Role of bacterial plaque in dental

caries
n Definition
n Composition
n Clinical appearance
n Mechanism of formation
n Factors affecting plaque formation
n Role of plaque matrix
n Acid production (Stephan’s experiment)
n Biochemical reactions in the dental plaque.
Definition
n “Plaque is a tenaciously adherent
deposit that forms on the areas of
food stagnation on the teeth”.

n Dental palque is an example of a

[BIOFILM].
Composition
Ø Micro-organisms: up to(60% to 70%by
volume).
Ø Amorphous matrix:
Ø Mucin: proteins derived from the salivary
mucoids.
Ø Glucans: extracellular bacterial
polysaccharides.
Ø Carbohydrates: (dextran, levan, amylopectin)
Ø Inorganic content: calcium, phosphate and
fluorides
Ø Food debris are also entrapped within plaque.
Ø Leucocytes and desquamated epithelial cells.
Clinically:
ü Dental plaque is a thin yellow film on
the surface of the teeth.
ü It becomes visible, particularly on the
labial surface of incisors when tooth
brushing is stopped for 12-24 hours.
ü With time, it undergoes mineralization
to form dental calculus.
ü Plaque cannot be removed by rinsing.
It resists the friction of food during
mastication and can only be readily
removed by tooth brushing.
Stages of plaque
formation
Stage I:
ØDeposition of the acquired dental
pellicle. This a structure-less, cell-
free layer of salivary glycoproteins
adsorbed on the tooth surface (3µ
in thickness.
ØIt is not usually visible to the
naked eye.
N.B.
Ø The pellicle is enhanced by bacterial action
increasing the bulk of the pellicle.
Ø The bacteria reproduce and are joined by
other adherent bacteria.
Ø Actually if these bacteria are left
undisturbed, formation of dental plaque has
begun.
Ø The organisms at the tooth interface are
closely packed together whereas those
towards the outer plaque-saliva interface
are more loosely attached.
Stage II:
ØColonization of the acquired
pellicle by bacterial flora,
particularly by streptococcal
strains occurs. It comprise up to
95% of the total cultivable flora
of the plaque.
ØPlaque micro-organisms can
synthesize extra-cellular glucans
from dietary sugars which help
attach the plaque to the tooth.
Stage III:
Ø Maturation of the dental plaque
takes place by the proliferation of
the heterogeneous flora.
Ø The anaerobic filamentous micro-
organisms grow in long interlacing
threads arranged in parallel units
commencing at the deep surface of
the plaque on which smaller bacilli
and cocci become entrapped giving
the corn-cob appearance.
 Summary of Colonization
ØAttachment are single layer of
bacterial cells (the first 4 hours)
“Initial Community”
ØGrowth of the attached bacteria
lead to the formation of
microcolonies “intermediate
Community”[4 to48 hours]
ØMature community of plaque (2
weeks or older)
 Microbial Succession
ØSuccession is the replacement of
one type of community by another
in response to modifications in the
environment affecting the habitat.
ØMicrobial succession is a dynamic
process involving continuous
replacement of the microbial
communities according to the new
environmental conditions.
Factors affecting plaque formation:
1. Anatomy and position of tooth.

2. Presence of appliances.

3. Structure of tooth surface.

4. Friction from the diet and masticatory

movement.

5. Oral hygiene measures.

6. Composition of the diet

 Role of the plaque matrix
n Diffusion-limiting membrane:
– Retain acid : In a high concentration at
a particular site thus, allowing the
demineralization of enamel.
– Slowing down the arrival of the salivary
buffers from saliva thus delaying their
neutralizing action and allowing the
liberation of the mineral ions from the
hydroxyapatite crystals and their
diffusion into the plaque.
n Has an adhesive effect to the tooth
surface.
n Increases the bulk of the dental
plaque.
§ Dental plaque is important in the
mechanism of dental caries as
the microbiological enzymatic
reactions within the plaque lead
to the carious attack on enamel
(E), as follows:-

Bacterial enzymes Lactic acid,

Dietary sugars
Break them into Acetic acid
Biochemical reactions in
dental plaque:
1-Acid production in dental plaque.
2-Formation of extracellular
polysaccharides (glucan).
3-Formation of intracellular
polysaccharides (amylopectin).
4-Demineralization phase.
5-Remineralization phase.
Acid production in the plaque

Stephen curve
n It has been shown that after rinsing the
mouth with 10% glucose solution, the pH
falls within 2-5 minutes, often to a level
sufficient to decalcify enamel

n Sucrose diffuses rapidly into plaque and

acid production quickly follows.
n The high density of the acid produced in
the plaque contributes to a rapid fall in its
pH value by as much as 2 units within 10
minutes after the ingestion of sugar.
n The pH level remains at a low
level about 15-20 minutes.

n It returns gradually to the

resting level after about an hour.

n These changes are known as

(Stephen curve)
 The Sequence of Events
n Ingestion of sugar fall in pH due to acid
production by bacteria
n At a critical pH usually 5.5, mineral ions are
liberated from hydroxyapatite crystals of the
surface enamel and diffuse into the plaque.
n Around a neutral pH, the plaque is
supersaturated with mineral ions because of
the extra ions from the enamel. Some of the
excess ions in the plaque may be redeposited
on the enamel crystal surface
n Therefore, there is a see-sawing of ions across
the plaque enamel interface as the chemical
environment within the plaque changes.
 The rapidity with which the
pH falls in the plaque is due
to:
n Plaque allows the speedy
diffusion of sugar into it to be
fermented by bacteria and
produce acids.
 The slow reversion to resting pH
level may be due to:
n Continued metabolism of residual sugar
taken in by the plaque.
n Breakdown of the reserve
polysaccharides in the plaque
(amylopectin).
n Delayed diffusion of acid outwards into
the saliva or salivary buffers into the
plaque by the diffusion-limiting
properties of plaque and its thickness.
ØWhen the periods of demineralization
exceed those of remineralization then
caries is produced.

ØWhen the periods of remineralization is

more than the periods of
demineralization, the lesion becomes
resistant and arrested caries is
produced.
ØThis occurs when the sugar
intake stops and the oral
hygiene is established by good
tooth brushing.
 Dental Caries

ØDental caries is a dynamic

process.
ØIt consists of periods of
demineralization and periods of
remineralization.
 Role of saliva
üWhat is saliva?

üComposition?

üFunction?
 Saliva
Saliva is a critical regulatory factor in
the carious process.
1. Salivary glycoproteins:
– Forms the acquired enamel pellicle.
2. Washing effect of saliva:
– It has a cleaning effect.
– Rate of flow
A rapid flow (sialorrhia) rate has been found to be
accompanied by low caries activity.(mongolism).
In case of salivary gland aplsia and (xerostomia), increased
caries activity is the typical result.(sjogrens)
- Salivary Viscosity:
It was proved experimentally that the higher the
viscosity of saliva, the more the caries incidence.
3. Salivary Buffers:
n The buffering power of saliva
depends upon its bicarbonate
content. Also, it has been suggested
that high ammonia and urea levels in
saliva retards plaque formation and
neutralizes acids.
Salivary pH
n The normal salivary pH is neutral
[7.2] or slightly alkaline, a low pH
accelerates the demineralization of
enamel.
4. Inorganic components
(Availability of calcium , phosphorous and
fluoride ions)
These are essential for the re-
mineralization process, where the
calcium and phosphate ions are
exchanged between the enamel
surface and saliva.
5. Presence of antibacterial agents
Saliva contains lactoferrin and
lyzosymes. However, the
antibacterial substances in saliva
have little significant effect on
caries.
6. Salivary Immunoglobulin:
n Saliva contains secretory
immunoglobulins A (SIgA).
n It is produced by plasma cells found in
salivary glands.
n The main role of (SIgA)is:
1-killing of bacteria.
2-inhibition of its metabolic activity.
3-prevents adherence of bacteria to
tooth surface.