Objectives: To investigate whether systemic inflammation mediates the relationship between oral microbiome alterations and oral squamous cell carcinoma (OSCC) through multi-omics integration analyses.

Methods: Metagenomic sequencing of unstimulated saliva samples from 65 OSCC patients and 65 matched controls was performed. Plasma levels of 34 inflammatory cytokines were profiled using Luminex assay. Six machine learning models identified potential diagnostic microbial markers. Mediation analysis assessed whether inflammation serves as a mechanistic link between oral microbiota and OSCC.

Results: OSCC patients exhibited reduced species richness and significant beta diversity alterations. Among 155 differential species identified, 25 were enriched in OSCC, including Capnocytophaga sputigena, Gemella haemolysans, Staphylococcus aureus, and several Streptococcus species, with higher abundance in poor oral hygiene conditions. The Boruta-CatBoost model achieved exceptional diagnostic performance (bootstrap AUC = 0.991; 5-fold cross-validation AUC = 0.947). Functional profiling revealed 22 metabolic pathways over-represented in OSCC, notably lipopolysaccharide biosynthesis. Nine circulating cytokines (IL-22, IL-6, IL-2, CCL5, GM-CSF, IL-1β, TNF-α, IL-18, IFN-α) were significantly elevated in OSCC patients. Mediation analysis revealed that IL-22 partially mediated the effect of Staphylococcus aureus on OSCC risk, while CCL5 mediated associations of Gemella haemolysans and Streptococcus species with OSCC (mediation proportions: 29.9-50.1%).

Conclusion: Our multi-omics integration suggests that systemic inflammation, particularly through IL-22 and CCL5 upregulation, serves as a mechanistic link between specific oral bacteria and OSCC risk, which could provide new strategies for OSCC prevention and early intervention.