DENTAL

PLAQUE

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 Contents:
• Definitions
• Classification
• Composition of plaque
• Microbial complexes
• Formation of plaque
• Formation of plaque in relation to time
• Theories of plaque formation
• Criteria for identification of periodontal
pathogen
• Microbial shift from health to disease
• References
• Quiz time
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DENTAL PLAQUE
“Is a specific but highly variable structural
entity, resulting from sequential
colonization of microorganisms on tooth
surfaces, restorations & other parts of oral
cavity, composed of salivary components
like mucin, desquamated epithelial cells,
debris & microorganisms, all embedded in
extracellular gelatinous matrix.”
(WHO-1961)
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DENTAL CALCULUS
is an adherent calcified or calcifying mass that
forms on the surface of natural teeth & prosthesis.

MATERIA ALBA
is a deposit composed of aggregate of
microorganisms, leucocytes & dead exfoliated
epithelial cells , randomly organized & loosely
adherent to the surfaces of the teeth, plaque &
gingiva. 4
ANTONY VAN LEUWENHOEK - first one to describe dental
plaque biofilms and their resistance.

In 1899 G.V.BLACK coined the term "GELATINOUS MICROBIC

PLAQUE“

Waerhaug (1950) described bacterial plaque in the etiology

of
periodontal disease.

Loe et al (1965)- plaque is main etiological agent in

periodontal
diseases.

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 SUBGINGIVAL PLAQUE
• Sub gingival plaque
is found below the gingival
margin, between the tooth
and gingival sulcular tissue.

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 TOOTH UNATTACHE TISSUE
ATTACHE D ATTACHE
D D

Gram positive – rods Gram negative rods, Both

and cocci, filaments, spirochetes

Does not extend to JE Extend to JE Extend to JE

Calculus formation, Gingivitis Gingivitis, periodontitis

root caries

- May penetrate
May penetrate epithelium and
cementum connective tissue

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COMPOSITION OF DENTAL PLAQUE

INTERCELLULAR
MATRIX 20-
30% MICROORGANISM-
80%

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ORGANIC INORGANIC

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ORGANIC MATRIX INORGANIC MATRIX

Polysaccharide– produced by Predominantly

bacteria, Ca, P- major
e.g : dextran Na, K, F - trace

Protein -albumin source of inorganic material in

supra-gingival plaque is primarily
saliva.

Glycoprotein-from saliva source of inorganic material in sub

gingival plaque is GCF

Lipid
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 • One gram of plaque contains approximately
2 X 1011 bacteria.
(Socransky SS,1953), (Schroeder, De Boever-1970)

• More than 500 distinct microbial species found in dental

plaque- Moore 1994

Nonbacterial organisms
are:
MYCOPLASM
A YEAST
PROTOZOA
VIRUSES 14
Socransky et al in 1998, 7
closely associated
groups were recognized:

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 ACTINOMYCES
SPECIES
V. Parvula
A.odontolyticus
S.Mitis
S.Oralis
S.Sanguis
Streptococc
us sp.
S.gordonii PRIMARY
S.intermedius
COLONIZERS 14
16
 C.rectus
P.Intermedia
P.Nigrescen E.nodatum
s P.Micros
F.nucleatum
SECONDARY
COLONIZERS
C.showae
E.Corrodens P.Gingivali
Capnocyptophaga spp s
A.actinomycetemcomitans B.Forsythus
T.denticola
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16
SILVER COMPLEX • HSV type 1
• EBSTEIN
BARR VIRUS
•HUMAN
CYTOMEGAL
O VIRUS

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17
“ Matrix enclosed bacterial populations
adherent to each other and/or to
surface or interfaces.”
(Costerton, 1978)

Biofilms exist on any solid surface that

is exposed to bacteria containing fluid.

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SLIME LAYER

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 EXOPOLYSACCHARIDES –
the backbone of the biofilm

The bulk of the biofilm consists of the matrix, composed

predominantly of water and aqueous solutes.

Function :
Integrity of biofilm
Prevents attack by harmful agents
Assists in retention of extra cellular enzymes.
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Quorum sensing in bacteria ,‘‘involves the
regulation of expression of specific genes through the
accumulation of signaling compounds that mediate
intercellular communication.”
(Prosser
1999)

This is a method of intercellular communication.

Quorum sensing depends on cell density.

Once signaling compounds reach a threshold level,

gene expression is activated.
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 Q u o r u m sensing m a y give biofilms their
distinct properties:
Expression of genes for antibiotic resistance at high cell
densities may provide protection.

Has the potential to influence community structure, by

encouraging the growth of beneficial species (to the biofilm)
and discouraging the growth of competitors.

Alteration of physiological properties of bacteria in the

community through quorum sensing.
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🞂

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 I. FORMATION OF DENTAL
PELLICLE
• Acquired pellicle may be defined as a homogenous,
membranous, acellular film that covers the tooth surface
and frequently form the interface between the tooth ,the
dental and calculus .
plaque (SCHLUGER)

• `A fully established pellicle is found within 30 min.

Within 24 hr, the pellicle is around 0.1-0.8 µm in diameter.

• Derived from components of saliva and crevicular fluid as

as bacterial and host tissue cell products and food
well 30
debris.
• Consists of numerous components, including glycoprotein
(mucins), proline-rich proteins, phosphoproteins (e.g.,
statherin), histidine-rich proteins, enzymes (e.g., α-
amylase), and other molecules that can function as adhesion
sites for bacterial receptors.

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 FUNCTIONS OF DENTAL PELLICLE

Substrate to
Preventing which
Protective
Lubrication tissue bacteria
barrier
desiccation attaches

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 II. INITIAL ADHESION & ATTACHMENT
OF BACTERIA
• We cannot conclude a single mechanism that dictates the
adhesiveness of micro-organisms .
SCHEIE ( 1994)

TRANSPORT TO INITIAL
SURFACE ADHESION

COLONIZATIO
ATTACHMEN N OF SURFACE
& BIOFILM
T FORMATION 33
 A) TRANSPORT TO SURFACE
• The first stage involves the initial transport of the bacterium
to the tooth surface.

• Random contacts may occur

o Brownian motion (average displacement of 40 µm/hour)

o Sedimentation of microorganisms,

o Liquid flow

o Active bacterial movement (chemotactic activity).

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 B) INITIAL
• There isADHESION
an initial, reversible adhesion of the bacterium.

• It is initiated by the interaction between the bacterium and

the surface, from a certain distance (50 nm), through long-
range and short-range forces, including van der Waals
attractive forces and electrostatic repulsive forces.

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 C) 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 the bacteria & pellicle is mediated

by specific extracellular components of organisms &
complementary receptors on pellicle surface.

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 III. COLONIZATION
&
PLAQUE MATURATION

• The early colonizers (e.g., streptococci and

Actinomyces species) use oxygen and lower
the reduction-oxidation potential of the
environment, which then favors the growth of
anaerobic species. 37
34
 ACTINOMYCES
SPECIES
V. Parvula
A.odontolyticus
S.Mitis
S.Oralis
S.Sanguis
Streptococc
us sp.
S.gordonii PRIMARY
S.intermedius
COLONIZERS 35
16
• Secondary colonizers are the microorganisms that do not
initially colonize clean tooth surfaces, including
Prevotella intermedia, Prevotella loescheii,
Capnocytophaga spp., Fusobacterium nucleatum, and
Porphyromonas gingivalis.

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 C.rectus
P.Intermedia
P.Nigrescen E.nodatum
s P.Micros
F.nucleatum
SECONDARY
COLONIZERS
C.showae
E.Corrodens P.Gingivali
Capnocyptophaga spp s
A.actinomycetemcomitans B.Forsythus
T.denticola
37
16
`

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Well characterized interaction include the coaggregation
of:
• Fusobacterium nucleatum with
other human oral all
bacteria.
A. viscosus
• Prevotella loescheii A. viscosus
• Capnocytophaga
• ochraceus
Streptococci show intrageneric co-aggregation  bind
to the nascent monolayer of already bound
streptococci.

Later stages – coaggregation between different Gram

negative species seen – F. nucleatum & P. gingivalis or T.
denticola.
C O R N C O B formation – streptococci adhere to
filaments of Bacterionema species or F.nucleatum.

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CORNCOB STRUCTURE TEST TUBE BRUSH
As the plaque reaches maturity, it acquires a more filamentous
character.
During this, “invading” filamentous bacteria adheres to cells of
pioneer community.
The morphologic component of climax community are called
as “ Corncobs”.
The term coined by : Jones (1971) – resemblance to an ear of
corn.
First described by Vincentini (1897) – structures composed of a
single microbial species and named them Leptotrix racemosa.
(thought they are composed of single microbial species)
Socransky et al in 1998, 7
closely associated
groups were recognized:

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 COAGGREGATION BRIDGES

• A co-aggregation bridge is formed when the common

partner bears two or more types of coaggregation
mediators.

• These mediators can be various types of

polysaccharides or various adhesin or combination of
two

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 Bridging

A property of co-aggregating cells.

Refers to observation that two non-co-aggregating
strains may participate together in a multigeneric
aggregate if they recognize a common partner.
A.israelii does not co-aggregate with S.oralis.
However Prevotella loescheii co-aggregates with both
strains by means of different adhesions

A S

P
 DENTAL PLAQUE
FORMATION –
RELATION TO TIME
 1
• HOURto pellicle, and pellicle coats
Bacteria adhere
the enamel.
• Gram positive rods and cocci are laid down in
the first hour.
 24-48
HOUR
 Bacteria multiply and form mini-
colonies in layers upon the pellicle.
 The bacteria adhere and increase in
mass and thickness.
 7-14 DAYS
As the plaque continues to mature, vibrio,
spirochetes, and white blood cells
appear. The plaque becomes more gram
negative and anaerobic in the deeper
layers.
The signs of inflammation are
more pronounced. 48
 14-21 DAYS
• Vibrio and spirochetes continue to multiply.
• The bacteria become
 Highly organized
 Filamentous
 Perpendicular to the tooth surface
• The signs of inflamed gums are obvious
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 • Patterns of De Novo Supragingival plaque
formation

• Early undisturbed plaque formation on teeth follows

exponential curve.
• During 1st 24 hours after thorough scaling and root planing ,
the increase in amount of plaque is negligible (<3% of
buccal surface)
• Over next 3 days the increase is faster, then it slows down.
• After 96 hours of undisturbed growth, on average of 30 % of
total tooth crown is covered.
• After fourth day, its reported that bacterial composition will
shift towards a more anaerobic and a more Gram negative
flora, including an influx of fusobacteria, filaments, spiral
forms and spirochetes.
• The slow start of plaque growth curve – a single colony of
bacteria has to reach a certain size before it can be
clinically detected.
• Brecx et al (1983) illustrated that the early increase in
plaque mass originates from the proliferation of bacteria
already present, and only to limited extent from new
adhering species.
• During night – plaque growth rate is reduced by some 50
%
Early plaque growth follows a topographical growth pattern.

Initial growth along gingival margin

Extension in coronal direction

Also start from grooves, cracks or pits.

Rough intraoral surface- more plaque growth
 Plaque growth rate

• Increased plaque formation in lower jaw compared to

upper
• Higher rate of plaque formation in molar region compared
to front region and more on buccal surfaces
• Interdental surfaces >>buccal surfaces >>oral surfaces
• Intersubject differences in plaque growth – heavy and light
plaque formers
• After one day heavy plaque formers showed more plaque
and with a higher proportion of gram negative rods in 14
days old plaque compared to light plaque formers
 Factors influencing plaque growth

• Diet
• Chewing fibrous food
• Smoking
• Presence of copper amalgam
• Tongue and palate brushing
• Antimicrobial factors present in saliva
• Chemical composition of pellicle
• Retention depth of dentogingival areas
• Studies indicate in vivo plaque formation is more
rapid on tooth surfaces facing inflammed gingival
margins (increases crevicular fluid production)
• Variation withing the dentition: early plaque
formation occurs faster in the lower jaw compared
to upper jaw, im molar areas, on the buccal tooth
surface and in interdental region.

• Impact of gingival inflammation: more

rapid on tooth margins with gingival
inflammation suggesting increase in GCF
enhances plaque formation.
1. Antibiotic resistance

Quorum sensing – intercellular communication -

express gene for antibiotic resistance and growth of
species

conjugation – exchange of genes.

translocation
 DETECTION OF
PLAQUE
A disclosing agent is a preparation in liquid, tablet
or lozenge form which contains a dye or other
contouring agent.
 Iodine preparation
 Bismarck brown
 Erythrosine
 Fast green
 Basic fucshin
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 ECOLOGICAL
PLAQUE
SPECIFIC HYPOTHESIS
PLAQUE
HYPOTHESIS

NON-SPECIFIC
PLAQUE
HYPOTHESIS
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(Theilade 1976) held that the entire bacterial flora in
plaque played a role in periodontal destruction rather
than specific bacteria.

The nonspecific plaque hypothesis maintains that

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

Thus it lead to concept that control of periodontal disease

depends on control of the amount of plaque
accumulation. 60
Specific plaque hypothesis- Walter
Loesche 1979
states that only certain plaque is
pathogenic, and its pathogenicity depends on
the presence of or increase in specific
microorganisms.
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Plaque harboring specific bacterial pathogens
results in periodontal disease.

A. actinomycetemcomitans is a pathogen in
aggressive periodontitis.

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 ECOLOGICAL PLAQUE
HYPOTHESIS
• A change in a key environmental factor (or factors)
will trigger a shift in the balance of the resident plaque
microflora, and this might predispose a site to disease.
( PD Marsh 1994)

• This hypothesis is based on the theory that the unique

local microenvironment influences the composition
of the oral microflora.

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64
 In the 1870s, Robert
Koch postulated the
criteria by which an
organism can be judged
to be causative agent
in human infections

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Pathogen must be Must produce a
routinely isolated Must be grown similar disease when
from the diseased in pure culture inoculated into susceptible
individuals. in the laboratory. lab animals.

Must be recovered
from lesions in a
diseased laboratory
animals.

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Association- Elimination Host response

Must be capable of
causing disease
Virulence factors in experimental
animal models.
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1) Gm + ve to Gm –ve
2) Cocci to rods to spirochaetes
3) Non- motile to motile bacteria
4) Facultative anaerobes to obligate anaerobes

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 PERIODONTAL HEALTH

• BACTERIA ASSOCIATED WITH PERIODONTAL HEALTH ARE PRIMARILY

GRAM-POSITIVE FACULTATIVE SPECIES AND MEMBERS OF THE GENERA
• STREPTOCOCCI
• ACTINOMYCES SPECIES
ACTINOMYCES VISCOSUS
ACTINOMYCES NAESLUNDII
GRAM NEGATIVE SPECIES LIKE
P.INTERMEDIA
F.NUCLEATUM
CAPNOCYTOPHAGA
NEISSERIA
VEILLONELLA
ORGANISMS ASSOCIATED WITH
SPECIFIC PERIODONTAL DISEASE
 CHRONIC GINGIVITIS

• THE MICROBIOTA OF DENTAL PLAQUE INDUCED

GINGIVITIS CONSIST OF APPROX EQUAL PROPORTIONS
OF GRAM POSITIVE AND GRAM NEGATIVE SPECIES AS
WELL AS FACULTATIVE AND ANAEROBIC. PREDOMINANT
GRAM POSITIVE SPECIES INCLUDE S.SANGUIS, S.MITIS,
S.ORALIS, A.VISCOSUS, A.NAESLUNDII, P.MICROS.
• PREDOMINANT GRAM NEGATIVE INCLUDE
• FUSOBACTERIUM NUCLEATUM , P INTERMEDIA,
V.PARVULA, HAEMOPHILUS, CAPNOCYTOPHAGA AND
CAMPYLOBACTER SPECIES.
• PREGNANCY ASSOCIATED GINGIVITIS – P. INTERMEDIA
• MICROBIALCHRONIC
SHIFT PERIODONTITIS
GRAM POSITIVE -> GRAM NEGATIVE
COCCI -> RODS -> SPIROCHETES
NON MOTILE -> MOTILE
FACULTATIVE -> OBLIGATE ANAEROBES
FERMENTATING -> PROTEOLYTIC
 PREDOMINANT SPECIES IN CHRONIC PERIODONTITIS

A.ACTINOMYCETEMCOMITANS
B.FORSYTHUS
F.NUCLEATUM
P.MICROS
P.INTERMEDIA
P.GINGIVALIS
EUBACTERIUM SPECIES
C.RECTUS
STREPTOCOCCUS INTERMEDIUS
TREPONEMA SPECIES
• PERIODONTALLY ACTIVE SITES (COMPARED
WITH INACTIVE SITES) – C.RECTUS,
P.GINGIVALIS, F.NUCLEATUM, T. FORSYTHIA.
• DISEASE PROGRESSION – P.GINGIVALIS,
P.INTERMEDIA, T.FORSYTHIS, C.RECTUS,
A.ACTINIMYCETEMCOMITANS AND THEIR
ELIMINATION IS IMPROVED CLINICAL
RESPONSE
• RECENT STUDIES – VIRAL MICROORGANISMS
OF THE HERPESVIRUS GROUP, EBV-1, HCMV.
 LOCALIZED
AGGRESSIVE PERIODONTITIS

• PREDOMINANTLY : GRAM NEGATIVE, CAPNOPHILIC,

ANAEROBIC RODS.
• ALL DISEASE SITES HARBOUR A.ACTINOMYCETEMCOMITANS.
• OTHER ORGANISMS FOUND ARE : P.GINGIVALIS, E.CORREDENS,
C.RECTUS, F.NUCLEATUM, B.CAPILLUS, EUNACTERIUM BRACHY,
CAPNOCYTOPHAGA & SPIROCHETES. EBV-1, HCMC
 NECROTIZING PERIODONTAL
DISEASE

Necrotizing
ulcerative Necrotizing
gingivitis ulcerative
P.intermedia,
periodontitis
Fusobacterium,
Spirochetal Differ from NUG
microorganisms. in loss of clinical
In advance areas of attachment and
tissue destruction, bone in affected
Spirochetes areas.
infiltrate. Clinical
presentation and
etiologic factors
same.
ABSCESSES OF PERIODONTIUM

• F.NUCLEATUM
• P.INTERMEDIA
• P.GINGIVALIS
• P.MICROS
• T.FORSYTHIA
• PREVOTELLA MELANINOGENICA
• C.RECTUS
PERIIMPLANTITIS

• A.ACTINYMYCETEMCOMITANS, P.GINGIVALIS, T.FORSYTHIA,

P.MICROS, C.RECTUS, FUSOBACTERIUM, CAPNOCYTOPHAGA
ISOLATED FROM FAILING SITES.
• OTHER SPECIES SUCH AS PSEUDOMONAS AERUGINOSA,
ENTEROBACTERIACEAE, CANDIDA ALBINACANS &
STYPHOLOCOCCI ARE ALSO FREQUENTLY DETECTED.
 REFERENCES
• Clinical Periodontology - Carranza (9th & 10th edn)

• Clinical Periodontology- Jan Lindhe, Thorklid Karring , Niklaus P

Lang

• Clinical Periodontology : Listgarten

• Periodontal microbial ecology - Perio 2000,Vol. 38, 2005, 135–

187

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• Are dental diseases examples of ecological catastrophes? - P. D.
Marsh - Microbiology (2003), 149, 279–294

• Dental biofilms: difficult therapeutic targets - Periodontology

2000, Vol. 28, 2002, 12–55

• Dental biofilms: difficult therapeutic targets - Periodontology

2000, Vol. 28, 2002, 12–55

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 DENTAL PLAQUE MCQs
1. Defintion of dental plaque given by :
a.WHO 1974
b. WHO 1961.
c. WHO 1984
d. WHO 1955
Ans. B

2.Marginal plaque is a type of:

a.Subgingival plaque
b.Supragingival plaque
c.both
d.None of the above
Ans. B
3. Subgingival plaque is rich in-
a.GM +ve microbes
b.GM-ve microorganisms
c.Fungi
d.none
Ans-b

4. Microbial
complexes were
given by-
a. Socransky
b. Loe
c. Pierre Fauchard
d. Glickman
5. RED complex contains which one?
a. A. actinomycetemcomitans
b. P. gingivalis
c. Streptococcus sp.
d. Vellionella sp.
Ans-b

6. Which complex is associated with

bleeding on probing?
a. RED
b. BLUE
c. PURPLE
d. GREEN
Ans- a
7. Specific
plaque hypothesis given by-
a. Walter Loesche
b. Thelaide
c. Marsh
d. None
Ans-a

8. Transport of bacteria to the tooth

surface occurs by-
a. Brownian motion
b. Liquid flow
c. sedimentation
d. All of the above
Ans- d
9. Which is a primary colonizer?
a. P.gingivalis
b. T.denticola
c. Streptococcus
d. None of the above
Ans-c

10 which is an example of bacterial

interactions–
a. Quorum sensing
b. Corncob formation
c. Test-tube brush formations
d. All of the above
Ans- d
68