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Article

The Oral Bacteriome

by
Soukaina Ghaouas
1 and
Sanaa Chala
2,*
1
Laboratory of Research on Oral Biology and Biotechnology, Faculty of Dental Medicine, Mohammed V University, Rabat 10000, Morocco
2
Faculty of Dental Medicine, Mohammed V Military Teaching Hospital, Laboratory of Biostatistics Clinical and Epidemiological Research, Mohammed V University, Rabat 10000, Morocco
*
Author to whom correspondence should be addressed.
Microbiol. Res. 2025, 16(9), 194; https://doi.org/10.3390/microbiolres16090194
Submission received: 9 July 2025 / Revised: 15 August 2025 / Accepted: 25 August 2025 / Published: 1 September 2025
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Abstract

The oral microbiome has garnered significant interest in recent years. Its profound implications for oral and systemic diseases have led to a considerable amount of research and analysis aimed at providing deeper insights into its composition. This study aimed to characterize oral bacterial communities comprehensively based on microorganisms indexed in the Human Oral Microbiome Database, which was systematically analyzed, and its taxonomic classification was used to describe the diversity of indexed bacteria in the oral cavity. A total of 522 bacteria were considered for the analysis. Among these, 49.04% were named, whereas 29.12% represent uncultivated phylotypes. The taxonomic characterization revealed that more than 80% of total taxa are distributed across five phyla: Bacillota, Bacteroidota, Actinomycetota, Pseudomonadota, and Fusobacteriota. Of these, Bacillota and Bacteroidota are the dominant ones with, respectively, 166 (31.80%) and 96 (18.39%) bacterial taxa. With the recent advances in genomics and bioinformatics, the HOMD is constantly updated, further enhancing our understanding of the bacterial community of the oral microbiome. However, the considerable diversity of the oral microbiome may present analytical challenges and the possible misperception of the implications of closely related species/subspecies in oral and systemic health.

1. Introduction

The oral cavity is a distinct ecological niche that hosts a diverse microbiota reflecting its complexity [1]. This oral microbiota includes bacteria, fungi, viruses, and archaea, which inhabit various niches. These microbial communities play a key role in maintaining oral homeostasis and modulating host immune responses. The complex microbiome within the oral cavity plays a pivotal role in maintaining oral health; however, it can also contribute to systemic diseases. The ability of microbial species to colonize different niches in the mouth and form biofilms is a key factor in their pathogenicity.
Bacterial identification and classification have undergone remarkable evolution. Traditionally, bacteria were identified and classified primarily by their morphological and biochemical characteristics and their growth requirements. However, these fundamental methods had significant limitations such as insufficient precision to discriminate between closely related bacteria and being restricted to only culturable species. The advent of molecular approaches such as 16S rRNA gene sequencing, whole-genome sequencing, mass spectrometry, and computational approaches enabled the comprehensive profiling of the bacterial communities by uncovering uncultivated phylotypes, reducing redundancies, and refining the accuracy of the taxonomic classification, and revealed phylogenetic relationships that were overlooked by traditional culture-based approaches alone. These advancements have enabled taxonomic comprehension and assisted the evolving of reclassification. However, the resolution of fine-scale taxonomy remains complex and the diversity and complexity of the oral microbiome may hinder data analysis and interpretation [2,3,4,5].
Comprehensive databases serve as the foundation for sequences comparison and accurate taxonomic identification. The expanded Human Oral Microbiome Database (eHOMD) represents an important database that is widely used in studying and characterizing the oral microbiome. which provides comprehensive taxonomic and genomic data, functional insights that are not completely covered in general microbial databases [6]. The present paper aims to use the taxonomic description of oral bacteria from the expanded Human Oral Microbiome Database (eHOMD) to present an overview of the composition of oral bacteria.

2. Materials and Methods

The data used in this paper was obtained from the expanded Human Oral Microbiome Database (eHOMD) (https://www.homd.org, accessed on 7 April 2025 and updated on 20 June 2025). This openly accessible database provides data on microorganisms distributed throughout the oral cavity and aerodigestive tract, identified from both healthy individuals and subjects with various oral health conditions such as dental caries, periodontal disease, and oral cancer.
Considering the marked predominance of bacteria in this database (833 out of 834 of total indexed taxa), this paper focused exclusively on bacterial taxa. To this end, the following approach was used to gather information related to all registered and indexed bacteria.
The retrieved data from eHOMD were restricted to the oral cavity, which was selected as the primary body site. No limitations were applied to the bacterial abundance within the selected body site data; therefore, all abundance categories were included, ranging from high abundance taxa to those with no available data. Taxa were classified into four categories based on their log-transformed percentage abundance values: scarce (0.001% to <0.01%), low (0.01% to <0.1%), medium (0.1% to <1%), and high (>1%). Both body site specificity and abundance information in this database were determined through beta diversity analysis. The taxonomic status included named/cultivated, named/uncultivated, and unnamed/cultivated taxa, as well as phylotypes. Non-bacterial taxa, specifically archaea (only one indexed taxon), were excluded from the dataset.
The resulting bacterial taxa were processed and reclassified, and the microbial diversity and flora composition were analyzed and presented in this paper.

3. Results

A total of 522 bacterial taxa were identified within the oral microbiome (Figure 1). Among them, 49.04% were named, 19.16% were unnamed but cultivated, whereas 29.12% are uncultivated phylotypes (Table 1).
These bacterial taxa are distributed across 10 phyla, of which five phyla (Bacillota, Bacteroidota, Actinomycetota, Pseudomonadota, and Fusobacteriota) account for more than 80% of total bacteria. Among these, Bacillota and Bacteroidota are the dominant ones with, respectively, 166 (31.80%) and 96 (18.39%) bacterial taxa (Table 1).
The Bacillota phylum is composed of four distinct classes, among which the Clostridia (39%) and Negativicutes (30%) classes exhibit the highest bacterial taxa richness. The genera Selenomonas (44%) and Veillonella (22%) constitute over half the bacterial taxa of the Negativicutes class (Figure 2).
The Bacteroidota phylum predominantly comprises Gram-negative bacteria, categorized into two classes: Bacteroidia (82%) and Flavobacteriia (18%) (Figure 3).
The Actinomycetota encompasses several genera, characterized by their metabolic diversity. These genera include Actinomyces, Scardovia, and Corynebacterium species (Figure 4).
The Pseudomonadota phylum of the oral cavity (Formerly Proteobacteria) comprises four classes: the Betaproteobacteria (54%), Gammaproteobacteria (31%), Deltaproteobacteria (3%), and Epsiloproteobacteria (12%) (Figure 5).
The Fusobacteriota phylum comprises two main families: Fusobacteriaceae (42%) and Leptotrichiaceae (58%) (Figure 6).
The Patescibacteria phylum mainly includes two classes: Patescibacteria [C1] (18%) and Saccharimonodia (82%) (Figure 7).

4. Discussion

A total of 522 oral bacterial taxa were extracted and analyzed. Among these bacteria, 80.66% are distributed across five phyla: Bacillota, Bacteroidota, Actinomycetota, Pseudomonadota, and Fusobacteriota, which are recognized as the dominant phyla of the healthy oral microbiome [7].
The phylum Bacillota (formerly Firmicutes), is one of the major phyla of the oral microbiome. The Streptococcus genus within the Bacilli class plays pivotal roles in both oral health and disease [4]. With the increasing availability of whole genome sequences, the oral streptococci have been reclassified and include new unnamed species such as Streptococcus sp. HMT-056 and Streptococcus sp.HMT-057. The oral streptococci are currently categorized into six major groups: The Mutans, Mitis, Anginosus, Sanguinis, Salivarius, and Downei groups [8]. These Gram-positive cocci are among the primary colonizers of the oral cavity and play a fundamental role in dental biofilm formation [9]. Moreover, they significantly contribute to the landscape ecology of the oral cavity. As facultative anaerobes, the early colonizers Streptococci contribute to oxygen gradient formation by consuming oxygen in the outermost layer of the biofilm, thereby creating a microenvironment for anaerobic species [10]. Additionally, their ability to produce organic acids as byproducts from carbohydrate fermentation is directly associated with the development of dental caries. However, some species modulate pH fluctuations and contribute to its homeostasis through alkali generation from the catabolism of amino acids [8,11].
Moreover, Streptococci possess remarkable immunomodulatory properties [12]. These immunomodulatory effects are exerted through several mechanisms such as the production of hydrogen peroxide, quorum sensing molecules, as well as the interaction with macrophages [12,13,14]. For instance, it has been demonstrated that the hydrogen peroxide (H2O2) produced by Streptococcus mitis and Streptococcus oralis inhibit the nuclear-factor-kappa-light-chain-enhancer of activated B cells (NFκB), a pro-inflammatory response mediator [15]. This inhibition has been shown to suppress the secretion of a pro-inflammatory chemokine CXCL8 (IL-8) by epithelial cells, and also attenuate the pro-inflammatory response in macrophages by inducing the oxidative stress response [16,17]. However, while 30% of oral Streptococci displayed anti-inflammatory effects, others are more associated with pro-inflammatory responses [17]. Notably, Streptococcus anginosus and Streptococcus gordonii. S. anginosus stimulate a robust pro-inflammatory response in macrophages, which is associated with (NFκB) activation and increased levels of inflammatory mediators, such as inducible nitric oxide synthase (iNOS), cyclooxygenase 2 (Cox2), and pro-inflammatory cytokines (IL-1β, IL-6, and TNF) [14]. S. gordonii may induce inflammatory responses in several cells such as oral epithelial cells and periodontal ligament cells, characterized by IL-8 production [18,19]. The ambivalent capacities of oral Streptococcus contribute to oral homeostasis as well as to the development of oral and systemic diseases [20].
The Veillonella genus represents anaerobic Gram-negative cocci and have significant implications for both oral and systemic health [21,22]. The Veillonella genus exhibits niche specialization. For example, Veillonella parvula mainly proliferate in dental biofilms, while Veillonella atypica, Veillonella rogosae, and Veillonella dispar thrive on tongue dorsum [23].
A symbiotic interaction exists between Veillonella and saccharolytic Streptococcus through sugar metabolism and cross-feeding [24]. Veillonella spp. are nitrite-producing commensals, with different species exhibiting varied levels of nitrite-producing potential [25]. This activity may be promoted by several environmental factors such as lactate availability as well as anaerobic and acidic conditions [21]. The produced nitrite displayed antibacterial activity against acidogenic bacteria such as Streptococcus mutans and also inhibited its acid production, thus mitigating dental plaque acidification [24,26]. The interaction of Veillonella spp., especially V. parvula with S. mutans, is particularly noteworthy, contrary to the expected beneficial effect of Veillonella in the biofilm: it has been demonstrated that its presence along with S. mutans does not necessarily lead to pH homeostasis, but rather appears to promote the cariogenic potential of the biofilm, by promoting the growth, the aciduricity, the acid production, and the extracellular polysaccharides synthesis of S. mutans, thereby enhancing the structural stability and integrity of the biofilm, as well as its antimicrobial resistance [27,28,29,30].
Selenomonas are frequently identified in dental biofilm, primarily the subgingival biofilm [31,32]. Due to their implications in periodontal disease, Selenomonas noxia and Selenomonas sputigena represent the most extensively studied species within the Selenomonas genus [31,33]. S. sputigena may contribute to periodontitis through several mechanisms. Its ability to adhere to the surface of gingival keratinocytes triggers pro-inflammatory responses such as the secretion of cytokines (IL-6, IL-8, TNF-α) and chemokines (CXCL1, CXCL10), along with the production of matrix metalloproteases (MMP9, MMP13) [34].
Selenomonas spp., have also been isolated among caries-affected subjects [35,36,37]. Selenomonas spp. possesses fermentative metabolism and may interact with S. mutans to enhance their cariogenic potential through cooperative interaction. When both species are co-cultured, S. sputigena modifies the spatial distribution of the biofilm by forming a “dense honeycomb-like superstructure” that encapsulates S. mutans. This unique spatial distribution enhances the acidogenicity and aciduricity of the biofilm, ultimately exacerbating the cariogenic potential of the biofilm [38,39].
The Prevotella genus represents the abundant genus within the Bacteroidota phylum. It is commonly identified in the oral cavity and particularly in mucosal surfaces, dental biofilms, and saliva [40]. This genus is highly diverse and encompasses several species that play different ecological roles in the oral ecosystem, influencing both oral and systemic health [40,41].
Prevotella species display remarkable metabolic diversity, influencing their ability to thrive in diverse ecological niches and contributing to their possible adaptation to the fluctuating environmental conditions within the oral cavity [42,43]. Prevotella species such as Prevotella intermedia, Prevotella nigrescens, and Prevotella denticola exhibit both saccharolytic and proteolytic activities, enabling them to persist in both healthy and dysbiotic supragingival and subgingival biofilm [41], and they are significant contributors to periodontal disease and dental caries [43,44,45]. While the precise involvement and contribution to dental caries is not well characterized as in periodontal disease, it has been reported that the symbiotic interaction between P. denticola and S. mutans may shift the oral microbiome toward a dysbiotic state, contributing to the pathogenesis of dental caries [46].
Furthermore, it is likely that the functional and genetic heterogeneity within the Prevotella genus may influence the ecological role and distribution of the species [40,45]. For instance, Prevotella multisaccharivorax, Prevotella histicola, and P. nigrescens show variations in their ecological distribution according to the pH gradient within dentinal lesions, with P. nigrescens colonizing neutral and mildly acidic environments, whereas P. histicola and P. multisaccharivorax are more associated with acidic caries lesions [47]. While P. intermedia may promote oral health (isolated from healthy supragingival plaque) [48], it can also act as a pathobiont contributing to periodontal diseases within dysbiotic biofilm [43,45]. This considerable diversity within the Prevotella genus and the variant implications of its different species and strains (whether commensals, potentially protective, or pathobiont) highlight the importance of detailed taxonomic identification (species- and strain-level) to clarify their niche-specific contributions to the oral microbiome and their distinct role in oral diseases [40,41,45].
The Porphyromonas genus encompasses a “keystone” periodontal pathogen: Porphyromonas gingivalis. This bacterium is characterized by several virulence factors that are crucial for its survival and collectively enable its colonization and facilitate host tissue invasion and evasion while sustaining inflammation and promoting dysbiosis, therefore contributing to periodontitis and systemic diseases [49,50]. Its remarkable genetic diversity and plasticity, through several mechanisms such as horizontal gene transfer, natural competence, and CRISPR/cas systems, enable its adaptability, persistence, and pathogenicity in the dynamic and complex environment of the oral cavity [51,52,53].
Although P. gingivalis is mainly associated with periodontal disease, it may also be detected in healthy sites, albeit at a lower relative abundance and prevalence compared to the diseased sites [54,55]. However, the commonly identified genotype of P. gingivalis in healthy sites tend to be avirulent: “fimA type I genotype” [55,56].
P. gingivalis can form highly complex biofilms, often in consortium with other periodontal pathogens such as treponema denticola, Tannerella forsythia or with other opportunistic pathogens, enhancing its virulence and pathogenicity [57,58,59,60]. P. gingivalis induces a pro-inflammatory environment and reshapes the biofilm composition favoring proteolytic pathobionts, perpetuating dysbiosis and pathogenic resilience [50,61].
However, not all microbial interactions with P. gingivalis are synergistic; interactions with some commensal species may mitigate its pathogenicity [62,63,64]. Streptococcus cristatus antagonizes P. gingivalis by suppressing its virulence gene expression [64].
P. gingivalis has also been associated with various systemic diseases such as cardiovascular and neurodegenerative diseases and rheumatoid arthritis, mainly through inflammatory mechanisms and bacterial translocation [65,66,67,68].
The genus Capnocytophaga of the Flavobacteriia class is distinguished by its gliding motility and mainly colonize dental biofilm [69]. Among Capnocytophaga species, Capnocytophaga orchracea has been particularly studied for its biofilm-forming capacity, involving both quorum sensing pathways (mediated by the LuxS enzyme and autoinducer-2 signaling molecules) and the type IX secretion system (T9SS), which facilitates bacterial motility and biofilm development [70,71]. The (T9SS) has also been studied in Capnocytophaga gingivalis and it was reported that this system could facilitate the transport of other non-motile microorganisms across the dental biofilm, thereby potentially contributing to the modification of dental biofilm biogeography [72,73].
Capnocytophaga species have also been associated with several diseases. C. gingivalis was associated with gingivitis and the development of oral squamous cell carcinoma, whereas C. ochracea have been isolated from healthy individuals as well as individuals with periodontal disease, and it was also linked to poor oral hygiene along with Capnocytophaga sputigena, particularly in elderly populations [74,75,76,77].
The Actinomycetota phylum encompasses several genera, characterized by their metabolic diversity and significant contributions to oral health and disease dynamics. These genera include Actinomyces, Scardovia, and Corynebacterium species [78].
The Actinomyces species, in particular Actinomyces naeslundii, Actinomyces viscosus, Actinomyces gerencseriae, and Actinomyces oris, are the early colonizers of dental surfaces [79], and with other species, are able to create a fundamental basis for the subsequent attachment of secondary and late colonizers [79,80,81]. Several Actinomyces species, such as A. naeslundii, A. viscous, and A. israelii, were been identified in carious lesions comprising root caries lesions [82,83,84,85,86].
Within the oral microbiome, two species of Scardovia have been identified: Scardovia wiggsiae and Scardovia inopinata [87,88,89]. Moreover, S. wiggsiae is characterized by its dual metabolic pathway that enables the production of different byproducts (acids) according to environmental pH; at neutral pH, S. wiggsiae produces mainly acetic acid via the acetate pathway, whereas in the acidic environment, it also produces lactic acid via the lactate-formate pathway [89,90]. This flexibility may enable S. wiggsiae to be metabolically active under variable environmental conditions [89,90]. Furthermore, S. wiggsiae may interact with other cariogenic bacteria and enhance the overall cariogenic potential of the biofilm [89,91].
The Corynebacterium genus plays a fundamental role in the microbial ecology of the oral cavity, which contributes to the biofilm biogeography and promotes oral health [92]. In the oral microbiota, this genus comprises Corynebacterium durum and Corynebacterium matruchotii. This commensal is renowned for its ability to form filamentous structures in dental biofilms. Notably, the filamentous growth pattern of C. matruchotii contributes considerably to the biogeography of the supragingival biofilm, and contributes to the formation of the “hedgehogs” and “corncob” biofilm structure, thus creating a scaffold for the microbial community [92,93,94]. These structures contribute to the ecology of the oral microbiome; these enable the stratification of the bacterial community, creating microhabitats with distinct microenvironment conditions [92,93].
Moreover, Corynebacterium spp. engage in the synergistic interactions of commensal bacteria, particularly oral Streptococci [95,96]. They produce extracellular membrane vesicles which play a crucial role in biofilm formation, intracellular communication, and long-distance signaling within the oral microbiome [97]. Corynebacterium species also contribute to the survival of hydrogen peroxide-producing bacteria and may also modulate host immune responses, thus preventing pathogen dominance and promoting oral health [93,95,96].
As commensal of the oral cavity, the presence and abundance of the Neisseria genus in the microbial community can promote oral health. This genus includes several species that exhibit site-specific colonization. For example, Neisseria mucosa and Neisseria elongata predominantly colonize the dental biofilm, whereas Neisseria subflava is primarily detected on the tongue dorsum. Additionally, Neisseria oralis is primarily identified in dental biofilm, but could also be detected occasionally on tongue dorsum and mucosal sites [98]. This site-specific colonization is likely driven by the metabolic functions and genomic adaptation of the species. These metabolic functions not only reflect their niche adaptations but may also suggest their possible ecological role within their microbial communities. For instance, the denitrification and the nitrate reduction ability of “the dental biofilm specialist” may attenuate the acidification of the biofilm, thus promoting oral homeostasis as well as the growth of health-associated microbiota [98,99,100]. Actually, several studies have reported the predominance of Neisseria in caries-free samples, and its absence or significantly reduced abundance in the biofilm of patients with severe carious lesions support its potential role in maintaining oral health, as its decrease correlates with dental caries [101,102,103,104]. Moreover, the presence of Neisseria in the oral microbiota can antagonize some opportunistic pathogens that can promote oral diseases, such as P. gingivalis [105]. However, the identification of Neisseria species in both the healthy and diseased state may indicate a complex role within the oral microbiome [106].
Within the Betaproteobacteria class of the Pseudomonadota phylum, the Lautropia genus comprises two species: Lautropia mirabilis and Lautropia dentalis. This genus is able to ferment sucrose and to reduce nitrate and nitrite [107,108]. L. mirabilis has recently been identified as the cause of cases of peritoneal dialysis-associated peritonitis [109,110]. Overall, the pathogenicity of Lautropia spp. and their possible involvement in infections remain understudied, and thus further studies are warranted to elucidate its possible contributions to biofilm dynamics and opportunistic infections.
The Haemophilus genus of the Gammaproteobacteria class is among the prevalent commensals of the oral cavity [111]. The genomic plasticity and metabolic versatility of Haemophilus species contributes to their ecological distribution, in which some species can colonize various ecological niches within the oral cavity and other species are more site-specific [112,113]. Yet, the pangenomic subgroups of Haemophilus parainfluenzae, a “habitat-generalist”, display clear ecological specialization with the distinct metabolic adaptation. For instance, the two subgroups—supragingival plaque and tongue dorsum—exhibit distinct functional profiles, with certain metabolic pathways uniquely identified in each subgroup [113,114]. Specifically, key genes involved in biotin biosynthesis have been detected exclusively in the supragingival plaque subgroup, whereas the oxaloacetate decarboxylase operon appears to be limited to the tongue dorsum subgroup. This metabolic diversity might result from environmental adaptation, suggesting that the distinct metabolic pathways may in turn contribute to ecological specialization [113,114].
The immunomodulatory properties of H. parainfluenzae along with the microbial interactions with commensal bacteria such as S. mitis may promote the stability and resilience of the microbial communities [111,112,115,116]. Moreover, the significantly decreased abundance of H. parainfluenzae in saliva during periodontitis initiation suggest its potential role as a biomarker for the disease [117].
Nevertheless, the opportunistic pathogenicity of H. parainfluenzae can manifest beyond the oral cavity, causing various systemic infections when conditions permit its dissemination throughout the body [118].
The Fusobacteriota phylum comprises two main families: Fusobacteriaceae and Leptotrichiaceae. The Fusobacterium genus of the Fusobacteriaceae family represent a pivotal component of the oral cavity, playing an integral role in biofilm formation and ecology, particularly Fusobacterium nucleatum [119]. This bacterium acts as a “bridging organism”, connecting a broad range of microorganisms that can be phenotypically and metabolically distinct (early and late colonizers with varying oxygen requirements), thus contributing to biofilm stratification and integrity [119]. This versatile coaggregation along with the ability to adhere to host surfaces are mediated by its multiple outer membrane proteins (e.g., RadD, FomA, Fap2, and CmpA) and adhesin (FadA) [120,121,122].
F. nucleatum (Fn) is classified into four subspecies: nucleatum, polymorphum, animalis, and vincentii [123,124]. Commonly identified in dental biofilm, these subspecies demonstrated distinct biofilm-forming capacity and behaviors within the in vitro biofilms, influencing the biofilm structural integrity and biogeography [123,125]. While F. nucleatum subsp nucleatum thrives in vitro biofilms and supports periodontal pathogens growth [123,126], it shows low abundance and prevalence in the oral microbiota [124]. Among the subspecies, Fn. polymorphum is more prevalent in healthy biofilm; yet, it can also be identified in disease lesions, while Fn. animalis is more associated with inflammatory conditions [126]. Moreover, F. nucleatum subspecies display distinct immunomodulatory properties, affecting neutrophil activity and cytokine production, thereby influencing their pathogenic potential [127].
Nonetheless, according to several pangenomic and phylogenetic analyses, F. nucleatum subspecies are likely genetically divergent; thus, it has been suggested that these subspecies should be considered distinct species [128,129,130].
The Leptotrichia genus of the Leptotrichiaceae family predominantly inhabits the oral cavity. This bacterium is saccharolytic [131,132] and can also withstand acidic environments [101].
While 522 bacterial taxa have been identified, 29.12% are unnamed phylotypes, which are not cultivated yet. This part of the oral microbiome that has not been thoroughly characterized may be considered as the bacterial “dark matter” of the oral microbiome [133,134]. The Patescibacteria phylum constitutes a significant component of this bacterial dark matter. Although 48.48% of its species exhibit high or moderate abundance in the oral cavity, more than 50% of species remain underexplored due to the challenges associated with their cultivation. The Patescibacteria phylum, also referred to as “Candidate Phyla Radiation (CPR)” [4], represents a unique division of the bacteria domain, whose unique characteristics and potential impact on oral health have attracted considerable scientific interest [133]. The Patescibacteria phylum mainly includes two classes: Patescibacteria [C1] (18%) and Saccharimonadia (82%). They are distinguished by their small cell and genome sizes, with limited metabolic abilities. Due to these limited capabilities, they are often epibionts, and depend on their host for their survival [135]. These characteristics not only set them apart from other bacteria but have also hindered their in vitro cultivation, limiting our understanding of their potential ecological roles and functions within the microbiome [135].
Nanosynbacter lyticus (formerly Saccharibacteria TM7x) represents the first co-isolated strain of the CPR [135]. Actually, N. lyticus establishes dynamic and complex interactions with its host, notably Schaalia odontolytica XH001, in order to ensure its survival. These interactions involve both epibiotic–parasitic and episymbiotic interactions [135,136,137]. Since its genome is largely reduced and lacks essential biosynthetic pathways which limits its growth autonomously, N. lyticus attaches to the surface of S. odontolytica to ensure its survival in a parasitic way [138]. Although this parasitic interaction negatively affects the growth of S. odontolytica, resulting in cell death, the surviving cells undergo morphological and transcriptional adaptation to sustain their episymbiotic niche and to persist together within the oral cavity [136,138,139,140]. This episymbiotic interaction allows N. lyticus to rely on its host for essential nutrients and energy and also increases the expressions of pili and arginine metabolism genes, while S. odontolytica upregulates peptidoglycan biosynthesis, cell cycle, and stress–response genes [138,139,141].
Several species within the Saccharimonadia class have been identified in gingivitis and periodontitis [142,143,144]. However, its potential role in periodontal disease remains controversial. While several studies reported its abundance in inflammatory conditions [142,143,144], suggesting a potential pathogenic role, O. Chipashvili et al. [145] demonstrated that TM7 can modulate the pathogenicity of its host in order to decrease gingival inflammation and bone loss in a mouse model, suggesting a protective role in inflammatory diseases [145]. Overall, further studies are warranted to elucidate the precise role of this epibiont in health and disease and to investigate its potential as a therapeutic target for disease management [145].

Author Contributions

Conceptualization, S.G. and S.C.; methodology, S.G. and S.C.; validation S.G. and S.C.; formal analysis, S.G. and S.C.; investigation, S.G. and S.C.; data curation, S.G. and S.C.; writing—original draft preparation, S.G. and S.C.; writing—review and editing, S.G. and S.C.; visualization, S.G. and S.C.; supervision, S.C. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

The original contributions presented in this study are included in the article. Further inquiries can be directed to the corresponding author.

Conflicts of Interest

The authors declare no conflicts of interest.

References

  1. Iyer, P. Oral Cavity Is the Gateway to the Body: Role of Oral Health Professionals: A Narrative Review. J. Calif. Dent. Assoc. 2023, 51, 2193372. [Google Scholar] [CrossRef]
  2. Benn, A.M.L.; Heng, N.C.K.; Broadbent, J.M.; Thomson, W.M. Studying the Human Oral Microbiome: Challenges and the Evolution of Solutions. Aust. Dent. J. 2018, 63, 14–24. [Google Scholar] [CrossRef]
  3. Byrne, S.J.; Butler, C.A.; Reynolds, E.C.; Dashper, S.G. Taxonomy of Oral Bacteria. Methods Microbiol. 2018, 45, 171–201. [Google Scholar]
  4. Parks, D.H.; Chuvochina, M.; Waite, D.W.; Rinke, C.; Skarshewski, A.; Chaumeil, P.A.; Hugenholtz, P. A Standardized Bacterial Taxonomy Based on Genome Phylogeny Substantially Revises the Tree of Life. Nat. Biotechnol. 2018, 36, 996–1004. [Google Scholar] [CrossRef]
  5. Braga, P.A.C.; Tata, A.; Gonçalves Dos Santos, V.; Barreiro, J.R.; Schwab, N.V.; Veiga Dos Santos, M.; Eberlin, M.N.; Ferreira, C.R. Bacterial Identification: From the Agar Plate to the Mass Spectrometer. RSC Adv. 2013, 3, 994–1008. [Google Scholar] [CrossRef]
  6. Escapa, I.F.; Chen, T.; Huang, Y.; Gajare, P.; Dewhirst, F.E.; Lemon, K.P. New Insights into Human Nostril Microbiome from the Expanded Human Oral Microbiome Database (EHOMD): A Resource for the Microbiome of the Human Aerodigestive Tract. mSystems 2018, 3, e00187-18. [Google Scholar] [CrossRef]
  7. Zaura, E.; Keijser, B.J.; Huse, S.M.; Crielaard, W. Defining the Healthy “Core Microbiome” of Oral Microbial Communities. BMC Microbiol. 2009, 9, 259. [Google Scholar] [CrossRef]
  8. Abranches, J.; Zeng, L.; Kajfasz, J.K.; Palmer, S.R.; Chakraborty, B.; Wen, Z.T.; Richards, V.P.; Brady, L.J.; Lemos, J.A. Biology of Oral Streptococci. Microbiol. Spectr. 2018, 6. [Google Scholar] [CrossRef]
  9. Kolenbrander, P.E.; Palmer, R.J.; Rickard, A.H.; Jakubovics, N.S.; Chalmers, N.I.; Diaz, P.I. Bacterial Interactions and Successions during Plaque Development. Periodontol 2000 2006, 42, 47–79. [Google Scholar] [CrossRef] [PubMed]
  10. Simon-Soro, A.; Ren, Z.; Krom, B.P.; Hoogenkamp, M.A.; Cabello-Yeves, P.J.; Daniel, S.G.; Bittinger, K.; Tomas, I.; Koo, H.; Mira, A. Polymicrobial Aggregates in Human Saliva Build the Oral Biofilm. mBio 2022, 13, e00131-22. [Google Scholar] [CrossRef] [PubMed]
  11. Zuber, P.; Kreth, J. Aspects of Oral Streptococcal Metabolic Diversity: Imagining the Landscape Beneath the Fog. Mol. Microbiol. 2023, 120, 508–524. [Google Scholar] [CrossRef]
  12. Erttmann, S.F.; Gekara, N.O. Hydrogen Peroxide Release by Bacteria Suppresses Inflammasome-Dependent Innate Immunity. Nat. Commun. 2019, 10, 3493. [Google Scholar] [CrossRef]
  13. Medapati, M.R.; Singh, N.; Bhagirath, A.Y.; Duan, K.; Triggs-Raine, B.; Batista, E.L.; Chelikani, P. Bitter Taste Receptor T2R14 Detects Quorum Sensing Molecules from Cariogenic Streptococcus mutans and Mediates Innate Immune Responses in Gingival Epithelial Cells. FASEB J. 2021, 35, e21375. [Google Scholar] [CrossRef] [PubMed]
  14. Kumar, S.S.; Gunda, V.; Reinartz, D.M.; Pond, K.W.; Thorne, C.A.; Santiago Raj, P.V.; Johnson, M.D.L.; Wilson, J.E. Oral Streptococci S. anginosus and S. mitis Induce Distinct Morphological, Inflammatory, and Metabolic Signatures in Macrophages. Infect. Immun. 2024, 92, e00536-23. [Google Scholar] [CrossRef]
  15. Tang, Y.L.; Sim, T.S.; Tan, K.S. Oral Streptococci Subvert the Host Innate Immune Response through Hydrogen Peroxide. Sci. Rep. 2022, 12, 656. [Google Scholar] [CrossRef]
  16. Matsushima, H.; Kumagai, Y.; Vandenbon, A.; Kataoka, H.; Kadena, M.; Fukamachi, H.; Arimoto, T.; Morisaki, H.; Fujiwara, N.; Okahashi, N.; et al. Microarray Analysis of Macrophage Response to Infection with Streptococcus Oralis Reveals the Immunosuppressive Effect of Hydrogen Peroxide. Biochem. Biophys. Res. Commun. 2017, 485, 461–467. [Google Scholar] [CrossRef] [PubMed]
  17. Myers, S.; Do, T.; Meade, J.L.; Tugnait, A.; Vernon, J.J.; Pistolic, J.; Hancock, R.E.W.; Marsh, P.D.; Trivedi, H.M.; Chen, D.; et al. Immunomodulatory Streptococci That Inhibit CXCL8 Secretion and NFκB Activation Are Common Members of the Oral Microbiota. J. Med. Microbiol. 2021, 70, 001329. [Google Scholar] [CrossRef] [PubMed]
  18. Kim, A.R.; Ahn, K.B.; Kim, H.Y.; Seo, H.S.; Kum, K.Y.; Yun, C.H.; Han, S.H. Streptococcus Gordonii Lipoproteins Induce IL-8 in Human Periodontal Ligament Cells. Mol. Immunol. 2017, 91, 218–224. [Google Scholar] [CrossRef]
  19. Peyyala, R.; Kirakodu, S.; Novak, K.F.; Ebersole, J.L. Epithelial Interleukin-8 Responses to Oral Bacterial Biofilms. Clin. Vaccine Immunol. 2011, 18, 1770–1772. [Google Scholar] [CrossRef]
  20. de Toledo, A.; Nagata, E.; Yoshida, Y.; Oho, T. Streptococcus Oralis Coaggregation Receptor Polysaccharides Induce Inflammatory Responses in Human Aortic Endothelial Cells. Mol. Oral Microbiol. 2012, 27, 295–307. [Google Scholar] [CrossRef]
  21. Wicaksono, D.P.; Washio, J.; Abiko, Y.; Domon, H.; Takahashi, N. Nitrite Production from Nitrate and Its Link with Lactate Metabolism in Oral Veillonella Spp. Appl. Environ. Microbiol. 2020, 86, e01255-20. [Google Scholar] [CrossRef]
  22. Rajasekaran, J.J.; Krishnamurthy, H.K.; Bosco, J.; Jayaraman, V.; Krishna, K.; Wang, T.; Bei, K. Oral Microbiome: A Review of Its Impact on Oral and Systemic Health. Microorganisms 2024, 12, 1797. [Google Scholar] [CrossRef]
  23. Giacomini, J.J.; Torres-Morales, J.; Dewhirst, F.E.; Borisy, G.G.; Mark Welch, J.L. Site Specialization of Human Oral Veillonella Species. Microbiol. Spectr. 2023, 11, e04042-22. [Google Scholar] [CrossRef] [PubMed]
  24. Yamamoto, Y.; Washio, J.; Shimizu, K.; Takahashi, N. Effects of Nitrate and Nitrite on Plaque PH Decrease and Nitrite-Producing and -Degrading Activities of Plaque In Vitro. Caries Res. 2024, 58, 552–561. [Google Scholar] [CrossRef]
  25. Sato-Suzuki, Y.; Washio, J.; Wicaksono, D.P.; Sato, T.; Fukumoto, S.; Takahashi, N. Nitrite-Producing Oral Microbiome in Adults and Children. Sci. Rep. 2020, 10, 16652. [Google Scholar] [CrossRef]
  26. Radcliffe, C.E.; Akram, N.C.; Hurrell, F.; Drucker, D.B. Effects of Nitrite and Nitrate on the Growth and Acidogenicity of Streptococcus mutans. J. Dent. 2002, 30, 325–331. [Google Scholar] [CrossRef]
  27. Liu, S.; Chen, M.; Wang, Y.; Zhou, X.; Peng, X.; Ren, B.; Li, M.; Cheng, L. Effect of Veillonella parvula on the Physiological Activity of Streptococcus mutans. Arch. Oral Biol. 2020, 109, 104578. [Google Scholar] [CrossRef]
  28. Li, G.; Liu, Y.; Zhang, M.; Ning, J.; Wu, L.; Jian, L.; Wu, H.; Cheng, X. Veillonella parvula Promotes Root Caries Development through Interactions with Streptococcus mutans and Candida albicans. Microb. Biotechnol. 2024, 17, e14547. [Google Scholar] [CrossRef]
  29. Luppens, S.B.I.; Kara, D.; Bandounas, L.; Jonker, M.J.; Wittink, F.R.A.; Bruning, O.; Breit, T.M.; Ten Cate, J.M.; Crielaard, W. Effect of Veillonella parvula on the Antimicrobial Resistance and Gene Expression of Streptococcus mutans Grown in a Dual-Species Biofilm. Oral Microbiol. Immunol. 2008, 23, 183–189. [Google Scholar] [CrossRef]
  30. Wei, Y.; Zhang, Y.; Zhuang, Y.; Tang, Y.; Nie, H.; Haung, Y.; Liu, T.; Yang, W.; Yan, F.; Zhu, Y. Veillonella parvula Acts as a Pathobiont Promoting the Biofilm Virulence and Cariogenicity of Streptococcus mutans in Adult Severe Caries. Microbiol. Spectr. 2024, 12, e04318-23. [Google Scholar] [CrossRef] [PubMed]
  31. McDaniel, J.; McDaniel, S.; Samiano, B.J.; Marrujo, M.; Kingsley, K.; Howard, K.M. Microbial Screening Reveals Oral Site-Specific Locations of the Periodontal Pathogen Selenomonas Noxia. Curr. Issues Mol. Biol. 2021, 43, 353–364. [Google Scholar] [CrossRef]
  32. Drescher, J.; Schlafer, S.; Schaudinn, C.; Riep, B.; Neumann, K.; Friedmann, A.; Petrich, A.; Göbel, U.B.; Moter, A. Molecular Epidemiology and Spatial Distribution of Selenomonas Spp. in Subgingival Biofilms. Eur. J. Oral Sci. 2010, 118, 466–474. [Google Scholar] [CrossRef]
  33. Oliveira, R.R.D.S.; Fermiano, D.; Feres, M.; Figueiredo, L.C.; Teles, F.R.F.; Soares, G.M.S.; Faveri, M. Levels of Candidate Periodontal Pathogens in Subgingival Biofilm. J. Dent. Res. 2016, 95, 711–718. [Google Scholar] [CrossRef] [PubMed]
  34. Hawkes, C.G.; Hinson, A.N.; Vashishta, A.; Read, C.B.; Carlyon, J.A.; Lamont, R.J.; Uriarte, S.M.; Miller, D.P. Selenomonas sputigena Interactions with Gingival Epithelial Cells That Promote Inflammation. Infect. Immun. 2023, 91, e00319-22. [Google Scholar] [CrossRef]
  35. Yang, Z.; Cai, T.; Li, Y.; Jiang, D.; Luo, J.; Zhou, Z. Oral Microbial Communities in 5-Year-Old Children with versus without Dental Caries. BMC Oral Health 2023, 23, 400. [Google Scholar] [CrossRef]
  36. Zhou, J.; Jiang, N.; Wang, S.; Hu, X.; Jiao, K.; He, X.; Li, Z.; Wang, J. Exploration of Human Salivary Microbiomes—Insights into the Novel Characteristics of Microbial Community Structure in Caries and Caries-Free Subjects. PLoS ONE 2016, 11, e0147039. [Google Scholar] [CrossRef] [PubMed]
  37. Becker, M.R.; Paster, B.J.; Leys, E.J.; Moeschberger, M.L.; Kenyon, S.G.; Galvin, J.L.; Boches, S.K.; Dewhirst, F.E.; Griffen, A.L. Molecular Analysis of Bacterial Species Associated with Childhood Caries. J. Clin. Microbiol. 2002, 40, 1001–1009. [Google Scholar] [CrossRef] [PubMed]
  38. Shouche, Y.S.; Dighe, A.S.; Dhotre, D.P.; Patole, M.S.; Ranade, D.R. Selenomonas. In Bergey’s Manual of Systematics of Archaea and Bacteria; Wiley: Hoboken, NJ, USA, 2015; pp. 1–12. [Google Scholar] [CrossRef]
  39. Cho, H.; Ren, Z.; Divaris, K.; Roach, J.; Lin, B.M.; Liu, C.; Azcarate-Peril, M.A.; Simancas-Pallares, M.A.; Shrestha, P.; Orlenko, A.; et al. Selenomonas sputigena Acts as a Pathobiont Mediating Spatial Structure and Biofilm Virulence in Early Childhood Caries. Nat. Commun. 2023, 14, 2919. [Google Scholar] [CrossRef]
  40. Tett, A.; Pasolli, E.; Masetti, G.; Ercolini, D.; Segata, N. Prevotella Diversity, Niches and Interactions with the Human Host. Nat. Rev. Microbiol. 2021, 19, 585–599. [Google Scholar] [CrossRef]
  41. Sharma, G.; Garg, N.; Hasan, S.; Shirodkar, S. Prevotella: An Insight into Its Characteristics and Associated Virulence Factors. Microb. Pathog. 2022, 169, 105673. [Google Scholar] [CrossRef]
  42. Accetto, T.; Avguštin, G. Polysaccharide Utilization Locus and CAZYme Genome Repertoires Reveal Diverse Ecological Adaptation of Prevotella Species. Syst. Appl. Microbiol. 2015, 38, 453–461. [Google Scholar] [CrossRef]
  43. Ibrahim, M.; Subramanian, A.; Anishetty, S. Comparative Pan Genome Analysis of Oral Prevotella Species Implicated in Periodontitis. Funct. Integr. Genom. 2017, 17, 513–536. [Google Scholar] [CrossRef]
  44. Kressirer, C.A.; Chen, T.; Lake Harriman, K.; Frias-Lopez, J.; Dewhirst, F.E.; Tavares, M.A.; Tanner, A.C.R. Functional Profiles of Coronal and Dentin Caries in Children. J. Oral Microbiol. 2018, 10, 1495976. [Google Scholar] [CrossRef]
  45. Könönen, E.; Fteita, D.; Gursoy, U.K.; Gursoy, M. Prevotella Species as Oral Residents and Infectious Agents with Potential Impact on Systemic Conditions. J. Oral Microbiol. 2022, 14, 2079814. [Google Scholar] [CrossRef]
  46. Niu, Y.; Zhang, C.; Sun, Y.; Dong, L.; Si, Y.; Yang, J.; Zhu, P.; Yang, F. Symbiotic Relationship between Prevotella Denticola and Streptococcus mutans Enhances Virulence of Plaque Biofilms. Arch. Oral Biol. 2023, 151, 105714. [Google Scholar] [CrossRef] [PubMed]
  47. Kianoush, N.; Adler, C.J.; Nguyen, K.A.T.; Browne, G.V.; Simonian, M.; Hunter, N. Bacterial Profile of Dentine Caries and the Impact of PH on Bacterial Population Diversity. PLoS ONE 2014, 9, e92940. [Google Scholar] [CrossRef]
  48. Chen, L.; Qin, B.; Du, M.; Zhong, H.; Xu, Q.; Li, Y.; Zhang, P.; Fan, M. Extensive Description and Comparison of Human Supra-Gingival Microbiome in Root Caries and Health. PLoS ONE 2015, 10, e0117064. [Google Scholar] [CrossRef]
  49. Chen, W.A.; Dou, Y.; Fletcher, H.M.; Boskovic, D.S. Local and Systemic Effects of Porphyromonas gingivalis Infection. Microorganisms 2023, 11, 470. [Google Scholar] [CrossRef]
  50. Hajishengallis, G.; Diaz, P.I. Porphyromonas gingivalis: Immune Subversion Activities and Role in Periodontal Dysbiosis. Curr. Oral Health Rep. 2020, 7, 12–21. [Google Scholar] [CrossRef] [PubMed]
  51. Tribble, G.D.; Kerr, J.E.; Wang, B.Y. Genetic Diversity in the Oral Pathogen Porphyromonas gingivalis: Molecular Mechanisms and Biological Consequences. Futur. Microbiol. 2013, 8, 607–620. [Google Scholar] [CrossRef] [PubMed]
  52. Watanabe, T.; Shibasaki, M.; Maruyama, F.; Sekizaki, T.; Nakagawa, I. Investigation of Potential Targets of Porphyromonas CRISPRs among the Genomes of Porphyromonas Species. PLoS ONE 2017, 12, e0183752. [Google Scholar] [CrossRef]
  53. Tribble, G.D.; Rigney, T.W.; Dao, D.H.V.; Wong, C.T.; Kerr, J.E.; Taylor, B.E.; Pacha, S.; Kaplan, H.B. Natural Competence Is a Major Mechanism for Horizontal DNA Transfer in the Oral Pathogen Porphyromonas gingivalis. mBio 2012, 3, e00231-11. [Google Scholar] [CrossRef]
  54. Ingalagi, P.; Bhat, K.; Kulkarni, R.; Kotrashetti, V.; Kumbar, V.; Kugaji, M. Detection and Comparison of Prevalence of Porphyromonas gingivalis through Culture and Real Time-Polymerase Chain Reaction in Subgingival Plaque Samples of Chronic Periodontitis and Healthy Individuals. J. Oral Maxillofac. Pathol. 2022, 26, 288. [Google Scholar] [CrossRef]
  55. Zhao, L.; Wu, Y.F.; Meng, S.; Yang, H.; OuYang, Y.L.; Zhou, X.D. Prevalence of FimA Genotypes of Porphyromonas gingivalis and Periodontal Health Status in Chinese Adults. J. Periodontal. Res. 2007, 42, 511–517. [Google Scholar] [CrossRef]
  56. Kugaji, M.; Muddapur, U.; Bhat, K.; Joshi, V.; Manubolu, M.; Pathakoti, K.; Peram, M.R.; Kumbar, V. Variation in the Occurrence of Fima Genotypes of Porphyromonas gingivalis in Periodontal Health and Disease. Int. J. Environ. Res. Public Health 2020, 17, 1826. [Google Scholar] [CrossRef]
  57. Bartnicka, D.; Karkowska-Kuleta, J.; Zawrotniak, M.; Satała, D.; Michalik, K.; Zielinska, G.; Bochenska, O.; Kozik, A.; Ciaston, I.; Koziel, J.; et al. Adhesive Protein-Mediated Cross-Talk between Candida albicans and Porphyromonas gingivalis in Dual Species Biofilm Protects the Anaerobic Bacterium in Unfavorable Oxic Environment. Sci. Rep. 2019, 9, 4376. [Google Scholar] [CrossRef]
  58. Soto, C.; Rojas, V.; Yáñez, L.; Hidalgo, A.; Olivera, M.; Pacheco, M.; Venegas, D.; Salinas, D.; Bravo, D.; Quest, A.F.G. Porphyromonas gingivalis-Helicobacter Pylori Co-Incubation Enhances Porphyromonas gingivalis Virulence and Increases Migration of Infected Human Oral Keratinocytes. J. Oral Microbiol. 2022, 14, 2107691. [Google Scholar] [CrossRef] [PubMed]
  59. Yamada, M.; Ikegami, A.; Kuramitsu, H.K. Synergistic Biofilm Formation by Treponema Denticola and Porphyromonas gingivalis. FEMS Microbiol. Lett. 2005, 250, 271–277. [Google Scholar] [CrossRef] [PubMed]
  60. Periasamy, S.; Kolenbrander, P.E. Mutualistic Biofilm Communities Develop with Porphyromonas gingivalis and Initial, Early, and Late Colonizers of Enamel. J. Bacteriol. 2009, 191, 6804–6811. [Google Scholar] [CrossRef]
  61. Hajishengallis, G. Porphyromonas gingivalis-Host Interactions: Open War or Intelligent Guerilla Tactics? Microbes Infect. 2009, 11, 637–645. [Google Scholar] [CrossRef] [PubMed]
  62. Van Hoogmoed, C.G.; Geertsema-Doornbusch, G.I.; Teughels, W.; Quirynen, M.; Busscher, H.J.; Van Der Mei, H.C. Reduction of Periodontal Pathogens Adhesion by Antagonistic Strains. Oral Microbiol. Immunol. 2008, 23, 43–48. [Google Scholar] [CrossRef]
  63. Tenorio, E.L.; Klein, B.A.; Cheung, W.S.; Hu, L.T. Identification of Interspecies Interactions Affecting Porphyromonas gingivalis Virulence Phenotypes. J. Oral Microbiol. 2011, 3, 8396. [Google Scholar] [CrossRef]
  64. Wang, Q.; Wang, B.-Y.; Pratap, S.; Xie, H. Oral Microbiome Associated with Differential Ratios of Porphyromonas gingivalis and Streptococcus cristatus. Microbiol. Spectr. 2024, 12, e03482-23. [Google Scholar] [CrossRef]
  65. Aleksijević, L.H.; Aleksijević, M.; Škrlec, I.; Šram, M.; Šram, M.; Talapko, J. Porphyromonas gingivalis Virulence Factors and Clinical Significance in Periodontal Disease and Coronary Artery Diseases. Pathogens 2022, 11, 1173. [Google Scholar] [CrossRef] [PubMed]
  66. de Jongh, C.A.; de Vries, T.J.; Bikker, F.J.; Gibbs, S.; Krom, B.P. Mechanisms of Porphyromonas gingivalis to Translocate over the Oral Mucosa and Other Tissue Barriers. J. Oral Microbiol. 2023, 15, 2205291. [Google Scholar] [CrossRef]
  67. Mei, F.; Xie, M.; Huang, X.; Long, Y.; Lu, X.; Wang, X.; Chen, L. Porphyromonas gingivalis and Its Systemic Impact: Current Status. Pathogens 2020, 9, 944. [Google Scholar] [CrossRef]
  68. Huang, Z.; Hao, M.; Shi, N.; Wang, X.; Yuan, L.; Yuan, H.; Wang, X. Porphyromonas gingivalis: A Potential Trigger of Neurodegenerative Disease. Front. Immunol. 2025, 16, 1482033. [Google Scholar] [CrossRef] [PubMed]
  69. Hayashi, F.; Okada, M.; Zhong, X.; Miura, K. PCR Detection of Capnocytophaga Species in Dental Plaque Samples from Children Aged 2 to 12 Years. Microbiol. Immunol. 2001, 45, 17–22. [Google Scholar] [CrossRef] [PubMed]
  70. Hosohama-Saito, K.; Kokubu, E.; Okamoto-Shibayama, K.; Kita, D.; Katakura, A.; Ishihara, K. Involvement of LuxS in Biofilm Formation by Capnocytophaga ochracea. PLoS ONE 2016, 11, e0147114. [Google Scholar] [CrossRef]
  71. Kita, D.; Shibata, S.; Kikuchi, Y.; Kokubu, E.; Nakayama, K.; Saito, A.; Ishihara, K. Involvement of the Type IX Secretion System in Capnocytophaga ochracea Gliding Motility and Biofilm Formation. Appl. Environ. Microbiol. 2016, 82, 1756–1766. [Google Scholar] [CrossRef]
  72. Ratheesh, N.K.; Zdimal, A.M.; Calderon, C.A.; Shrivastava, A. Bacterial Swarm-Mediated Phage Transportation Disrupts a Biofilm Inherently Protected from Phage Penetration. Microbiol. Spectr. 2023, 11, e00937-23. [Google Scholar] [CrossRef]
  73. Shrivastava, A.; Patel, V.K.; Tang, Y.; Yost, S.C.; Dewhirst, F.E.; Berg, H.C. Cargo Transport Shapes the Spatial Organization of a Microbial Community. Proc. Natl. Acad. Sci. USA 2018, 115, 8633–8638. [Google Scholar] [CrossRef]
  74. Idate, U.; Bhat, K.; Kotrashetti, V.; Kugaji, M.; Kumbar, V. Molecular Identification of Capnocytophaga Species from the Oral Cavity of Patients with Chronic Periodontitis and Healthy Individuals. J. Oral Maxillofac. Pathol. 2020, 24, 397. [Google Scholar] [CrossRef]
  75. Pudakalkatti, P.; Baheti, A.; Hattarki, S.; Kambali, S.; Naik, R. Detection and Prevalence of Capnocytophaga in Periodontal Health and Disease. J. Orofac. Sci. 2016, 8, 92. [Google Scholar] [CrossRef]
  76. Shigeishi, H.; Hamada, N.; Kaneyasu, Y.; Niitani, Y.; Takemoto, T.; Ohta, K. Prevalence of Oral Capnocytophaga Species and Their Association with Dental Plaque Accumulation and Periodontal Inflammation in Middle-Aged and Older People. Biomed. Rep. 2024, 20, 99. [Google Scholar] [CrossRef] [PubMed]
  77. Zhu, W.; Shen, W.; Wang, J.; Xu, Y.; Zhai, R.; Zhang, J.; Wang, M.; Wang, M.; Liu, L. Capnocytophaga Gingivalis Is a Potential Tumor Promotor in Oral Cancer. Oral Dis. 2022, 30, 353–362. [Google Scholar] [CrossRef] [PubMed]
  78. Dewhirst, F.E.; Chen, T.; Izard, J.; Paster, B.J.; Tanner, A.C.R.; Yu, W.H.; Lakshmanan, A.; Wade, W.G. The Human Oral Microbiome. J. Bacteriol. 2010, 192, 5002–5017. [Google Scholar] [CrossRef] [PubMed]
  79. Li, J.; Helmerhorst, E.J.; Leone, C.W.; Troxler, R.F.; Yaskell, T.; Haffajee, A.D.; Socransky, S.S.; Oppenheim, F.G. Identification of Early Microbial Colonizers in Human Dental Biofilm. J. Appl. Microbiol. 2004, 97, 1311–1318. [Google Scholar] [CrossRef]
  80. Soria, S.; Angulo-Bejarano, P.I.; Sharma, A. Biofilms: Development and Molecular Interaction of Microbiome in the Human Oral Cavity. In New and Future Developments in Microbial Biotechnology and Bioengineering: Microbial Biofilms Current Research and Future Trends in Microbial Biofilms; Elsevier: Amsterdam, The Netherlands, 2019. [Google Scholar]
  81. Zijnge, V.; Van Leeuwen, M.B.M.; Degener, J.E.; Abbas, F.; Thurnheer, T.; Gmür, R.; Harmsen, H.J.M. Oral Biofilm Architecture on Natural Teeth. PLoS ONE 2010, 5, e9321. [Google Scholar] [CrossRef]
  82. Yang, R.; Zou, J.; Li, J.Y. Study of the Relationship between Oral Actinomyces and Childhood Caries. West China J. Stomatol. 2007, 25, 568–570. [Google Scholar]
  83. Struzycka, I. The Oral Microbiome in Dental Caries. Pol. J. Microbiol. 2014, 63, 127–135. [Google Scholar] [CrossRef]
  84. Dame-Teixeira, N.; Parolo, C.C.F.; Maltz, M.; Tugnait, A.; Devine, D.; Do, T. Actinomyces Spp. Gene Expression in Root Caries Lesions. J. Oral Microbiol. 2016, 8, 32383. [Google Scholar] [CrossRef] [PubMed]
  85. Brailsford, S.R.; Lynch, E.; Beighton, D. The Isolation of Actinomyces Naeslundii from Sound Root Surfaces and Root Carious Lesions. Caries Res. 1998, 32, 100–106. [Google Scholar] [CrossRef]
  86. Tang, G.; Samaranayake, L.P.; Yip, H.K.; Chu, F.C.S.; Tsang, P.C.S.; Cheung, B.P.K. Direct Detection of Actinomyces Spp. from Infected Root Canals in a Chinese Population: A Study Using PCR-Based, Oligonucleotide-DNA Hybridization Technique. J. Dent. 2003, 31, 559–568. [Google Scholar] [CrossRef]
  87. Isaac, R.D.; Sanjeev, K.; Subbulakshmi, C.L.; Amirtharaj, L.V.; Sekar, M. Identification of a Novel Bacterium Scardovia Wiggsiae in High Caries Risk Adolescence: A Metagenomic and Melt Curve Analysis. J. Conserv. Dent. 2022, 25, 297–305. [Google Scholar] [CrossRef] [PubMed]
  88. McDaniel, S.; McDaniel, J.; Howard, K.M.; Kingsley, K. Molecular Screening and Analysis Reveal Novel Oral Site-Specific Locations for the Cariogenic Pathogen Scardovia Wiggsiae. Dent. J. 2021, 9, 73. [Google Scholar] [CrossRef] [PubMed]
  89. Kressirer, C.A.; Smith, D.J.; King, W.F.; Dobeck, J.M.; Starr, J.R.; Tanner, A.C.R. Scardovia Wiggsiae and Its Potential Role as a Caries Pathogen. J. Oral Biosci. 2017, 59, 135–141. [Google Scholar] [CrossRef]
  90. Kameda, M.; Abiko, Y.; Washio, J.; Tanner, A.C.R.; Kressirer, C.A.; Mizoguchi, I.; Takahashi, N. Sugar Metabolism of Scardovia Wiggsiae, a Novel Caries-Associated Bacterium. Front. Microbiol. 2020, 11, 479. [Google Scholar] [CrossRef]
  91. Shao, Q.; Feng, D.; Yu, Z.; Chen, D.; Ji, Y.; Ye, Q.; Cheng, D. The Role of Microbial Interactions in Dental Caries: Dental Plaque Microbiota Analysis. Microb. Pathog. 2023, 185, 106390. [Google Scholar] [CrossRef]
  92. Welch, J.L.M.; Rossetti, B.J.; Rieken, C.W.; Dewhirst, F.E.; Borisy, G.G. Biogeography of a Human Oral Microbiome at the Micron Scale. Proc. Natl. Acad. Sci. USA 2016, 113, E791–E800. [Google Scholar] [CrossRef]
  93. Li, Q.; Zhou, F.; Su, Z.; Li, Y.; Li, J. Corynebacterium matruchotii: A Confirmed Calcifying Bacterium with a Potentially Important Role in the Supragingival Plaque. Front. Microbiol. 2022, 13, 940643. [Google Scholar] [CrossRef]
  94. Morillo-Lopez, V.; Sjaarda, A.; Islam, I.; Borisy, G.G.; Mark Welch, J.L. Corncob Structures in Dental Plaque Reveal Microhabitat Taxon Specificity. Microbiome 2022, 10, 145. [Google Scholar] [CrossRef]
  95. Kreth, J.; Helliwell, E.; Treerat, P.; Merritt, J. Molecular Commensalism: How Oral Corynebacteria and Their Extracellular Membrane Vesicles Shape Microbiome Interactions. Front. Oral Health 2024, 5, 1410786. [Google Scholar] [CrossRef]
  96. Almeida, E.; Puri, S.; Labossiere, A.; Elangovan, S.; Kim, J.; Ramsey, M. Bacterial Multispecies Interaction Mechanisms Dictate Biogeographic Arrangement between the Oral Commensals Corynebacterium matruchotii and Streptococcus mitis. mSystems 2023, 8, e00115-23. [Google Scholar] [CrossRef]
  97. Briaud, P.; Carroll, R.K. Extracellular Vesicle Biogenesis and Functions in Gram-Positive Bacteria. Infect. Immun. 2020, 88, e00433-20. [Google Scholar] [CrossRef] [PubMed]
  98. Giacomini, J.J.; Torres-Morales, J.; Dewhirst, F.E.; Borisy, G.G.; Mark Welch, J.L. Spatial Ecology of the Neisseriaceae Family in the Human Oral Cavity. Microbiol. Spectr. 2025, 13, e03275-24. [Google Scholar] [CrossRef] [PubMed]
  99. Feng, J.; Liu, J.; Jiang, M.; Chen, Q.; Zhang, Y.; Yang, M.; Zhai, Y. The Role of Oral Nitrate-Reducing Bacteria in the Prevention of Caries: A Review Related to Caries and Nitrate Metabolism. Caries Res. 2023, 57, 119–132. [Google Scholar] [CrossRef]
  100. Moran, S.P.; Rosier, B.T.; Henriquez, F.L.; Burleigh, M.C. The Effects of Nitrate on the Oral Microbiome: A Systematic Review Investigating Prebiotic Potential. J. Oral Microbiol. 2024, 16, 2322228. [Google Scholar] [CrossRef] [PubMed]
  101. Richards, V.P.; Alvarez, A.J.; Luce, A.R.; Bedenbaugh, M.; Mitchell, M.L.; Burne, R.A.; Nascimento, M.M. Microbiomes of Sitespecific Dental Plaques from Children with Different Caries Status. Infect. Immun. 2017, 85, e00106-17. [Google Scholar] [CrossRef]
  102. Gross, E.L.; Beall, C.J.; Kutsch, S.R.; Firestone, N.D.; Leys, E.J.; Griffen, A.L. Beyond Streptococcus mutans: Dental Caries Onset Linked to Multiple Species by 16S RRNA Community Analysis. PLoS ONE 2012, 7, e47722. [Google Scholar] [CrossRef]
  103. Peterson, S.N.; Snesrud, E.; Liu, J.; Ong, A.C.; Kilian, M.; Schork, N.J.; Bretz, W. The Dental Plaque Microbiome in Health and Disease. PLoS ONE 2013, 8, e58487. [Google Scholar] [CrossRef]
  104. Tanner, A.C.R.; Kressirer, C.A.; Faller, L.L. Understanding Caries From the Oral Microbiome Perspective. J. Calif. Dent. Assoc. 2016, 44, 437–446. [Google Scholar] [CrossRef] [PubMed]
  105. Fukuda, S.; Akatsu, T.; Fujii, A.; Kawano, S.; Minegishi, Y.; Ota, N. Commensal Neisseria Inhibit Porphyromonas gingivalis Invasion of Gingival Epithelial Cells. Oral Health Prev. Dent. 2024, 22, 609–616. [Google Scholar] [CrossRef] [PubMed]
  106. Gross, E.L.; Leys, E.J.; Gasparovich, S.R.; Firestone, N.D.; Schwartzbaum, J.A.; Janies, D.A.; Asnani, K.; Griffen, A.L. Bacterial 16S Sequence Analysis of Severe Caries in Young Permanent Teeth. J. Clin. Microbiol. 2010, 48, 4121–4128. [Google Scholar] [CrossRef] [PubMed]
  107. Gerner-Smidt, P.; Keiser-Nielsen, H.; Dorsch, M.; Stackebrandt, E.; Ursing, J.; Blom, J.; Christensen, A.C.; Christensen, J.J.; Frederiksen, W.; Hoffmann, S.; et al. Lautropia mirabilis Gen. Nov., Sp. Nov., a Gram-Negative Motile Coccus with Unusual Morphology Isolated from the Human Mouth. Microbiology 1994, 140, 1787–1797. [Google Scholar] [CrossRef]
  108. Lim, Y.K.; Park, S.N.; Lee, W.P.; Shin, J.H.; Jo, E.; Shin, Y.; Paek, J.; Chang, Y.H.; Kim, H.; Kook, J.K. Lautropia Dentalis Sp. Nov., Isolated from Human Dental Plaque of a Gingivitis Lesion. Curr. Microbiol. 2019, 76, 1369–1373. [Google Scholar] [CrossRef]
  109. Calheiros Cruz, G.; Sousa, M.; Vilela, S.; Teixeira E Costa, F.; Silva, F.J. Lautropia mirabilis: An Exceedingly Rare Cause of Peritoneal Dialysis-Associated Peritonitis. Case Rep. Nephrol. Dial. 2022, 12, 81–84. [Google Scholar] [CrossRef]
  110. Tan, R.Y.P.; Tan, B.Q.; Rao, N. The First Case of Peritoneal Dialysis-Associated Peritonitis Due to Lautropia mirabilis. Nephrology 2021, 26, 634–635. [Google Scholar] [CrossRef]
  111. Perera, D.; McLean, A.; Morillo-López, V.; Cloutier-Leblanc, K.; Almeida, E.; Cabana, K.; Mark Welch, J.; Ramsey, M. Mechanisms Underlying Interactions between Two Abundant Oral Commensal Bacteria. ISME J. 2021, 16, 948–957. [Google Scholar] [CrossRef]
  112. de Palma, T.H.; Powers, C.; McPartland, M.J.; Mark Welch, J.; Ramsey, M. Essential Genes for Haemophilus parainfluenzae Survival and Biofilm Growth. mSystems 2024, 9, e00674-24. [Google Scholar] [CrossRef]
  113. Giacomini, J.J.; Torres-Morales, J.; Tang, J.; Dewhirst, F.E.; Borisy, G.G.; Mark Welch, J.L. Spatial Ecology of Haemophilus and Aggregatibacter in the Human Oral Cavity. Microbiol. Spectr. 2024, 12, e04017-23. [Google Scholar] [CrossRef] [PubMed]
  114. Utter, D.R.; Borisy, G.G.; Eren, A.M.; Cavanaugh, C.M.; Mark Welch, J.L. Metapangenomics of the Oral Microbiome Provides Insights into Habitat Adaptation and Cultivar Diversity. Genome Biol. 2020, 21, 293. [Google Scholar] [CrossRef]
  115. Tseng, Y.C.; Yang, H.Y.; Lin, W.T.; Chang, C.B.; Chien, H.C.; Wang, H.P.; Chen, C.M.; Wang, J.T.; Li, C.; Wu, S.F.; et al. Salivary Dysbiosis in Sjögren’s Syndrome and a Commensal-Mediated Immunomodulatory Effect of Salivary Gland Epithelial Cells. npj Biofilms Microbiomes 2021, 7, 21. [Google Scholar] [CrossRef] [PubMed]
  116. Tseng, Y.C.; Liao, K.S.; Lin, W.T.; Li, C.; Chang, C.B.; Hsu, J.W.; Chan, C.P.; Chen, C.M.; Wang, H.P.; Chien, H.C.; et al. A Human Oral Commensal-Mediated Protection against Sjögren’s Syndrome with Maintenance of T Cell Immune Homeostasis and Improved Oral Microbiota. Npj Biofilms Microbiomes 2025, 11, 18. [Google Scholar] [CrossRef]
  117. Diao, J.; Yuan, C.; Tong, P.; Ma, Z.; Sun, X.; Zheng, S. Potential Roles of the Free Salivary Microbiome Dysbiosis in Periodontal Diseases. Front. Cell. Infect. Microbiol. 2021, 11, 711282. [Google Scholar] [CrossRef]
  118. Wajid, S.; Farrukh, L.; Rosenberg, L.; Faiz, M.; Singh, G. Systemic Haemophilus parainfluenzae Infection Manifesting with Endocarditis and Membranoproliferative Glomerulonephritis. Cureus 2023, 15, e41086. [Google Scholar] [CrossRef]
  119. Jenkinson, H.F.; Lamont, R.J. Oral Microbial Communities in Sickness and in Health. Trends Microbiol. 2005, 13, 589–595. [Google Scholar] [CrossRef]
  120. Chen, Y.; Shi, T.; Li, Y.; Huang, L.; Yin, D. Fusobacterium Nucleatum: The Opportunistic Pathogen of Periodontal and Peri-Implant Diseases. Front. Microbiol. 2022, 13, 860149. [Google Scholar] [CrossRef] [PubMed]
  121. Kaplan, C.W.; Lux, R.; Haake, S.K.; Shi, W. The Fusobacterium Nucleatum Outer Membrane Protein RadD Is an Arginine-Inhibitable Adhesin Required for Inter-Species Adherence and the Structured Architecture of Multispecies Biofilm. Mol. Microbiol. 2009, 71, 35–47. [Google Scholar] [CrossRef]
  122. Coppenhagen-Glazer, S.; Sol, A.; Abed, J.; Naor, R.; Zhang, X.; Han, Y.W.; Bachrach, G. Fap2 of Fusobacterium Nucleatum Is a Galactose-Inhibitable Adhesin Involved in Coaggregation, Cell Adhesion, and Preterm Birth. Infect. Immun. 2015, 83, 1104–1113. [Google Scholar] [CrossRef]
  123. Thurnheer, T.; Karygianni, L.; Flury, M.; Belibasakis, G.N. Fusobacterium Species and Subspecies Differentially Affect the Composition and Architecture of Supra- and Subgingival Biofilms Models. Front. Microbiol. 2019, 10, 1716. [Google Scholar] [CrossRef] [PubMed]
  124. Hao, H.; Nambu, T.; Liang, Y.; Kato, J.; Shinkawa, A.; Uchida, H.; Zhang, R.; Zheng, J.; Okinaga, T.; Takahashi, K. Phylogenetic Analysis and Subspecies Distribution of Fusobacterium Nucleatum Isolated from Interdental Plaque. Nano Biomed. 2024, 16, 109–115. [Google Scholar] [CrossRef]
  125. Muchova, M.; Balacco, D.L.; Grant, M.M.; Chapple, I.L.C.; Kuehne, S.A.; Hirschfeld, J. Fusobacterium Nucleatum Subspecies Differ in Biofilm Forming Ability In Vitro. Front. Oral Health 2022, 3, 853618. [Google Scholar] [CrossRef] [PubMed]
  126. Krieger, M.; AbdelRahman, Y.M.; Choi, D.; Palmer, E.A.; Yoo, A.; McGuire, S.; Kreth, J.; Merritt, J. Stratification of Fusobacterium Nucleatum by Local Health Status in the Oral Cavity Defines Its Subspecies Disease Association. Cell Host Microbe 2024, 32, 479–488.e4. [Google Scholar] [CrossRef]
  127. Muchova, M.; Kuehne, S.A.; Grant, M.M.; Smith, P.P.; Nagi, M.; Chapple, I.L.C.; Hirschfeld, J. Fusobacterium Nucleatum Elicits Subspecies-Specific Responses in Human Neutrophils. Front. Cell. Infect. Microbiol. 2024, 14, 1449539. [Google Scholar] [CrossRef]
  128. Kook, J.K.; Park, S.N.; Lim, Y.K.; Cho, E.; Jo, E.; Roh, H.; Shin, Y.; Paek, J.; Kim, H.S.; Kim, H.; et al. Genome-Based Reclassification of Fusobacterium Nucleatum Subspecies at the Species Level. Curr. Microbiol. 2017, 74, 1137–1147. [Google Scholar] [CrossRef] [PubMed]
  129. Ma, X.; Sun, T.; Zhou, J.; Zhi, M.; Shen, S.; Wang, Y.; Gu, X.; Li, Z.; Gao, H.; Wang, P.; et al. Pangenomic Study of Fusobacterium Nucleatum Reveals the Distribution of Pathogenic Genes and Functional Clusters at the Subspecies and Strain Levels. Microbiol. Spectr. 2023, 11, e05184-22. [Google Scholar] [CrossRef]
  130. Krieger, M.; Guo, M.; Merritt, J. Reexamining the Role of Fusobacterium Nucleatum Subspecies in Clinical and Experimental Studies. Gut Microbes 2024, 16, 2415490. [Google Scholar] [CrossRef]
  131. Eribe, E.R.K.; Olsen, I. Leptotrichia Species in Human Infections II. J. Oral Microbiol. 2017, 9, 1368848. [Google Scholar] [CrossRef]
  132. Thompson, J.; Pikis, A. Metabolism of Sugars by Genetically Diverse Species of Oral Leptotrichia. Mol. Oral Microbiol. 2012, 27, 34–44. [Google Scholar] [CrossRef]
  133. Khelaifia, S.; Virginie, P.; Belkacemi, S.; Tassery, H.; Terrer, E.; Aboudharam, G. Culturing the Human Oral Microbiota, Updating Methodologies and Cultivation Techniques. Microorganisms 2023, 11, 836. [Google Scholar] [CrossRef]
  134. Bhandary, R.; Venugopalan, G.; Ramesh, A.; Tartaglia, G.M.; Singhal, I.; Khijmatgar, S. Microbial Symphony: Navigating the Intricacies of the Human Oral Microbiome and Its Impact on Health. Microorganisms 2024, 12, 571. [Google Scholar] [CrossRef] [PubMed]
  135. He, X.; McLean, J.S.; Edlund, A.; Yooseph, S.; Hall, A.P.; Liu, S.Y.; Dorrestein, P.C.; Esquenazi, E.; Hunter, R.C.; Cheng, G.; et al. Cultivation of a Human-Associated TM7 Phylotype Reveals a Reduced Genome and Epibiotic Parasitic Lifestyle. Proc. Natl. Acad. Sci. USA 2015, 112, 244–249. [Google Scholar] [CrossRef]
  136. Bor, B.; Poweleit, N.; Bois, J.S.; Cen, L.; Bedree, J.K.; Zhou, Z.H.; Gunsalus, R.P.; Lux, R.; McLean, J.S.; He, X.; et al. Phenotypic and Physiological Characterization of the Epibiotic Interaction Between TM7x and Its Basibiont Actinomyces. Microb. Ecol. 2016, 71, 243–255. [Google Scholar] [CrossRef]
  137. Bedree, J.K.; Bor, B.; Cen, L.; Edlund, A.; Lux, R.; Mclean, J.S.; Shi, W.; He, X. Quorum Sensing Modulates the Epibiotic-Parasitic Relationship Between Actinomyces Odontolyticusand Its Saccharibacteria Epibiont, a Nanosynbacter LyticusStrain, TM7x. Front. Microbiol. 2018, 9, 2049. [Google Scholar] [CrossRef] [PubMed]
  138. Hendrickson, E.L.; Bor, B.; Kerns, K.A.; Cen, L.; Shi, W.; He, X.; McLean, J.S. Ultrasmall Epibiont Nanosynbacter Lyticus Strain TM7x and Host Bacteria Transcriptional Activity after Initial Host Parasitism. J. Oral Microbiol. 2024, 16, 2287349. [Google Scholar] [CrossRef] [PubMed]
  139. Hendrickson, E.L.; Bor, B.; Kerns, K.A.; Lamont, E.I.; Chang, Y.; Liu, J.; Cen, L.; Schulte, F.; Hardt, M.; Shi, W.; et al. Transcriptome of Epibiont Saccharibacteria Nanosynbacter Lyticus Strain TM7x During the Establishment of Symbiosis. J. Bacteriol. 2022, 204, e00112-22. [Google Scholar] [CrossRef]
  140. Bor, B.; McLean, J.S.; Foster, K.R.; Cen, L.; To, T.T.; Serrato-Guillen, A.; Dewhirst, F.E.; Shi, W.; He, X. Rapid Evolution of Decreased Host Susceptibility Drives a Stable Relationship between Ultrasmall Parasite TM7x and Its Bacterial Host. Proc. Natl. Acad. Sci. USA 2018, 115, 12277–12282. [Google Scholar] [CrossRef]
  141. Dong, P.T.; Tian, J.; Kobayashi-Kirschvink, K.J.; Cen, L.; McLean, J.S.; Bor, B.; Shi, W.; He, X. Episymbiotic Saccharibacteria Induce Intracellular Lipid Droplet Production in Their Host Bacteria. ISME J. 2024, 18, wrad034. [Google Scholar] [CrossRef]
  142. Papapanou, P.N.; Park, H.; Cheng, B.; Kokaras, A.; Paster, B.; Burkett, S.; Watson, C.W.M.; Annavajhala, M.K.; Uhlemann, A.C.; Noble, J.M. Subgingival Microbiome and Clinical Periodontal Status in an Elderly Cohort: The WHICAP Ancillary Study of Oral Health. J. Periodontol. 2020, 91, S56–S67. [Google Scholar] [CrossRef]
  143. Kharitonova, M.; Vankov, P.; Abdrakhmanov, A.; Mamaeva, E.; Yakovleva, G.; Ilinskaya, O. The Composition of Microbial Communities in Inflammatory Periodontal Diseases in Young Adults Tatars. AIMS Microbiol. 2021, 7, 59–74. [Google Scholar] [CrossRef] [PubMed]
  144. Brinig, M.M.; Lepp, P.W.; Ouverney, C.C.; Armitage, G.C.; Relman, D.A. Prevalence of Bacteria of Division TM7 in Human Subgingival Plaque and Their Association with Disease. Appl. Environ. Microbiol. 2003, 69, 1687–1694. [Google Scholar] [CrossRef] [PubMed]
  145. Chipashvili, O.; Utter, D.R.; Bedree, J.K.; Ma, Y.; Schulte, F.; Mascarin, G.; Alayyoubi, Y.; Chouhan, D.; Hardt, M.; Bidlack, F.; et al. Episymbiotic Saccharibacteria Suppresses Gingival Inflammation and Bone Loss in Mice through Host Bacterial Modulation. Cell Host Microbe 2021, 29, 1649–1662.e7. [Google Scholar] [CrossRef] [PubMed]
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Figure 1. Overview of the bacterial taxonomy in the oral microbiome. Taxa are categorized under 7 levels: Phylum, Class, Order, Family, Genus, Species, and Subspecies, when identified.
Figure 1. Overview of the bacterial taxonomy in the oral microbiome. Taxa are categorized under 7 levels: Phylum, Class, Order, Family, Genus, Species, and Subspecies, when identified.
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Microbiolres 16 00194 g002
Figure 2. Composition of the oral Bacillota phylum. Taxa are categorized under 6 levels: Class, Order, Family, Genus, Species, and Subspecies, when identified.
Figure 2. Composition of the oral Bacillota phylum. Taxa are categorized under 6 levels: Class, Order, Family, Genus, Species, and Subspecies, when identified.
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Microbiolres 16 00194 g003
Figure 3. Composition of the oral Bacteroidota phylum. Taxa are categorized under 5 levels: Class, Order, Family, Genus, and Species.
Figure 3. Composition of the oral Bacteroidota phylum. Taxa are categorized under 5 levels: Class, Order, Family, Genus, and Species.
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Microbiolres 16 00194 g004
Figure 4. Composition of the oral Actinomycetota phylum. Taxa are categorized under 6 levels: Class, Order, Family, Genus, Species, and Subspecies, when identified.
Figure 4. Composition of the oral Actinomycetota phylum. Taxa are categorized under 6 levels: Class, Order, Family, Genus, Species, and Subspecies, when identified.
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Microbiolres 16 00194 g005
Figure 5. Composition of the oral Pseudomonadota phylum. Taxa are categorized under 6 levels: Class, Order, Family, Genus, Species, and Subspecies, when identified.
Figure 5. Composition of the oral Pseudomonadota phylum. Taxa are categorized under 6 levels: Class, Order, Family, Genus, Species, and Subspecies, when identified.
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Microbiolres 16 00194 g006
Figure 6. Composition of the oral Fusobacteriota phylum. Taxa are categorized under 5 levels: Class, Order, Family, Genus, and Species.
Figure 6. Composition of the oral Fusobacteriota phylum. Taxa are categorized under 5 levels: Class, Order, Family, Genus, and Species.
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Microbiolres 16 00194 g007
Figure 7. Composition of the Patescibacteria phylum. Taxa are categorized under 5 levels: Class, Order, Family, Genus, and Species.
Figure 7. Composition of the Patescibacteria phylum. Taxa are categorized under 5 levels: Class, Order, Family, Genus, and Species.
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Table 1. Composition and distribution of the oral bacteria at the phylum level.
Table 1. Composition and distribution of the oral bacteria at the phylum level.
PhylumNo. (%)
Taxa 1Status (Name and Culture)Abundance 3
Named 2Unnamed CultivatedUncultivated PhylotypesHighMediumLow
Bacillota166 (31.80%)85 (51.20%)36 (21.69%)40 (24.10%)24 (14.46%)55 (33.13%)37 (22.29%)
Bacteroidota96 (18.39%)49 (51.04%)14 (14.58%)32 (33.33%)19 (19.79%)41 (42.71%)15 (15.63%)
Actinomycetota62 (11.88%)41 (66.13%)14 (22.58%)4 (6.45%)18 (29.03%)17 (27.42%)9 (14.52%)
Pseudomonadota61 (11.69%)45 (73.77%)6 (9.84%)10 (16.39%)19 (31.15%)23 (37.70%)5 (8.20%)
Spirochaetota52 (9.96%)13 (25%)4 (7.69%)35 (67.31%)-14 (26.92%)18 (34.62%)
Fusobacteriota36 (6.90%)15 (41.67%)13 (36.11%)7 (19.44%)7 (19.44%)17 (47.22%)6 (16.67%)
Patescibacteria33 (6.32%)-12 (36.36%)17 (51.52%)3 (9.09%)13 (39.39%)4 (12.12%)
Mycoplasmotota8 (1.53%)6 (75%)-2 (25%)-1 (12.50%)1 (12.50%)
Synergistota7 (1.34%)2 (28.57%)-5 (71.43%)-1 (14.29%)4 (57.14%)
Chloreflexota1 (0.19%)-1 (100%)---1 (100%)
Total522 (100%)256 (49.04%)100 (19.16%)152 (29.12%)90 (17.24%)182 (34.87%)99 (18.97%)
Phylogenetic distribution of 522 oral bacterial taxa, identified from both healthy subjects and those with various oral diseases. Data extracted and analyzed from https://www.homd.org/, accessed on 20 June 2025. 1: shows the number of identified taxa per phylum and their percentage of total identified taxa, and refers to all identified taxa regardless of nomenclatural status, including the named but not validly published (NVP) and the taxa whose name was recently retracted; 2: refers only to the taxa with validly published names and excludes those that are (NVP) or have retracted names; 3: refers to the relative abundance to total taxa of the phylum, where abundance is classified as high, medium, or low, taxa have scarce (limited presence) and unknown abundance in the oral cavity were excluded from the relative abundance analyzes.
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Ghaouas, S.; Chala, S. The Oral Bacteriome. Microbiol. Res. 2025, 16, 194. https://doi.org/10.3390/microbiolres16090194

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Ghaouas S, Chala S. The Oral Bacteriome. Microbiology Research. 2025; 16(9):194. https://doi.org/10.3390/microbiolres16090194

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Ghaouas, Soukaina, and Sanaa Chala. 2025. "The Oral Bacteriome" Microbiology Research 16, no. 9: 194. https://doi.org/10.3390/microbiolres16090194

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Ghaouas, S., & Chala, S. (2025). The Oral Bacteriome. Microbiology Research, 16(9), 194. https://doi.org/10.3390/microbiolres16090194

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