Download application~~vnd.ms-powerpoint~~dental plaque part 1

DENTAL PLAQUE
Contents
Introduction
Definition and structure
Composition
Classification
Stages of plaque formation
 Plaque as a biofilm
Human fetus →sterile
oral cavity.
Hours after
birth→Facultative aerobic
bacteria.
Second day→anaerobic
bacteria .
Two weeks→nearly
mature microbiota in the
gut
Oral cavity - >500 bacterial species,
mostly commensal & beneficial
Open growth system
periodontal diseases unusual human
infection. major reason anatomic feature of
a mineralized structure, the tooth, partly
exposed to the external environment and
partly in the connective tissues
Teeth & implants – hard non shedding
surfaces, continually held in immediate
proximity to the soft tissues of the
periodontium
Provide port of entry
Dental Plaque - Definitions
“ A soft deposit that form the biofilm adhering
to the tooth surfaces in the oral cavity
including removable and fixed restorations.
Diverse community of microorganism found on
tooth surface as biofilm embeded in an
extracellular matrix of polymers of host and
microbial origin (Marsh 2004)
Clinically plaque is def as structured
resilient, yellow grayish substance that
adheres tenaciously to the intraoral hard
surfaces including removable and fixed
restorations
Accumulates in the gingival third and in
pits, cracks, fissures, overhanging
restorations and around malaligned tooth
Methods of detecting plaque
 Probing with a
periodontal probe.
 Disclosing solution.
Materia Alba - Soft accumulations of bacteria
and tissue cells that lack the organised
structure of dental plaque and are easily
displaced by water spray.
Calculus – Hard deposit that forms by
mineralisation of dental plaque and is generally
covered by a layer of unmineralised plaque
Composition
•
•
Water: 80-85% plaque mass ;
•



Cells: primarily bacteria, 1 gm (wet weight)= 1011 bacteria
Non bacterial: Mycoplasma spp, yeasts, protozoa,
viruses
(conteras 2000)
Host cells : epithelial cells, macrophages & leucocytes
•
Matrix:
Organic
•
Inorganic
 Matrix : 20-30% plaque mass
1. Organic:
Carbohydrates: Dextrans, levans, polysaccharides,
galactose
Lipids
Proteins: Albumin, glycoproteins
Misc: cxtracellular bacterial products, cell remnants,
food
2. Inorganic:
Calcium
Phosphorus/ phosphate
Na, Cl, F
Classification
SUPRAGINGIVAL PLAQUE
 Gram –positive cocci and short rods predominate at the
tooth surface area,
 Gram –ve rods filaments as well as spirochaetes
pedominate the outer surface of mature plaque mass.
SUBGINGIVAL PLAQUE
TOOTH ASSOCIATED ( Attached Plaque)
 Cervical part : densely arranged consists of gram
+ve rods and cocci including Streptococcus mitis ,
Streptococcus sanguis, Actinobacillus Viscosus, A.
naeslundi and Eubacterium species .
Deeper parts filamentous forms are fewer
Apical border of plaque mass is separated from
junctional epithelium by a layer of host leukocytes.
increased concentration of gram negative rods,
spirochetes
TISSUE / EPITHELIUM ASSOCIATED PLAQUE
-Loosely
arranged
- Comprises of Gram-negative rods and cocci, large
number of filaments, flagellated rods, spirochaetes.
Presence of Porphyromonas gingivalis, Prevotella
Intermedia, Tannerella Forsythia , Fusobacterium
Nucleatum are predominant
-

Clinical signifance
 Marginal plaque→ gingivitis
 Supragingival and tooth associated subgingival
plaque→calculus formation
 Tissue associated subgingival plaque→periodontal tissue
destruction
 Subgingival tooth attached plaque→calculus formation and root
caries
Characteristic Supragingival
plaque
+/MOS
Subgingival plaque
Dominated by -
Morph types
Cocci, branching
rods, filaments,
spirochetes
Dominated by rods and
spirochetes
Energy
metabolism
Facultative with some Dominated by anaerobes
anaerobes
Energy
sources
Generally ferment
carbohydrates
Many proteolytic forms
Causes
Can cause caries and
gingivitis
Can cause gingivitis and
periodontitis
Plaque formation
3 major phases of plaque formation
MECHANISMS OF PLAQUE FORMATION
Formation of pellicle
 Pellicle – Glycoprotein derived from components of saliva and
GCF as well as bacterial and host tissue cell products and
debris.
 Forms within nanoseconds after vigorous brushing
 Contains – glycoproteins (mucins), Phosphoproteins, Histidine
rich proteins, enzymes (α- amylase)
 Forms by selective adsorption of the environmental
macromolecules
 mechanisms involved in enamel pellicle formation include
electrostatic, van der Waals, and hydrophobic forces
.
 Can be removed by polishing .
 Recurs soon after removal.
 Fully established pellicle – in 30 minutes.
Initial Adhesion and Attachment of Bacteria
Phase I: Transport to the surface
 Random contacts through brownian motion.
 Sedimentation of microorganisms
 Through liquid flow
 Active bacterial movement ( chemotactic
activity).
Phase 2 ; Initial adhesion
Reversible adhesion of bacterium to the
surface
Through long and short range forces like
van der Waals attractive and elecrostatic
repulsive forces, hydrogen bonding

Phase 3 : Attachment
Firm anchorage→ specific interactions (
covalent, hydrogen bonding )
Direct contact or bridging through specific
extracellular proteinecious components of
organisms and complementory receptors (
proteins and glycoproteins or
polysaccharides on the surface )
S. sanguis ( principle early coloniser )bind
to proline rich proteins
A. viscosus posses fimbriae →adhesins
→proline rich proteins .
.
Colonisation and plaque maturation
 Plaque increases by two mechanisms.
- Multiplication of bacteria already attached to the tooth
surface.
- Subsequent attachment and multiplication of new
bacterial species to cells of bacteria already present in
the plaque mass.
Coaggregation
 Coaggregation - defined as the specific cell-to-cell
recognition that occurs between genetically distinct
cell types
 Occurs primarily through highly specific
stereochemical interaction of protein and carbohydrate
molecules located on the bacterial cell surface.
 Less specific interactions from hydrophobic,
electrostatic and vanderWaals forces also occur.
Early stages, coaggregation occurs
among different gram positive species
and between gram positive and gram
negative species.
Later stages between different gram
negative species . Eg: E.nucleatum,P.
gingivalis and T. denticola
Primary colonizers are taught to prepare a
favorable environment for secondary colonizers
They are gram +ve aerobic micro organisms
secondary colonizers do not initially colonize
on to the clean tooth surface but adhere to
bacteria already in the plaque mass
They are gram -ve anaerobic micro organisms
Secondary colonizers
 Gram negative species- Fusobacterium nucleatum,
Prevotella intermedia , Porphyromonas gingivalis,
Prevotella loeschii and capnocytophaga species.
 Adehere to the gram positive species already
present in the plaque..
Tertiary colonisers
After one week of plaque accumulation other gram
negative species may also appear
P gingivalis, C rectus., E corrodens A A Comitans and the
oral spirochaetes( Treponema species)
Spatiotemporal model of Oral bacterial colonization
Kolenbrander et al
Perio 2000 vol-42
 Socransky etal →13000 plaque samples
Used cluster analysis and community coordination
techniques to demonstrate the presence of specific
microbial groups.
DNA hybridisation methodology defined “ complexes” of
periodontal microorganisms
Yellow complexes -streptococcus species.
 Purple complex consisting of Veillonella parvula
and Actinomyces odontolyticus.
Green Complex: E corrodens, A.
actinomycetemcomitans serotype a, and
Capnocytophaga species.
Orange Complex : Fusobacterium , prevotela and
Campylobacter species.
Red Complex: P gingivalis, Tanerella forsythus
and T denticola.
They are aasociated with bleeding on probing.
Actinomyces
species
V.parvula
A.odontolyticus
SUBJECTS - 185
PLAQUE SAMPLES- 13,261
40 subgingival microorganisms
DNA-hybridization
Socransky et al - 1998
P.intermedia
P.nigrescens
P.micros
F.nucleatum
C.rectus
P.gingivalis
T.forsythia
T.denticola
BOP
Physiological properties of dental plaque
 Early colonisers use oxygen and reduce the redox
potential which then favours anaerobic species.
 gram +ve species use sugars as energy source and
saliva as carbon source.
 Mature plaque bacteria use aminoacids and small
peptides as energy source
Metabolic interactions among plaque bacteria
Lactate and formate→by products of
streptococci and actinomyecetes , used by
other microbes.
Growth of P gingivalis is enhanced by
succinate from Capnocytophaga and
protoheme by Campylobacter rectus.
Hemin from breakdown of hemoglobin is
important in the metabolism of P gingivalis.
Steroid hormones→proportions of P
intermedia in subgingival plaque.
Microorganisms generally exhibit two
distinct modes of behavior
 The first is the familiar free floating, or
planktonic form in which single cells float
or swim independently in some liquid
medium.
 The second is an attached state in which
cells are closely packed and firmly
attached to each other in the form of a
biofilm
Plaque as a biofilm
 Defn: Matrix enclosed bacterial populations
adherent to each other and/or to surfaces and
inter-surfaces
 Biofilm are organized structures composed of
microcolonies of bacterial cells nonrandomly
distributed in a shaped matrix or glycocalyx

Nutrients penetrate by molecular diffusion

Dental plaque →heterogenous structure fluid filled
channels running across the plaque.

Nutrients contact with sessile microcolonies by
diffusion from water channels to the microcolony.
Nature Of Biofilms
Cooperating community of various types of
microorganisms
Microorganisms are arranged in microcolonies
Microcolonies are surrounded by protective
matrix
Properties of biofilm
Structure
microcolonies of bacterial cells (15–20% by
volume), non-randomly distributed in a shaped
matrix or glycocalyx (75–80% volume)
presence of voids or water channels
Nutrients diffuse from the water channel to the
microcolony rather than from the matrix.
Microbial specificity of periodontal diseases
Nonspecific Plaque Hypothesis
Specific Plaque Hypothesis
Ecological plaque hypothesis
Nonspecific Plaque Hypothesis
Non specific and specific hypotheses
was proposed by Walter Loesche in 1976
Supported by epidemiologic studies that
correlated pts age & amount of plaque with
evidence of periodontitis (Russel 1967,
lovadal 1958)
 Periodontal disease results from the “ Elaboration of
noxious products by the entire plaque flora”.
According to this hypothesis, when only small
amounts of plaque are present, the 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
defenses.
 According to this concept the control of periodontal
disease depends on control of amount of plaque
accumulation.
Specific Plaque Hypothesis
States that only certain plaque is pathogenic,
and its pathogenicity depends on the presence
of or increase in specific microorganisms
Plaque harboring specific bacterial pathogens
results in periodontal disease
Recognition of A.a as pathogen in localized
aggressive periodontitis
Ecological shift hypothesis
“Pathogenic bacteria is directly coupled to the
changes in the environment.”
Disease can be prevented not only by
targeting the putative pathogens directly but
also by interfering with their environment
Factors affecting plaque formation
Saliva
Diet
Oral Hygiene Habits
Other local factors.
Saliva.
Non immune and immune ( secretary IgA)
components of saliva provide an initial protective
barrier against the invasion of foreign substances
and pathogens in the oral cavity.
 Several studies have shown that bacterial
attachment to the tooth surface is mediated by
salivary glycoprotein that coat the tooth surface as
part of the acquired enamel pellicle.
DIET
 Consistency and texture: fibrous foods may be
beneficial in periodontal health than soft, sticky
foods.
 Chewing fibrous food exerts a natural cleaning
action , particularly with respect to the removal of
the plaque from gingival half of the tooth.
Oral Hygiene Status
In the absence of oral hygiene measures ,
plaque continues to accumulate until a
balance is reached between the forces of
plaque removal and those of plaque
formation.
Other local factors
 Margins of restorations: Overhanging margins of
restorations changes the ecological balance of the
gingival sulcus to an area that favours the growth of
disease associated organisms
 Also inhibit the patients access to remove accumulated
plaque.
 Subgingival margins are associated with large amounts
of plaque accumulation , gingival inflammation and the
rate of gingival fluid flow.
 Margins placed at the level of the gingival margin induce
less severe inflammation.
 Supragingival margins →periodontal health.
Contours
Over contoured crowns and restorations→more plaque
accumulation.
ill fitting dentures
Quantitative and qualitative changes in plaque
Emergence of spirochaetal microrgnisms.
Malocclusion
Plaque control becomes more difficult.
Orthodontic Therapy
 Retain plaque and food debris
 Increases P. melaninigenica , P intermedia, Actinimyces
odontolyticus
 Direct injury to the gingiva as a result of overextented
bands
 Exessive force → bone loss →increased mobility of teeth
calculus
 Nidus for plaque formation
 Maintains and accentuates periodontal disease.
 Keeps plaque in close contact with the gingiva.
 Creates areas where plaque removal is impossible.
Growth dynamics of plaque
 First 2-8 hours→pioneering streptococci , cover 3-30% OF
ENAMEL SURFACE
 One day , it can be called biofilm.
 After 4 days 30% of the tooth crown is covered by plaque.
Variation within dentition
Early plaque formation occurs faster in
 The lower jaw compared to upper jaw.
 In molar areas
 On buccal tooth surfaces compared to oral site
 Interdental regions
Impact on gingival inflammation
 More rapid in tooth margins facing the inflamed gingival
margins than adjacent healthy gingiva.
Hence it is suggested that crevicular fluid enhances plaque
accumulation.
Impact on patient’s age
 Fransson etal detected no differences in amount or
composition between a group of young( 20-25 years ) and
older ( 65-68)
 plaque in older patients however resulted in more severe
gingival inflammation.
Microbial shift during disease
Gram + to Gram –
From cocci to rods to spirochetes
Nonmotile to motile
Facultative anaerobes to obligate anaerobes
Fermenting to proteolytic
Criteria for identification of periodontal
pathogen
Koch’s postulates
Must be routinely isolated from diseased
individuals
Must be grown in pure culture in lab
Must produce similar disease when inoculated
into susceptible lab animal
Must be recovered from lesions in a diseased
lab animal
In case of periodontitis, 3 specific problems
are
1. Inability to culture all organisms
2. Difficulties in defining active sites
3. Lack of good animal model system
Criteria for periodontal pathogen
1. Must be associated with disease
2. Decreased in sites that show clinical
resolution of disease after treatment
3. Must demonstrate a host response
4. Capable of causing disease in
experimental animal models
5. Must demonstrate virulence factors
Virulence factors of bacteria associated
with periodontal infection
Virulence factors
Mechanism of action
Fimbriae, pilli
Used as attachment ,
prevention of bacterial
phagocytosis
Protection from
complement & immune
system
Activation of cytokine,
↑bone resorption
capsule
Lps
Virulence factors
Mechanism of action
Peptidoglycan
Induction of
inflammatory mediators
Breakdown of host c/t,
Host tissue invasion
Proteolytic enzymescollagenase,
hyluronidase, hydrogen
sulfides
Microorganisms associated with specific
periodontal diseases
Periodontal health
Actinomyeces(Viscosus and naeslundi)
Streptococcus ( S.mitis and S sanguis
Veillonella parvula, small amounts of gram negative species.
Chronic gingivitis
Gram positive ( 56%) , Gram negative ( 44%)
Facultative -59% , Anaerobic-41%
Gram positive are Actinomyeces(Viscosus and naeslundi)
Streptococcus ( S.mitis and S sanguis)
Gram negative –F nucleatum, P intermedia , V Parvula ,
Hemophilus, Capnocytophaga, Campylobacter species
Chronic Periodontitis
Anaerobic- 90% and Gram negative – 75%
P gingivalis
P intermedia
C rectus
E corrodens
Viruses-EBV-1
F nucleatum
Human cytomegalo
 A A comitans
virus
P streptococcus micros
Treponema
Eubacterium species
Localised aggressive Periodontitis









AA comitans
P gingivalis
E corrodens
C rectus
F nucleatum
Bacteroides capillus
Eubacterium brachy
Capnocytophaga
Herpes virus
Generalised aggressive
periodontoitis
A A comitans
P gingivalis
P intermedia
Capnocytophaga
E corrodens
Neisseria
Key characteristics of Specific Periodontopathogens
Actinobacillus actinomyecetemcomitans
New name
Aggregatibacter actinomyecetemcomitans
 Small ,straight or curved rod with rounded end
 Nonmotile and gram negative,capnophilic
 Forms ; five serotypes( a to e ) , based on differences in
polysaccharide composition.
 Grows in white translucent ,smooth, nonhemolytic colony on
blood agar.
 Possess virulence factors like lipopolysaccharide,
leukotoxin,collagenase and protease.
Tannerella forsythia
 Nonmotile,spindle shaped, highly pleomorphic
rod,
 Gram negative obligate anaerobe
 Grows slowly only in anaerobic conditions and
needs several growth factors from other
species.
 Produce several proteolytic enzymes that are
able to destroy immunoglobulns and factors of
the complement system.
 Induces apoptotic cell death.
Porphyromonas gingivalis
 Nonmotile , pleomorphic rod, gram negative
obligate anaerobe
 Different forms are present based on their
genotype.
 Grows in anerobic medium with dark
pigmentation ( brown, dark green or black ) on
blood agar.
 Has strong proteolytic activity.
 Aggressive periodontal pathogen- fimbriae
mediate adhesion and capsule defend against
phagocytosis.
 Produces proteases , collagenases , hemolysins
 Potential to invade soft tissues.
Prevotella intermedia, Prevotella nigrescens
 Short rounded gram negative rods,
 Grow anaerobically with dark pigmentation.
Campylobacter rectus.




Rare motile organism
Gram negative, short rod, curved or helical
Motility→polar flagellum
Grows anaerobically with dark pigmentationwhen
sulphide is added. Gets transformed in to greyish FeS
 Produces leukotoxin
 Less virulent and less proteolytic
Fusobacterium nucleatum
 Gram negative, cigar shaped bacilli with pointed ends.
 Several subspecies are present
 Grows anaerobically in blood agar.
 Can trigger the release of cytokines.,elastase and oxygen
radicals from leukocytes
 Coaggregates with most of the oral microorganisms.
 Bridging organism between primary and secondary
colonisers.
Spatiotemporal model of Oral bacterial colonization
Kolenbrander et al
Perio 2000 vol-42
Peptostreptococcus micros
 Rare cocci in periodontitis
 Gram positive and grows obligate anaerobically.
Eubacterium species.
 Gram positive , obligate anaerobic , small pleomorphic
rod
 Several forms are classified including E nodatum, E
timidum, E brachy.
 Grow anaerobically but with difficulty in standard blood
agar.
Spirochaetes






Diverse group of spiral and motile organisms
Helical rods 5-15µm long , diameter 0.5µm
Have 3 to 8 irregular spirals
Cell wall is gram negative , but they stain poorly.
Forms: T denticola, T. Vincenti , T socranski, T pallidum
Able to travel through viscous enviroment like GCF and
penetrate epithelium and connective tissue
 Some have the capacity to degrade collagen and even
dentin
 T denticola produces proteolytic enzymes that can
destroy immunoglobulins( IgA, IgM, IgG) or complement
factors
Antiplaque agents
 Depending on efficacy and substantivity , they are
classified as.
First generation agents- reduce plaque score by
20- 50 percent, efficacy is limited because of poor
substantivity.eg- antibiotics, , quarterinary ammonium
compunds, sanguinarine. Should be used 4 to 6 times
daily.

Second generation agents- retained longer in
the tissues, slow release property provides overall
reduction in plaque score by 70 to 90 percent ( should be
used twice daily)eg- chlorhexidiene, triclosan with either
copolymer or zinc citrate.
Third generation agents: Should be
effective against specific periodontopathic
organisms. The most promising agent is
Delmopinol which is a surface active agent
.Weak antimicrobial agent , can exert its effect by
binding to salivary proteins and thereby alters
the cohesive and adhesive properties of the film
formed.
QUARTERNARY AMMONIUM COMPOUNDS
 Cetylpyridinium chloride (0.05%)
 Cationic and rapidly binds to oral tissues
 Rapidly released , hence not as effective as
chlorhexidiene.
 Rupture of cell wall and alteration of cytoplasmic
contents.
 Side effects are similar to that of chlorhexidiene.
SANGUINARINE
 Used as both mouth rinse and tooth paste.
 Alkaloid extract from blood root plant (Sangiunaria
Canadensis)
 Contain the extract at 0.03% and 0.2 % Zinc chloride
 Plaque reduction of 17-42 %, reduction in gingivitis is 1742%
 Burning sensation
BISGUANIDES:
 Chlorhexidiene gluconate→most widely used 0.12% or
0.2%
 Rupture of bacterial cell walls and precipitation of the
cytoplasmic content.
 Reduces plaque by 50-55% and gingivitis by 45%.
 Should be used twice daily.
 Brown staining of teeth, taste alteration, oral
desquamation, increase in calculus formation
ESSENTIAL OILS
 Listerine→Neutral in electric charge.
 Combination of phenol related essential oils , thymol
and eucalyptol , mixed with menthol and methyl
salicylate.
 Cell wall destruction, inhibition of bacterial enzymes
 Plaque reduction of 20 -34 % was noticed.
 Initial burning sensation
TRICLOSAN
 Available as mouthrinses and dentrifices.
 Bisphenol and nonionic germicide with low toxicity and
broad spectrum antibacterial activity.
 Widely used in soaps, antiperspirants and cosmetic
toiletries.
 Various formulations enhance their ability to bind to
plaque and teeth.
 Zinc citrate →antiplaque affect
Copolymer of methoxyethylene and maleic acid→increase
retention time.
Pyrophosphates →enhance anticalculus properties.
Conclusion
Bacterial plaque is regarded as one of the main
aetiological factors in the initiation and
promotion of periodontal disease ie gingivitis
and periodontitis . The knowledge of the fact has
been derived from epidmological studies as well
as clinical experiments . Several clinical studies
established the direct cause and effect
relationship between plaque and inflammation.
Thus it is of paramount importance to understand
the complex structure of plaque and its inter
relation and influence on the development of
oral diseases.