Oral microflora / dental implant courses by Indian dental academy

ORAL MICROFLORAORAL MICROFLORA
INDIAN DENTAL ACADEMY
Leader in continuing Dental Education
www.indiandentalacademy.comwww.indiandentalacademy.com

CONTENTS OF THE SEMINAR
Introduction.
Ecological Terminologies.
Mouth as a habitat for microbial growth.
Factors affecting the growth of the micro-
organisms in the oral cavity.
Distribution of the resident oral micro flora.
Adhesion, acquisition, metabolism.
Dental plaque.
Microflora in disease.
Opportunistic infections.
Conclusion. www.indiandentalacademy.comwww.indiandentalacademy.com

Introduction
The mouth is continually exposed to organisms
from the external environment ,beginning with
the passage through the birth canal. In time a
ecological balance is reached that serves to
establish a resident microbial flora that remains
fairly stable throughout life.

In general, these microflora’s live in harmony
with humans and, indeed, all parties benefit from the
association. It has been proposed recently that this
harmonious relationship is a result of complex
molecular signaling between members of the
resident microflora and host cells.

It has been estimated that the human body is
made up of over 1014
cells of which only around 10%
are mammalian. The remainder are the micro-
organisms that comprise the resident microflora of
the host. This resident microflora does not have
merely a passive relationship with its host.

ECOLOGICAL TERMINOLOGIES

THE INDIGENOUS (RESIDENT) FLORA
The indigenous flora comprise those indigenous
species that are almost always present in high
numbers, that is, greater than 1 percent of the
total viable count .
SUPPLEMENTAL FLORA
The supplemental flora are those bacterial species
that are nearly always present, but in low
numbers, that is, less than 1 percent of the total
viable count . www.indiandentalacademy.comwww.indiandentalacademy.com

TRANSIENT FLORA
Transient flora comprise organisms "just passing
through" a host. At any given time a particular
species may or may not be represented in the
flora.
AUTOCHTHONOUS
Species found characteristically in a particular
habitat.
ALLOCHTHONOUS
organisms which originate from elsewhere and
are generally unable to colonize successfully
unless the ecosystem is severely disturbed.www.indiandentalacademy.comwww.indiandentalacademy.com

SYMBIOSIS
When both the host and the bacteria benefit from
their inter-relationship it is termed "symbiotic."
ANTIBIOSIS
An antibiotic relationship is the opposite of a
symbiotic relationship. Instead of helping each
other, the bacteria and the host are antagonistic
to, each other.

PATHOGENS
Micro-organisms that have the potential to cause
disease are termed pathogens.
OPPORTUNISTIC PATHOGENS
Micro-organisms that cause disease only under
exceptional circumstances .
TRUE PATHOGENS
Micro-organisms that are consistently associated with a
particular disease .

AEROBIC
Micro-organisms that require oxygen for growth.
ANAEROBIC
Micro-organisms that require reduced condition for
growth .
CAPNOPHILIC
Micro-organisms that require carbon dioxide for
growth.
HABITAT
Site where the micro-organisms grow.www.indiandentalacademy.comwww.indiandentalacademy.com

MICRO- AEROPHILIC
Micro-organisms that require low concentration of
oxygen for their growth.
FACULTATIVE
Micro-organisms that can grow in the presence or
absence of a specific environment
E.g. facultative aerobes
OBLIGATORY
Micro- organisms that require a specific environment
for growth.
E.g. obligatory anaerobeswww.indiandentalacademy.comwww.indiandentalacademy.com

The Mouth As a Habitat For Microbial GrowthThe Mouth As a Habitat For Microbial Growth
Not all of the micro-organisms that enter the mouth
are able to colonize. The properties of the mouth
make it ecologically distinct from all other surfaces of
the body, and dictate the types of microbe able to
persist. Habitats that provide obviously different.
ecological conditions include mucosal surfaces (such
as the lips, cheek, palate and tongue) and teeth.

Ecological conditions within the mouth will also
vary during the change from the primary to the
permanent dentition. and following the extraction of
teeth, the insertion of prostheses such as dentures,
and any dental treatment, including scaling, polishing
and fillings.

Transient fluctuations in the stability of the
oral ecosystem may be induced by the frequency
and type of food ingested, variations in saliva flow
and periods of antibiotic therapy.

Four features that make the oral cavity distinct
from other areas of the body are:
 Teeth
 Specialized mucosal surfaces
 Saliva
 Gingival crevicular fluid (GCF).

TEETHTEETH
Is the only normally accessible site in the body
that has hard non-shedding surface for microbial
colonization. These unique tissues allow the
accumulation of large masses of micro-organisms
(predominantly bacteria) and their extra cellular
products, termed dental plaque.www.indiandentalacademy.comwww.indiandentalacademy.com

Plaque is an example of a biofilm, and, while it
is found naturally in health, it is also associated with
dental caries and periodontal disease. In disease,
there is a shift in the composition of the plaque
microflora away from the species that predominate
in health.

The ecological complexity of the mouth is
increased still further by the range of habitats
associated with the tooth surface. Teeth do not
provide a uniform habitat but possess several
distinct surfaces, each of which is optimal for
colonization and growth by different populations
of micro-organisms.

MUCOSAL SURFACESMUCOSAL SURFACES
Although the mouth is similar to other ecosystems in
the digestive tract in having mucosal surfaces for
microbial colonization, the oral cavity does have
specialized surfaces which contribute to the diversity
of the microflora at certain sites.

The papillary structure of the dorsum of the
tongue provides refuge for many micro-organisms
which would otherwise be removed by mastication
and the flow of saliva. Such sites on the tongue can
also have a low redox potential, which enables
obligatory anaerobic bacteria to grow. Indeed, the
tongue may act as a reservoir for some of the Gram-
negative anaerobes. www.indiandentalacademy.comwww.indiandentalacademy.com

The mouth also contains keratinized (e.g. the
palate) as well as non-keratinized, stratified
squamous epithelium which may affect the intra-oral
distribution of micro-organisms.

Distinct microbial habitats within the mouthDistinct microbial habitats within the mouth
SiteSite CommentsComments
Lips, cheek, palateLips, cheek, palate Biomass restricted by desquamation;Biomass restricted by desquamation;
different surfaces have specialized hostdifferent surfaces have specialized host
cell types.cell types.
TongueTongue Highly papillated surface; acts as aHighly papillated surface; acts as a
reservoir for anaerobes.reservoir for anaerobes.
TeethTeeth Non-shedding surface enabling largeNon-shedding surface enabling large
masses of microbes to accumulate (e.g.masses of microbes to accumulate (e.g.
biofilms such as dental plaque). Teethbiofilms such as dental plaque). Teeth
have distinct surfaces for microbialhave distinct surfaces for microbial
colonization; each surface (e.g. fissures,colonization; each surface (e.g. fissures,
smooth surfaces, approximal, gingivalsmooth surfaces, approximal, gingival
crevice) will support a distinct microfloracrevice) will support a distinct microflora
because of their intrinsic biologicalbecause of their intrinsic biological
properties.properties.www.indiandentalacademy.comwww.indiandentalacademy.com

SALIVASALIVA
The mouth is kept moist and lubricated by
saliva which flows over all the internal surfaces of
the oral cavity. Saliva enters the oral cavity via ducts
from the major paired parotid, submandibular and
sublingual glands as well as from the minor glands
of the oral mucosa (labial, lingual, buccal and palatal
glands) where it is produced.

There are differences in the chemical
composition of the secretions from each gland, but the
complex mixture is termed 'whole saliva'. Saliva
contains several ions including sodium, potassium,
calcium, chloride, bicarbonate and phosphate .

Some of these ions contribute to the buffering
property of saliva which can reduce the cariogenic
effect of acids produced from the bacterial
metabolism of dietary carbohydrates. Bicarbonate is
the major buffering system in saliva but phosphates,
peptides and proteins are also involved.

The mean pH of saliva is between pH 6.75 and
7.25, although the pH and buffering capacity will vary
with the flow rate. Within a mouth, the flow rate and
the concentration of components such as proteins and
calcium and phosphate ions have circadian rhythms,
with the slowest flow of saliva occurring during sleep.

Whole SalivaWhole Saliva
ConstituentsConstituents RestingResting StimulatedStimulated GCFGCF
ProteinProtein 220220 280280 7x107x1033
IgAIgA 1919 110*110*
IgGIgG 11 350*350*
IgMIgM <1<1 25*25*
C3C3 trtr trtr 4040
AmylaseAmylase 3838 --
LysozymeLysozyme 2222 1111 ++
AlbuminAlbumin trtr trtr ++

SodiumSodium 1515 6060 204204
PotassiumPotassium 8080 8080 7070
CalciumCalcium 66 66 2020
MagnesiumMagnesium <<11 <<11 11
PhosphatePhosphate 1717 1212 44
BicarbonateBicarbonate 3131 200200 --

GINGIVAL CREVICULAR FLUID (GCF)GINGIVAL CREVICULAR FLUID (GCF)
Serum components can reach the mouth by
the flow of a serum-like fluid through the junctional
epithelium of the gingivae .The flow of GCF is
relatively slow at healthy sites, but increases during
inflammation.

GCFGCF can influence the site by acting as a novel
source of nutrients, while its flow will remove non-
adherent microbial cells. Many bacteria from sub-
gingival plaque are proteolytic and interact
synergistically to break down the host proteins and
glycoprotein's to provide peptides, amino acids and
carbohydrates for growth.

GCFGCF also contains components of the host
defenses which play an important role in regulating
the microflora of the gingival crevice in health and
disease. The neutrophils in GCF are viable and can
phagocytose bacteria within the crevice.

Factors affecting the growth of
micro-organisms in the oral
cavity
Temperature
Redox potential
pH
Nutrients
Adherence and agglutination
Anti-microbial agents.
Host defence
Host genetics www.indiandentalacademy.comwww.indiandentalacademy.com

TEMPERATURETEMPERATURE
The human mouth is kept at a relatively
constant temperature (35-36 ◦
C), which provides
conditions suitable for the growth and metabolism of
a wide range of micro-organisms. Temperature can
also affect key parameters associated with the
habitat, such as pH, ion activity, aggregation of
macro-molecules and gas solubility.www.indiandentalacademy.comwww.indiandentalacademy.com

Periodontal pockets with active disease have a higher
temperature (up to 390
C) compared with healthy
sites (mean value 36.80
C). Such changes in
temperature affect gene expression in periodontal
pathogens, such as Porphyromonas gingivalis.

A large rise in temperature down-regulates
expression of fimbriae (which mediate attachment of
the bacterium to host cells) and the major proteases
of this micro-organism, and up regulates synthesis of
superoxide dismutase, which neutralizes toxic
oxygen metabolites.

Temperature has been shown to vary between
different sub gingival sites, even within the same
individual, and may influence the proportions of
certain bacterial species, such as the putative
periodontal pathogens P. gingivalis, Bacteroides
forsythus' and Campylobacter rectus.

REDOX POTENTIALREDOX POTENTIAL
It is the level of the electrical potential of a site
relative to a standard hydrogen electrode. This
potential, called the Eh, is the tendency for a medium
or compound to oxidize or reduce an introduced
molecule by the removal or addition of electrons..

Tissues or microbes that need a positive Eh for
viability are termed "aerobes," and those that need a
negative Eh are "anaerobes”. Despite the easy
access to the mouth of air with an oxygen
concentration of approximately 20%, it is perhaps
surprising that the oral microflora comprises few, if
any, truly aerobic specieswww.indiandentalacademy.comwww.indiandentalacademy.com

The majority of organisms are either
facultatively anaerobic or obligately anaerobic .
Anaerobic species require reduced conditions for
their normal metabolism; therefore, it is the degree
of oxidation-reduction (redox potential, Eh) at a site
that governs their survival.

Some anaerobes can survive at aerobic
habitats by existing in close partnership with oxygen
consuming species. Obligate anaerobes also
possess specific molecular defence mechanisms
that enable them to cope with low redox potential
(highly reduced).

The development of plaque in this way is
associated with a specific succession of micro-
organisms . Early colonizers will utilize O2 and
produce CO2; later colonizers may produce H2 and
other reducing agents such as sulphur containing
compounds and volatile fermentation products,

Thus, as the redox potential is gradually
lowered, sites become suitable for the survival and
growth of a changing pattern of organisms, and
particularly anaerobes. Differences have been found
between the Eh of the gingival crevice in health and
disease.

Periodontal pockets are more reduced ( - 48
m V) than healthy gingival crevices in the same
individuals (+ 73 m V). Approximal areas (between
teeth) will also have a low Eh although values for
the redox potential at these sites have not been
reported. Gradients of O2 concentration and Eh will
exist in the oral cavity, particularly in a thick biofilm
such as plaque. www.indiandentalacademy.comwww.indiandentalacademy.com

Thus, plaque will be suitable for the growth of
bacteria with a range of oxygen tolerances. The
redox potential at various depths will be influenced
by the metabolism of the organisms present and
the ability of gases to diffuse in and out of plaque.

Similarly, the redox potential will also affect
bacterial metabolism, e.g. the activity intracellular
glycolytic enzymes and the pattern of fermentation
products of Streptococcus mutants varies under
strictly anaerobic conditions. Thus, modifications to
the habitat that disturb such gradients may
influence the composition and metabolism of the
microbial community.

pHpH
Many micro-organisms require a pH around
neutrality for growth, and are sensitive to extremes
of acid or alkali. The pH of most surfaces of the
mouth is regulated by saliva so that, in general,
optimum pH values for microbial growth are
provided at sites bathed by this fluid.

Bacterial population shifts within the plaque
microflora can occur following fluctuations in
environmental pH After sugar consumption, the
pH in plaque can fall rapidly to below pH 5.0 by
the production of acids (predominantly lactic acid)
by bacterial metabolism the pH then recovers
slowly to base-line values.

Depending on the frequency of sugar intake, the
bacteria in plaque will be exposed to varying
challenges of low pH. Many of the predominant
plaque bacteria from healthy sites can tolerate only
brief conditions of low pH, and are inhibited or killed
by more frequent or prolonged exposures to acidic
conditions. www.indiandentalacademy.comwww.indiandentalacademy.com

This can result in the enhanced growth of, or
colonization by, acid-tolerant species, especially
mutans streptococci and Lactobacillus species,
which are normally absent or only minor components
in dental plaque at healthy sites. Such a change in
the bacterial composition of plaque predisposes a
surface to dental caries.www.indiandentalacademy.comwww.indiandentalacademy.com

In contrast, the pH of the gingival crevice becomes
alkaline during the host inflammatory response in
periodontal disease, e.g. following deamination of
amino acids and ammonia production. The mean
pH may rise to between pH 7.2 and 7.4 during
disease, with a few patients having pockets with a
mean pH of around 7.8.

This degree of change may perturb the balance of
the resident microflora of gingival crevice by
favouring the growth and metabolism of periodontal
pathogens, such as Porphyromonas gingivalis, that
have pH optima for growth above pH 7.5.

NUTRIENTSNUTRIENTS
The association of an organism with a particular
habitat is direct evidence that all of the necessary
growth-requiring nutrients are present. The mouth
can support a microbial community of great
diversity and satisfy the requirements of many
nutritionally demanding bacterial population.

ENDOGENOUS NUTRIENTSENDOGENOUS NUTRIENTS
The persistence and diversity of the resident oral
microflora is due primarily to the metabolism of the
endogenous nutrients provided by the host, rather
than by exogenous factors in the diet. The main
source of endogenous nutrients saliva, which
contains amino acids, peptides, proteins and
glycoproteins, vitamins and gases.www.indiandentalacademy.comwww.indiandentalacademy.com

In addition, the gingival crevice is supplied with GCF
which, in addition to delivering components of the
host defences, contains potential sources of novel
nutrients, such as albumin and other host proteins
and glycoproteins, including haeme containing
molecules. The difference in source of endogenous
nutrients is one of the reasons for the variation in the
microflora of the gingival crevice compared with
other oral sites . www.indiandentalacademy.comwww.indiandentalacademy.com

Plaque bacteria produce glycosidase and
proteases, and interact synergistically to
breakdown these endogenous nutrients as no
single species has the full enzyme complement to
totally metabolize these nutrients.

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Superimposed upon these endogenous nutrients is
the complex array of food stuffs ingested
periodically in the diet. Fermentable carbohydrates
are the main class of compounds that influence
markedly the ecology of the mouth. Such
carbohydrates can be broken down to acids while,
additionally,

sucrose can be converted by bacterial enzymes into
two classes of polymer (glucans and fructans)
which can be used to consolidate attachment or act
as extra cellular nutrient storage compounds,
respectively. Dairy products (milk, cheese) have
some influence on the ecology of the mouth.

The ingestion of milk or milk products can
protect the teeth of animals against caries This
may be due to the buffering capacity of milk
proteins or due to decarboxylation of amino acids
after proteolysis since several bacterial species
can metabolize casein.

Sugar substitutes are sweet-tasting
compounds that cannot be metabolized to acid by
oral bacteria. XylitolXylitol, for example, is inhibitory to
the growth of S.S. mutansmutans, and lower levels of this
species are found in plaque and saliva of those that
frequently consume products containing this
alternative sweetener.

ADHERENCE AND AGGLUTINATIONADHERENCE AND AGGLUTINATION
Chewing and the natural flow of saliva (mean rate =
19 ml/h) will detach microorganisms not firmly
attached to an oral surface. Although saliva contains
between 108
and 109
viable micro-organisms per ml,
these organisms are all derived from the teeth and
mucosa, with plaque and the tongue being the main
contributors.

Salivary components can aggregate certain bacteria
which facilitates their removal from the mouth by
swallowing. Bacteria are unable to maintain
themselves in saliva by cell division because they
are lost at an even faster rate by swallowing.

The molecules responsible for agglutination
are mucins. Mucins are high molecular weight
glycoprotein's. These Mucins not only agglutinate
oral bacteria, but can also interact with exogenous
pathogens such as Staphylococcus aureusStaphylococcus aureus and
Pseudomonas aeruginosaPseudomonas aeruginosa, as well as viruses (e.g.
influenza virus)

Dental plaque formation involves an ordered
colonization by a range of bacteria. The early
colonizers interact with, and adhere to, saliva coated
enamel, while later colonizers bind to already
attached species (co-aggregation).

ANTIMICROBIAL AGENTS AND INHIBITORSANTIMICROBIAL AGENTS AND INHIBITORS
Anti-plaque agents are distinguished from
antimicrobials on the basis of their mode of action.
Anti-plaque agents remove already attached cells, or
prevent adhesion of new cells to the tooth surface.
Unlike antimicrobials which are designed to kill
(bactericidal) or inhibit the growth (bacteriostatic) of
the bacteria.

Both types of agent can be delivered from
toothpastes (dentifrices) and mouthwashes.
Antibiotics given systemically or orally for problems
at other sites in the body will enter the mouth via
saliva or GCFGCF and affect the stability of the oral
microflora

Within a few hours of taking prophylactic high
doses of penicillin's, the salivary microflora can be
suppressed permitting the emergence of antibiotic-
resistant bacteria.

Host defencesHost defences
The health of the mouth is dependent on the integrity
of the mucosa (and enamel) which acts as a physical
barrier to prevent penetration by micro-organisms or
antigens . The host has a number of additional
defence mechanisms which play an important role in
maintaining the integrity of these oral surfaces.www.indiandentalacademy.comwww.indiandentalacademy.com

HOST GENETICSHOST GENETICS
Gender and race can influence disease
susceptibility, and possibly also affect the microflora.
In an adult periodontitis group, P. gingivalis and
Peptostreptococcus anaerobius were associated
more with black subjects whereas, Fusobacterium
nucleatum was found more commonly in white
individuals.

The reasons for this are unknown, but may
reflect some variation in the local immune response.
The microflora of twin children living together was
more similar than that of unrelated children of the
same age. Further analysis showed that the micro
flora of identical twins was more similar than that of
fraternal twins, suggesting some genetic control.

ACQUISITIONACQUISITION

ACQUISITION OF THE RESIDENT ORAL
MICROFLORA

The foetus in the womb is normally sterile.
During delivery the baby comes into contact with
the normal microflora of the mother's uterus and
vagina, and at birth with the micro-organisms of the
atmosphere and of the people in attendance.

Despite the widespread possibility of
contamination, the mouth of the new born baby is
usually sterile. From the first feeding onwards,
however, the mouth is regularly inoculated with
micro-organisms and the process of acquisition of
the resident oral microflora begins.

Acquisition depends on the successive
transmission of micro-organisms to the site of
potential colonization. Initially, in the mouth, this is by
passive contamination from the mother, from food,
milk and water, and from the saliva of individuals in
close proximity to the baby. S. salivariusS. salivarius, mutansmutans
streptococcistreptococci and some other species are
transmitted from mother to child via saliva.

Mutans streptococciMutans streptococci found in children appeared
identical to those of their mothers in 71 % of 34
infant-mother pairs examined. No evidence of
father to infant transmission of mutansmutans
streptococcistreptococci was observed, although transmission
between spouses may occur with some periodontal
pathogens, such as P. gingivalisP. gingivalis.

The first micro-organisms to colonize are termed
pioneer species, and collectively they make up the
pioneer microbial community. These pioneer
species continue to grow and colonize until
environmental resistance is encountered. This can
be due to several limiting forces (including physical
and chemical factors) which act as barriers to
further development.

In the oral cavity, physical factors include the
shedding of epithelial cells (desquamation), and the
shear forces from chewing and saliva flow. Nutrient
requirements, redox potential, pH, and the
antibacterial properties of saliva can act as chemical
barriers limiting growth. One genus or species is
usually predominant during the development of the
pioneer community. www.indiandentalacademy.comwww.indiandentalacademy.com

The pioneer micro-organisms are S. salivarius, S.S. salivarius, S.
mitis and S. oralis.mitis and S. oralis. With time, the metabolic activity
of the pioneer community modifies the environment
providing conditions suitable for colonization by a
succession of other populations, by:
Changing the local Eh or pH.
Modifying or exposing new receptors for
attachment.
Generating novel nutrients.

Eventually a stable situation is reached with a high
species diversity; this is termed the climax
community. A climax community reflects a highly
dynamic situation and must not be regarded as a
static state. The diversity of the pioneer oral
community increases during the first few months of
life, and several Gram-negative anaerobic species
appear . www.indiandentalacademy.comwww.indiandentalacademy.com

When the infants were followed longitudinally during
the eruption of the primary dentition, gram-negative
anaerobic bacteria were isolated more commonly,
and a greater diversity of species were recovered
from around the gingival margin of the newly
erupted teeth (infant mean age = 32 months).

These findings confirmed that the eruption of
teeth has a significant ecological impact on the oral
environment, and its resident microflora. The
acquisition of some bacteria may occur optimally
only at certain ages.

Studies of the transmission of mutans streptococci
to children have identified a specific ''window ofwindow of
infectivityinfectivity'' between 19 and 31 months (median
age = 26 months). This opens up the possibility of
targeting preventive strategies over this critical
period to reduce the likelihood of subsequent
colonization in the infant.www.indiandentalacademy.comwww.indiandentalacademy.com

ALLOGENIC AND AUTOGENIC SUCCESSION
The development of a climax community at an
oral site can involve examples of both allogenic and
autogenic succession. In allogenic succession,
factors of non microbial origin are responsible for an
altered pattern of community development.

For example, species such as mutansmutans
streptococcistreptococci and S. sanguisS. sanguis only appear in the
mouth once teeth have erupted .The increase in
number and diversity of obligate anaerobes once
teeth are present is an example of autogenic
succession in which community development is
influenced by microbial factors

AGEING AND THE ORAL
MICROFLORA
Birth
Infancy and early childhood
Adolescence
Adulthood

DECIDUOUS
DENTITION
PERMANENT
DENTITION

HUMAN ORAL FLORA
Gram-positive facultativeGram-positive facultative
coccicocci
Gram-negative facultativeGram-negative facultative
rodsrods
StaphylococcusStaphylococcus
epidermidisepidermidis
Staph. aureusStaph. aureus
Streptococcus mutansStreptococcus mutans
Strep. sanguisStrep. sanguis
Strep. MitisStrep. Mitis
Strep. SalivariusStrep. Salivarius
Strep. FaecalisStrep. Faecalis
Beta-hemolytic streptococciBeta-hemolytic streptococci
EnterobacteriaceaeEnterobacteriaceae
Hemophilus influenzaeHemophilus influenzae
Eikenella corrodensEikenella corrodens
ActinobacillusActinobacillus
ActinomycetemcomitansActinomycetemcomitans

Gram-positiveGram-positive
anaerobic coccianaerobic cocci
Gram-positive anaerobicGram-positive anaerobic
rodsrods
Peptostreptococcus spPeptostreptococcus sp Actinomyces israeliiActinomyces israelii
A. odonotolyticusA. odonotolyticus
A. ViscosusA. Viscosus
LactobacillusLactobacillus
Gram- negitiveGram- negitive
Gram-negative aerobicGram-negative aerobic
or facultative coccior facultative cocci
DiphtheroidsDiphtheroids
CorynebacteriumCorynebacterium
EubacteriumEubacterium
Neisseria siccaNeisseria sicca
N. FlavescensN. Flavescens

Gram-negativeGram-negative
Gram-negative anerobic rodsGram-negative anerobic rods
Veillonella alcaescensVeillonella alcaescens
V. parvulaV. parvula
Bacteroides asaccharolyticusBacteroides asaccharolyticus
B. GingivalisB. Gingivalis
B. FragilisB. Fragilis
Fusobacterium periodonticumFusobacterium periodonticum
F.nucleatumF.nucleatum

SpirochetesSpirochetes YeastsYeasts
Treponema denticolaTreponema denticola
T. MicrodentiumT. Microdentium
Candida albicansCandida albicans
Geotrichum sp.Geotrichum sp.
ProtozoaProtozoa MycoplasmaMycoplasma
Entamoeba gingivalisEntamoeba gingivalis
Tirchomonas tenaxTirchomonas tenax
Mycoplasma oraleMycoplasma orale
M. pneumoniaeM. pneumoniae

DISTRIBUTION OF THE RESIDENTDISTRIBUTION OF THE RESIDENT
ORAL MICROFLORAORAL MICROFLORA

Host receptors
Bacterial adhesins
FACTORS AFFECTING THE DISTRIBUTION OF
ORAL MICRO-ORGANISMS

CELL WALL OF STREPTOCOCCUSCELL WALL OF STREPTOCOCCUS

METABOLISM OF ORAL BACTERIA

PLAQUE

DEFENITIONDEFENITION
Dental plaqueDental plaque can be defined as the soft deposits
that form the biofilm adhering to the tooth surfaces
or other hard surfaces in the oral cavity, including
removable and fixed prosthesis.
The term BiofilmBiofilm is used to describe communities
of micro-organisms attached to a surface.

Steps in formation of
plaque

Bacteria attached to Enamel Pellicle

Initial colonization

Biofilm Formation

Colonies of Rods and Filamentous Bacteria

Mature plaque (Corncob Formation)

PLAQUE AS SEEN
WITH NAKED EYES
AFTER STAINING WITH
ERYTHROCINE

MICRO-ORGANISMS FOUND IN
PLAQUE

Predominant microflora of the dental plaque

CLASSIFICATION OF PLAQUE BASED
ON THE SITE
Supra gingival (Smooth surface) plaque.
Sub gingival plaque.
Approximal plaque
Fissure plaque
Denture plaque

Gradients in dental Plaque

Microbial homeostasis in dental plaque

Factors involved in break down of microbial
homostasis

Factors involved in microbial interaction in dental
plaque

MICROFLORA IN DISEASE
INFECTIONS OF THE MOUTHINFECTIONS OF THE MOUTH
InfectionInfection OrganismOrganism
Dental cariesDental caries Streptococcus mutansStreptococcus mutans
Periodontal diseasesPeriodontal diseases Bacteroides, ActinomycesBacteroides, Actinomyces
Surgical infectionSurgical infection
a)a) Dry socketDry socket
b)b) Dental abscessDental abscess
c)c) OsteomyelitisOsteomyelitis
d)d) Ludwig’s anginaLudwig’s angina
e)e) PericoronitisPericoronitis
ActinomycesActinomyces
Oral streptococciOral streptococci
Staphylococcus aureusStaphylococcus aureus
ββ --haemolytic streptococcihaemolytic streptococci
BacteroidesBacteroides

Soft tissue infectionsSoft tissue infections
a)a) DiphtheriaDiphtheria
b)b) ANUGANUG
c)c) Cancrum orisCancrum oris
d)d) TuberculosisTuberculosis
e)e) LeprosyLeprosy
C. DiphtheriaeC. Diphtheriae
Fuso-spirochaetesFuso-spirochaetes
Fuso-spirochaetesFuso-spirochaetes
M. TuberculosisM. Tuberculosis
M. LepraeM. Leprae
Viral infectionsViral infections
a)a) Herpetic stomatitisHerpetic stomatitis
b)b) Herpes ZosterHerpes Zoster
c)c) MumpsMumps
d)d) MeaslesMeasles
Herpes simplexHerpes simplex
Varicella-zosterVaricella-zoster
Mumps virusMumps virus
Measles virusMeasles virus

Fungal infectionsFungal infections
a)a) CandidosisCandidosis
b)b) HistoplasmosisHistoplasmosis
c)c) SporotrichosisSporotrichosis
Candida albicansCandida albicans
H. CapsulatumH. Capsulatum
Sporotrichum schenkiiSporotrichum schenkii
MiscellaneousMiscellaneous
a)a) Erythema multiformeErythema multiforme
b)b) StevensJohnsonStevensJohnson
syndromesyndrome

MICROFLORA IN DISEASE
Interrelationship that leads to dental disease

Dental caries
Property

Acids produced in caries

Bacteria in caries

PLAQUE HYPOTHESIS

PERIODONTAL DISEASE

Hypothesis in periodontal
disease

Mechanism of tissue distruction in periodintal disease

BACTERIA IN GINGIVITIS

GINGIVITIS

BACTERIA IN CHRONIC PERIODONTITIS

PERIODONTITIS

Bacterial invasion

OPPORTUNISTIC INFECTIONS

Virulance factor of candida albicans

Predisposing factors of oral candidosis

Classification of primary oral candidiasis

Principal fungi affecting the oral cavity

REVIEW OF LITTERATURE

Budtz-Jorgensen E, Theilade. E, Theilade J:
Quantitative relationship between yeasts and
bacteria in denture induced stomatitis. (1983)
They conducted an electron microscope study on
denture plaque. A smear was prepared from
denture scraping and examined by light
microscope. Most organisms were gram negative
cocci or rods, Some filaments were also seen. In
one subject only yeast were seen. The acquired
deposits was not seen to invaginate the denture
base. www.indiandentalacademy.comwww.indiandentalacademy.com

Further he concluded that denture plaque may be
present without clinically demonstrable signs of
stomatitis.
He also stated that the presence of denture plaque
constitutes the principal cause leading to the
inflammation of the palatal mucosa.

Thomas E Rams, Thomas W, Roberts, Helt
tatun & Paul H.Keyer(1984) conducted a
study on the subgingival microbial flora
associated with human dental implants. They
concluded that the microorganisms around
protruding dental implants are similar to the
bacterial population around natural teeth.

FRANK R. M. et. aI, Transmission electron
microscopy of plaque accumulations in denture
stomatitis(1985)
They found that in general the ultrastructure of
denture plaque in patients with denture stomatitis,
was quite different from that of dental plaque with
respect to the pellicle and plaque matrix, as well
as the distribution and nature of the organisms
present. www.indiandentalacademy.comwww.indiandentalacademy.com

R.Holt,M.G.Newman,F.Kratochvil,S.Jeswani,
M.Bugler,S.Khorsandi and M.Sanz,1986
Implants are subjected to many of the same
bacterial etiologic factors as natural teeth and
their placement and maintenance should be
subject to same standard of periodontal
treatment as natural teeth.

Michael G, Newman ThomasF, Flemig 1988
The microbiota associated with stable and
failing implants is similar to the microbiota of
periodontally healthy and diseased teeth
respectively

Quirynen M, Listgarten MA, 1990 No
significant changes in the distribution of bacterial
morphotypes could be found between implants
and natural teeth.
Srinivas Koka, Michael E.Razzog,Thomas
J.Blocess, Salam Syed (1993)
Conducted a study on the microbial colonization
of dental implants in partially edentulous
subjects. They concluded that Branemark dental
implants placed in partially edentulous patients
may be colonized by disease associated bacteria
within 14 days of second stage surgery.www.indiandentalacademy.comwww.indiandentalacademy.com

Hajishengallis G, Michalek SM.( 1999)
Current status of a mucosal vaccine against dental caries
Research efforts towards developing an effective and safe
caries vaccine have been facilitated by progress in molecular
biology, with the cloning and functional characterization of
virulence factors from mutans streptococci, the principal
causative agent of dental caries, and advancements in mucosal
immunology, including the development of sophisticated
antigen delivery systems and adjuvants that stimulate the
induction of salivary immunoglobulin A antibody responses.www.indiandentalacademy.comwww.indiandentalacademy.com

Cell-surface fibrillar proteins, which mediate
adherence to the salivary pellicle, and,
glycosyltransferase enzymes, which synthesize
adhesive glucans and allow microbial
accumulation, are virulence components of
mutans streptococci, and primary canidates for a
human caries vaccine

Ueta E, Tanida T, Yoneda K, Yamamoto T, Osaki T
(2001)
Increase of Candida cell virulence by anticancer drugs
and irradiation.
The influence of anticancer drugs and irradiation on
Candida cell proliferation, adherence to HeLa cells
and susceptibility to antifungal drugs (amphotericin B
IIld miconazole) and neutrophils were examined using
two Candida albicans.

Correspondingly, surviving Candida cells after these
treatments were resistant to nentrophils, with a reduction to
half of the killing.
These results indicate that anti-cancer drugs and irradiation
potentiate the virulence of Candida cells, or eliminate
Candida cells with low virulence, thereby enhancing the risk
of oral and systemic candidiasis.

Ling L-J, Hung S-L, Tseng S-C, Chen Y-T, Chi L-
Y, Wu K-M, Lai Y-L. (2001)
Association between betel quid chewing,
periodontal status and periodontal pathogens.
This investigation examined whether an
association exists between betel quid chewing
and signs of periodontal disease and
determined the prevalence of Actinobacillus
actinomycetemcomitans and Porphyromonas
gingivalis by polymerase chain reaction .www.indiandentalacademy.comwww.indiandentalacademy.com

This investigation examined whether an
association exists between betel quid chewing and
signs of periodontal disease and determined the
prevalence of Actinobacillus
actinomycetemcomitans and Porphyromonas
gingivalis by polymerase chain reaction . The
periodontal status of 34 betel quid chewers and 32
non-betel quid chewers were compared.

A significantly higher prevalence of bleeding
on probing was found in betel quid chewers
than non-chewers among the subjects with
higher plaque level, greater gingival
inflammation, deeper probing depth or greater
attachment loss. Also, the results suggested
that betel quid chewers may harbor higher
levels of infection with A.
actinomycetemcomitans and P.gingivalis than
non-betel quid chewers.www.indiandentalacademy.comwww.indiandentalacademy.com

Vitkov L, Krautgartner WD, Hannig M, Weitgasser R,
Stoiber W (2002)
Candida attachment to oral epithelium.
Inflamed oral mucosa biopsies from patients with
thrush and high candidal density were observed in a
transmission electron microscope (TEM) using ultra-
histochemical staining with ruthenium red for
glycocalyx visualization. Candida adhesion itself is
assumed to induce mucosal inflammation

Ersin NK, Kocabas EH, Alpoz AR, Uzel A.(2004 )
Transmission of Streptococcus mutans in a group
of Turkish families
.
Eight mothers who had high S. mutans levels in
unstimulated saliva and 8 children aged between 2
and 3 years participated in the study. Plaque
samples from each child were collected with the
tips of sterile toothpicks for S. mutans counts.
Although not part of the original study design, S.
mutans samples were also obtained from the
unstimulated saliva of the three fathers who
shared the same households. .The mothers or the
fathers could be the source for the transmission
of S. mutans to their children.www.indiandentalacademy.comwww.indiandentalacademy.com

CONCLUSION

The mouth has a resident microflora with a
characteristic composition that exists, for the most
part, in harmony with the host. This microflora is of
benefit to the host and contributes to the normal
development of the physiology and host defences.
Components of this microflora can act as
opportunistic pathogens when the habitat is
disturbed or when micro-organisms are found at
sites not normally accessible to them. Dental
diseases, caused by imbalances in the resident
microflora, are highly prevalent and extremely costly
to treat.

“PREVENTION IS BETTER THAN CURE”
Emphasis has to be given for
maintenance of good oral
hygiene

References –
1.Oral Microbiology 4 th
edition
Philip Marsh, Michael V Martin.
2. Oral Microbiology and Immunology
Newman and Nisengard .
3. Microbiology for Dental students 3 rd
edition
T H Melville and C Russell.
4. Basic Medical Microbiology
Robert F Boyd and Brian G .
5. Oral Microbiology and Infectious disease.3rd
ed
Schuster

6. Kees Mcyoledjh, Menny J.A Merija, Wila
A.Vas der rcijcles Gerry M.Raghobar, Arjan
Vissis, Boundwijn stegesga “Microbiota around
root-forms endosseous implants’ a review of
the literature Int. J.Oral Maxillofacial implants
2002; 17:829-838 .
7. Mombelli A, Buser, D Lang N.P ”Colonization
of osseointgrated titanium implants in
edentulous patients early results” Oral
Microbiology & Immunology 1988; 3-113-120
8. Quirjnen M listgarters M.A” the distribution of
bacterial morphotoypes around natural teeth
and titanium implants ad modum branemark”.
Clinical oral Implants Research 1990; 1:8-12.www.indiandentalacademy.comwww.indiandentalacademy.com

9. Sreenivas Koka, Michael Razziig, Thomas
J.Bolem, Salam Syed , “ Microbial colonization
of dental implants in partially edentulous
subjects” J.Prosthet Dent 1993; 70;141-4
10.Thomas E, Rams, Thomas W.Roberts, Helt
Tatum & Paul H.Keys “The Gingival microbial
flora associated with human dental implants”.
J.Prosthet Dent 1984
11.Budtz-Jorgensen E , Theilade E, Theilade J “
Quantative relationship between yeast and
bacteria in denture induced stomatitis. J Dent
Research 1983; 91; 134 – 142.www.indiandentalacademy.comwww.indiandentalacademy.com

12. Frank RM et al Transmission electron
microscopy of plaque accumulation in denture
stomatitis. JPD 1985 ; 53: 115-124

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