Oral bacteria species-Oral microbiology - Wikipedia

The mouth contains a wide variety of oral bacteria, but only a few specific species of bacteria are believed to cause tooth and gum infections. List the types of bacteria and issues associated with oral bacteria: Streptococci spp and Lactobaccilus acidophilus. Dental caries, also known as tooth decay or cavity, is a bacterial infection that causes demineralization and destruction of the hard tissues enamel, dentin, and cementum. This usually happens from the production of acid by bacterial fermentation of the food debris accumulated on the tooth surface. If demineralization exceeds saliva and other remineralization factors, such as from calcium and fluoridated toothpastes, these hard tissues progressively break down, producing dental caries cavities, holes in the teeth.

Oral bacteria species

Oral bacteria species

Oral bacteria species

Are dental diseases examples of ecological catastrophes? Clin Vaccine Immunol ; 20 : — These conditions make the gingival sulcus an excellent environment for anaerobic microbes to inhabit. Also, eating foods that are known to promote healthy bacteria will help you Elanas model your teeth and mouth healthy for Oral bacteria species lifetime. The labial frenulum attaches the inside of your upper lip to the upper Oral bacteria species of your gums. The affect of supragingival plaque control on the subgingival microflora in human periodontitis. Heart J. Actinomyces naeslundii is a facultative anerobic pathogen that contributes to gingivitis, mild periodontitis, and root surface tooth decay [C17]. Oral streptococcal colonization of infants. Sultana, H.

Latex making an acknowledgement section. MATERIALS AND METHODS

Author information Article notes Copyright and License information Disclaimer. Pornstar aspen bbw and fissure caries. International Dental Journal. Medicine portal Biology portal. It Oral bacteria species in your mouth and feeds on the Oral bacteria species and starches that you eat. Bacteria were first detected under the microscopes of Antony van Leeuwenhoek in the 17th century. Zehnder M, Guggenheim B. Subgingival microorganism those that exist under the gum line colonize the periodontal pockets and cause further inflammation in the gum tissues and progressive bone loss. Plaque is a biofilm on the surfaces of the teeth. Saitou, N. Dark field microscopy Impedance microbiology Microbial cytology Microbiological culture Staining. Enterococcus faecalis from patients with chronic periodontitis: virulence and antimicrobial resistance traits and determinants. The oral cavity of the newborn baby does not contain bacteria but rapidly becomes colonized with bacteria such as Streptococcus salivarius.

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  • Enterococci are considered as transient constituent components of the oral microbiome that may cause a variety of oral and systemic infections.
  • Biofilms are masses of microorganisms that bind to and multiply on a solid surface, typically with a fluid bathing the microbes.
  • Our purposes were i to utilize culture-independent molecular techniques to extend our knowledge on the breadth of bacterial diversity in the healthy human oral cavity, including not-yet-cultivated bacteria species, and ii to determine the site and subject specificity of bacterial colonization.
  • Oral ecology refers to the organisms that live in a mouth.

Thank you for visiting nature. You are using a browser version with limited support for CSS. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. We are not distinct entities from our microbiome, but together we form a 'superorganism' or holobiont, with the microbiome playing a significant role in our physiology and health.

Through recent advances in technology, we have started to unravel the complexities of the oral microbiome and gained new insights into its role during both health and disease. Perturbations of the oral microbiome through modern-day lifestyles can have detrimental consequences for our general and oral health.

In dysbiosis, the finely-tuned equilibrium of the oral ecosystem is disrupted, allowing disease-promoting bacteria to manifest and cause conditions such as caries, gingivitis and periodontitis. For practitioners and patients alike, promoting a balanced microbiome is therefore important to effectively maintain or restore oral health.

This article aims to give an update on our current knowledge of the oral microbiome in health and disease and to discuss implications for modern-day oral healthcare. Highlights existing strategies to preserve a balanced oral microbiome for practitioners and patients to follow.

Humans, like all complex multicellular eukaryotes, are not autonomous organisms, but biological units that include numerous microbial symbionts and their genomes. Together with our symbiotic microbial residents, we form a 'superorganism', or holobiont. The microbial component of the human holobiont is substantial, and at least equals the number of our own cells.

The relationship between microbiome and host is dynamic, and influenced by many aspects of modern lifestyle, such as diet, tobacco consumption and stress, which can alter our microbiome and its properties, and induce a state in which this finely tuned ecosystem is no longer in balance. To address this divergence and maintain a harmonious state to protect health and prevent disease, we must not focus on the host and its residents as separate units, but instead consider the holobiont as one.

Several distinct habitats within the oral cavity support heterogeneous microbial communities that constitute an important link between oral and general health. The purpose of this article is to update oral healthcare practitioners on our current knowledge of the oral microbiome in health and disease, to review how molecular methods of microbial characterisation have advanced our understanding, and to discuss potential implications for clinical practice.

For an introduction to key terms used throughout the text highlighted in bold , please see the glossary in Table 1. There is evidence that resident microbes have been performing metabolic functions in animals for at least million years. In humans, coevolution has also resulted in minor, but important, differences between ethnic groups. Throughout human evolution, our environment has continuously shaped the composition of our microbiome, increasingly so during Neolithic, industrial revolution and modern eras.

A study of calcified dental plaque samples from the time of transition from hunter-gather to Neolithic societies, and from the industrial revolution has proposed a compositional shift and declining microbial diversity around each of these evolutionary milestones.

Introduction of refined sugar to our diet in the early times of agriculture caused certain oral bacteria to genetically evolve their metabolism to adapt to 'post-agricultural' changes in our diet. For example, Streptococcus mutans was able to successfully compete against other oral bacterial species by developing defences against increased oxidative stress and resistance against the acidic by-products of its own new efficient carbohydrate metabolism.

Bacteria within a biofilm can communicate with each other by producing, detecting and responding to small diffusible signal molecules in a process called quorum sensing, which confers benefit for host colonisation, biofilm formation, defence against competitors and adaptation to changes in the environment.

The endogenous human microbial communities contribute to critical metabolic, physiological and immunological functions, including: 21 , 22 , 23 , Development and regulation of the immune system and fine-tuning of its reaction pattern, that is, the balance between pro-inflammatory and anti-inflammatory processes.

Perturbations to the function and composition of the microbiome can have significant consequences for human health. The composition of our microbiome shows great diversity between compartments in the body, and is highly variable within and between people. The mouth is not a homogeneous environment for the resident microbiota, but offers several distinct habitats for microbial colonisation, 30 such as teeth, gingival sulcus, attached gingiva, tongue, cheek, lip, and hard and soft palate.

These oral habitats form a highly heterogeneous ecological system and support the growth of significantly different microbial communities. A detailed study of 9 oral sites in 26 subjects using DNA sequencing revealed a mean of species-level taxa in each individual, while taxa were found among the 26 subjects unpublished data; Dr Floyd Dewhirst, personal communication. During birth, the mother transmits microbes to the child, and delivery mode vaginal versus caesarean is therefore a determinant for the type of microorganisms that a child is initially exposed to.

Once established, the oral microbiome is maintained by host- and microbe-derived factors, involving processes that are still not fully understood. Resident bacteria have both pro- and anti-inflammatory activities that are crucial for maintaining homeostasis at heavily colonised sites such as the oral cavity.

Both saliva and GCF provide nutrients for microbial growth and contain components with antimicrobial activities. A large number of salivary components, including secretory immunoglobulin A, lactoferrin, lactoperoxidase, lysozyme, statherin and histatins, directly and indirectly regulate the microbiome, keeping it in balance. Hypothiocyanite exerts direct antimicrobial effects by inhibiting bacterial glycolysis.

Nitrite is further reduced to nitric oxide that can inhibit growth of cariogenic bacteria and thus may help to protect against caries. Proteins, including enzymes, lipids and other components carbohydrates, nucleic acids , mainly from saliva, but also derived from GCF, the oral mucosa and bacteria, form the acquired pellicle, which modulates attachment of bacteria to dental and epithelial surfaces and protects the tooth surfaces against acid attacks.

Saliva not only helps to maintain an environment that allows biofilms to flourish, but also modulates the layers of plaque with the help of numerous proteins, including enzymes and glycoproteins, and minerals, which control biofilm build-up and activity. A variety of conventional methods have been used to analyse the composition of the oral microbiome, including microscopy, cultural analysis, enzymatic assays and immunoassays. However, many oral bacteria are fastidious and slow-growing, and require complex growth media, specific atmospheric requirements and long incubation times.

Many oral bacteria are strict anaerobes, and expert care must be taken in sample collection, transport and incubation to prevent exposure to oxygen. Comprehensive cultural analysis of samples is difficult and only allows for the processing of small sample numbers.

Selective bacteriological media have proven useful for studying particular species of interest, but may have biased our understanding of microbial aetiology of oral disease, attributing disease characteristics to species that happen to thrive under such culture conditions, while others remain undetected. The advent of culture-independent methods has greatly improved the detection of microorganisms, many of which cannot yet be grown in culture. If a match for the sequence is found on the database, the microorganism can be identified; if there is no matching entry on the database, the sequence can be added as a record for a previously unknown phylotype.

The traditional method of 16S rRNA gene sequencing was costly, laborious and time-consuming. The advent of NGS methods such as pyrosequencing which is currently being phased out and Illumina MiSeq have enabled a massively increased sample throughput, with up to 27 million sequences being generated in a single run compared with a few hundred with the traditional method. The simplicity and relative affordability of NGS has led to enormous data generation and an explosion in publications, with accompanying challenges for data analysis and interpretation.

Great care has to be taken in the conduct of NGS studies to avoid contamination of clinical samples with bacterial DNA present in some extraction kits, laboratory reagents and sample collection tools, which can significantly influence the outcome of studies. Culture-independent methods have provided great insight into the diversity of the microbiome, but to investigate the properties and potential of an organism, it needs to be grown in culture.

Currently, up to a third of the species in the oral microbiome are only known by their 16S rRNA gene sequence, 62 and there is an ongoing quest to develop new methods for growing currently 'uncultivatable' microorganisms. The application of such novel culturing methods, along with emerging molecular biological and bioinformatics approaches and increased computational power, will not only grow our understanding of the oral microbiome, but also help us devise interventional strategies to maintain health and target disease in future.

The oral microbiota contributes to oral and general well-being Fig. An example of this is the effect of nitrate-reductase-expressing oral bacteria, which have been shown to catalyse the conversion of dietary nitrates to nitrite. After being swallowed, salivary nitrite is further converted to nitric oxide, a potent vasodilator with antimicrobial activity which plays a critical role in sustaining cardiovascular health.

The complex equilibrium between resident species in the oral cavity is responsible for the maintenance of a healthy state in symbiosis or a state associated with disease in dysbiosis. A dysbiotic microbiome is one in which the diversity and relative proportions of species or taxa within the microbiota is disturbed. In health, the majority of the bacteria have a symbiotic relationship with the host; for simplicity, these microorganisms are shown in green.

Potentially cariogenic or periodontopathic bacteria shown in red with dotted outlines have been detected at healthy sites at low levels that are not clinically relevant; they may also be acquired from close partners transmission , but again, their levels would be extremely low relative to the bacteria associated with health. In disease, there is an increase in the numbers and proportions of cariogenic or periodontopathic bacteria, and there may be increased biomass especially in gingivitis.

The factors driving this selection need to be recognised and addressed for adequate and consistent disease prevention. It is now an accepted concept that the bacteria historically considered as oral 'pathogens' can be found in low numbers at healthy sites, and oral disease occurs as a consequence of a deleterious change to the natural balance of the microbiota rather than as a result of exogenous 'infection'.

Alterations in the pattern of biofilm formation may result in dysbiotic microenvironments in the many distinct habitats in the mouth. The distinct, non-shedding structure of teeth smooth surfaces, pits and fissures, proximal sites and exposed root surfaces enables large masses of microbes to accumulate as dental plaque biofilm. Different theories on the relationship between plaque and dental disease have evolved over time.

Initially, the NSPH speculated that dental infections were caused by the nonspecific over-growth of all bacteria in dental plaque. The NSPH was further extended to stipulate that destructive periodontitis was the result of subgingival colonisation, favoured by ecological changes associated with plaque accumulation, gingivitis and gingival exudate. These changes increase the numbers of microorganisms and alter their proportions, but no single species appears in active sites that is not also commonly present in inactive sites.

The observation that kanamycin was particularly effective against caries-associated species, such as streptococci, led to the emergence of the 'specific plaque hypothesis', which proposed that only a few species in the oral microbiome are involved in the disease process, and that targeting these species with antibiotics could cure or prevent disease initially caries and later periodontitis. Following a renewed interest in the NSPH in the s, an ecological plaque hypothesis was proposed to explain the relationship between the resident oral microbiota, the host environment and oral diseases Fig.

In caries, carbohydrates are fermented to organic acids for example, lactic acid , which lower the local pH resulting in net demineralisation of the tooth surface.

This drives the selection of efficient acid-producing and acid-tolerating bacteria dysbiosis. The biofilm undergoes multiple pH cycles during the day, resulting in enamel de- and remineralisation showed by ion efflux and influx into the enamel in the diagram. If fluoride ions are present in the biofilm, F— is then taken up in the superficial layer of enamel during the remineralisation phase, slowing down demineralisation during the acid challenge. The ecological plaque hypothesis was further refined by the proposal that certain low-abundance microbial pathogens can cause inflammatory disease by interfering with the host immune system and remodelling of the microbiota, leading to gingivitis and periodontitis.

Figure 7 shows a contemporary model of host-microbe interactions in the pathogenesis of gingivitis and periodontitis. It is now recognised that complex interactions between immune response mediators and the biofilm are necessary requirements that lead to disease progression from gingivitis to periodontitis.

The resulting conditions are conducive for periodontitis-associated species such as Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans to survive and flourish.

Clinical health assumes some mild inflammatory changes that are proportionate to maintaining a resident 'health-promoting' periodontal microbiota. The relationship is symbiotic, with the host living harmoniously with its microbes.

For example, Porphyromonas gingivalis requires iron from haem and can start to establish itself and contribute to the dysbiosis, because as local inflammation increases it provides iron from gingival bleeding. In gingivitis, the host response remains proportionate, but due to the maturing biofilm, the associated inflammation does not resolve so easily and becomes chronic in nature, supporting the dysbiosis.

Dependent upon various genetic, environmental and lifestyle risk factors, some susceptible patients will progress to periodontitis. The latter is driven by disproportionate and exaggerated host inflammatory immune responses that cause the majority of host tissue damage and drive a frank dysbiosis with failed resolution of the chronic destructive inflammation. A vicious cycle develops that sustains the disequilibrium, but symbiosis may be restored by regular and thorough biofilm disruption to help resolve the inflammation.

The degree by which biofilm accumulation promotes periodontitis varies between individuals, 82 according to their risk profile.

In patients not susceptible to periodontitis, the inflammatory response in gingivitis is proportionate and self-resolving, but in susceptible patients, multiple genetic, epigenetic or patient-modifiable factors tobacco, alcohol, diet, unregulated diabetes, stress, etc can trigger an exaggerated, yet ineffective and chronic, non-resolving inflammation in the connective tissues supporting the teeth.

The coevolution to a harmonious coexistence is only valid as long microbes remain in their natural habitat and are not disseminated to other body sites, where they can cause disease. Dysbiosis in periodontal disease as a trigger of bacteraemia likely facilitates systemic dissemination of oral bacteria, and good oral hygiene is therefore crucial for controlling the total bacterial load.

It is well established that severe periodontitis adversely affects glycaemic control in diabetes and glycaemia in subjects who do not have diabetes. Severe periodontitis poses an increased risk for the onset of type 2 diabetes, and there is a direct and dose-dependent relationship between the severity of periodontitis and diabetic complications. Analysis of the oral cavity and its microbiome may be a useful tool to diagnose systemic diseases that have periodontal manifestations.

Good oral hygiene to control the total microbial load is important to prevent dissemination to other body sites. The diverse community that makes up the oral microbiome is finely tuned by nature to protect from disease, and it is of great importance to maintain its natural diversity.

Modern lifestyles can disturb and upset the natural balance of our oral microbiome, and our clinical goal should be to re-establish its symbiotic equilibrium by whatever means are necessary and appropriate in the individual patient. Thus, it is pivotal that both patients and healthcare professionals embrace the concept of a balanced oral microbiome and its importance in oral and systemic health.

For example, Lactobacillus or Leuconostoc are typically found in foods such as yogurt and wine. Other common preventative measures center on reducing sugar intake. PLoS One. Food Chemistry. Identity of viridans streptococci isolated from cases of infective endocarditis. Journal of Young Investigators.

Oral bacteria species

Oral bacteria species

Oral bacteria species

Oral bacteria species

Oral bacteria species. Navigation menu

As a result, S. In discussing the evolution of S. As humans evolved anthropologically, the bacteria evolved biologically. It is widely accepted that the advent of agriculture in early human populations provided the conditions S. These new foods introduced new bacteria to the oral cavity and created new environmental conditions. For example, Lactobacillus or Leuconostoc are typically found in foods such as yogurt and wine.

This new acidic habitat would select for those bacteria that could survive and reproduce at a lower pH. Another significant change to the oral environment occurred during the Industrial Revolution. This provided S. From Wikipedia, the free encyclopedia. Streptococcus mutans Stain of S. Scientific classification Domain: Bacteria.

Sherris Medical Microbiology 4th ed. McGraw Hill. In Baron S; et al. Baron's Medical Microbiology 4th ed. University of Texas Medical Branch. In: The Oral Environment, online tutorial". Archived from the original on Retrieved Canadian Journal of Microbiology. Archives of Oral Biology. PLoS Pathogens. Brock Biology of Microorganisms 11th ed. Prentice Hall. European Journal of Epidemiology.

Molecular Oral Microbiology. Caister Academic Press. Scientific Reports. Bibcode : NatSR Journal of Young Investigators. Archived from the original on 21 December Retrieved 21 December European Journal of Oral Sciences. Antimicrobial Agents and Chemotherapy. Journal of Clinical Microbiology. Bibcode : PLoSO Journal of Medical Internet Research. BMC Oral Health. International Dental Journal. Journal of Dental Research.

Pediatric Dentistry. Journal of Dentistry. The Journal of the Association of Physicians of India. Clinical Preventive Dentistry. Materia Socio-Medica. Mechanisms of action of fluoride for caries control. Monographs in Oral Science. Evidence-Based Dentistry. The Journal of the American Dental Association. International Journal of Pharma and Bio Sciences.

Entwicklung eines quantitativen Testes zum Nachweis von Streptococcus mutans auf Basis der "Real-time"-quantitativen Polymerase-Kettenreaktion" [Xylitol-containing chewing gum and the oral bacterial flora. Junge Wissenschaft Young Researcher in German. Archived from the original PDF on 23 January Retrieved 23 January International Journal of Oral Science. Clinical Microbiology Reviews. Phytotherapy Research.

Food Chemistry. Indian Journal of Dental Research. Biochip Journal. International Journal of Oral and Maxillofacial Pathology. International Journal of Dental Hygiene. Current Microbiology. Journal of Bacteriology. Infection, Genetics and Evolution. Frontiers in Microbiology.

Applied and Environmental Microbiology. Molecular Biology and Evolution. August D Thesis. University of Glasgow. Viridans streptococci : S. Streptococcus iniae Cutaneous Streptococcus iniae infection. Bacillus anthracis Anthrax Bacillus cereus Food poisoning. Listeria monocytogenes Listeriosis. Clostridium difficile Pseudomembranous colitis Clostridium botulinum Botulism Clostridium tetani Tetanus.

Clostridium perfringens Gas gangrene Clostridial necrotizing enteritis. Peptostreptococcus magnus. Ureaplasma urealyticum Ureaplasma infection Mycoplasma genitalium Mycoplasma pneumoniae Mycoplasma pneumonia. Erysipelothrix rhusiopathiae Erysipeloid. Biology portal. Subjects did not suffer from severe halitosis.

The periodontia were healthy in that all periodontal pockets were less than 3 mm deep with no redness or inflammation of the gums.

Subjects did not have active white spot lesions or caries on the teeth. The subjects had not used antibiotics for the last 6 months. Samples from the following nine sites were analyzed for each subject: dorsum of the tongue, lateral sides of the tongue, buccal fold, hard palate, soft palate, labial gingiva and tonsils of soft tissue surfaces, and supragingival and subgingival plaques from tooth surfaces.

Microbiological samples of supragingival and subgingival plaque samples were taken with a sterile Gracey curette. Other samples were collected with sterile swab brushes. Detection of species is dependent upon obtaining DNA that can be amplified. Thus, a difficult-to-lyse bacterium may not be detected. However, by using our lysis technique, we were able to detect many hard-to-lyse species, such as species of Actinomyces and Streptococcus.

The PCR primers do not necessarily include all bacterial species. Nevertheless, a wide range of phylogenetic types were obtained in this study and our previous studies by using this universal primer set 3 , 15 , 21 - DNA was stained with ethidium bromide and visualized under short-wavelength UV light. Transformation was done with competent Escherichia coli TOP10 cells provided by the manufacturer.

The primers used for sequencing have been described previously A total of 2, clones with an insert of the correct size of approximately 1, bases were analyzed.

The number of clones per subject that were sequenced ranged from 42 to 69, with an average of A sequence of approximately bases was obtained first to determine identity or approximate phylogenetic position. Full sequences of about 1, bases were obtained by using five to six additional sequencing primers 15 for those species deemed novel. For identification of closest relatives, the sequences of the unrecognized inserts were compared to the 16S rRNA sequences of over 10, microorganisms in our database and over , sequences in the Ribosomal Database Project 7 and the GenBank databases.

The similarity matrices were corrected for multiple base changes at single positions by the method of Jukes and Cantor Phylogenetic trees were constructed by the neighbor-joining method of Saitou and Nei Chimeric sequences were identified by using the Chimera Check program in the Ribosomal Database Project, by treeing analysis, or by base signature analysis. Species identification of chimeras was obtained, but the sequences were not examined for phylogenetic analysis.

The complete 16S rRNA gene sequences of clones representing novel phylotypes defined in this study, sequences of known species not previously reported, and published sequences are available for electronic retrieval from the EMBL, GenBank, and DDBJ nucleotide sequence databases under the accession numbers shown in Fig.

Bacterial profiles of the buccal epithelium of healthy subjects. GenBank accession numbers are provided. Bacterial profiles of the subgingival plaque of healthy subjects. Novel phylotypes identified in this study are indicated in bold. It has long been known that oral bacteria preferentially colonize different surfaces in the oral cavity as a result of specific adhesins on the bacterial surface binding to complementary specific receptors on a given oral surface 11 , Indeed, the profiles of 40 cultivable bacterial species differed markedly on different oral soft tissue surfaces, saliva, and supragingival and subgingival plaques from healthy subjects The purpose of this study was to define the predominant bacterial flora of the healthy oral cavity by identifying and comparing the cultivable and the not-yet-cultivated bacterial species on different soft tissues and supra- and subgingival plaques.

Based on the analysis of 2, 16S rRNA clones, the bacterial diversity of the microflora from nine different sites of five clinically healthy subjects was striking—a total of different bacterial taxa representing six different bacterial phyla were detected. Thirteen new phylotypes see Fig.

Aas, S. Dardis, A. Griffen, L. Stokes, A. Lee, I. Olsen, F. Dewhirst, E. Leys, and B. Consequently, it is important to identify both the cultivable and not-yet-cultivated bacterial flora in a given environment before we can ascribe association to health or disease status.

There is no evidence to suggest that the not-yet-cultivated segment is any less important than the cultivable segment. Bacterial profiles of the maxillary anterior vestibule of healthy subjects. Bacterial profiles for each site tested for each subject are shown in nine phylogenetic trees see Fig.

In these dendrograms, the distribution of bacterial species or phylotypes in each subject can be observed at a glance. For example, it is clear that Streptococcus mitis , S. Similarly, the predominant bacterial flora for the other eight oral sites was examined. In the maxillary anterior vestibule, S.

On the tongue dorsum, several species of Streptococcus , such as S. On the lateral tongue surface Fig. It is interesting that there were considerable differences in the bacterial profiles of the tongue dorsum and the lateral tongue surface.

For example, S. Conversely, S. This was not surprising, because these surfaces are known to be different in ultrastructure and function. For instance, the lateral side of the tongue has a smooth nonkeratinized surface, in contrast to the dorsum of the tongue, which is a keratinized, highly papillated surface with a large surface area and underlying serous glands. These anatomic differences likely influence the ecology of these habitats and create microbial environmental differences.

Bacterial profiles of the tongue dorsum of healthy subjects. Bacterial profiles of the lateral tongue surface of healthy subjects. On the hard palate, the predominant bacterial species included S. On the soft palate, S. The tonsil bacterial flora Fig. On the tooth surface, several species of Streptococcus , including Streptococcus sp.

Finally, in subgingival plaque, several species of Streptococcus and Gemella were often found Fig. Bacterial profiles of the hard palate of healthy subjects. Bacterial profiles of the soft palate of healthy subjects. Bacterial profiles of the tonsils of healthy subjects. Bacterial profiles of the tooth surfaces of healthy subjects. The number of cultivable and not-yet-cultivable species detected in each subject for each site is also shown in Fig.

For example, in Fig. A common question asked is how many bacterial species are present in the oral cavity of a single individual. Note that in this study, S. Both S. In addition, they are now recognized as frequent causes of infection in immunocompromised patients, particularly immediately after tissue transplants and in neutropenic cancer patients A high mortality rate for endocarditis by G.

As already discussed, several species, such as S. For example, R. Some species appeared to have a predilection for soft tissue, e. On the other hand, Neisseria spp. Simonsiella muelleri colonized only the hard palate. Indeed, S. For example, P. Prevotella sp. This clone was also found in lower proportions on the soft palate and tonsils of another subject Fig. Site specificity of predominant bacterial species in the oral cavity. In general, bacterial species or phylotypes were selected on the basis of their detection in multiple subjects for a given site.

In conclusion, there is a distinctive bacterial flora in the healthy oral cavity which is different from that of oral disease. For example, many species specifically associated with periodontal disease, such as Porphyromonas gingivalis , Tannerella forsythia , and Treponema denticola , were not detected in any sites tested.

In addition, the bacterial flora commonly thought to be involved in dental caries and deep dentin cavities, represented by Streptococcus mutans , Lactobacillus spp. As noted in this study on healthy subjects, some species are site specific at one or multiple sites, while other species are subject specific. As we have previously asserted 21 , to rigorously assess the association of specific species or phylotypes with oral health or disease, it is necessary to analyze larger numbers of clinical samples for the levels of essentially all oral bacteria in well-controlled clinical studies.

The bacterial complexes involved in periodontal disease as defined by Socransky et al. We are currently developing DNA probes for approximately known bacterial species and novel phylotypes for use in similar studies.

Boches, A. Lee, B. Paster, and F. Dewhirst, J. Our intent was to first establish the full bacterial diversity of the oral cavity and then to determine variation and reproducibility using the microarrays. It is necessary to first define the bacterial flora of the healthy oral cavity before we can determine the role of oral bacteria in disease. National Center for Biotechnology Information , U. Journal List J Clin Microbiol v. J Clin Microbiol. Paster , 1, 3 Lauren N.

Stokes , 1 Ingar Olsen , 2 and Floyd E. Dewhirst 1, 3. Bruce J. Lauren N. Floyd E. Author information Article notes Copyright and License information Disclaimer. Phone: 47 Fax: 47 E-mail: on. This article has been cited by other articles in PMC. Sample collection. Sample lysis. Cloning procedures. Nucleotide sequence accession numbers. Open in a separate window.

TABLE 1. Number of predominant bacterial species per site and subject. Subject no. Total no. Albandar, J. Brunelle, and A. Destructive periodontal disease in adults 30 years of age and older in the United States, Beck, J. Garcia, G. Heiss, P. Vokonas, and S. Periodontal disease and cardiovascular disease. Becker, M. Paster, E. Leys, M. Moeschberger, S. Kenyon, J. Galvin, S. Boches, F. Dewhirst, and A. Molecular analysis of bacterial species associated with childhood caries.

Berbari, E. Cockerill III, and J. Infective endocarditis due to unusual or fastidious microorganisms. Mayo Clin. Bouvet, A. New bacteriological aspects of infective endocarditis. Heart J. C : Buduneli, N. Baylas, E. Buduneli, O. Turkoglu, T. Kose, and G. Periodontal infections and pre-term low birth weight: a case-control study.

Oral Bacteria in Mouth | Colgate® Oral Care

The dark, wet, and warm environment of the mouth, with the occasional meal running through it, makes it an excellent niche for microbes to live. Over the past 40 years, scientists have been arduously working to discover the over different species of bacteria in and around the mouth known today. The mouth is comprised of an oral cavity, which includes the teeth and gums, surrounded by the lips, cheeks, tongue, palate, and throat. Each of these habitats offers differing environmental conditions, and as such, is colonized by a different microbial flora.

The oral environment is constantly in flux. From birth to around age 12, when the permanent dentition is complete, the local oral conditions are continuously changing as teeth are shed and new ones erupt [A1]. In addition, environmental factors such as, nutrition, diet, hygiene, smoking, dehydration, and even stress, alter the ecological conditions of mouth. Saliva covers all surfaces and serves various important functions, mechanical and nutritional, digestive, swallowing, cleansing, lubricative, bactericidal, and excretory in the oral cavity.

The typical resting pH 6. While salivary flora does not necessarily represent the microbial composition of the different components of the mouth, it does impact which microbes can live within the oral cavity, and has recently been the target of research in early disease detection.

The bacteria within the mouth not only have to communicate with all the different species living within the biofilm, but they must obtain a strong adherence to a surface in order to not be washed away by saliva. These nutrients provide carbohydrates, proteins, and glycoproteins needed for the growth [B3]. The mouth conditions change throughout the day depending on saliva flow, food, and oxygen levels.

This fluctuation of oral conditions causes the population of the biofilm within the mouth to also change because it will affect the bacteria-bacteria interactions.

These prominent bacteria are responsible for the plaque formation due to their interactions with each other and the tooth surface. In the mouth, the tooth forms its own layer of protection known as the acquired pellicle. While protection is its main purpose, it also serves as lubrication for the enamel surface and acts as a semi-permeable membrane [B7].

Some of these proteins are the phosphoproteins: statherin, histatin, and proline-rich proteins PRPs. Although these have been commonly found to form the initial layer of the acquire pellicle, studies have shown that there may be other interactions, such as Van der Waal forces and hydrophobic interactions, that also play an important role in protein-enamel interactions.

Like the biofilm, the pellicle is constantly undergoing modifications depending on the host enzymes and microbial metabolites within the mouth. The pellicle is able to form a protective layer around the enamel surface because of its many antimicrobial components. The bacteria that live on the tooth surface form multi-specie communities known as a biofilm.

A biofilm can be called a community because the bacteria work together to organize themselves in such a way to maintain homeostasis by resisting changes in their environment. Biofilms can resist antimicrobial agents, bacterial enzymes, pH changes to some degree due to the different components of the overall structure of the biofilm and individual contributions each species of bacteria contributes [B3] [B6]. When the microbe is still some distance to the pellicle-coated enamel, long-rang physicochemical forces allow for weak, reversible attachment.

Adhesins are molecular components of the binding structures: pili, fibrils and fimbriae. This process happens through strong-range sterochemical forces. These bacteria must be able to withstand high oxygen concentrations and abrasion [B6].

As these attach themselves, they in turn provide new surface receptors that adhesin proteins of later colonizers can bind. These earlier colonizers deplete the oxygen within the local environment, and allow for anaerobes to bind to the biofilm [B3] [B10]. A notable secondary colonizer is Fusobacterium nucleatum which is important base for tertiary and further layers because it forms a bridge between the early and late colonizers.

This dictates the overall population and spatiotemporal formation of the biofilm. The biofilm is able to withstand environmental pressures because they form a protective outer layer. As the Streptococci and other primary colonizers begin their attachment they utilize sugars mainly sucrose to start polysaccharide production.

When sucrose is broken down it has two components fructose and glucose, further enzymes and bacterial reactions creates bonds between multiple fructose molecules forming fructan. The same is done with glucose which is called glucan. Glucan and fructan are than brought into the cell and can later be broken down and used as an energy source [B13]. The microbes also use these polysaccharides as a glue-like substance to further secure their attachment to the pellicle-coated enamel and also to form one of the staple components in any mature biofilm, the extracellular matrix [B1] [B12].

The matrix provides structural support that allows the microbes to attach in a columnar fashion and also gives the biofilm a strong attachment to the pellicle to prevent it from washing away. One would tend to believe that the extracellular matrix is a solid structure surrounding the cell, but on the contrary it is very open with channels and voids running along it. This is to help the biofilm retain nutrients and water; it also allows them to pass these nutrients in between the channels to other microbes in the community.

However, the biofilm is not just a simple community where bacteria can easily bind to nascent surfaces to build upon. The biofilm must maintain homeostasis, constant environmental conditions, in order to maintain a healthy mouth. The commensal bacteria compete with their neighbors in order to dictate the conditions of the biofilm [B3].

Studies are still ongoing to fully understand how the oral microflora is able to from such diverse and complex communities, but it is agreed that communication is essential. For the early colonizers, who withstand many factors from both the environment and their neighbors, they must have a variety of different receptors and adhesins to perform all their functions.

For example, S. Other early colonizers like actinomyces, capnoyctophagae, haemophili, prevotellae, propionibacteria, and veillonellae also recognize the components in the acquired pellicle through specific cell surface adherence proteins [B11]. However, studies have shown that individual attachment and growth of monospecies can survive within the mouth.

Bacteria-bacteria interactions increase their affinity for a communal lifestyle. Without coaggregation and coadhesion, the multi-specie biofilms would not be able to form. Coaggregation is the recognition and communication between bacteria in suspension that will clump together to form an aggregate that can bind to the biofilm; while coadhesion is the adhesion of individual bacteria cell in suspension with a cell that is already a member of the biofilm.

These interactions are mediated by complementary protein-adhesin and saccharide-receptors [B10]. Coaggregation between streptococci and actinomcyes, initial colonizers, help them bind to the acquired pellicle as well as manipulate spatiotemperoral development of plaque.

Cell-cell interactions are formed through lectin-like receptors; which involves a protein adhesion recognizing the streptococcal receptor polyscahharide RPS. Coaggregations also occur between different genuses; for example, Gn and G RPS on streptococci is recognized by the protein adhsin type 2 fimbriae on actinomyces [B15]. Without coaggregation, both S.

The earlier colonizers are essential to the formation of the biofilm because they change the environmental conditions for the next layer of bacteria to adhere. After S. The presence of these proteins promotes its ability to bind to salivary agglutinin as well as the coaggregation of S.

However, since S. The initial colonizers will determine which colonizers will be able to adhere later. For example, if S. Some interactions promote synergistic behavior. Some bacteria act as a bridge between bacteria that would not normally coadhere or coaggregate with each other [B9] [B2].

The bacteria send diffusible signals to their neighbors in order to communicate. One method, quorum sensing, involves the signaling molecule, autoinducer-2 AI-2 produced from the gene LuxS. This is frequently found in both gram-positive and gram-negative bacteria and is suggested to have a wide range of functions for the community. In biofilms that do not have properly working AI-2 molcules, or those similar, are not able to maintain homeostasis.

Gene exchange allows the inhabitants the ability share. If a cell lyses, the free DNA can be up taken into a competent cell and incorporated into its own genome, can be used as a nutrient source, or just as a means of communication [B9].

The transfer of conjugative transposons, jumping genes, can allow for horizontal gene transfer, between different geniuses. Oral bacterial metabolism is not only important for one species growth and development but important for the entire biofilm as well. For example, Streptococci spp. Veillonellae in turn uses the lactic acid produced by Streptococci to promote its own growth. Studies have shown that when Streptococci are absent Veillonellae is not able to grow, so this shows that Veillonellae growth is dependent on Streptococci metabolism [B10].

Metabolism by bacteria in the mouth also produces by products that protect the mouth from incoming pathogens and acid build up. As mentioned already Veillonellae takes up lactic acid which prevents high build up of lactic acid and allowing the mouth to maintain a constant pH.

The elevated levels of hydrogen peroxide inhibit growth of A. Dental plaque is present in both a healthy and diseased mouth, but its only when homeostasis is not maintained that problems arise. Diseased mouth have a greater number of gram negative cocci, rods, filaments, and anaerobic bacteria [B3] [B6].

These changes allow the commensal bacteria to be taken over by the pathogenic bacteria. Now the pathogenic bacteria present in the dental plaque can begin to induce changes in neighboring bacteria gene expression that will allow itself to rapidly increase its own numbers to cause diseases [B3].

An example of this is when metabolic products of the bacteria lead to dental caries, better known as cavities. The increase in acids decreases the pH on the teeth. Once the pH has dropped below 5. The saliva is full of calcium and phosphate that is used to re-mineralize minor chips. However, if carbon sources are depleted and the saliva becomes unsaturated, the pH cannot readjust and neutralize leading to tooth decay [B18] [B3].

Changes in the supragingival plaque have been shown to influence the subgingival plaque as well. The biofilms in both the supra- and sub-gingival areas have many of the same bacteria with similar interactions. Many of the Streptococci spp. The mucus membrane that conceals the alveolar bone, or in other words, the gingiva, is affected by all the environmental and developmental factors which the oral cavity as a whole encounters. The Gingiva is divided into the free gingiva, attached gingiva, and alveolar mucosa by two imaginary lines at the base of the gingival sulcus also known as gingival crevice and the mucogingival junction, respectively.

The free gingiva is the epithelial tissue from the gingival margin to the imaginary line extending from the cementoenamel junction of the gingival sulcus. Width of the gingival sulcus usually ranges from 0.

Attached gingiva, comprised of the epithelial tissue, supraalveolar connective tissue, and alveolar bone, continues from the imaginary cementoenamel junction of the gingival sulcus to the mucogingival junction. Finally the alveolar mucosal covers the base of the alveolar bone and continues to the floor of the mouth and the vestibule. Its unique topography, position, and adjacent community of the teeth, serve as a mechanical retention of bacterial plaque, impervious to cleaning by a simple toothbrush [C3].

In addition, the gingival crevice has the lowest oxidation-reduction potential Eh , as well as a low overall oxygen level, and alkaline pH [C4].

Oral bacteria species