Dental plaque

1. DENTAL PLAQUE
BY- DR.SWAPNA EDIGA

2. DEFINITION
Dental plaque
is defined clinically as a structured, resilient, yellow-
grayish substance that adheres tenaciously to the intraoral
hard surfaces, including removable and fixed
restorations.(Caranzza)

3. Material
Alba Calculus
Material Alba – soft accumulations of bacteria and tissue cells that
lack the organized structure of dental plaque & it is easily displaced
with a water spray
Calculus – is a hard deposit that form by mineralization of dental
plaque & it is generally covered by a layer of unmineralized plaque

4. Supra-
gingival
At/above gingival margin
Sub gingival
Below gingival margin &
gingival pocket epithelium
CLASSIFICATION
If in direct contact
with gingival margin
c/as MARGINAL
PLAQUE
Tooth associated
Tissue associated

5. Composed primarily of microorganisms.
>500 distinct microbial species found in
dental plaque
Composition
Non-bacterial species
-mycoplasma species
-yeasts
-protozoa
-viruses
Micro-org exist
within an
intracellular matrix
that also contains
few host cells
Epithelial
cells
Macrophag
es
Leuckocyte
s

6. SUPRA-GINGIVAL PLAQUE
 Stratified organization of
multilayered accumulation
of bacterial morphocytes
 Gram +ve cocci
 Short rods
 Gram –ve rods
 Filaments & spirochetes
Predominate at
tooth surface
Predominate at
outer surface of
maute plaque

7. SUB-GINGIVAL PLAQUE
Subgingival composition differs from supragingival plaque
>Low oxidation-reduction (redox) potential with characteristics of anaerobic
environment
>Local availability of blood products
Environmental parameter differ from those of supragingival plaque
>Gingival crevice/pocket – bathed by the flow of GCF which contains many substances
that bacteria may use  nutrients
>Host inflammatory cells + mediators have considerate influence on the
establishment & growth of bacteria in subgingival region

8. TOOTH ASSOCIATED SUB-GINGIVAL PLAQUE
 Adheres to root Cementum.
 Generally does not differ greatly
from that observed in gingivitis.
Dominance : filamentous micro-organism but cocci, rods
also occur
Gram +ve
rods, cocci
Streptococc
us mitis
S. Sanguis
Actinomyce
s viscous
A Naeslundi
Eubacterium
species
 Deeper part : filamentous
 Apically : virtually absent
(instead smaller micro-
organisms without proper
orientation)
Apical border of plaque mass is
separated from JE by  a layer of
host leucocytes
Concentration of gram –ve rods
Thus composition of sub gingival plaque
depends upon the pocket depth
APICAL – spirochets, cocci, rods
CORONAL – more filamentous

9. TISSUE ASSOCIATED SUB-GINGIVAL PLAQUE
 Lacks a definite intermicrobial matrix &
contains primarily
 Gram –ve rods & cocci
 Also large no of filamentous, flagellated rods
and spirochetes
Studies done
by Dibart et
al & Dzink et
al indicate
predominanc
e of
- Streptococcus oralis
- Strptococcus
intermedius
-Peptostreptococcus
micros
- Porphyromonas
Gingivalis
- Prevotella Intermedia
- Fusobaterium
nucleatum
Host tissue cells (e.g WBC’s , Epithelial cells)

10.  Between subgingival plaque & tooth an electron – dense organic
material is interposed  “Cuticle”
 This cuticle is porbably contains the remains of the epithelial
attachment lamina, originally connecting J.E to the tooth, with
addition of the material deposited from gingival exudate.
{ Frank & Cimasoni 1970, Lie & Selvig 1975, Eide et al 1983 }
 Schroeder & Listgarten 1977 – suggested the cuticle represents
a severity product of the adjacent epithelial cells

11.  Thus there are 4 different subgingival ecologic niches which are
probably different in their composition
subgingival
ecologic niches
Tooth/implant
surface
Gingival
exudate fluid
medium
Surface of
epithelial cells
Superficial
portion of
the pocket
epithelium

12. Characteristic
s
Supragingival Subgingival
Location At or above the gingival margin
Marginal plaque
Below the gingival margin
Between the tooth and gingival pocket
epithelium
Gram reaction +/- Dominated by -
Morphotypes Gm +ve Cocci, short rods, -
at tooth surface
Gm-ve rods & filaments
predominate in outer
surface of mature plaque
Dominated by rods and
spirochetes
Energy
metabolism
Facultative aerobic with
some anaerobes
Dominated by anaerobes
( due to local availability of blood products ,
low red-ox potential )
Energy sources Generally ferment
carbohydrates
Many proteolytic forms
Motility Firmly adherent to plaque
matrix
Adherence less pronounced with
many motile forms
12

13. The intercellular matrix consists or organic and inorganic
materials derived from saliva, gingival crevicular fluid, and
bacterial products.
INTERCELLULAR MATRIX:
ORGANIC CONSTITUENTS INORGANIC COMPONENTS
- Albumin - Predominantly
calcium and
- Lipid material phosphorous.
- Glycoproteins - trace amt, of
sodium,
- Polysaccharides-dextran potassium, and
fluoride.
The source of inorganic constituents:
Supragingival plaque - primarily saliva
Subgingival plaque – Crevicular fluid (a serum
transudate).
The fluoride component of plaque is largely derived
from external sources such as fluoridated toothpastes,
Organic content source:
1. Albumin – GCF
2. Lipid – disrupted
membrane of acteria &
host cells
3. Glycoprotein – saliva
4. polysaccharide-
produced by bacteria

14. SITE SPECIFICITY OF PLAQUE
Marginal Plaque
Supragingival
plaque + tooth
ass. Plaque
Tissue associated
subgingival plaque

15. FORMATION OF DENTAL PLAQUE
Formation of
the pellicle.
Initial
adhesion and
attachment of
bacteria
Colonization
and plaque
maturation.

16. THE FORMATION OF THE PELLICLE &
BIOFILM ON THE TOOTH SURFACES
• All The Surfaces Of The Oral Cavity Are Coated With A Pellicle.
• Within Nanoseconds After Vigorously Polishing The Teeth, A Thin Saliva
Derived Layer, Called Acquired Pellicle (Term No Longer Used Since
Misleading), Covers The Tooth Surface.
• The Pellicle Forms By Selective Adsorption Of The Environment
Macromolecules.
• Electrostatic, Vanderwaals & Hydrophobic Forces

17. INITIALADHESION & ATTACHMENT OF BACTERIA
• Microbial Adhesion To Surfaces In An Aquatic Environment
As A Four Stages Sequences:
I. Transport To The Surface.
II. Initial Adhesion.
III. Attachment.
IV. Colonization Of The Surface And Biofilm Formation.

18. PHASE I: TRANSPORT TO THE SURFACE
-Transport Of Bacterium To The Tooth Surface.
- Random Contact May Occur, Through:
- Brownian Motion.
- Sedimentation Of Microorganisms
- Liquid Flow
- Active Bacterial Movement.

19. PHASE II : INITIALADHESION.
- Initially Adhesion Of Bacterium By Long Range
Force (50nm) Ie, Reversible.
- Later By Short Range Forces ( Less Than 2 Nm)
Ie, Irreversible.
- These Includes Electrostatic Repulsive Forces( E)
And
Vanderwals Attractive Forces ( A).

20. • PHASE III: ATTACHMENT:
- Here Firm Anchorage Between Bacterium And Surface Will Be
Established By Specific Interactions
(Covalent, Ionic, Or Hydrogen Bonding).
- This Is Followed By Direct Contact Or Bridging Through Extra
Cellular Filamentous Appendages.
- The Bonding Between Bacteria And Pellicle Is Mediated By
Specific Extrcellular Proteinaceous Components ( Adhesions) Of
The Organisms And Complementary Receptors( Ie Proteins,
Glycoprotein, Or Polysaccharides) On The Surfaces ( E.G.,
Pellicle) And Is Species Specific.

21. COLONIZATION AND PLAQUE MATURATION
• Here Early Colonizers Start Growing And Allow For Newly Formed Bacterial
Clusters Remain Attached, Micro Colonies And Biofilm Can Develop.
• New Mechanism Involved Characterized By Inter Bacterial Connections.
• 18 Genera From The Oral Cavity Shows Co Aggregation
• ( Cell-to-cell Recognition Of Genetically Distinct Partner Cell Types).
• Co Aggregation Is Interaction Of Protein And Carbohydrate Molecules Located On
The Bacterial Cell Surfaces. Hydrophobic, Electrostatic, Vanderwals Forces Also
Participates.

22. SECONDERY COLONIZATION AND PLAQUE
MATUARATION
SECONDARY COLONIZERS
PROVETELLA INTERMEDIA ,PREVOTELLA
LOESCHII,
CAPNOCYTOPHAGA,FUSOBACTERIUM
NUCLEATUM &P.GINGIVALIS
• CO-AGGREGATION
ABILITY OF DIFFERENT SPECIES & GENERA OF
PLAQUE MICROORGANISMS TO ADHERE TO
ONE OTHER
EG F. NUCLEATUM WITH S.SANGUIS
P.LOESCHII WITH A .VISCOSUS
C.OCHRACEA WITH A .VISCOSUS
F.NUCLEATUM WITH P.GINGIVALIS
F.NUCLEATUM WITH T.DENTICOLA

23. LATER STAGE COAGGREGATION BETWEEN THE
GRAM –VE SPECIES PREDOMINATE:
• F. NULEATUM WITH P. GINGIVALIS OR T.
DENTICOLA.
• “CORNCOB” FORMATION (STREPTOCOCCI WITH
B. MATRUCHOTII OR ACTINOMYCES.
• “TEST TUBE BRUSH” FILAMENTOUS TO GRAM –
VE RODS.

24. 24

25. PATHOGENIC POTENTIAL OF DENTAL PLAQUE IN
PERIODONTAL DISEASES
specific
plaque
hypothesis
ecological
plaque
hypothesis
Non-
specific
plaque
hypothesis

26. FACTORS AFFECTING PLAQUE FORMATION
Topography of
supragingival plaque
Surface micro-roughness
Individual variables
Variations in dentition
Gingival inflammation
Age

27.  Early Plaque Formation On Teeth Initial Growth Along The Gingival Margin And
From The Interdental Space. (Protected From Shear Forces). Later Extend In
Coronal Direction
 Plaque Formation Can Also Start From Surface Irregularities Like Grooves, Cracks,
Perikymata, Or Pits
 By Multiplication, The Bacteria Subsequently Spread Out From These Initial Areas
As A Relatively Even Monolayer.

28. SURFACE MICROROUGHNESS
Rough Intraoral Surfaces (E.G. Crowns, Implant Abutments, Denture Bases)
Accumulate And Retain More Plaque And Calculus In Terms Of Thickness,
Area, And Colony Forming Units. (Quirynen And Bollen ,1995).
 Smoothing An Intraoral Surface Decreases The Rate Of Plaque Formation.
 Threshold Level For Surface Roughness (About 0.2 µm), Above Which
Bacterial Adhesion Will Be Facilitated.

29. INDIVIDUAL VARIABLES INFLUENCING
PLAQUE FORMATION.
Plaque
formers
Heavy(Fast)
Light(slow)

30. Noticed only minor
differences between
the groups -
Simonsson et al
( 1987)
After one day, the
heavy plaque formers
showed more plaque
with a more complex
supragingival
structure.
From 1- 14 days,
there were no
discernible
differences between
both groups, except
for a more prominent
inter microbial matrix
in the group of fast
growers.
Higher level of Gram
–ve rods in 4 day old
plaque-Zee KY et al (
1996,97)

31. Factors
such as
Diet
Chewing
fibrous
foods
Smoking
Restorations
Tongue
and palate
brushing
The colloidal
stability of
bacteria in the
saliva
Antimicrobial
factors present
in the saliva
Chemical
composition of
pellicle
Ainamo J
et al
(1979)

32. VARIATION WITHIN THE DENTITION:
EARLY PLAQUE FORMATION OCCUR FASTERS IN:
• In The Lower Jaw Compare To The Upper Jaw.
• In The Molar Areas.
• On Buccal Tooth Surfaces Compare To Oral Sites.
• In The Interdental Areas Compare To Strict Buccal Or Oral
Surfaces.
QUIRYNEN M ( 1986)

33. IMPACT OF GINGIVAL INFLAMMATION:
• Plaque Formation Is More Rapid On Tooth Surfaces Facing
Inflammed Gingival Margins Than On Those Adjacent To
Healthy Gingiva
• Increase In Crevicular Fluid Production Enhances Plaque
Formation.
Ramberg P, Et Al (1994)

34. IMPACT OF PATIENTS AGE :
• Could Detect No Differences In De Nevo Plaque Formation, Either In
Amount Or In Composition Between A Group Of Young And Older
Subjects.
FRANSSON ET AL (1996)

35. 35
PERI IMPLANT PLAQUE
Mombelli etal -1988
Quirynen and Listgarten et al 1990
Apse et al 1984
Studies characterized deposits of plaque in human
peri-implant sulcus but no study has documented
the structure of supramucosal and submucosal
(peri-implant ) microbiota
However ,similarities between peri-implant and sub
gingival microbial deposits 
Mombelli 1987, 1995,
Pontoreiro 1994
Also recently  QUIRYNEN et al 2005
complex subgingival microbiota
( periopathogens ) is established in 1 week after
abutment insertion which increase with time

36. Characteristics of sub-gingival
flora around implant
Degree of
periodonitis in
remaining
dentition
Presence of
remaining
teeth
Smoothness of
abutments(
<0.2 um)25
times less
flora then
rough ones

37. 37
BIOFILM CONTROL
doxycycline
Authors like  bonito etal 2005 confirmed
that tetracycline , minocycline most effective
 in terms of PD reduction & CAL gain
locally
Under systemic antibiotics amox –metro
combination beneficial otcomes  6 months
after FMD. Also beneficaial are tetracyclines
and metronidazole haffajee, 2003, hererra
2002, cionca 2009

38. CONCLUSION
• Because Of The Various Risk Factors That Contribute To Periodontitis, It Is Possible That
There Will Be No Magic Bullet Treatment.
• It Is Also Probably True That The Underlying Cause Of Periodontitis Is Different In
Different Patients.
• For Instance, One Patients Periodontitis May Be Due To A Shift In The Oral Microflora
Due To Poor Hygiene, While Another Patients Periodontitis May Be Due To An
Underlying Genetic Abnormality That Leads To A Destructive Immune Response.
• In Light Of This, Periodontitis Is Perhaps Better Described Not As A Disease But As A
Symptom Of An Underlying Condition.
• For Successful Treatment, It Is Imperative That This Underlying Cause Is Being
Identified And Addressed.

39. THANK
YOU