ORAL BIOFILM-

DENTAL PLAQUE
 Dental Plaque-A Host associated
biofilm.

Bowen W.H. in the year

1976 defined dental plaque
clinically as a structured,
resilient, yellow-grayish
substance that adheres
tenaciously to the intraoral
hard surfaces, including
removable and fixed
restorations.
2
 WHO in the year 1978
defined it as a specific but
highly variable structural
entity resulting from
colonization and growing
microorganisms on surfaces
of teeth and consisting of
numerous microbial species
and stains embedded in a
extracellular matrix. 3
Other tooth deposits found on
the tooth surfaces
Materia alba

Calculus.

4
 Materia alba:
Refersto soft accumulations
of bacteria and tissue cells
that
lack the organized structure
of
dental plaque, and it is easily
displaced with a water
spray.
5
 CALCULUS:

It is a hard
deposit that
forms by
mineralization
of dental plaque,
and it is
generally covered by a layer
of unmineralized plaque.
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 Cuticle:
It is an electon dense material present in
between subgingival plaque and the tooth.
It contains:
Remains of epithelial attachment lamina.
It represents:
Secretory product of the adjacent
epithelial cells.

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 TYPES:
Dental Plaque

Supragingival
Periimplant plaque
Plaque Subgingival plaque

Marginal plaque Fissure plaque Tooth associated Tissue associated

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 SUPRAGINGIVAL PLAQUE

Is found at or above the

gingival margin.
Plaque found in direct contact
with
the gingival margin is known as
marginal plaque.
When found in the pit and
fissure
areas of the tooth surface ,it is
called fissure plaque.
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 Subgingival plaque
Is found below the
gingival margin, between
the tooth and the gingival
pocket epithelium.
When in contact with the
tooth surface it is called
tooth associated plaque.
When in contact with the
epithelial surface it is called
tissue associated plaque. 10
 Characteristic feature of
subgingival plaque:

Is that the apical border of

plaque mass is separated from
the junctional epithelium by a
layer of host leukocytes and
the bacteria of this region
show an increased
concentration of gram-ve rods.

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 Difference between tooth and
tissue associated plaque:
TOOTH ASSOCIATED TISSUE ASSOCIATED
FACES THE SOFT TISSUE.
ADHERS TO THE ROOT CEMENTUM.
M.O.PRESENT IN AN LACK A DEFINITE
INTERMICROBIAL MATRIX. INTERMICROBIAL MATRIX.
CONTAINS GRAM VE RODS
DOMINATED BY FILAMENTS ,BUT AND COCCI AS WELL AS
RODS AND COCCI ALSO OCCUR. SPIROCHETES AND
FLAGELLATED RODS.
APICAL BORDER IS DOMINATED BY DOMINATED BY
GRAM VE RODS. SPIROCHETES ,COCCI AND
CRITICAL IN CALCULUS RODS .
FORMATION AND ROOT CARIES. IMPORTANT IN THE TISSUE
DISTRUCTION AND
DIFFERENT FORMS OF
PERIODONTITIS

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 Tooth Similar to supragingival plaque
attached Associated with calculus formation,
plaque root caries and root resorption

Epithelial
Similar to subgingival plaque
associated periodontitis
plaque

Unattached Rapid periodontal destruction

plaque
Supragingival plaque Subgingival plaque

50% matrix Little or no matrix

Mostly gram +ve Gram -ve
Few motile Common motile
bacteria bacteria
Aerobic Highly anaerobic
Metabolism is Predominantly
mostly protein
carbohydrates metabolism
 Periimplant plaque:

It is found on artificial
surfaces exposed to
the oral
environment.e.g.(oral
implants)
Structure resembles
that encountered in
the subgingival
environment.
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 Composition of dental plaque:
Dental plaque is composed
primarily of microorganisms.
1 gm of plaque consists of
approx 1.2x1011 bacteria
and nonbacterial species.

The microorganisms exist

within an
extracellular matrix that
also contains a few host
cells,such as epithelial
cells,macrophages and
leukocytes.
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 The Non Bacterial microorganisms are:

Mycoplasma species
Yeasts
Protozoa
Viruses

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 Plaque matrix:
The intercellular matrix
accounts for
approximately 20%-30% of the
plaque mass.
It consists of:
1. Organic material.
2. Inorganic materials.
3. Degenerating or dead
bacteria
4. Few host cells like:
Epithelial cells
Macrophages
Leukocytes

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 Sources of intermicrobial matrix:
Plaque microorganisms
Saliva
Gingival crevicular fluid
Types of intermicrobial matrix:
Fibrillar:in the matrix between gram positive cocci
Granular
Homogenous
May be characterized by the presence of small vesicles
surrounded by trilaminar membrane .Mostly seen in the
case of gram-ve bacteria.

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Functions of intercellular matrix:
Acts as a barrier.
Protects the resident bacteria.
Confers specialised properties on
bacteria.
Contains nutrient chanals
Maintains the integrity .

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 Organic constituents:
Protein-polysacchride complexes
Lipids
Carbohydrates such as:
1. Dextran
2. Mutan
3. Levan
4. Galactose
5. Methylpentose
Albumin
Murramic acid(obtained from bacterial remnants.)

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 The carbohydrate content of plaque matrix
is as follows:

Dextran (polymer of glucose) - 9.5%

Hexosamine - 4%

Methylpentose - 3.1%

Galactose - 2.6%

Levan (polymer of fructose) - 0.4%

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 Inorganic content:
Calcium
Phosphorous
Trace amounts of
Magnesium
Sodium
Potassium
Flouride(obtained from external sources
like toothpaste)

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 Plaque bacteria:

At the outset :
facultative cocci and rods
(Neisseria, Nocardia and
Streptococcus) are seen.
Streptococcus sanguis
predominate.

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 Second to third day :

Gram-negative cocci and rods.

Increase
in numbers and percentage
(from approximately 7 to 30 per cent),
of which approximately 15 per cent are
anaerobic rods.

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Fourth to fifth day :

Fusobacterium
Actinomyces and
Veillonella

all strict anaerobes, increase in number

with Veillonella comprising
approximately 16 per cent of the flora.

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 As the plaque matures:
After eleven days:
spirella and spirochetes appear in small
numbers.
Filamentous organisms continue to increase
Actinomyces Naeslundii increases from 1 to
14 per cent from the fourteenth to the
twenty-first day.
Streptococci diminish from approximately 50%
to 30-40%.
Rods ,particularly the filamentous form
increase to 50%.
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PLAQUE GROWS BY:

MULTIPLICATION OF
BACTERIA.
ADDITION OF BACTERIA.
ACCUMALATION OF
BACTERIAL PRODUCTS.

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 Mature plaque
2.51011 bacteria per gram (by total
microscopic count).
Anaerobes comprise 4.6 1010 per gram of
plaque.
Facultative and anaerobic bacteria consist of
approx. 40% gram positive cocci ,10% gram -ve
cocci,40%
gram +ve rods ,and 10% gram ve rods.

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 Bacterial Enzymes and Toxins
Hyaluronidase an enzyme produced by
Streptococci .
Bacterial collagenases- produced by
clostridial species and pophyromonas
melaninogenicus .
Lipopolysaccharide (LPS), an endotoxin.
Other Bacterial Cell Wall Products:
Lipoproteins.
Murray dipeptide .
Lipid A .
Teichoi acids.
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BACTERIAL BEHAVIOUR IN
BIOFILMS
Bacteria growing in microbial
communities adherent to a surface do not
behave the same as bacteria in a
planktonic.

For example, the resistance of bacteria to

antimicrobial agents is dramatically
increased in the biofilm.

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 SUPRAGINGIVAL PLAQUE:
Tooth surfaces ,enamel, and exposed
cementum are covered by a thin layer of
acquired pellicle.
First cellular material adhering to the
pellicle are:
1. Ccocoid bacteria
2. Epithelial cells
3. Polymophonuclear leukocytes.

32
 Factors modifying the number of
bacteria in early plaque deposits:
Procedure applied to the sample before
examination.

Presence of gingivitis.

Microorganism harbored in minute

irregularities(in which they are
protected from the natural cleaning of
the tooth surface.)
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 Topography of supragingival plaque:

Initial growth starts the gingival margin and from the

interdental areas and then it extends further coronally.
Plaque formation can also start from the grooves ,
cracks or pits.

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 Surface Microroughness:

Rough intraoral surfaces e.g. crowns, denture

bases,implant abutments accumalate and retain
more amount of plaque and calculus in terms
of thickness,area and colony forming unit.

35
 Individual variables influencing
plaque formation:
Rate of plaque formation varies between different subjects.Two
Groups are considered :
1. Heavy plaque formers.
2. Light plaque formers.

This variation can also be

explained by factors such as:

Diet
Chewing fibrous foods
Smoking
Presence of copper amalgam
Tongue and palate brushing
Stability of bacteria in saliva.

36
 Variation within the
dentition:
Early plaque formation can be seen
in:
1. In the lower jaw than in the upper
jaw.
2. In the molar areas.
3. On the buccal tooth surfaces .
4. In the interdental areas .

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Impact of gingival inflammation:

Increase in the crevicular fluid increases

plaque formation.This may be because
some substance from
this exudate
(proteins,carbohydrate,minerals) favors
the initial adhesion and the growth of
the early colonizing bacteria.

38
 Impact of patients age:

There is no difference in plaque formation

with age,
however in the older age group the
developed plaque results in more severe
gingival inflammation.This seems to indicate
an increased susceptibility to gingivitis with
aging.

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 Spontaneous tooth cleaning:
There is only negligible difference in
plaque extension before and after eating.

Even in the occlusal surface of the molars

,plaque remains even after chewing
fibrous food.

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Contt

 THE PLAQUE THEORIES:

Specific plaque hypothesis:
was given by Loesche in the year 1979.
According to this concept onlycertain plaque is
pathogenic and its pathogenicity depends on the
presence of or increase of specific micro
organisms.
Shortcomings in this theory were:
There were occasions when either disease was
diagnosed in the absence of the putative
pathogens or when pathogens are present with
no evidence of disease.
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 Non specific hypothesis:

Given by Theilade in the year 1986.He

described plaque as a biomass.

According to this hypothesis periodontal

disease results from the elaboration of
noxious products by the entire plaque
flora.

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 Shortcomings:
Some individuals with constant amount of
plaque & calculus never developed destructive
periodontitis.
Individuals who did present with periodontitis
demonstrated considerable site specificity in
the pattern of the disease.
Some sites were not affected, where as
advanced disease was found in adjacent sites.

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Unified theory:
Given by Theilade in 1986.
IT is the modern version of the two
theories.
Any composition of plaque in
sufficient quantity in the gingival
crevice causes gingivitis but only in
some cases does it lead to
periodontitis.
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Ecological plaque hypothesis:

According to this any change in

the nutrient status of a pocket i.e.
physical and chemical change to
the habitat are considered the
primary cause for overgrowth of
pathogens.

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 STRUCTURE OF DENTAL PLAQUE:

A high degree of specificity is found in

the interactions between bacteria in
dental plaque.

Highly specific cell-to-cell interactions

are evident from the corncob
structures.

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 Plaque as a true Biofilm :
Plaque like a Biofilm has an organized strucure.

Composed of microcolonies of bacterial cells non

randomly distributed in a shaped matrix glycocalyx.

It has a hetergenous structure with clear evidance of

open fluid filled channels running through them

Quorum Sensing Bacteria have the capacity to

communicate with each other.

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 Like biofilms other modes of gene transfer
are also seen:
Conjugation

Transformation

plasmid transfer and

transposon transfer

Also co-aggregation amongst the various plaque

bacteria is seen.
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Various phases in the plaque formation are

The formation of the pellicle on the tooth

surface.
Initial adhesion and attachment of bacteria,
and
Colonization and plaque maturation.
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 Formation of the Pellicle:
Pellicle is a thin (0.5mm) smooth, colourless & translucent film
which adheres firmly to the tooth surface & can be removed
only by positive friction.It is formed by the selective adsorption of
environment macromolecules. (the amino-acid conc. of the pellicle
was different from that of saliva)

Electrostatic affinity between hydroxyapatite and glycoprotein

seem to be the cause for pellicle formation.

Forms on the tooth surface within nanoseconds.

0.05-0.8 micron thick.

Initially it is bacteria free.

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Mechanism of Pellicle Formation :
This includes

Electrostatic forces.

Van der waals forces.

Hydrophobic forces

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 Functions of the Pellicle:
Protective.
Helps to reduce toothwear.
Restricts the diffusion of acids products of
sugar breakdown.
It can bind various inorganic ions e.g.,
calcium, phosphate & fluoride & contains
antibacterial factors including IgG,IgA,IgM,
complement and lysozyme
Nidus for a bacteria attachment of calculus

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Initial Adhesion and
Attachment of Bacteria:
Phase 1 : Transport to the
surface.
Phase 2 : Initial adhesion.

Phase 3 : Attachment.

Phase 4 : Colonization of
the surface and biofilm
formation.
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 Phase 1 : Transport to the surface.
It involves the initial transport of the
bacterium to the tooth surface .
Random contacts may occur, through
Brownian motion or through active bacterial
movement (chemotatic activity),or by
sedimentation.

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 Phase 2 : Initital adhesion
The second stage results
in an initial, reversible
adhesion of the bacterium,
initiated by the interaction
between the bacterium
and the surface.
Long-range and short-
range forces, including van
der waals attractive forces
and electrostatic repulsive
forces.
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 Phase 3 :
Attachment

After initial adhesion, a firm anchorage between

bacterium and surface will be established by
specific interactions (covalent, ionic, or hydrogen
bonding).
The bonding between bacteria and pellicle is
mediated by:
Specific extracellular proteinanceous components
(adhesions) of the organism and
Complementary receptors (i.e., proteins,
glycoproteins, or polysaccharides) on the surface
(e.g., pellicle).
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 Phase 4 : Colonization of the
surface and biofilm formation.
Now intrabacterial
connections occur.
Coaggregation is seen.
Secondary colonizers
Prevotella intermedia
1. Prevotella loescheii
2. Capnocytophaga species
3. Fusobacterium nucleatum
4. Porphyromonas gingivalis.
adhere to cells of bacteria
already in the plaque mass.

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 Growth Dynamics of Dental
Plaque :

Changes in the plaque growth rate can be detected

within the first 24 hours.
Undisturbed plaque formation on teeth follows
an exponential growth curve:
During the first 2 to 8 hours:
Streptococci saturate the salivary pellicular
binding sites and cover 3% to 30% of the enamel
surface.
After 1 day: the term biofilm is fully deserved
because organization of bacteria takes place
within it
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 After3 days:The thickness of the plaque
increases slowly with time increasing to 20
to 30 mm.

After the fourth day: plaque does not seem to increase

substantially
The slow start of the plaque growth curve is because of
a colony of bacteria needs a certain size before it can be
clinically detected.
The leveling of the slope from day 4 onward is due to
the lengthening of the microbial generation time (1
hour for initial plaque to 12 hours for 3-day-old plaque)

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Gingivitis model:

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 Plaque Architecture :
Inthe first few days:
plaque appears as a dense meshwork
of cocci with occasional rod.

As the plaque matures:

filaments and threads gradually
increase while coccal forms decrease.

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 On the inner surface:
they are aligned in a perpendicular
palisade arrangement in tuft-like groups
separated by cocci.

As the surface is approached:

the filaments and threads appear singly
and less regularly arranged and colonies
of cocci accumulate on the surface. 63
 Physiologic Properties of
Dental plaque:
A change from gram+ve to gram-ve is seen
due to physiologic transition.
The early colonisers (e.g., streptococci,
Actinomyces species) use oxygen and lower the
redox potential of the environment.
Gram+ve species use sugars as an energy source.
Lactate and formate are the byproducts of the
metabolism of streptococci and actinomycetes.
The metabolic byproducts produced by one
bacteria are used as nutrients for another
bacteria.
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The host also functions as
an important source of
nutrients .

Hemin iron from the

breakdown of host
hemoglobin may be an
important in the metabolism
of P. gingivalis.
Physiological interactions
occurs both between
different microorganisms in
plaque and between the
host and plaque
microorganisms. 65
 Spatiotemporal
model of dental
plaque:

This shows the

colonization of oral bacteria,
which recognises the salivary
pellicle receptors by
early colonizing bacteria
and coaggregations
between early colonizers,
fusobacteria, and
late colonizers of the
tooth surface.

66
 Microbial complexes:
These show the presence of specific microbial groups
within dental plaque .
Shown by Socransky in the year 1998.
Done on the basis of cluster analysis and community
ordination techniques.
Yellow complex consists of members of the genus
Streptococcus.
Green complex consists of Capnocytophaga
species,Actinobacillus actinomycetemcomitams
,E.corrodens and Campylobacter concisus.
PURPLE complex consists of v.paruvla and actinomyces
odontolyticus.
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Orange complex
consists of :
Camplyobacter gracilis,
C. rectus,C.showe,
E.nodatum,F.nucleatum,
P.intermedia,P.nigresence
And S.constellatus.
Red complex consists of:
B.forsythus,P.gingivalis,T.denticola.
These two complexes are comprised of the species
thought to be the major etiologic agent of periodontal
disease. 68
 The Role of Ingested
Nutrients in Plaque Formation
:
Dental plaque is not a food residue, and the rate of
plaque formation is not related to the amount of
food
consumption.
Dental plaque forms more rapidly during sleep.
Forms rapidly on soft diets.
Hard chewy food retard it.
Dietary supplements of sucrose increase plaque
formation and affect its bacterial composition.
Plaque formation can also occur on:
High protein diets and
Carbohydrate free diets but in small amounts.

70
 Significance of Site specificity of
plaque
Marginal plaque : is of prime importance
in the development of gingivitis.
Supragingival plaque & tooth associated
are critical in calculus formation & root
caries.
Tissue associated subgingival plaque is
important in the soft tissue destruction
that characterise different forms of
periodontium. 71
 Gingival and periodontal disease
producing:

In general, small amounts of bacterial plaque can be controlled by

the bodys defense mechanisms without destruction, but when the
balance between bacterial load and host response is disturbed,
periodontal destruction may occur.
This may result when the subject
is extremely susceptible by a large
amount of bacteria or
By an extremely pathogenic
microbiota.

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 CONCLUDING THOUGHTS:
Many different biofilms exist in nature ;some are useful and
others are associated with harmful effects.Dental plaque is a
naturally occurring biofilm that has the potential to cause
disease.Dental plaque has many properties in common with
biofilms found in other locations.It is rightly said that the

BACTERIA AFFECT THEIR HABITAT AND THE

HABITAT AFFECTS THE BACTERIA

so that the elimination of pockets or the removal of supragingival

plaque will provide a less favorable environment for the
growth of subgingival species ,particularly those associated
with disease.Thus ,the therapist can potentially affect
periodontal infections at several levels improving the possibility
for long term periodontal stability.
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Thank you