Indian Dental Academy Seminar Explores Oral Microflora Ecology

ORAL MICROFLORA
INDIAN DENTAL ACADEMY
Leader in continuing dental education
www.indiandentalacademy.com

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

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

resident microflora and host cells.

members

of

the

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 microorganisms that comprise the resident microflora of
the host. This resident microflora does not have
merely a passive relationship with its host.

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 .

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
habitat.

in a particular

ALLOCHTHONOUS
organisms which originate from elsewhere and
are generally unable to colonize successfully
unless the ecosystem is severely disturbed.

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.

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 anaerobes

The 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).

TEETH
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.

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 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 Gramnegative anaerobes.

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 mouth
Site

Comments

Lips, cheek, palate Biomass restricted by desquamation;
different surfaces have specialized host
cell types.
Tongue

Highly papillated surface; acts as a
reservoir for anaerobes.

Teeth

Non-shedding surface enabling large
masses of microbes to accumulate (e.g.
biofilms such as dental plaque). Teeth
have distinct surfaces for microbial
colonization; each surface (e.g. fissures,
smooth surfaces, approximal, gingival
crevice) will support a distinct microflora
because of their intrinsic biological
properties.

SALIVA
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 Saliva
Constituents
Protein
IgA
IgG
IgM
C3
Amylase

Resting
220
19
1
<1
tr
38

Stimulated GCF
280
7x103
110*
350*
25*
tr
40
-

Lysozyme

22

11

+

Albumin

tr

tr

+

Sodium

15

60

204

Potassium

80

80

70

Calcium

6

6

20

Magnesium

<1

<1

1

Phosphate

17

12

4

Bicarbonate

31

200 -

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.

GCF can influence the site by acting as a novel
source of nutrients, while its flow will remove nonadherent microbial cells. Many bacteria from subgingival

plaque

are

proteolytic

and

interact

synergistically to break down the host proteins and
glycoprotein's to provide peptides, amino acids and
carbohydrates for growth.

GCF 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

TEMPERATURE
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.

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,

oxygen metabolites.

which

neutralizes

toxic

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 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 species

The

majority

facultatively anaerobic

of

organisms

are

either

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 microorganisms . Early colonizers will utilize O 2 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.

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.

pH
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
slowly to base-line values.

the pH then recovers

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.

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.

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.

NUTRIENTS
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 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.

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 .

Plaque

bacteria

proteases,

and

produce

glycosidase

interact

synergistically

and
to

breakdown these endogenous nutrients as no
single species has the full enzyme complement to
totally metabolize these nutrients.

E
X
O
G
E
N
O
U
S

N
U
T
R
I
E
N
T
S

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. Xylitol, for example, is inhibitory to
Xylitol
the growth of S. mutans, and lower levels of this
species are found in plaque and saliva of those that
frequently

consume

alternative sweetener.

products

containing

this

ADHERENCE 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 aureus and
Pseudomonas aeruginosa, as well as viruses (e.g.
aeruginosa
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 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 GCF 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 antibioticresistant bacteria.

Host 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.

HOST 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.

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. salivarius, mutans
salivarius
streptococci

and

some

other

species

transmitted from mother to child via saliva.

are

Mutans streptococci found in children appeared
identical to those of their mothers in 71 % of 34
infant-mother
father

to

pairs examined. No evidence of
infant

transmission

of

mutans

streptococci was observed, although transmission
between spouses may occur with some periodontal
pathogens, such as P. gingivalis.
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.

The pioneer micro-organisms are S. salivarius, S.
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 .

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 of

infectivity' 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.

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

mutans

streptococci and S. 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 facultative
cocci

Gram-negative facultative
rods

Staphylococcus
epidermidis
Staph. aureus
Streptococcus mutans
Strep. sanguis
Strep. Mitis
Strep. Salivarius
Strep. Faecalis
Beta-hemolytic streptococci

Enterobacteriaceae
Hemophilus influenzae
Eikenella corrodens
Actinobacillus
Actinomycetemcomitans

Gram-positive
anaerobic cocci

Gram-positive anaerobic
rods

Peptostreptococcus sp

Actinomyces israelii
A. odonotolyticus
A. Viscosus
Lactobacillus

Gram- negitive
anaerobic cocci

Gram-negative aerobic
or facultative cocci

Diphtheroids
Corynebacterium

Eubacterium
Neisseria sicca
N. Flavescens

Gram-negative
anaerobic cocci

Gram-negative anerobic rods

Veillonella alcaescens Bacteroides asaccharolyticus
V. parvula
B. Gingivalis
B. Fragilis
Fusobacterium periodonticum
F.nucleatum

Spirochetes

Yeasts

Treponema denticola
T. Microdentium

Candida albicans
Geotrichum sp.

Protozoa

Mycoplasma

Entamoeba gingivalis
Tirchomonas tenax

Mycoplasma orale
M. pneumoniae

DISTRIBUTION OF THE RESIDENT
ORAL MICROFLORA

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

DEFENITION
Dental 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 Biofilm is used to describe communities
of micro-organisms attached to a surface.

Bacteria attached to Enamel Pellicle

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

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 MOUTH
Infection
Dental caries
Periodontal diseases
Surgical infection
a) Dry socket
b) Dental abscess
c) Osteomyelitis
d) Ludwig’s angina
e) Pericoronitis

Organism
Streptococcus mutans
Bacteroides, Actinomyces
Actinomyces
Oral streptococci
Staphylococcus aureus
β -haemolytic streptococci
Bacteroides

Infection
Organism
Soft tissue infections
a) Diphtheria
C. Diphtheriae
b) ANUG
Fuso-spirochaetes
c) Cancrum oris
Fuso-spirochaetes
d) Tuberculosis
M. Tuberculosis
e) Leprosy
M. Leprae
Viral infections
a) Herpetic stomatitis
b) Herpes Zoster
c) Mumps
d) Measles

Herpes simplex
Varicella-zoster
Mumps virus
Measles virus

Infection
Organism
Fungal infections
a) Candidosis
Candida albicans
b) Histoplasmosis
H. Capsulatum
c) Sporotrichosis
Sporotrichum schenkii
Miscellaneous
a) Erythema multiforme
b) StevensJohnson
syndrome

MICROFLORA IN DISEASE
Interrelationship that leads to dental disease

Hypothesis in periodontal
disease

Mechanism of tissue distruction in periodintal disease

BACTERIA IN CHRONIC PERIODONTITIS

Virulance factor of candida albicans

Predisposing factors of oral candidosis

Classification of primary oral candidiasis

Principal fungi affecting the oral cavity

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.

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.

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

treatment as natural teeth.

of

periodontal

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

healthy

and

diseased

teeth

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.

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.
151

Cell-surface fibrillar proteins, which mediate
adherence

to

the

salivary

pellicle,

and,

glycosyltransferase enzymes, which synthesize
adhesive

glucans

accumulation,

are

and
virulence

allow

microbial

components

of

mutans streptococci, and primary canidates for a
human caries vaccine

152

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.
153

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.

154

Ling L-J, Hung S-L, Tseng S-C, Chen Y-T, Chi LY, 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 .

155

This

investigation

examined

whether

an

association exists between betel quid chewing and
signs of periodontal disease and determined the
prevalence

of

actinomycetemcomitans

Actinobacillus
and

Porphyromonas

gingivalis by polymerase chain reaction . The
periodontal status of 34 betel quid chewers and 32
non-betel quid chewers were compared.
156

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.

157

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 ultrahistochemical staining with ruthenium red for
glycocalyx visualization. Candida adhesion itself is
assumed to induce mucosal inflammation
158

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.
159

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.

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

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.3 rd 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.

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.

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

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