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Dental Plaque
1. Dental plaque : composition, biochemistry, initiation, morphology,
metabolism & pathogenesis.
By-
Dr. Sudeep M. Chaudhary
PG 1st
Year
Dept. of Paedodontics &
Preventive Dentistry
2. Contents
â˘Introduction
â˘Classification of soft deposits
â˘Definitions
â˘Classification of dental plaque
â˘Composition
â˘Formation/development of dental plaque
⢠Plaque as a biofilm
â˘Morphology of dental plaque
â˘Factors affecting plaque formation
â˘Metabolism
â˘Pathogenesis
â˘Conclusion
â˘References
3. Dental plaque is a complex community of microorganisms that
forms on the surfaces of teeth and restorations and has been
implicated as the primary etiological factor in the development
of periodontal diseases. So far, more than 700 different
bacterial species have been identified from the human oral
cavity and the majority of them are associated with dental
plaque.
Introduction
4. âHuman fetus is sterile.
âColonization starts at birth.
âWithin hours â facultative & aerobic bacteria.
â2nd day â anaerobic bacteria.
âWithin 2 weeks â mature microbiota established in gut.
âAfter weaning - 1014
microorganisms with 400 different type of
bacteria.
âThere are 10 times more bacteria than human cells.
5. â Establishing microbiota - harmony with the host.
â Constant renewal microorganisms - Prevents the
accumulation of microorganisms.
â Teeth provide hard, non-shedding surfaces - accumulation &
metabolism of bacteria on hard oral surfaces is considered
the primary cause of dental caries, gingivitis, periodontitis
and peri-implant infections.
â In the oral cavity, the bacterial deposits have been termed
dental plaque or bacterial plaque.
6. Classification of soft deposits
â A non-cellular thin film
â An organized transparent deposit
which is primarily composed of
bacteria and their products
â Soft, whitish deposit with no
specific architecture, which can
be removed by water spray
â Retained food which is usually
removed by saliva and oral
muscular action
Dental Plaque
Acquired Pellicle
Materia Alba
Food Debris
7. DEFINITIONS
Plaque is a specific but highly variable structural entity
resulting from colonization and growth of microorganisms on
surfaces of teeth and consisting of numerous microbial
species and their products embedded in a extracellular matrix.
{WHO (1978)}
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. (Carranza, 11th Edition)
9. Composition
â Consist of densely packed bacteria which are embedded in
an amorphous material called plaque matrix
â 60 â 70% bacterial cells
â 30 â 40% matrix
11. Intercellular matrix -
âImpart structural integrity to the microbial masses
â80% water & remaining (20%) solids
âBacterial & salivary proteins comprise about one half of the dry
weight of plaque
âLipids
âCarbohydrates (25% dry weight) â glucans, fructose,
heteropolysaccherides
â˘play a role in bacterial attachment & cohesion
â˘Reservoir of fermentable substrates which are metabolized
by bacteria
13. âFluoride 5 â 10 ppm as
compared to saliva 0.01 â 0.05
ppm
âMost of fluoride is probably
bound on or within bacteria but
some may be in form of calcium
fluoride or fluorapatite.
âConcentration of Ca &
phosphate in plaque is several
magnitudes higher than in
saliva. (Dawes & Jenkins, 1962)
âHigher concentration is thought
to be due to infiltration of
salivary proteins which probably
includes â statherin.
14. Element High DMFS
mean
Low DMFS
mean
Fluoride (ppm) 12.4 36.0
Calcium (%) 0.416 2.158
Magnesium (%) 0.156 0.158
Phosphorus (%) 1.58 2.11
Table- The relationship between caries experience & palque
mineral concentrarion (Schamschula et al., 1980-82)
15. Formation/development of dental plaque
1)Pellicle formation
2)Initial adhesion/attachment of bacteria
3)Colonization & plaque maturation
16. 1)Pellicle formation
âPellicle is the initial stucture that forms on the surfaces the
teeth & artificial prosthesis
âInvolves attachment of positively charged salivary proteins to
apetite surface which has negatively charged phosphate
group
17. 2)Initial adhesion/attachment of bacteria
âWithin a few hours, bacteria are found on the dental pellicle.
The initial bacteria colonizing the pellicle coated tooth surface
are predominantly gram - positive facultative microorganisms
such as Actinomyces viscosus and Streptococcus sanguis.
âThese initial colonizers
adhere to the pellicle,
through specific molecules,
termed adhesins, on the
bacterial surface that
interact with receptors in
the dental pellicle.
Actinomyces spp
S.mitis
S.oralis
S.sanguis
S.gordonii
S.intermedius
V.parvula
A.odontolyticus
Primary colonizers
18. âThere is a transition from the early aerobic environment
characterized by gram-positive facultative species to a highly
oxygen-deprived environment in which gram-negative
anaerobic microorganisms predominate.
19. 3)Colonization & plaque maturation
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.
These microorganisms adhere
to cells of bacteria already in
the plaque mass.
C.showae
C.rectus
E.nodatum
P.intermedia
P.nigrescens
P.micros
F.nucleatum
E.corrodens
Capnocytophaga spp
A.actinomycetemcomitans
P.gingivalis
B.forsythus
T.denticola
Secondary
Colonizers
20. âExtensive laboratory studies have documented the ability of
different species and genera of plaque microorganisms to
adhere to one another, a process known as coaggregation.
This process occurs primarily through the highly specific
stereochemical interaction of protein and carbohydrate
molecules located on the bacterial cell surfaces, in addition to
the less specific interactions resulting from hydrophobic,
electrostatic, and van der Waals forces.
21. âMost studies of coaggregation have focused on interactions
among different gram-positive species and between gram-
positive and gram-negative species.
âIn the latter stages of plaque formation, coaggregation
between different gram-negative species is likely to
predominate. Examples of these types of interactions are the
coaggregation of F. nucleatum with P. gingivalis or Treponema
denticola.
22. âFirst 2-8 hoursâpioneering streptococci, cover 3-30% of
enamel surface
âNext 20 hrsâshort period of rapid growth.
âOne day, it can be called biofilm.
âAs bacterial densities approach 2-6 million bacteria /mm2,
a
marked increase in growth rate can be observed up to 32
million bacteria/mm2
âThickness slowly increases with time to 20- 30 Âľm after 3
days.
âAfter 4 days 30% of the tooth crown is covered by plaque.
23.
24.
25. Morphology of dental plaque
âSupragingival plaque typically demonstrates a stratified
organization of the bacterial morphotypes. Gram-positive cocci
and short rods predominate at the tooth surface, whereas
Gram-negative rods and filaments as well as spirochetes
predominate in the outer surface of the mature plaque mass.
âHighly specific cell-to-cell interactions are also evident from
the âcorncobâ structures often observed. Corncob formations
have been observed between rod-shaped bacterial cells (e.g.
Bacterionema matruchotii or F. nucleatum) that form the inner
core of the structure and coccal cells (e.g., streptococci or P.
gingivalis) that attach along the surface of the rodshaped cell.
26. Development of dental plaque on a clean enamel surface. Coccal bacteria attach to the enamel
pellicle as pioneer species (A) and multiply to form microcolonies (B), eventually resulting in biofilm
formation embedded in a matrix of extracellular polymers of bacterial and salivary origin (C). With
time, the diversity of the microflora increases and rod and filament-shaped bacteria colonize (D
27. Long-standing supragingival plaque near the gingival margin demonstrates âcorncobâ
arrangement. A central gramnegative filamentous core supports the outer coccal cells, which
are firmly attached by interbacterial adherence or coaggregation.
28. Plaque as a biofilm
âAs the bacteria attach to a surface and to each other, they
cluster together to form sessile, mushroom-shaped
microcolonies that are attached to the surface at a narrow
base.
âEach microcolony is a tiny, independent community
containing thousands of compatible bacteria.
âDifferent microcolonies may contain different combinations of
bacterial species.
29. âBacteria in the center of a microcolony may live in a strict
anaerobic environment, while other bacteria at the edges of
the fluid channels may live in an aerobic environment.
âThus, the biofilm structure provides a range of customized
living environments (with differing pH
, nutrient availability and
oxygen concentrations) within which bacteria with different
physiological needs can survive.
30. âThe extracellular slime layer is a protective barrier that
surrounds the mushroomshaped bacterial microcolonies.
âThe slime layer protects the bacterial microcolonies from
antibiotics, antimicrobials and host defense mechanisms.
âA series of fluid channels penetrates the extracellular slime
layer.
31. âThese fluid channels provide nutrients and oxygen for the
bacterial micro colonies and facilitate movement of bacterial
metabolites, waste products and enzymes within the biofilm
structure.
âEach bacterial
microcolony uses
chemical signals to
create a primitive
communication system
used to communicate
with other bacterial
microcolonies Fluid
channel
32. Quorum sensing
âInvolves the regulation of expression of specific genes
through the accumulation of signaling compounds that
mediate intercellular communication.
âDependent on cell density and mediated through signaling
compounds.
âQuorum sensing gives biofilms their distinct properties
Cell â cell communication
33. Quorum sensing is involved in the regulation of -
a)Genetic competence
b)Mating
c)Bacteriocin production
d)Sporulation
e)Stress responses
f)Virulence expression
g)Biofilm formation
35. Plaque formation occurs faster -
âLower jaw > upper jaw
âMolar region > anterior region
âBuccal surface > palatal surface (especially in upper jaw)
âInterdental region > buccal/palatal surface
Variations in dentition -
36. Impact of gingival inflammation -
âPlaque formation is more rapid on tooth surfaces facing
inflamed gingival margins, than those facing healthy gingivae.
âIncrease in crevicular fluid production enhances plaque
formation, it favors initial adhesion & colonization of bacteria.
37. Ageing -
âFollowing tooth eruption the isolation frequency of
spirochetes & black pigmented anaerobes increases.
âIncreased prevalence of spirochetes & black pigmented
anaerobes is found in teenagers, this is due to hormones
entering gingival crevice & acting as a novel nutrient source.
38. Nutrients
Bacteria
degrade host
proteins to
release
ammonia which
is used by
another baceria
as a nitrogen
source.
P. gingivalis -
uses hemin
iron from the
breakdown of
Host
haemoglobin.
Prevotella
intermedia -
Proportions
increases with
steroid increase in
host.
39. Metabolism
âHeterogeneity & complexity of the chemical and the microbial
composition of the dental plaque has been emphasized
â A very wide range of metabolic reactions may be detected in
plaque
âDegradative reactions whereby bacteria convert organic
substances to metabolites & thereby derive energy are readily
detectable.
âOpposite biochemical processes also occur which utilize the
energy
40. Glycolysis
âAnaerobic catabolism of
carbohydrates predominates in
plaque which have a reduced
oxygen tension.
âBacteria of plaque â capable of
using different carbohydrates â
starch, disaccherides &
monosaccherides â as a
substrate.
â1 molecule of glucose â2
molecules of lactic acid + 2 ATP
Polyglucose
Glucose-1-phosphate
Glucose-6-phosphate
Glucose-1,6-diphosphate
Pyruvic acid
Lactic acid
ATP
ADP
ADP
41. âHomorofermentors â some
streptococci & many
lactobacilli â produced 90%
lactic acid
âHeterofermentors â produce
mixure of metabolite â
propionic acid, butyric acid,
succinic acid & ethanol.
Polyglucose
Pyruvic acid
Lactic acid
Propionic acid/butyric acid/
succinic acid
CO2
42. âThe proportion of lactic acid or other organic acids formed by
plaque may be markly affected by growth conditions & by the
bacterial types present.
âWhen the concentration of cariogenic bacteria & sugars in
plaque is high the pathway leading to lactic acid formation is
dominent. On other hand, when carbohydrate is limited the
latter reaction is favored. (Yamada & Carlsson, 1975)
43. Base production
âpH
of plaque is usually highest upon wakening in the morning
& it is higher than pH
of saliva.
âDue to production of ammonia, amines & other basic
components by bacterial degradation of proteins, peptides,
urea & other nitrogenous compounds. (Kleinberg & Jenkins,
1964)
45. 1. Nonspecific plaque hypothesis
âThis hypothesid was delineated in the 1976 by Walter
Loesche
âThe nonspecific plaque hypothesis maintains that periodontal
disease results from the âelaboration of noxious products by
the entire plaque flora.â
âAccording to this thinking, when only small amounts of plaque
are present, noxious products are neutralized by the host.
âSimilarly, large amounts of plaque would produce large
amounts of noxious products, which would essentially
overwhelm the host's defenses.
46. âNonspecific plaque hypothesis is the concept that control of
periodontal disease depends on control of the amount of
plaque accumulation.
âTreatment 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.
47. 2. Specific plaque hypothesis
âProposed by Walter Loesche(1976)
âThe specific plaque hypothesis states that only certain plaque
is pathogenic, and its pathogenicity depends on the presence
of or increase in specific microorganisms.
âThis concept predicts that plaque harboring specific bacterial
pathogens results in periodontal disease because these
organisms produce substances that mediate the destruction of
host tissues.
48. 3. Ecologic plaque hypothesis
âIn 1994, Philip D. Marsh proposed a hypothesis that
combined key concepts of the earlier hypotheses.
âDisease is the result of an imbalance in the total microflora
due to ecological stress, resulting in an enrichment of some
oral pathogens or disease-related micro-organisms
âThis hypothesis is based on the theory that the unique local
microenvironment influences the composition of the oral
microflora.
49. âThis hypothesis postulated dynamic relationship between
environmental cause & ecological shifts within the biofilm.
âIt also introduced the concept that the disease can be
prevented not only by inhibiting the putative pathogens, but
also interfering with the environmental factors driving the
selection & enrichment of these bacteria.
50. Bacteria associated with health & disese
Health
â102
to 103
bacteria/mm2
.
âCertain bacterial species have been
proposed to be beneficial to the host,
including S. sanguis, Veilonella
parvula, and C. ochraceus
âBacteria associated with periodontal diseases are often found
in the subgingival microflora at healthy sites, although they are
normally present in small proportions.
âNonmotile nature.
51. Gingivitis
â10 4 to 10 6 bacteria/mm2
.
âGram-negative bacteria.
âCompared with healthy sites,
noticeable increase also occur
in the numbers of motile
bacteria, including cultivable and
uncultivable treponemas
(spirochetes).
âPregnancy associated gingivitis is accompanied by dramatic
increases in levels of P. intermedia, which uses the steroid as
growth factors.
52. Chronic periodontitis
âCampylobacter rectus, Porphyromonas
gingivalis, Provella intermedia,
Fusobacterium nucleatum and Tannerella
forsythia were found to be elevated in the
active sites.
âSites with chronic periodontitis will be
populated with greater proportions of gram-
negative organisms and motile bacteria.
âCertain gram-negative bacteria with pronounced virulence properties
have been strongly implicated as etiologic agents e.g. Porphyromonas
gingivalis and Tannerella forsythus.
53. Localized aggresive periodontitis
âGram negative, and anaerobic rods.
âThe most numerous isolates are several species from
the genera Eubacterium, Actinomyces naeslundii,
Fusobacterium nucleatum, Campylobacter rectus and
Veillonella parvula.
âIn some populations, a strong case can be made for Aggregatibacter
actinomycetemcomitans playing a causative role in LAP, especially in cases
in which patients harbor highly leukotoxic strains of the organism.
âHowever, some populations of patients with LAP do not harbor A.
actinomycetemcomitans, and in still others Porphyromonas gingivalis may
be etiologically more important.
54. Generalized aggressive periodontitis
âThe sub-gingival flora in patients
with generalized aggressive
periodontitis resembles that in
other forms of periodontitis.
âThe predominant subgingival
bacteria in patients with generalized
aggressive periodontitis are P.
gingivalis, T. forsythis, A.
actinomycetemcomitans and
Campylobacter species.
55. Periodontal abscess
âThe bacteria isolated from abscesses are similar to
those associated with chronic and aggressive forms of
periodontitis.
âAn average of approximately 70% of the cultivable
flora in exudates from periodontal abscesses are
gram-negative and about 50% are anaerobic rods.
âPeriodontal abscesses revealed a high prevalence of the following putative
pathogens: F. nucleatum (70.8%), Peptostreptococcus micros (70.6%), P.
intermedia (62.5%), P. gingivalis (50.0%) and T. forsythis (47.1%).
âEnteric bacteria, coagulase-negative staphylococci and Candida albicans have
also been detected.
56. Necrotizing ulcerative gingivitis & periodontitis
âMore than 50% of the isolated species were strict anaerobes
with P. gingivalis and F. nucleatum accounting for 7-8% and
3.4%, respectively.
57. Conclusion
âDental plaque biofilm cannot be eliminated permanently.
âDental plaque is regarded as one of the main etiological
factors in the initiation and promotion of periodontal disease
i.e. gingivitis and periodontitis & dental caries.
âHowever, the pathogenic nature of the dental plaque biofilm
can be reduced by reducing the bioburden and maintaining a
normal flora with appropriate oral hygiene methods that
include daily brushing,flossing and rinsing with antimicrobial
mouthrinses.
âThis can result in the prevention or management of the
associated sequelae, including the development of periodontal
diseases
58. References
â Newman MG, Takei H, Klokkevold PR, Carranza FA.
Carranza's clinical periodontology (Vol-1). 11th
edition
Elsevier health sciences; 2011 Feb 14.
â Reddy S. Essentials of Clinical Periodontology &
Periodontics. JP Medical Ltd; 2017 Nov 30.
â Nikiforuk G. Understanding Dental Caries. 1. Etiology and
Mechanisms, Basic and Clinical Aspects. 1985:125-7.