Dental plaque

INTRODUCTION
 1 mm3 of dental plaque, weighing about 1
mg contains more than 200 million bacteria
Index
 Definition
 Classification
 Composition
 Clinical feature
 Formation
 Clinical significance
 Diagnosis & treatment
 Conclusion
 References
 Definition
 IT IS A MICROBIAL ECOSYSTEM OR
BIOFILM COMPOSED OF DENSELY PACKED
MICROBIAL STRUCTURE INSOLUBLE
SALIVARYGLYCOPROTEIN , MICROBIAL
INTRACELLULAR PRODUCT & TO SOME
EXTENT EPITHELIAL CELLS & DEBRIES
ARRANGED IN AN ORGANISED COMPLEX
INTER CELLULAR MATRIX.
- BY WHO
 CLASSIFICATION
 by location on tooth

supra gingival plaque sub gingival plaque

coronal marginal attached unattached

tooth asso. tissue asso.

 By pathogenic effects

Cariogenic periodontal ds’ calculogenic

plaque producing plaque plaque
 COMPOSITION
 PRIMARILY OF MICRO-ORGANISMS
Gram +ve -
s.mutans
s.Sanguis
s.Milleri
s.Salivarius
Gram –ve -
a.Viscosus
a.Naslundi
a.Israelli
Gram –ve anaerobic cocci –
Vellionellae
v.parvula
 Organic : -
Polysaccharide
Protein
Glycoprotein
Lipid
Albumin
 Inorganic : -

Phosphorous
Sodium
Pottasium
Fluoride
calculus
PLAQUE MICRO-ORGANISMS

 DAY :- 1-2
Early plaque is consisted of streptococci which
dominates bacterial population include, s.
mutans, s.sanguis
 Day :- 2-4
cocci r still dominate & increase in no of
filamentous may be seen. gradually filamentous
form grows into cocci layer & replace them.
 Day : - 6-10
filamentous increase in no.along with rods,
spirilia, & fusobacteria.
Plaque near the gingival margin is thicker &
develops more mature flora earlier with spirochete
& vibrios
As plaque matures- more gram –ve & anaerobic
organism appear. During the period when this is
happening, signs of inflmmation begin to observe
in the gingiva.
 Older plaque :- spirochete & vibrios r prevalent
along with cocci & filamentous m.o arranged
themselves perpendicular to the tooth surface in a
palisade
 FORMATION
 DENTAL PLAQUE IS A MICROBIAL
BIOFILM.
 Biofilms – “ defined as matrix enclosed
bacterial populations adherent to each
other and/or to surfaces or interfaces.”
( costerton,1994 )
 Biofilm can be formed by a single bacterial
species or multiple bacterial species as well
as other organisms & debris.
 It can form on any surfaces that is wet.
 It can exist on any solid surfaces that is
exposed to bacteria-containing fluid.
Biofilm structure
 The bacteria in a biofilm r
not distributed evenly,
they cluster to gether to
form sessile mushroom
shaped microcolonies.

 Each microcolony is an
independent community
with its own customised
living environment.
 A protective extra cellular slime layer surrounds
the microcolonies.
 A series of fluid channels penetrate the slime
layer & facilitate the movement of nutrients &
bacterial products throughout the biofilm
 A primitive communication system of chemical
signals allows communication bt. the bacterial
microcolonies.
 Bacteria in the center
of a microcolony may
live in a strict
anaerobic
environment, while
other bacteria at the
edges of the fluid
channel may live in an
aerobic environment.
 Fluid channels provide
nutrients & oxygen for
the bacterial
microcolonies, waste
products & enzymes
within the biofilm
structure
 The bacterial
microcolonies use
“chemical signals” to
communicate with
each other.
 Bacterial microcolonies r protected by one
another or by extracellular slime layer & r
usually resistant to antibiotics &
antimicrobials, & the body’s defense
system.
 Can be destroyed by simply wipping off
them.
FORMATION OF DENTAL
PLAQUE BOIFILMS
 THE PATTERN OF PLAQUE BIOFILM
CAN BE DIVIDED INTO 3 PHASES :
1. Attchment of bacteria to the solid surface
2. Formation of microcolonies on the surface
3. Formation of the mature subgingival
plaque biofilms
1.Initial attachment of bacteria
 Pellicle formation –
defined as “an acellular layer of salivary
proteins & other macromolecules,
aproximately 2 to 10 micrometer thick,
adsorbed on to the enamel surface.”
It has important role in protecting the enamel
from abrasion and attrition but it also serves
as diffusion barrier.
 A thin, bacteria free layer forms within
minutes on a cleaned tooth surface.
 The purpose is to protect the enamel from
acidic activity.
 Acts like a double sided adhesive tape with
their amino- terminal segments to the tooth
surface,leaving their carboxy-terminal
regions directed towards the oral
cavity,where they may interact with oral
micro-organisms
 Initial colonization of the tooth surface :
within few hours bacteria connect to the
pellicle & each other with hundreds of hair
like structures called fimbriae.
Stimulate other free floating bacteria to join
the community
 4 hrs. after cleaning, there r 103 to 104 bacteria /
1 mm2 of tooth surface,predominently streptococci
& actinomycetes.
 Within a day a no. of bacteria increases, due to
growth of streptococci
 The initial bacteria r called “pioneer bacteria”
 It is interection bt. Pr. Adhesion on the surface of
colonizing bacteria & carbo. Receptor on the
salivary components adsorbed to the tooth
surface.
If within 2 days no further cleaning is undertaken,
the tooth surface is colonized predominantly by
gram +ve facultative cocci, which r primarily
streptococci.
 Extra cellular slime layer formation :

The act of attaching to the solid surface stimulate

the bacteria to excrete a slimy glue like substance
that helps to anchor them to the surface &
provides protection for attached bacteria
2.Microcolony formation
 Bacterial growth :-
primarily through cell division of the adherent
bacteria(rather than attachment of new bacteria)
Next proliferating bacteria begin to grow away from
the tooth.
Plaque doubling time are rapid in early development
& slow in more mature biofilms.
Bacterial blooms - r periods when specific species
or grp. Of species grow at rapidly accelerated
rate
Coaggregation into mushroom shaped
microcolonies
 It is ability of new bacterial colonizer to
adheres to previously attached cells
 Forms sessile, mushroom shaped
microcolonies that r attached to tooth
surface at a narrow base & gives “corn cob”
appearance or “taste tube brushes.”
 Central rod
shaped bacterium
becomes
surrounded by
many round cocci
 “bristles” of taste
tube brush
formation r
composed of
gram –ve rods.
3. Formation of mature subgingival
plaque biofilm
 Sub gingival
plaque biofilm
 Relationship of plaque
biofilm to alveolar bone

 The distance bt. Apical

edge of calculus & crest of
alveolar bone in human pd
pocket is constant, having
mean length of 1.97 mm.

(indicates that bacteria r

capable of producing bone
resorbing activity only in alv.
Bone no further than 2.7mm
away from biofilm.
 Microbial
interactions
 Although bacteria initiate the periodontal
disease process, it is the body’s own immune
response that is actually responsible for the
breakdown of periodontal tissues.
 Immune system complex in periodontitis
1. Phagocytes ( the army )
2. Lymphocytes ( the air force )
3. The complement system ( the navy )
Neutrophil
 Macrophage
Lymphocyte
Complementary system
 3 major function
1. Recruitment of phagocytic cells
2. Facilitation of phagocytosis by
opsonization
3. Direct killing of bacteria by puncturing the
bacterial cell membrane
Phagocytosis
Sequence of events
in host response
 Early bacterial
accumulation phase
 Plaque over growth
phase : acute
inflammation
 Sub gingival plaque
phase
 Tissue destruction
phase
 Tissue
destruction in
periodontitis
 DETECTION OF PLAQUE

1. Direct vision : -

Thin plaque – may be translucent & therefore

not visible
Stained plaque – may be acquired
e.g tobacco stained
Thick plaque – tooth may appear dull & durty
2.USE OF EXPLORER : -
Tactile Examination – when calcification has
started it appears slightly rough, otherwise
it may feel slippery due to coating of soft ,
slimy plaque
Removal Of Plaque – when no plaque is
visible , an explorer can be passed over
the tooth surface & when plaque is
present it will adhere to explorer tip.this
technique is used when evaluating plaque
index.
Use of disclosing solutions -
CLINICAL SIGNIFICANCE
 SUPRA GINGIVAL PLAQUE
1. Occlusal surface leads to caries
2. Gingivitis
 SUB GINGIVAL PLAQUE
1. Periodontitis
2. Other periodontal disease
Treatment

 Several investigations r being carried out to

develop plaque inhibiting agents which could be
applied as mouth rinse, tooth paste,& chewing
gums.
 They interfere in plaque formation by
1. Prevention of plaque formation or alteration of
plaque microflora by anti microbial substance
2. Prevention or absorption of organic matrix of the
teeth
3. By means of enzymes capable of decomposing
the inter microbial substance
Surface treatment

 Chemical plaque inhibition is very little

successful
 Antibiotics
 Other antimicrobial substance like chemical
disinfectant
 Chlorhexidine longer time use is not
preferable because it causes discoloration
of mucus membrane
 CONCLUSION
PLAQUE + TIME = GINGIVITIS
GINGIVITIS +TIME = PERIODONTITIS
PERIODONTITIS + TIME = TOOTH LOSS
REFERENCES
 FOUNDATION OF PERIODONTICS
- By donald E. willmann
 DIAGNOSIS & RISK PREDICTION OF
PERIODONTAL DISEASE
- per axelson,dds,odont dr
 CLINICAL PERIODONTOLOGY
- caranza ( 9 th edition)