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Dental plaque.ppt
1.
2. The human fetus inside the uterus after passing
through the birth canal acquires vaginal and
fecal microorganisms.
The colonization of the oral cavity also starts
about the time of birth.
3. Plaque is a specific but highly variable structural
entity resulting from the colonization of micro-
organisms on the tooth surfaces, restorations & other
parts of the oral cavity which consists of salivary
components like mucin, desquamated epithelial
cells, debris & micro- organisms all embedded in a
gelatinous extra cellular matrix. {WHO}
4. • Acc to Carranza dental plaque is defined
clinically as a structured, resilient, yellow-
grayish substance that adheres tenaciously to
the intra-oral hard surfaces including removable
& fixed restorations.
8. Sub gingival plaque can be divided into 2
regions
Tooth
associated
cervical
plaque
Tissue
associated
9.
10.
11. Biofilms are defined as “matrix-enclosed
bacterial populations adherent to each
other and/or to surfaces or interfaces”
(Richard et al)
Have an organized structure
Composed of microcolonies of bacterial cells
nonrandomly distributed in shaped matrix or
glycocalyx.
15. The intercellular matrix consists of organic &
inorganic materials
Derived from
16. Organic materials include - polysaccharides, proteins,
glycoproteins & lipid material.
Inorganic components include calcium & phosphorus
& trace amounts of sodium, potassium & fluoride
17. As the mineral content increases, the plaque mass
calcifies to form calculus.
Sub gingival calculus is typically dark green or
dark brown probably reflecting the presence of
blood products associated with sub gingival
hemorrhage.
18. Increased resistance of biofilms to antimicrobial agents up to
2-1000 fold.
The surface of a biofilm may restrict the penetration of an
antimicrobial agent
Environment in the depth may be unfavorable for optimal
action of certain drugs
A susceptible pathogen may be rendered resistant if
neighboring cells produce a neutralizing or drug degrading
enzyme.
In addition biofilms provide an ideal environment for
transfer of resistance genes.
19. THE PROCESS OF PLAQUE FORMATION CAN BE
DIVIDED INTO 3 MAJOR PHASES :-
1. FORMATION OF PELLICLE ON THE TOOTH
SURFACE
2. INITIAL ADHESION & ATTACHMENT OF THE
BACTERIA
3. COLONIZATION & PLAQUE MATURATION
20. 1. FORMATION OF THE PELLICLE
All surfaces of the oral cavity are coated with a
pellicle.
This pellicle (saliva derived layer) consists of
phosphoproteins, glycoproteins , proline rich proteins,
histidine rich proteins, enzymes & other molecules that
can function as adhesion sites for bacteria (receptors).
Forces which are used electrostatic, vanderwall force,
hydrophobic force
21. 2. INITIAL ADHESION & ATTACHMENT OF THE
BACTERIA
Occurs in 4 phases:
a) transport to the surface
b) initial adhesion
c) attachment
d) colonization
22. a) Transport to the surface
Initial transport of bacteria to the tooth surface
Random contacts occur through Brownian motion,
sedimentation of micro organisms, through liquid
flow or through active bacterial
movement(chemotactic activity)
23. b) Initial adhesion:
Reversible adhesion of the bacterium
Initiated by interaction between the bacterium &
the surface from a certain distance (50nm)
through long range & short range forces used-
including van der Waals attractive forces &
electrostatic repulsive forces.
24. Derjaguin, Landau, Verwey, & Overbeek (DLVO)
postulated that above a separation distance of
1nm, the summation of the previous 2 forces
describes the total long range interaction.
Total interaction energy also called as total Gibbs
energy Gtot = GA+GE
25. c) Attachment
After initial adhesion
a firm anchorage between bacterium & the surface
The bonding between bacteria & pellicle is
mediated by specific extra cellular protein
components (adhesins) of the organism &
complementary receptors on the surface & is species
specific.
26.
27. 3. COLONIZATION & PLAQUE MATURATION
When the firmly attached microbes
start growing & the newly formed
bacterial clusters remain attached,
biofilms develop.
28. Now intra bacterial connections start occurring
leading to coaggregation.
Essentially all oral bacteria possess surface
molecules that foster some type of cell – to – cell
interaction.
Fusobacterium coaggregates with all other oral
bacteria. Veillonella, Capnocytophage &
Provetella binds to Streptococci &
Actinomycetes.
29. • Most coaggregation are mediated
by nectin-like adhesins & can be
inhibited by lactose &
galactosides
30.
31.
32. • Special e.g. of coaggregation
are the “corncob” formation
(streptococci with
Bacterionema matruchotii or
Actinomyces species);
• “test tube brush” composed
of filamentous bacteria to
which gram negative rods
adheres
33. Secondary colonizers do not initially colonize clean
tooth surface but adheres to bacteria already in the
plaque mass.
Examples of interaction of secondary colonizers with
early colonizers include coaggregation of
Fusobacterium nucleatum with S. sanguis and
Prevotella loescheii & Capnocytophage ochraceus with
A. viscosus.
34. YELLOW COMPLEX : Streptococcus species
PURPLE COMPLEX- Veillonella Parvula,
Actinomyces odontolyticus
GREEN COMPLEX- Eikinella corrodens, A.
actinomycetimcomitans serotype a &
Capnocytophage species
35. RED COMPLEX – P. gingivalis, T. forsythia &
Treponema denticola
ORANGE COMPLEX- Fusobacterium,
Prevotella & Campylobacter species
36.
37. THE RED COMPLEX IS OF PARTICULAR
IMPORTANCE BECAUSE IT IS ASSOCIATED
WITH BLEEDING ON PROBING WHICH IS A
IMPORTANT CLINICAL PARAMETER OF
DESTRUCTIVE PERIODONTAL DISEASE.
38. During the first 24hrs,(<3%)
During the following 3 days(rapid rate then slows
down)
After 4 days 30% of the tooth crown area will be
covered with plaque & a shift towards anaerobic &
gram negative flora.
During night :50% less production of plaque
39. Early plaque formation on teeth follows a typical
topographic pattern with initial growth along the
gingival margin & interdental space.
Later further extension in the coronal direction can be
observed.
Surface irregularities
Shear force
40.
41. Rough intraoral surfaces (crown, abutments,
denture bases) accumulate & retain more
plaque & calculus in terms of thickness, area &
colony- forming units.
Threshold level of surface roghness: 0.2 um
42.
43. In general, early plaque formation occurs faster
1) in the lower jaw compared to upper jaw
2) in molar areas
3) on the buccal tooth surfaces compared to oral sites
(especially in the upper jaw)
4) in the interdental regions compared to strict oral or
buccal surfaces
44. Non Specific Plaque Hypothesis
Specific Plaque Hypothesis
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45. The nonspecific and specific plaque hypotheses were delineated in
1976 by Walter Loesche
The nonspecific plaque hypothesis maintains that periodontal
disease results from the "elaboration of noxious products by the
entire plaque flora.
According to this thinking, when only small amounts of plaque
are present, noxious products are neutralized by the host.
Similarly, large amounts of plaque would produce large amounts
of noxious products, which would essentially overwhelm the
host's defenses.
Nonspecific plaque hypothesis is the concept that control of
periodontal disease depends on control of the amount of plaque
accumulation.
Treatment of periodontitis by debridement (nonsurgical or
surgical) and oral hygiene measures focuses on the removal of
plaque and its products and is founded in the nonspecific plaque
hypothesis.
12/27/2011 DENTAL PAQUE 45
46. The specific plaque hypothesis states that only
certain plaque is pathogenic, and its
pathogenicity depends on the presence of or
increase in specific microorganisms.
This concept predicts that plaque harboring
specific bacterial pathogens results in
periodontal disease because these organisms
produce substances that mediate the
destruction of host tissues.
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