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Oral microbialflora

Oral microbiology is the study of the microorganisms of the oral cavity and the interactions between the oral microorganisms with each other and with the host. Of particular interest is the role of oral microorganisms in the two major dental diseases: dental caries and periodontal disease.
Microbiology began in the mouth: Antony van Leeuwenhoek developed and used the first microscope to examine material collected from teeth, and described motile “animalcules”Microbes include higher and lower organisms, although Oral Microbiology concerns mainly bacteria, some viruses and few fungi: The mouth harbors a diverse, abundant and complex microbial community. This highly diverse  microflora  inhabits the various surfaces of the normal mouth. Bacteria accumulate on both the hard and soft oral tissues in biofilms. Bacterial adhesion is particularly important for oral bacteria.Oral bacteria have evolved mechanisms to sense their environment and evade or modify the host. Bacteria occupy the ecological niche provided by both the tooth surface and gingival epithelium. However, a highly efficient innate host defense system constantly monitors the bacterial colonization and prevents bacterial invasion of local tissues. A dynamic equilibrium exists between dental plaque bacteria and the innate host defense system.
Oral bacteria
Oral bacteria include streptococci, lactobacilli, staphylococci, corynebacteria, and various anaerobes in particular bacteroides. The oral cavity of the new-born baby does not contain bacteria but rapidly becomes colonized with bacteria such as Streptococcus salivarius. With the appearance of the teeth during the first year colonization by Streptococcus mutans and Streptococcus sanguis occurs as these organisms colonise the dental surface and gingiva. Other strains of streptococci adhere strongly to the gums and cheeks but not to the teeth. The gingival crevice area (supporting structures of the teeth) provides a habitat for a variety of anaerobic species. Bacteroides and spirochetes colonize the mouth around puberty.
Treponema denticola
The levels of oral spirochetes are elevated in patients with periodontal diseases. Among this group, Treponema denticola is the most studied and is considered as one of the main etiological bacteria of periodontitis. Treponema denticola is a motile and highly proteolytic bacterium.
  Porphyromonas gingivalis
Porphyromonas gingivalis is a Gram-negative oral anaerobe strongly associated with chronic adult periodontitis. The bacterium produces a number of well-characterized virulence factors and can be manipulated genetically. The availability of the genome sequence is aiding our understanding of the biology of P. gingivalis and how it interacts with the environment, other bacteria and the human host.
  Aggregatibacter actinomycetemcomitans
Aggregatibacter actinomycetemcomitans is considered an oral pathogen due to its virulence factors, its association with localized aggressive periodontitis in young adolescents, and studies indicating that it can cause bone loss.
Some Lactobacillus species have been associated with dental caries although these bacteria are normally symbiotic in humans and are found in the gut flora.  
 Dental plaque
Dental plaque is the material that adheres to the teeth and consists of bacterial cells (mainly S. mutans and S. sanguis), salivary polymers and bacterial extracellular products. Plaque is a biofilm on the surfaces of the teeth. This accumulation of microorganisms subjects the teeth and gingival tissues to high concentrations of bacterial metabolites which results in dental disease. If not taken care of, via brushing or flossing, the plaque can turn into tartar (its hardened form)and lead to gingivitis or periodontal disease.
  Cell-cell communication
Most of the bacterial species found in the mouth belong to microbial communities, called biofilms, a feature of which is inter-bacterial communication. Cell-cell contact, is mediated by specific protein adhesins and often, as in the case of inter-species aggregation, by complementary polysaccharide receptors. Another method of communication invoves cell-cell signalling molecules, which are of two classes: those used for intra-species and those used for inter-species signalling. An example of intra-species communication is quorum sensing. Oral bacteria have been shown to produce small peptides, such as competence stimulating peptides, which can help promote single-species biofilm formation. A common form of inter-species signalling is mediated by 4, 5-dihydroxy-2, 3-pentanedione (DPD) or Autoinducer-2 (Al-2).
  Vaccination against oral infections
Dental caries and periodontitis have an infectious etiology and immunization has been proposed as a means of controlling them. However, the approaches vary according to the nature of the bacteria involved and the mechanisms of pathogenesis for these two very different diseases. In the case of dental caries, proteins involved in colonization of teeth by Streptococcus mutans can produce antibodies that inhibit the cariogenic process. Periodontal vaccines are less well developed, but some antigenic targets have been identified. :

The Mouth as a Habitat 
Host defences associated with the tooth surfaces:-
The host defences associated with oral mucosal surfaces:-
Specific and non-specific host defence factors in the mouth.
Specific FactorMain functionNon-specific factorMain function
Intra-epithelial lymphocytesCellular barrier to bacteria ± antigensSaliva flowphysical removal of organisms
Langerhans cell
Prevents adhesion & metabolismMucin/agglutininsphysical removal of organisms
IgG, IgA, IgMprevent adhesion, opsonise, complement Lysozyme-protease-anion systemcell lysis
Complementactivates neutrophils, bactericidalLactoferriniron sequestration
Neutrophils, macrophagesphagocytosisApo-lactoferrinCell killing

Sialoperoxidase systemNeutral pH: hypothiocyanite
Acid pH: hypocyanous acid

Histatinsantibacterial and antifungal

Growth and Death of Oral Microorganisms

  • Reproduction and growth of bacteria
  • Measurement of growth
  • Growth curves
  • Environmental factors affecting growth and survival
  • Introduction to sterilisation and disinfection
Growth of a biological system or of a living organism, or part of one, may be defined as an increase in mass or size (in any direction) accompanied by the synthesis of macromolecules, leading to the production of a newly organised structure. Measurement of the growth of some organisms is dictated by the nature of the organism; actinomycetes and fungi exist as hyphae, which increase in length by extension of the zone behind the hyphal tip. A fungal colony will increase in diameter with most growth occurring at the margin. Yeasts and some bacteria reproduce by budding. Growth when applied to bacteria normally refers to an increase in the number of individual cells and so is a measure of population density, denoting an increase in number beyond that in the original inoculum. Bacterial growth can be very rapid (a culture of Escherichia coli can double in size in 20 minutes in a rich medium) and this characteristic is especially important in vivo when nutrients may be extremely scarce.
Measurement of Growth
Growth may be estimated as an increase in the number of bacteria, cell mass, or any cellular constituent. When measuring populations counting methods can be divided into two broad groups: total counts, including both living and dead bacteria, and viable counts in which only cells able to grow in the conditions provided are counted. Both types of procedures are used commonly to enumerate and evaluate oral bacteria. Total counts give much higher numbers of organisms in plaque, not only because dead cells are counted, but also because many of the organisms in plaque cannot yet be cultivated in the lab (eg many oral spirochaetes, which can be seen by microscopy and their nucleic acids can be detected, are non-cultivable).
Environmental Factors Influencing Growth
Microorganisms in their natural environments and in the laboratory are subjected to a wide variety of environmental influences, which combine to determine whether growth can occur and the rate at which it can occur. Organisms which are best adapted to the environment will grow best and will consequently be selected from a mixed population. For example, as organisms in subgingival plaque grow and the periodontal pocket deepens, conditions become increasingly anaerobic so the bacteria which come to predominate in periodontal pockets do not require oxygen for metabolism.
Temperature: Temperature primarily affects the enzymes of a microorganism: a rise in temperature increases enzyme activity and allows a faster growth rate, until key enzymes are denatured. The temperatures at which these events occur vary widely amongst microbes, which all have characteristic maximum, minimum and optimum temperatures for growth. Organisms which inhabit the human body as commensals and/or pathogens are mesophiles, and grow most rapidly within the range 20·C to 45·C, with growth optima between 35·C and 40·C.
pH: Most bacteria have an optimum pH for growth in the range 6.5 - 7.5 with limits somewhere between 5 and 9. Acidophilic bacteria can grow at a low pH, and such organisms are very important in Oral Microbiology as the causative agents of caries: lactobacilli and mutans streptococci produce acid as end products of metabolism of dietary sugars, and are able to survive and grow in the acidic conditions created (aciduric). The organisms found in periodontal disease are usually not aciduric as they tend to rely for growth on protein/peptide breakdown and this produces slighlty alkaline end products.
Oxygen: Bacteria vary widely in their requirements for oxygen, ranging from obligate aerobes through facultative anaerobes and microaerophiles to obligate anaerobes. Because oxygen and its derivatives are toxic and can lethally damage certain cellular components, aerobic and facultative organisms have evolved protective enzyme systems: superoxide dismutase (SOD) eliminates superoxide radicals and hydrogen peroxide can be removed by catalase and peroxidase enzymes. In general, anaerobes lack protective mechanisms.
Aerobic bacteria use oxygen as the terminal electron acceptor in respiration, and obligate aerobes have an absolute requirement for oxygen to grow.
Microaerophilic (eg. Campylobacter spp.) organisms require a low concentration of oxygen for growth, and are sensitive to atmospheric concentrations.
Facultative anaerobes, such as streptococci and Neisseria, use oxygen but also grow in its absence although growth is usually slower without oxygen.
An obligately anaerobic organism is one whose energy generating and synthetic pathways do not require molecular oxygen, and which demonstrates a high degree of adverse sensitivity to oxygen. Because of their extreme sensitivity, obligate anaerobes must be cultivated in the absence of atmospheric oxygen and a low redox potential (Eh) must be maintained in the growth medium (Eh is a measure of the tendency of a solution to give up or receive electrons). These conditions can be acheived using specialised techniques, such as incubation in anaerobic jars or cabinets. These cultivation techniques, and anaerobic sampling methods, are essential in Oral Microbiology when examining samples from, for example, periodontal pockets or abscesses which contain high numbers of obligately anaerobic bacteria.
Control of microorganisms
Control of the growth and spread of microorganisms is acheived in three main ways (apart from by developments in sanitation, water purification etc.).
Chemotherapy: most successful antimicrobial agents are antibacterial, with target sites in the cell wall, the bacterial ribosome, nucleic acid synthetic pathways or the cell membrane. They may be bactericidal (kill bacteria) or bacteriostatic (inhibit growth, thereby limiting numbers of infecting organisms to levels which the host defences can control). There are far fewer antifungal drugs available; because fungi are eukaryotic, there are fewer target sites within fungal cells which differ sufficiently from host cells to ensure non-toxicity of the antifungal agent. Similarly, development of antiviral drugs is difficult because interference with viruses is often impossible without damage to host cells.
Immunisation: vaccines have been of enormous importance in controlling, and in some cases (eg. smallpox) eradicating, significant diseases. In Oral Microbiology the diseases to be controlled are often caused by too many different organisms to make vaccination a realistic option, but much work has been done on a vaccine based on Streptococcus mutans to control dental caries.
Sterilisation and disinfection: excluding sources of infection from equipment, dressings, medicines, water supplies etc. is of paramount importance in infection control within hospitals/clinics/practices.
Sterilisation means the process of killing or removing all viable organisms. Sterilisation may be acheived by:
heat - moist heat, more often used than dry heat, is used within autoclaves where saturated steam under pressure ensures sufficient killing and penetration of heat into materials to be sterilised. The usual sterilisation cycle of 121·C for 15 minutes is sufficient to kill all vegetative bacterial cells and the heat resistant endospores of clostridia and Bacillus spp.
irradiation - gamma irradiation is used to sterilise needles, syringes, gloves, vaccines and heat-sensitive items and equipment. Free radicals are produced by the irradiation and these attack target sites such as DNA.
chemical agents - the gases, ethylene oxide and formaldehyde, are alkylating agents which damage proteins and nucleic acids. Many chemical agents are capable of disinfecting but few are capable of rendering articles sterile.
filtration - passing fluids through nitrocellulose membranes with pore sizes of 0.6 or 0.22mm removes microbial cells as well as particles and pyrogens. Filtration may also be used to isolate very small numbers of organisms from large volumes of fluid, for example when looking for pathogens in water supplies.
Disinfection is a process which kills most, but not all, viable organisms. It may employ a chemical agent which kills pathogens, but does not kill viruses or endospores, or a physical process such as boilong water to reduce the viable microbial load. Antiseptics, a particular group of disinfectants, reduce the number of organisms on the skin.
Pasteurisation eliminates pathogens and reduce the total numbers of viable microbes, but does not affect endospores. The original regime of 62·C for 30 min has been replaced by the “Flash” method of about 71·C for 15 seconds to pasteurise many bulk fluids.
Metabolism of Oral Microorganisms
Oral microorganisms derive nutrients from saliva and GCF. Additionally, exogenous substrates are provided intermittently in the diet. Thus, there is an enormous diversity in substrates available and in the metabolic activities of the organisms which colonise the mouth.
Carbohydrate metabolism (figure) has received much attention because of its role in caries production. End products of such fermentation in the mouth are varied e.g., Streptococcus mutans produces only lactic acid from sugars, some lactobacilli produce lactic acid and ethanol, whereas yeasts convert glucose to ethanol and CO2. The substrates used are also very varied and many of the anaerobes seen in the mouth are able to utilise amino acids as substrates for fermentation; therefore, periodontal organisms are predominantly proteolytic.

The Bacterial Flora of Humans

The Normal Flora

In a healthy animal, the internal tissues, e.g. blood, brain, muscle, etc., are normally free of microorganisms. However, the surface tissues, i.e., skin and mucous membranes, are constantly in contact with environmental organisms and become readily colonized by various microbial species. The mixture of organisms regularly found at any anatomical site is referred to as the normal flora, except by researchers in the field who prefer the term "indigenous microbiota". The normal flora of humans consists of a few eucaryotic fungi and protists, but bacteria are the most numerous and obvious microbial components of the normal flora.
The predominant bacterial flora of humans are shown in Table 1. This table lists only a fraction of the total bacterial species that occur as normal flora of humans. A recent experiment that used 16S RNA probes to survey the diversity of bacteria in dental plaque revealed that only one percent of the total species found have ever been cultivated. Similar  observations have been made with the intestinal flora.  Also, this table does not indicate the relative number or concentration of bacteria at a particular site.  .  (1) The staphylococci and corynebacteria occur at every site listed. Staphylococcus epidermidis is highly adapted to the diverse environments of its human host. S. aureus is a potential pathogen. It is a leading cause of bacterial disease in humans. It can be transmitted from the nasal membranes of an asymptomatic carrier to a susceptible host.
S. epidermidis. Scanning EM. CDC
(3) Streptococcus mutans is the primary bacterium involved in plaque formation and initiation of dental caries.  Viewed as an opportunistic infection, dental disease is one of the most prevalent and costly infectious diseases in the United States.
Streptococcus mutans. Gram stain. CDC
(5) Streptococcus pneumoniae is present in the upper respiratory tract of about half the population.  If it invades the lower respiratory tract it can cause pneumonia.  Streptococcus pneumoniae causes 95 percent of all bacterial pneumonia.
Streptococcus pneumoniae. Direct fluorescent antibody stain. CDC.
(6) Streptococcus pyogenes refers to the Group A, Beta-hemolytic streptococci. Streptococci cause tonsillitis (strep throat), pneumonia, endocarditis. Some streptococcal diseases can lead to rheumatic fever or nephritis which can damage the heart and kidney.
Streptococcus pyogenes. Gram stain.
(7) Neisseria and other Gram-negative cocci are frequent inhabitants of the upper respiratory tract, mainly the pharynx. Neisseria meningitidis, an important cause of bacterial meningitis, can colonize as well, until the host can develop active immunity against the pathogen.
Neisseria meningitidis. Gram stain.
 Lactobacilli in the oral cavity probably contribute to acid formation that leads to dental caries.  Lactobacillus acidophilus colonizes the vaginal epithelium during child-bearing years and establishes the low pH that inhibits the growth of pathogens.
Lactobacillus species and a vaginal squaemous epithelial cell. CDC
Normal Flora of the Oral Cavity The presence of nutrients, epithelial debris, and secretions makes the mouth a favourable habitat for a great variety of bacteria. Oral bacteria include streptococci, lactobacilli, staphylococci and corynebacteria, with a great number of anaerobes, especially bacteroides.The mouth presents a succession of different ecological situations with age, and this corresponds with changes in the composition of the normal floras birth, the oral cavity is composed solely of the soft tissues of the lips, cheeks, tongue and palate, which are kept moist by the secretions of the salivary glands. At birth the oral cavity is sterile but rapidly becomes colonized from the environment, particularly from the mother in the first feeding. Streptococcus salivarius is dominant and may make up 98% of the total oral flora until the appearance of the teeth (6 - 9 months in humans). The eruption of the teeth during the first year leads to colonization by S. mutans and S. sanguis. These bacteria require a nondesquamating (no epithelial) surface in order to colonize. They will persist as long as teeth remain. Other strains of streptococci adhere strongly to the gums and cheeks but not to the teeth. The creation of the gingival crevice area (supporting structures of the teeth) increases the habitat for the variety of anaerobic species found. The complexity of the oral flora continues to increase with time, and bacteroides and spirochetes colonize around puberty.

  Various streptococci in a biofilm in the oral cavity.
The normal bacterial flora of the oral cavity clearly benefit from their host who provides nutrients and habitat. There may be benefits, as well, to the host. The normal flora occupy available colonization sites which makes it more difficult for other microorganisms (nonindigenous species) to become established. Also, the oral flora contribute to host nutrition through the synthesis of vitamins, and they contribute to immunity by inducing low levels of circulating and secretory antibodies that may cross react with pathogens. Finally, the oral bacteria exert microbial antagonism against nonindigenous species by production of inhibitory substances such as fatty acids, peroxides and bacteriocins.On the other hand, the oral flora are the usual cause of various oral diseases in humans, including abscesses, dental caries, gingivitis, and  periodontal disease. If oral bacteria can gain entrance into deeper tissues, they may cause abscesses of alveolar bone, lung, brain, or the extremities. Such infections usually contain mixtures of bacteria with Bacteroides melaninogenicus often playing a dominant role. If oral streptococci are introduced into wounds created by dental manipulation or treatment, they may adhere to heart valves and initiate subacute bacterial endocarditis

Beneficial Effects of the Normal Flora

The effects of the normal flora are inferred by microbiologists from experimental comparisons between "germ-free" animals (which are not colonized by any microbes) and conventional animals (which are colonized with a typical normal flora). Briefly, some of the characteristics of a germ-free animals that are thought to be due to lack of exposure to a normal flora are:

1. vitamin deficiencies, especially vitamin K and vitamin B12
2. increased susceptibility to infectious disease
3. poorly developed immune system, especially in the gastrointestinal tract
4. lack of "natural antibody" or natural immunity to bacterial infection

Because these conditions in germ-free mice and hamsters do not occur in conventional animals, or are alleviated by introduction of a bacterial flora (at the appropriate time of development), it is tempting to conclude that the human normal flora make similar contributions to human nutrition, health and development. The overall beneficial effects of microbes are summarized below.

1. The normal flora synthesize and excrete vitamins in excess of their own needs, which can be absorbed as nutrients by their host. For example, in humans, enteric bacteria secrete Vitamin K and Vitamin B12, and lactic acid bacteria produce certain B-vitamins. Germ-free animals may be deficient in Vitamin K to the extent that it is necessary to supplement their diets.
2. The normal flora prevent colonization by pathogens by competing for attachment sites or for essential nutrients.  This is thought to be their most important beneficial effect, which has been demonstrated in the oral cavity, the intestine, the skin, and the vaginal epithelium.  In some experiments, germ-free animals can be infected by 10 Salmonella bacteria, while the infectious dose for conventional animals is near 106 cells.
3. The normal flora may antagonize other bacteria through the production of substances which inhibit or kill nonindigenous species. The intestinal bacteria produce a variety of substances ranging from relatively nonspecific fatty acids and peroxides to highly specific bacteriocins, which inhibit or kill other bacteria.
4. The normal flora stimulate the development of certain tissues, i.e., the caecum and certain lymphatic tissues (Peyer's patches) in the GI tract. The caecum of germ-free animals is enlarged, thin-walled, and fluid-filled, compared to that organ in  conventional animals. Also, based on the ability to undergo immunological stimulation, the intestinal lymphatic tissues of germ-free animals are poorly-developed compared to conventional animals.
5. The normal flora stimulate the production of natural antibodies. Since the normal flora behave as antigens in an animal, they induce an immunological response, in particular, an antibody-mediated immune (AMI) response.  Low levels of antibodies produced against components of the normal flora are known to cross react with certain related pathogens, and thereby prevent infection or invasion.  Antibodies produced against antigenic components of the normal flora are sometimes referred to as "natural" antibodies, and such antibodies are lacking in germ-free animals.

Harmful Effects of the Normal Flora

Harmful effects of the normal flora, some of which are observed in studies with germ-free animals, can be put in the following categories. All but the last two are fairly insignificant.
1. Bacterial synergism between a member of the normal flora and a potential pathogen. This means that one organism is helping another to grow or survive. There are examples of a member of the normal flora supplying a vitamin or some other growth factor that a pathogen needs in order to grow. This is called cross-feeding between microbes. Another example of synergism occurs during treatment of "staph-protected infections" when a penicillin-resistant staphylococcus that is a component of the normal flora shares its drug resistance with pathogens that are otherwise susceptible to the drug.
2. Competition for nutrients Bacteria in the gastrointestinal tract may get to some of our utilizable nutrients before we are able to absorb them. Germ-free animals grow more rapidly and efficiently than germ-free animals. The explanation and absurd rationale for incorporating antibiotics into the food of swine, cows and poultry is that they grow faster (and thereby get to market earlier).
3 Induction of a low grade toxemia Minute amounts of bacterial toxins (e.g. endotoxin) may be found in the circulation. Of course, it is these small amounts of bacterial antigen that stimulate the formation of natural antibodies.
4. The normal flora may be agents of disease. Members of the normal flora may cause endogenous disease if they reach  a site or tissue where they cannot be restricted or tolerated by the host defences.  Many of the normal flora are potential pathogens, and if they gain access to a compromised tissue from which they can invade, disease may result.
5. Transfer to susceptible hosts Some pathogens of humans that are members of the normal flora may also rely on their host for transfer to other individuals where they can produce disease. This includes the pathogens that colonize the upper respiratory tract such as Neisseria meningitidis, Streptococcus pneumoniae, Haemophilus influenzae and Staphylococcus aureus, and potential pathogens such as E. coli, Salmonella or Clostridium in the gastrointestinal tract.
Dental Caries, Gingivitis and Periodontal Disease: - The most frequent and economically-important condition in humans resulting from interactions with our normal flora is probably dental caries. Dental plaque, dental caries, gingivitis and periodontal disease result from actions initiated and carried out by the normal bacterial flora.
Dental plaque, which is material adhering to the teeth, consists of bacterial cells (60-70% the volume of the plaque), salivary polymers, and bacterial extracellular products. Plaque is a naturally-constructed biofilm, in which the consortia of bacteria may reach a thickness of 300-500 cells on the surfaces of the teeth. These accumulations subject the teeth and gingival tissues to high concentrations of bacterial metabolites, which result in dental disease.
The dominant bacterial species in dental plaque are Streptococcus sanguis and Streptococcus mutans, both of which are considered responsible for plaque. .
Plaque formation is initiated by a weak attachment of the streptococcal cells to salivary glycoproteins forming a pellicle on the surface of the teeth. This is followed by a stronger attachment by means of extracellular sticky polymers of glucose (glucans) which are synthesized by the bacteria from dietary sugars (principally sucrose). An enzyme on the cell surface of Streptococcus mutans, glycosyl transferase, is involved in initial attachment of the bacterial cells to the tooth surface and in the conversion of sucrose to dextran polymers (glucans) which form plaque.

Dental plaque, scanning electron micrograph illustrating the diversity of microbes in plaque.
Dental Caries is the destruction of the enamel, dentin or cementum of teeth due to bacterial activities. Caries are initiated by direct demineralization of the enamel of teeth due to lactic acid and other organic acids which accumulate in dental plaque. Lactic acid bacteria in the plaque produce lactic acid from the fermentation of sugars and other carbohydrates in the diet of the host. Streptococcus mutans and Streptococcus sanguis are most consistently been associated with the initiation of dental caries, but other lactic acid bacteria are probably involved as well. These organisms normally colonize the occlusal fissures and contact points between the teeth, and this correlates with the incidence of decay on these surfaces.
Cross section of a tooth illustrating the various structural regions susceptible to colonization or attack by microbes.
Streptococcus mutans in particular has a number of physiological and biochemical properties which implicate it in the initiation of dental caries.
1. It is a regular component of the normal oral flora of humans which occurs in relatively large numbers. It readily colonizes tooth surfaces: salivary components (mucins, which are glycoproteins) form a thin film on the tooth called the enamel pellicle. The adsorbed mucins are thought to serve as molecular receptors for ligands on the bacterial cell surface.
2. It contains a cell-bound protein, glycosyl transferase, that serves an adhesin for attachment to the tooth, and  as an enzyme that polymerizes dietary sugars into glucans that leads to the formation of plaque.
3. It produces lactic acid from the utilization of dietary carbohydrate which demineralizes tooth enamel. S. mutans produces more lactic acid and is more acid-tolerant than most other streptococci. 4. It stores polysaccharides made from dietary sugars which can be utilized as reserve carbon and energy sources for production of lactic acid. The extracellular glucans formed by S. mutans are, in fact, bacterial capsular polysaccharides that function as carbohydrate reserves. The organisms can also form intracellular polysaccharides from sugars which are stored in cells and then metabolized to lactic acid.
Streptococcus mutans appears to be important in the initiation of dental caries because its activities lead to colonization of the tooth surfaces, plaque formation, and localized demineralization of tooth enamel. It is not however, the only cause of dental decay. After initial weakening of the enamel, various oral bacteria gain access to interior regions of the tooth. Lactobacilli, Actinomyces, and various proteolytic bacteria are commonly found in human carious dentin and cementum, which suggests that they are secondary invaders that contribute to the progression of the lesions.

Actinomyces israelii
Periodontal Diseases are bacterial infections that affect the supporting structures of the teeth (gingiva, cementum, periodontal membrane and alveolar bone). The most common form, gingivitis, is an inflammatory condition of the gums. It is associated with accumulations of bacterial plaque in the area. Increased populations of Actinomyces have been found, and they have been suggested as the cause. Diseases that are confined to the gum usually do not lead to loss of teeth, but there are other more serious forms of periodontal disease that affect periodontal membrane and alveolar bone resulting in tooth loss. Bacteria in these lesions are very complex populations consisting of Gram-positive organisms (including Actinomyces and streptococci) and Gram-negative organisms (including spirochetes and Bacteroides). Themechanisms of tissue destruction in periodontal disease are not clearly defined but hydrolytic enzymes, endotoxins, and other toxic bacterial metabolites seem to be involved.The microbial flora of the oral cavity are rich and extremely diverse. This reflects the abundant nutrients and moisture, and hospitable temperature, and the availability of surfaces on which bacterial populations can develop. The presence of a myriad of microorganisms is a natural part of proper oral health. However, an imbalance in the microbial flora can lead to the production of acidic compounds by some microorganisms that can damage the teeth and gums. Damage to the teeth is referred to a dental caries.Microbes can adhere to surfaces throughout the oral cavity. These include the tongue, epithelial cells lining the roof of the mouth and the cheeks, and the hard enamel of the teeth. In particular, the microbial communities that exist on the surface of the teeth are known as dental plaque. The adherent communities also represent a biofilm. Oral biofilms develop over time into exceedingly complex communities. Hundreds of species of bacteria have been identified in such biofilms.Development of the adherent populations of microorganisms in the oral cavity begins with the association and irreversible adhesion of certain bacteria to the tooth surface. Components of the host oral cavity, such as proteins and glycoproteins from the saliva, also adhere. This early coating is referred to as the conditioning film. The conditioning film alters the chemistry of the tooth surface, encouraging the adhesion of other microbial species. Over time, as the biofilm thickens, gradients develop within the biofilm. For example, oxygen may be relatively plentiful at the outer extremity of the biofilm, with the core of the biofilm being essentially oxygen-free. Such environmental alterations promote the development of different types of bacteria in different regions of the biofilm.
This changing pattern represents what is termed bacterial succession. Examples of some bacteria that are typically present as primary colonizers include Streptococcus, Actinomyces, Neisseria, and Veillonella. Examples of secondary colonizers include Fusobacterium nucleatum, Prevotella intermedia, and Capnocytophaga species. With further time, another group of bacteria can become associated with the adherent community. Examples of these bacteria include Campylobacter rectus, Eikenella corrodens, Actinobacillus actinomycetemcomitans, and the oral spirochetes of the genus Treponema.
Under normal circumstances, the microbial flora in the oral cavity reaches equilibrium, where the chemical by-products of growth of some microbes are utilized by other microbes for their growth. Furthermore, the metabolic activities of some bacteria can use up oxygen, creating conditions that are favorable for the growth of those bacteria that require oxygen-free conditions.This equilibrium can break down. An example is when the diet is high in sugars that can be readily used by bacteria. The pH in the adherent community is lowered, which selects for the predominance of acid-loving bacteria, principally Streptococcus mutans and Lactobacillus species. These species can produce acidic products. The resulting condition is termed dental caries. Dental caries is the second most common of all maladies in humans, next only to the common cold. It is the most important cause of tooth loss in people under 10 years of age.Dental caries typically proceeds in stages. Discoloration and loosening of the hard enamel covering of the tooth precedes the formation of a microscopic hole in the enamel. The hole subsequently widens and damage to the interior of the tooth usually results. If damage occurs to the core of the tooth, a region containing what is termed pulp, and the roots anchoring the tooth to the jaw, the tooth is usually beyond saving. Removal of the tooth is necessary to prevent accumulation of bacterial products that could pose further adverse health effects.Dental caries can be lessened or even prevented by coating the surface of the tooth with a protective sealant. This is usually done as soon as a child acquires the second set of teeth. Another strategy to thwart the development of dental caries is the inclusion of  a chemical called fluoride in drinking water. Evidence supports the use of fluoride to lessen the predominance of acid-producing bacteria in the oral cavity. Finally, good oral hygiene is of paramount importance in dental heath. Regular brushing of the teeth and the avoidance of excessive quantities of sugary foods are very prudent steps to maintaining the beneficial equilibrium microbial equilibrium in the oral cavity.
  • There are estimated to be circa 100,000,000,000,000 cells in the human body, of which only 10% are of human origin. The remaining 90% comprise the commensal microbial flora. Different anatomical sites are associated with their own characteristic flora.
  • Some microbes that come into contact with the body are ill-equipped to exploit the ecological niche in which they land. These are easily removed and they make up the transient flora of a site.
  • Other microbes have evolved to adhere to and grow in a particular location. Once these become established they comprise the resident flora at a given site.
  • The mouth is the portal of entry of food. This also provides access to a wide array of microbes, the majority of which become part of the transient oral flora.

 Protection of the oral cavity

Saliva provides a washing mechanism that will help to remove microbes from the mouth. We swallow 30 times per hour, on average It has been estimated that saliva contains 1,000,000,000 bacteria per ml.
Saliva also contains digestive enzymes and a number of specifically antimicrobial compounds. These include secretory IgA, lysozyme and lactoferrin. Saliva thus helps to prevent colonisation with potentially pathogenic bacteria.
Measures designed to improve oral hygiene also remove microbes from the mouth. The commensal flora of the mouth is profoundly influenced by diet.
Despite these observations and practices, the mouth provides a number of distinct ecological sites and carries a diverse and rich commensal flora.
The presence of the oral commensal flora provides protection from overgrowth by pathogens including Streptococcus pyogenes, Streptococcus pneumoniae and Candida albicans.

Dental infection and the oral commensal flora

The commensal oral flora plays a significant role in dental infections. It is also in a constant and dynamic flux. This is partly in response to the intake of food and also influenced by oral hygiene measures including brushing of teeth and flossing.
·         The hard surfaces of the teeth and the gingival crevices are the sites of accumulation of dental plaque. This is a complex structure comprising microbes, microbial products, food particles, host secretions and host cells.
·         Plaque is continually altering in composition in response to micro-environmental changes. It differs in response to its location in the mouth and in response to the length of time that it has been established.
·         On the surface of a tooth, Streptococcus mutans is the first important coloniser; particularly in people with a high sucrose diet. This bacterium can metabolise sucrose to produce extracellular polysaccharide (glucans) that enable the bacterial cells to stick onto the surface of the tooth.
·         Metabolism of the sucrose by Streptococcus mutans also leads to the formation of large quantities of lactic acid. In turn this provides the low pH environment that favours colonisation by lactobacilli.
·         Next in the microbial succession are the actinomycetes. These are filamentous bacteria that provide a web of cells that can provide a niche for the colonisation of anaerobic bacteria, including those belonging to genera such as Bacteroides, Capnocytophaga, Veillonella as well as spirochaetes and fusobacteria. An array of poorly-characterised bacteria can also be found in plaque, which may contain up to 100,000,000,000 bacteria per gram wet weight.

Oral Microbial Ecology and the Role of Salivary Immunoglobulin A  *
In the oral cavity, indigenous bacteria are often associated with two major oral diseases, caries and periodontal diseases. These diseases seem to appear following an inbalance in the oral resident microbiota, leading to the emergence of potentially pathogenic bacteria. To define the process involved in caries and periodontal diseases, it is necessary to understand the ecology of the oral cavity and to identify the factors responsible for the transition of the oral microbiota from a commensal to a pathogenic relationship with the host. The regulatory forces influencing the oral ecosystem can be divided into three major categories: host related, microbe related, and external factors. Among host factors, secretory immunoglobulin A (SIgA) constitutes the main specific immune defense mechanism in saliva and may play an important role in the homeostasis of the oral microbiota. Naturally occurring SIgA antibodies that are reactive against a variety of indigenous bacteria are detectable in saliva. These antibodies may control the oral microbiota by reducing the adherence of bacteria to the oral mucosa and teeth. It is thought that protection against bacterial etiologic agents of caries and periodontal diseases could be conferred by the induction of SIgA antibodies via the stimulation of the mucosal immune system. However, elucidation of the role of the SIgA immune system in controlling the oral indigenous microbiota is a prerequisite for the development of effective vaccines against these diseases. The role of SIgA antibodies in the acquisition and the regulation of the indigenous microbiota is still controversial. Our review discusses the importance of SIgA among the multiple factors that control the oral microbiota. It describes the oral ecosystems, the principal factors that may control the oral microbiota, a basic knowledge of the secretory immune system, the biological functions of SIgA, and, finally, experiments related to the role of SIgA in oral microbial ecology.
 The oral microbial flora contains over 500 different microbial species that often interact as a means to compete for limited space and nutritional resources. Streptococcus mutans, a major caries-causing pathogen, is a species which tends to interact competitively with other species in the oral cavity, largely due to its ability to generate copious quantities of the toxic metabolite, lactic acid. However, during a recent clinical study, we discovered a novel oral streptococcal species, Streptococcus oligofermentans, whose abundance appeared to be inversely correlated with that of S. mutans within dental plaque samples and thus suggested a possible antagonistic relationship with S. mutans. In this study, we used a defined in vitro interspecies interaction assay to confirm that S. oligofermentans was indeed able to inhibit the growth of S. mutans. Interestingly, this inhibitory effect was relatively specific to S. mutans and was actually enhanced by the presence of lactic acid. Biochemical analyses revealed that S. oligofermentans inhibited the growth of S. mutans via the production of hydrogen peroxide with lactic acid as the substrate. Further genetic and molecular analysis led to the discovery of the lactate oxidase (lox) gene of S. oligofermentans as responsible for this biological activity. Consequently, the lox mutant of S. oligofermentans also showed dramatically reduced inhibitory effects against S. mutans and also exhibited greatly impaired growth in the presence of the lactate produced by S. mutans. These data indicate that S. oligofermentans possesses the capacity to convert its competitor's main 'weapon' (lactic acid) into an inhibitory chemical (H2O2) in order to gain a competitive growth advantage. This fascinating ability may be an example of a counteroffensive strategy used during chemical warfare within the oral microbial community.
The oral cavity is comprised of many surfaces, each coated with a plethora of bacteria, the proverbial bacterial biofilm (see figure below). Based on both culture and culture-independent molecular methods using sequence analysis of 16S rRNA genes, we and others have identified most of the predominant bacterial species in the oral cavity. Collectively speaking, there are about 550 oral bacterial species, of which about 60% have not yet been cultivated in vitro. These "uncultivables" are often termed phylotypes.

In order to make definitive bacterial associations with oral health and disease states, the microbial profiles of large numbers of clinical samples must be determined. 16S rRNA-based DNA probes have been designed and validated. We have developed the Human Oral Microbe Identification Microarray, or HOMIM, in order to examine complex oral microbial diversity in a single hybridization. This high throughput technology will allow the simultaneous detection about 300 bacterial species, including the "uncultivables".
Recently, it has been recognized that oral infection, especially periodontitis, may affect the course and pathogenesis of a number of systemic diseases, such as cardiovascular disease, bacterial pneumonia, diabetes mellitus, and low birth weight. The purpose of this review is to evaluate the current status of oral infections, especially periodontitis, as a causal factor for systemic diseases. Three mechanisms or pathways linking oral infections to secondary systemic effects have been proposed: 
(i) metastatic spread of infection from the oral cavity as a result of transient bacteremia, (ii) metastatic injury from the effects of circulating oral microbial toxins, and 
(iii) metastatic inflammation caused by immunological injury induced by oral microorganisms. Periodontitis as a major oral infection may affect the host's susceptibility to systemic disease in three ways: by shared risk factors; subgingival biofilms acting as reservoirs of gram-negative bacteria; and the periodontium acting as a reservoir of inflammatory mediators. Proposed evidence and mechanisms of the above odontogenic systemic diseases are given. 

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