Plaque - Nitika

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12/27/2011 DENTAL PAQUE

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Dental PLAQUE

By Dr. Nitika JainPost Graduate Student


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Guide : Dr. Dipika Mitra (HOD and Prof.)

Co guided by: Dr. Ashok KP, Dr. Jyoti,

Dr. Sweta, Dr. Sameer

Presented by: Dr. Nitika Jain ( 1st yr. PGstudent)

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Introduction - distinct habitats of oralcavity

Plaque definition, types.

Structure and Composition of DentalPlaque

Plaque Formation At Ultra structural LevelFormation of dental pellicle

Initial adhesion and Attachment

Colonization

Supragingival & Subgingival PlaqueFormation: Clinical Aspects

Physiologic Properties of Dental Plaque33DENTAL PAQUE12/27/2011


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Microbial habitats withinthe mouth*

On the basis of physical & morphologiccriteria, oral cavity can be divided in to 5major ecosystems:

1. Intraoral, supragingival, hard surfaces(teeth, implants, restorations &prosthesis)

2. Periodontal/periimplant pocket (with itscrevicular fluid, root cementum orimplant surface, & the pocket epithelium)

3. Buccal epithelium, palatal epithelium &

epithelium of floor of mouth. 44DENTAL PAQUE12/27/2011


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Distribution of ResidentOral Micro flora

TeethNon shredding

surfacesStagnant sites;

food impactionpossibleInfluenced by GCF

& salivaStreptococcus,

Actinomyces,Veillonella,

Fusobacteria,Prevotella,

Treponema,unculturable

TongueHighly papillated surfaces

Some anaerobic sites.

Facultative & obligateanaerobes

Cheeks, Lips,Palate

Microflora has

low diversitySome

periodontalpathogenspersist byinvading

buccal cells.Streptococcus

spp.

predominate 55DENTAL PAQUE12/27/2011


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Gram PositiveCocci Rods

Abiotrophia Actinobaculum

Enterococcus Actinomyces

Gemella Alloscardovia

Preptostreptococcus Bifidobacterium

Streptococcus Cornybacterium

Finegoldia Eubacterium

Granulicatella Filifactor

Lactobacillus

Propionibacterium 77DENTAL PAQUE12/27/2011


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Gram Negative

Cocci Rods

Anaeroglobu Aggregatibacter

Mega sphaera Campylobacter

Moraxella CantonellaNeisseria Capnocytophaga

Veillonella Centipeda

Eikenella

Leptotrichia

Prevotella

Porphyromonas

Tanerella 88DENTAL PAQUE12/27/2011

B t i l C iti f


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Bacterial Composition ofDental Plaque From

Different Sites

Tooth

Approxima

lGram

positive &gram

negative;facultative& obligateanaerobes:1. Neisseria2. Streptoco

Gingival

creviceGram

positive &gram

negative &obligateanaerobes:

1. Streptococcus

2. Prevotella

FissureGram

positive;Facultativeanaerobes

1. Streptoco

ccus2. Actinomy

ces



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Dental plaque

Definitions


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Definations

Dental plaque is defined clinically as astructured, resilient, yellow-grayishsubstance that adheres tenaciously tointraoral hard surfaces, including

removable or fixed restorations.

Bowen WH: Nature of plaque, Oral science review1976

Dental plaque is a general term forcomplex microbial community thatdevelops on the tooth surface, embeddedin a matrix of polymers of bacterial &

salivary origin.



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Dental plaque can be defined as the softdeposits that form the biofilm adhering tothe tooth surface or other hard surfaces

in the oral cavity, including removableand fixed restorations.

Carranza 9thedition



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1880 1900 1930 1960 19902000

Sp pathogens identified formany diseasesSearch begins for oralpathogens in plaque

Non sp plaqueHypothesisDiseaseslinked to

constitutionaldefects

Sp plaquehypothesis

Treatment aimedatCausative agent

Biofilm

Golden age of

microbiology

Plaque

control

Biofilm

CHANGING VIEWS OF PLAQUE



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Classification of dental plaque Listgarten (1976) Classified Dental Plaque According

to its Location as



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Dental plaque must be differentiated fromother tooth deposits, like materia alba andcalculus.

Materia Alba refers to soft accumulations ofbacteria and tissue cells that lack theorganized structure of dental plaque.

Calculus is hard deposits that form bymineralization of dental plaque and isgenerally covered by a layer of un mineralised

plaque. 1616DENTAL PAQUE12/27/2011


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Material alba Calculus



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12/27/2011 DENTAL PAQUECarranza 11th edition 1818DENTAL PAQUE12/27/2011


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Plaque can be defined as a complex microbialcommunity, with greater than 1010 bacteriaper milligram.

Socransky SS et al The micro biota of gingival

crevice area of man JCP 25:134, 1998

In addition to the bacterial cells, plaquecontains a small number of epithelial cells,leukocytes, and macrophages. The cells arecontained within an extracellular matrix,which is formed from bacterial products and

saliva. 1919DENTAL PAQUE12/27/2011


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Dental plaque

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Composition organic and in - organic

CHEMICAL COMPOSITION OF DENTAL PLAQUE


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CHEMICAL COMPOSITION OF DENTAL PLAQUE

80% water

20% solids, includes cells mainly bacteria making up 35%of the dry weight and extracellular components making 65%of the dry weight.

Other than bacteria, non bacterial organisms include: Mycoplasma Yeast Protozoa Viruses

Host cells in Dental plaque.

Epithelial cells Macrophages Leukocytes



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INTERCELLULAR MATRIX OFDENTAL PLAQUE



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ORGANIC CONSTITUENTS

Poly saccharides - dextran 95% (adhesion), levan5%, Sialic acid and fructose

Proteins - Albumin

Glycoproteins - saliva

Lipid materials - Membrane remnants of bacteria and host cells.



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INORGANIC CONSTITUENTS

Primarily - Calcium &Phosphate

Traces - Sodium, Potassiumand Fluoride

Fluoride - From external

sources likeis derived tooth paste, mouth

washes



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Dental plaque

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Formation


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DEVELOPMENT OF DENTALPLAQUE



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Formation of the pellicle

Within nanoseconds after a vigorouslypolishing the teeth, a thin, saliva derivedlayer called the acquired pellicle, covers

the tooth surface.

Consists of more than 180 peptides,

proteins, glyco proteins, includingkeratins, mucins, proline rich proteins,and other molecules can function asadhesion sites( receptors) for bacteria.



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ULTRA STRUCTURE OF DENTAL PELLICLE

Thickness - 30 - 100 nm

2 hr pellicle: Granular structures which form

globules, that connect to the Hydroxyapatite surface

via stalk like structures. 24 hrs Later: Globular structures get covered up by

fibrillar particles : 500 - 900 nm thick

36 hrs Later: The pellicle becomes smooth,globular



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Studies shows ( 2 hours) enamel pellicle,its amino acids composition differs fromthat of saliva, indicating that the pellicle

forms by selective adsorption* of theenvironmental macromolecules.

Scannapieo FA et al , saliva and dental pelliclescontemporary periodontics, 1990

Mechanism involved are:

q Electrostatic forces *

q Van der waals * 2929DENTAL PAQUE12/27/2011


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CHEMICAL COMPOSITION OF ACQUIRED PELLICLE(Mayhell & Butller 1976, Sonju 1975)

4.6% amino acids 2.7% Hexosamine

14% Total carbohydrates Lipids - in small amounts

Amino acids in the pellicle Pellicle contains more hydrophobic and less neutralamino acids than whole saliva (ie more leucine,alamine, tyrosine and sereine than saliva)

Hexosamines in the pellicle Glucosamine - 18%, Galactosamine -18%

Carbohydrates in the pellicle Glucose - 20%, Galactose - 27%Mannose- 9% Fructose - 18%

Salivary Molecules in the pellicle Acinar cell familiesMucins

Proline rich proteins - statherins

Cystatins, Amylases

Ductal & stromal products

Lactoferrin & Lysozyme



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Initial Adhesion &Attachment of Bacteria

This concept approaches microbialadhesion to surfaces in aquaticenvironment as 4 stage sequence:



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Clean

substratum

Molecula

radsorption(Phase1)

Single

organisms(Phase2)

Multiplication(Phase 3)

Sequentia

ladsorptionof

organisms(Phase 4)3333DENTAL PAQUE12/27/2011


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Transport to the surface

Random contacts occur through:

q Brownian motion ( 40 m/hour)*

q Sedimentation of organisms*

q Liquid flow

q Active bacterial movement (chemotactic

activity)*



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Initial adhesion

Reversible adhesion of the bacterium andthe surface

The proteins and carbohydrates that are

exposed on the bacterial cell surfacebecome important once the bacterial arein loose contact with the acquired enamelpellicle.



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It results in initial, reversible adhesion ofbacteria, initiated by interactions

between bacterium & surface throughlong range & short range forces,including Van der Waals attractive forces& electrostatic repulsive forces.

Derjaguin, Landau, Verwey, & Overbeek(DLVO) theory have been postulated thatabove a separation distance of 1nm, the

summation of previous two forces 3636DENTAL PAQUE12/27/2011


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The result of (GTOT=GA+GE )summationis function of a separation distancebetween negatively charged particle & a

negatively charged surface in a mediumionic strength suspension medium.

GTOT for most bacteria consists ofsecondary minimum (reversible binding

takes place: 5-20 nm from the surface), apositive maximum (located at


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Particles in aqueous suspension canacquire charge due to preferentialadsorption of ions from solution of certain

groups attached to pellicle or surface.

The charge on surface is always exactlybalanced by an equivalent number of

counter ions; the size of this electricaldouble layer is inversely proportional toionic strength of environment.

As particle approaches surface, itexperiences a weak van der Waalsattraction induced by fluctuating dipoleswithin the molecules of the twoapproaching surfaces. This attractionincreases as articles moves closer to 3838DENTAL PAQUE12/27/2011


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attachment

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Adhesins


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Attachment

A firm anchorage between bacterium andsurface will be established by specificinteractions ( ionic, covalent, or hydrogen

bonding)



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Adhesins

Adhesins can be subdivided into twomajor classes:

Fimbrial adhesins, including fimbriae, pili, curli

and type IV pili,Nonfimbrial adhesins, such as autotransporter,

outer membrane and secreted adhesins,

Those associated with biofilm formation

Periodontology 2000, Vol. 52, 2010, 12374141DENTAL PAQUE12/27/2011

i b i l dh i


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Fimbrial adhesins

Fimbrial adhesins of gram-negativebacteria are classified into five majorclasses

Chaperoneusher (CU) pili,Curli,

Type IV pili,

Type III secretion pili and

Type IV secretion pili based on theirbiosyntheticpathway


C li


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Curli

Curli are thin aggregative fimbriaeidentified as a new type of fimbrialadhesin expressed on the outer surfacesof some Enterobacteriaceae, such asEscherichia and Salmonella spp.

Curli promote bacterial adhesion to andinvasion of the host, as well as biofilm

formation, and they also function as apotent promoter of host pro-inflammatoryresponses.


Ch h ili


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Chaperoneusher pili

Pili (from Latin for hairs) and fimbriae(from Latin for threads) are thin,filamentous, proteinaceous surfaceappendages (hair-like organelles) thatprotrude from the surface of manydifferent bacterial species and areespecially prominent on gram-negative

bacteria where they are anchored withinthe outer membrane.


T IV ili


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Type IV pili

Type IV pili are extruded across the outermembrane and form long and flexiblesurface appendages expressed by majorhuman pathogens, such as

Neisseria gonorrhoeae,

Neisseria meningitidis,

Pseudomonas aeruginosa,

Vibrio cholerae,

Salmonella enterica,

Legionella pneumophila and4545DENTAL PAQUE12/27/2011


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Fimbriae:

Are proteinaceous hair like appendages Composed of protein subunits called fimbrillin Fimbriae also carry adhesins

Fimbriae of oral strain are thin, flexible and 2-3nm indiameter, thus differing from larger more rigid filmbriae

found on other bacteria such as eschericia coli

Fibrils are also found oral bacterialspecies

e.g. S. mitis, Prevotellaintermedia,

Prevotella nigrescens and S.mutans.



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A naeslundi is one of the most imp colonizing specieson tooth surfaces.

Two major types of fimbriae are presentType 1:- Are associated with adhesion

of A.naeslundi to salivary acidic rich

protein andto statherin deposited within salivary

pellicle.

Type 2: Are associated with attachmentto of

A.naeslundi to glycosidic receptors an

epithelial cells PMNs and oralstreptocci

The lectinase like adhesion to these substrates isinhibited by galactose and N. acetyl galactosamine



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The best characterized fimbriae of the oralG-ve bacteria are those of P-gingivalis

3 types arepresent

vThey are upto 3 m long and 5nm wide, the major classof which is composed of fimbrillin

vThe fimbrillin polypeptide binds proline rich proteinsstatherin, lactoferrin, oral epithelial cells, oralstreptococci

vFimbrae of P.g exhibit chaemotactic properties anddemonstrate cytokine induction, both of which arenecessary for P.g to invade epithelial cells


Host Bacterial Interactions


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Host Bacterial InteractionsInvolved In Adhesion

Bacterium Adhesin Receptor

Streptococcusspp

Antigen 1/11 Salivaryagglutinin

Streptococcusspp

LTA Blood groupreactive proteins

Mutansstreptococci

Glucan bindingprotein

Glucan

Streptococcusparasanguinis

35 kDAlipoprotein

Fibrin, pellicle

Actinomycesnaelslundii

Type 1 fimbriae Proline-richproteins

Porphyromonas 150 kDA protein FibrinogenOral microbiology 4th edition, Philip Marsh4949DENTAL PAQUE12/27/2011


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Other factors that help in attachment ofbacteria

Force generating movement is an important firststep in biofilm formation by G-ve bacteria

Active motility due to the production offlagella ortwitching mobility due to type IV pili are thought to

increase the no of initial interactions between bacterialcells and solid surfaces and to help overcome initialrepulsive forces between bacteria and the surface.

Cell surface proteins of staphylococcus epidermidis

andCaulobacter crescentus are imp in initial attachment.

Polysaccharide adhesion of S. epidermidis



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colonization

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Primary and secondary colonizersCo aggregation

Test tube brush

C l i ti d l


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Colonization and plaquematuration

Co aggregation -

cell to cell recognition of genetically distinctpartner cell types



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Primary colonizers

They provide new binding sites foradhesion by other oral bacteria.

The metabolic activity of the primary

colonizers modifies the local microenvironment which influences the abilityof other bacteria to survive in the dentalplaque biofilm.



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Primary colonizers



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Secondary colonizers

They do not initially colonize the cleantooth surface but adhere to bacteria

already in the plaque mass.



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Secondary colonizers



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Primary colonization by

predominantly Gram-positive facultativebacteria.Ss: Streptococcus

sanguis is most dominant.Av :

Actinomyces spp. are alsofound in 24h plaque. Gram-positive facultative

cocci and rods co- 5757DENTAL PAQUE12/27/2011


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Surface receptors on

theGram-positivefacultative cocciand rods allow the

subsequent adherenceof Gram-negativeorganisms, which havea poor ability todirectly adhere to the

pellicle. 5858DENTAL PAQUE12/27/2011


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The heterogeneity increasas plaque ages and maturAs a result of ecologicchanges, more Gram-negative

strictly anaerobic bacteriacolonizesecondarily and contributeto anincreased pathogenicity ofthe 5959DENTAL PAQUE12/27/2011


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Co aggregation

It was described by Gibbsons & Nygaard

Corncob formation - Streptococci adheresto filaments of bacterionema matruchotti

or actinomyces speciesTest tube brush composed of

filamentous bacteria to which gramnegative rods adhere.


Significance of co aggregation has been highlighted (Kollenbrander


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g gg g g g (1989, 1995, 1993) in various in vitro & in vivo studies.

F.nucleatum is central to the mechanism - since this organism canco aggregate with numerous other species.

Examplesv F.nucleatum -v S.sanguisv P. loescheii

v A.viscousv Capnocytophagav P.gingivalisv B.forsythusv T.denticola


18 new genera from oral cavity show co aggregation


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18 new genera from oral cavity show co aggregation

-Cell to cell recognition of genetically distinct partner celltypes (Kolen brander PE et al 1993)

-Through the highly specific steriochemical interaction ofprotein and carbohydrate molecules located on the bacterialcell surface.

-Mediated by lectinlike adhesins and can be inhibited by

lactose and other galactosides-Coaggregation concept opens new perspectives, especiallyfor the use of probiotics



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C OS ASSOC A


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S.mitis

S.oralis

S.sanguis

Streptococcus

spsS.gorondi,S.intermedius

EAR

LYCO

LONIZ

ERS

V.parvulaA.odontolyticus

P.intermedia

P.nigrescensP.microsF.nucleatum

C.rectus

E.nodatum

C.showae

E.corrodensCapnocytophaga

spsA.actinomycetocomitans

P.gingivalis

T.forsythusT.denticola

CLOSELY ASSOCIATEDCOMPLEXES IN THE ORALCAVITY

LATE COLONIZERS



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Socransky SS, Haffajee et al, micro bielcomplexes in subgingival plaque JCP 14: 588, 1987


Physiologic properties of


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Physiologic properties ofdental plaque


Host as important source


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Host as important sourceof nutrients


Ecological plaque


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Ecological plaquehypothesis

In 1990, Marsh et al developed theecologic plaque hypothesis

According to this, both the total no. of

dental plaque and the specific microbialcomposition of plaque may contribute tothe transition from health to disease.

A change in the nutrient status of apocket or chemical and physical changesto the habitat are thus considered the

primary cause for overgrowth by 6868DENTAL PAQUE12/27/2011


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New treatment concepts :

Alter the local environment by reducing thecrevicular flow rate, or

The site made less anaerobic by the use ofredox agents

12/27/2011 DENTAL PAQUE 6969

De Novo Supragingival


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p g gPlaque Formation: Clinical

Aspects During 1st 24 hrs, starting from a cleantooth surface, plaque growth is negligiblefrom clinical view point.

Following 3 days, plaque growthincreases at a rapid rate, then slowsdown.

After 4 days, on average 30% of totaltooth crown area will be covered withplaque. Plaque does not seem to increasesubstantially after 4th day.

There will be a shift towards anaerobic &7070DENTAL PAQUE12/27/2011

Topography of


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Topography ofsupragingival plaque:

Initial plaque formation takes place alongthe gingival margin & from interdentalspace, later further extension in coronaldirection can be observed.

Plaque formation can also start fromgrooves, cracks, perikymata, or pits

Scanning electron microscopy revealsthat early colonization of enamel surfacestarts from surface irregularities, wherebacteria escape shear forces allowingtime needed to change from reversible to



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Surface microroughness:

Rough intraoral surfaces accumulate &retain more plaque & calculus in terms ofthickness, area & colony forming unit.

Smoothing intraoral surfaces decreasesrate of plaque formation.

There seems to be threshold for surfaceroughness {Ra 0.2 micrometers}, abovewhich bacterial adhesion is facilitated.



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Variation within dentition:

Early plaque formation occurs faster.

1. In lower jaw, compared to upper jaw.

2. In molars areas.

3. On buccal tooth surfaces, compared tooral sites.

4. In interdental regions compared to strict

buccal or oral surface.


Impact of gingival


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Impact of gingivalinflammation:

Plaque formation is more rapid on toothsurfaces facing inflamed gingivalmargins, than those facing healthygingivae. Studies suggest that increase increvicular fluid production enhancesplaque formation, it favors initialadhesion & colonization of bacteria.



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Impact of patient age:

Subjects age does not influence de novoplaque formation.

Plaque developed in older patients

resulted in more severe gingivalinflammation, which indicates anincreased susceptibility to gingivitis withaging.


De Novo Subgingival


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De Novo SubgingivalPlaque Formation

Early studies, using culturing techniquesexamined changes in subgingivalmicrobiota during 1st week aftermechanical debridement, partialreduction followed by fast regrowth toalmost pre treatment levels within 7days.

This reveals that a high proportion oftreated tooth surfaces still harboredplaque & calculus after scaling, theseremaining bacteria were considered

primary source for subgingival 7676DENTAL PAQUE12/27/2011


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Oral implants have been used as modelto study impact of surface roughness onsubgingival plaque formation.

Bollen CM, et al The influence of abutment surface roughness on

plaque accumulation and peri impalnt mucositis clin oral implantsres 7: 201;1996

Smooth abutments were found to harbor25 times less bacteria than rough ones,

with a slightly higher density for coccoidcells.

Subgingival microflora was largelydependent on remaining presence of


A i & Mi fl


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Ageing & Microflora

Following tooth eruption the isolationfrequency of spirochetes & blackpigmented anaerobes increases.

Increased prevalence of spirochetes &black pigmented anaerobes is found inteenagers, this is due to hormonesentering gingival crevice & acting as a

novel nutrient source. Rise in P. intermedia in plaque during 2nd

trimester of pregnancy has been ascribeddue to elevated levels of oestradiol &



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Oralmicroflora

Directeffects Indirecteffects

Cell mediated

immunity wanesChanges in salivaryantibodiesHormonal changesAltered physiology oforal mucosa

Denture

wearingMedicationCancertherapyDietary

changes


Effects on oral microflora

Pl A Bi Fil


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Plaque As a BioFilm

The term biofilm describes the relativelyundefinable microbial communityassociated with a tooth surface or anyother hard, non-shedding material(Wilderer & Charaklis 1989)

Biofilms have an organized structure.

They are composed of micro colonies of

bacterial cells non randomly distributedin a shaped matrix or glycocalyx.

In lower plaques layers microbes are

bound together in polysaccharide matrix8080DENTAL PAQUE12/27/2011

Where can we find


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them?

P ti f Bi fil


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Properties of Biofilm

Survival of the bacterial communityas a whole

Metabolic cooperativity

Have a primitive circulatory system

Numerous microenvironments

Resistant to host defenses

B t i i bi fil


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Bacteria in bio - films

Resistant of bacteria to antimicrobialagents is increased in the biofilm.

Almost 1000 to 1500times more resistant

to antibiotics than in their planktonicstage

Why increased resistance?????

Nutrional status Growth rate

Temperature

pH 8383DENTAL PAQUE12/27/2011

Bi fil


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Bio film

Certain properties that resists diffusionlike; strongly charged or chemicallyhighly reactive agents fail to reach thedeeper part of bio film because biofilm

acts as an ion- exchange resin, removingsuch molecules from solution.

Recently super resistant bacteria were

identified; the cells have multidrugresistant pumps that can extrudeantimicrobial agents from the cell.



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Good morning


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Important Features ofBiofilm

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Communications in


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Biofilm Genetic expression is different in

biofilm bacteria when comparedto planktonic (free floating)bacteria.

Biofilm cells can coordinatebehavior

via intercellular "communicationusing biochemical signalingmolecules.

Q or m sensing


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Quorum sensing

Involves the regulation ofexpression of specific genesthrough the accumulation ofsignaling compounds that

mediate intercellularcommunication

Dependent on cell density and

mediated through signalingcompounds

Quorum sensing gives biofilmstheir distinct properties


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Quorum sensing is involved in theregulation of

genetic competencematingbacteriocin production

sporulationstress responsesvirulence expressionbiofilm formationbioluminescence


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Competence is a physiological state inwhich bacteria develop a capacity totake up exogenous DNA (Dubnau, 1991)

It is an elaborate process involvingmultiple protein components andsophisticated regulatory networks

It is important to ensure that a DNA poolis available when the cells becomecompetent.


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In S.mutans ,quorum sensing ismediated by a competencestimulating peptide (CSP)

This peptide also induces geneticcompetence so that thetransformation frequency of

biofilm grown S.mutans was 10to 600 fold greater than forplanktonic cells

Transmission,


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,Translocation OR Cross

Infection Intraoral transmission of bacteria from

one niche to another is called

translocation orcross infection. Christersson et al. demonstrated

translocation of A.a by periodontal probesin patients with localized aggressiveperiodontitis.


Translocation &


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Mechanical DebridementTo reduce the chance of intraoral

translocation one stage mouthdisinfectionwas introduced by Leuvengroup in 1990

This strategy attempts to eradicate, or atleast suppress periodontal pathogens in ashort time not only from periodontal

pocket, but also from their habitats. Several studies illustrate benefits of one

stage full mouth disinfection approach inrelation to:


Microbial Specificity of


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p yPeriodontal Diseases


Non Specific Plaque


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p qHypothesis

The nonspecific and specific plaquehypotheses were delineated in 1976 byWalter Loesche

The nonspecific plaque hypothesismaintains that periodontal diseaseresults 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 the9595DENTAL PAQUE12/27/2011

Specific Plaque Hypothesis


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The specific plaque hypothesis statesthat only certain plaque is pathogenic,and its pathogenicity depends on thepresence of or increase in specific

microorganisms.

This concept predicts that plaqueharboring specific bacterial pathogens

results in periodontal disease becausethese organisms produce substances thatmediate the destruction of host tissues.


Socransky's criteria for


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yperiodontal pathogens

ASSOCIATION: A pathogen should befound more frequently and in highernumbers in disease states than inhealthy states

ELIMINATION: Elimination of thepathogen should be accompanied byelimination or remission of thedisease.



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HOST RESPONSE: There should beevidence of a host response to a specificpathogen which is causing tissue

damage. VIRULENCE FACTORS: Properties of a

putative pathogen that may function todamage the host tissues should be

demonstrated. ANIMAL STUDIES: The ability of a

putative pathogen to function inproducing disease should bedemonstrated in an animal models stem. 9898DENTAL PAQUE12/27/2011


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The two periodontal pathogens that havemost thoroughly fulfilled Socransky'scriteria are Actinobacillusactinomycetemcomitans in the form of

periodontal disease known as LocalizedJuvenile periodontitis (LJP), andPorphyromonas gingivalis in the form ofperiodontal disease known as adultperiodontitis.


Evidence implicating as a periodontalpathogen(Adapted from Socransky,


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pa oge ( dap ed o Soc a s y,1992)

CRITERION OBSERVATIONS

Association Elevated in lesions of JuvenilePeriodontitis, and some lesions of AdultPeriodontitis

Elevated in "active" Localized Juvenile Periodontitis

(LJP) lesions Detected in apical region of periodontal pocket or in

tissues of LJP lesions

Unusual in health or gingivitis

Elimination Elimination associated with clinicalresolution of disease

Species found in recurrent lesions

Host Response Elevated systemic and local

antibody levels in Juvenile Periodontitis 100DENTAL PAQUE12/27/2011

Evidence implicating P. gingivalis as aperiodontal pathogen (Adapted from

Socransky 1992)


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Socransky, 1992)

CRITERION OBSERVATIONS

Association Microorganism is elevated inperiodontitis lesions Unusual in health orgingivitis

Elimination Suppression or elimination results inclinical resolution

Species found in recurrent lesions

Host Response Elevated systemic and local

antibody in periodontitis Virulence Factors Collagenase, trypsin-like

enzyme, fibrinolysin, immunoglobulin degradingenzymes, other proteases, phospholipase A,phosphatases, endotoxin, hydrogen sulfate,

ammonia, fatty acids and other factors thatcom romise PMN unction 101DENTAL PAQUE12/27/2011

WITHSPECIFIC PERIODONTAL


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SPECIFIC PERIODONTALDISEASESPERIODONTAL HEALTH

102 to 103 bacteria.

Certain bacterial species have been proposed to be beneficial to thehost, including S. sanguis, Veilonella parvula, and C.ochraceus(Carranza 10th)

Bacteria associated with periodontal diseases are often found in thesubgingival microflora at healthy sites, although they are normally

present in small proportions(Rose & Maeley, 6th)

Nonmotile nature.


GINGIVITIS


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104 to 106 bacteria.

Gram-negative bacteria. Compared with healthy sites, noticeable increase also occur in the

numbers of motile bacteria, including cultivable and uncultivabletreponemas (spirochetes).

Pregnancy associated gingivitis is accompanied by dramaticincreases in levels of P. intermedia, which uses the steroid asgrowth factors(Carranza,10th )


CHRONIC PERIODONTITIS


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C. rectus, P. gingivalis, P. intermedia, F. nucleatum and T. forsythia

were found to be elevated in the active sites(Carranza,10th ) Sites with chronic periodontitis will be populated with greater

proportions of gram-negative organisms and motile bacteria.

Certain gram-negative bacteria with pronounced virulence properties

have been strongly implicated as etiologic agents e.g. P. gingivalisand Tannerella forsythus.


LOCALIZED AGGRESSIVEPERIODONTITIS


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PERIODONTITIS Gram -ve, and anaerobic rods.

The most numerous isolates are several species from thegenera Eubacterium, A. naeslundii, F. nucleatum, C. rectus,and Veillonella parvula.

In some populations, a strong case can be made for Aa

playing a causative role in LAP, especially in cases in whichpatients harbor highly leukotoxic strains of the organism.

However, some populations of patients with LAP do notharbor Aa, and in still others P. gingivalis may be etiologically

more important.


GENERALIZED AGGRESSIVE


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PERIODONTITIS The sub-gingival flora in patients with generalized aggressive peri-odontitis resembles that in other forms of periodontitis.

The predominant subgingival bacteria in patients with generalizedaggressive periodontitis are P. gingivalis, T. forsythis A.actinomycetemcomitans, and Campylobacter species.


REFRACTORY CHRONIC


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PERIODONTITIS Unusually diverse and may contain enteric rods,

staphylococci, and Candida.

Persistently high levels are found of one or more of P.gingivalis, T. forsythis, S. inter-medius, P. intermedia,

Peptostreptococcus micros, and Eikenella corrodens. Persistence of Streptococcus constellatus has also been

reported.


NECROTIZING ULCERATIVE


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GINGIVITIS/PERIODONTITIS

More than 50% of the isolated species were strictanaerobes with P. gingivalis and F. nucleatumaccounting for 7-8% and 3.4%, respectively.


PERIODONTAL ABSCESSES


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The bacteria isolated from abscesses are similarto those associated with chronic and aggressiveforms of periodontitis.

An average of approximately 70% of the

cultivable flora in exudates from periodontalabscesses are gram-negative and about 50% areanaerobic rods.

Periodontal abscesses revealed a high prevalence

of the following putative pathogens: F. nucleatum(70.8%), P. micros (70.6%), P. intermedia (62.5%),P. gingivalis (50.0%), and T. forsythis (47.1%).

Enteric bacteria, coagulase-negative

staphylococci, and Candida albicans have also109DENTAL PAQUE12/27/2011

PERIIMPLANTITIS


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High proportion of anaerobic gram negativerods, motile organisms, and spirochetes).

Species such as Aa, Pg, Tf, P. micros, C. rectus,Fusobacterium, and Capnocytophaga are oftenisolated from failing sites.

Other species such as Pseudomonas aeruginosa,enterobacteriaceae, Candida albicans andstaphylococci, are also frequently detectedaround implants.


PEPTOSTREPTOCOCCUSMICROS


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MICROS P. micros is a Gram positive, anaerobic, small, asaccharolytic

coccus.

Two genotypes can be distinguished with the smoothgenotype being more frequently associated with periodontitislesions than the rough genotype (Kremer et al. 2000).

P. micros was found to be in higher numbers at sites ofperiodontal destruction as compared with healthy sites(Papapanou et al 2000, Riggio et al 2001).

It was shown that P. micros in combination with either P.intermedia or P. nigrescens could produce transmissible

abscesses (Van Dalen et al 1998).

Produce protease(Grenier 2006)


SALMONELLAS SPECIES


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The salmonellas spp. are Gram negative, curved, saccharolyticrods and may be recognized by their curved shape, tumblingmotility and, in good preparations, by the presence of a tuft offlagella inserted in the concave side.

Moore et al (1987) described six genetically andphenotypically distinct groups isolated from oral cavity andfound S. noxia at a higher proportion of shallow sites(PD>4mm) in chronic periodontitis.


EUBACTERIUM SPECIES


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Suggested as possible periodontal pathogens due totheir increased levels in disease sites. (Moore et al1985).

E. nodatum, Eubacterium brachy and Eubacteriumtimidum are Gram positive, strictly anaerobic, small

somewhat pleomorphic rods. Some of these species elicited elevated antibody

responses in subjects with destructive periodontitis.(Martin et al 1988)


MILLERI STREPTOCOCCI


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Some of the streptococcal species are

associated with and may contribute todisease progression.

Milleri streptococci, Streptococcusanginosus, S. constellatus and S. intermidius

might contribute to disease progression insubsets of periodontal patients.

These species was found to be elevated atsites which demonstrated recent disease

progression (Dzink et al 1988).


OTHER SPECIES


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Emphasis have been placed on enteric organisms, staphylococcalspecies as well as other unusual mouth inhabitants.

Slots et al (1990)


VIRUSES


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Contreras & Slots 2000, Kamma et al 2001



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Viral diseases of the oral mucosa and theperioral region are often encountered indental practice. Viruses are importantulcerogenic and tumorigenic agents of

the human mouth.



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Four major viral families are associatedwith the main viral oral diseases ofadults, as follows:

1. The group of herpesviruses containseight different members that all areenveloped double-stranded DNA viruses.

In the oral cavity, they are related todifferent ulcers, tumors, and other oralpathoses.



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3. Picornaviruses are all nonenveloped,single-stranded RNA viruses. In the oralcavity, they are related to ulcers anddifferent oral pathoses

4. Retroviruses are divided into sevengenera of which two are humanpathogens. All retroviruses are enveloped

single-stranded RNA viruses. In the oralcavity, they are related to differenttumors and oral pathoses.



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Herpesviruses are capable of infecting various types of cells,

including polymorphonuclear leukocytes, macrophages, andlymphocytes.

The diffuse invasion of Candida fungi and other opportunisticorganisms into the gingival tissue of AIDS patients has beendemonstrated to be a typical virus-mediated alteration of hostdefense mechanisms.

Shobha Prakash, Sushma Das (2006) concluded that HSV-1 and

EBV are significantly associated with destructive periodontaldisease including chronic and aggressive periodontitis. HSV-1detected sites in relation to pocket depth and clinical attachmentlevel were found to be significant indicating that it is associatedwith severity and progression of destructive periodontal disease.



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FUNGI


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Hannula J, Dogan B, Slots (2001) showed

geographical differences in the subgingivaldistribution ofC. albicans serotypes andgenotypes and suggested geographicclustering ofC. albicans clones in

Subgingival samples of ChronicPeriodontitis patients.

Reynaud AH (2001) found a weakcorrelation between yeasts in periodontal

pockets.


MIXED INFECTIONS


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At the pathogenic end of the spectrum, it is

conceivable that different relationships exist betweenpathogens.

The presence of two pathogens at a site could haveno effect or diminish the potential pathogenicity of

one or other of the species.

Alternatively, pathogenicity could be enhanced eitherin an additive or synergistic fashion.

It is not clear whether the combinations suggested inthe experimental abscess studies are pertinent tohuman periodontal diseases


ARCHAEA


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Single celled organism that are distinctfrom the bacteria.

Methanogenic archaea produce methane

gas from hydrogen gas, carbon dioxide Isolated from patients with periodontal

disease by enriching cultures with H2 andCO2.


References


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1.Dental Plaque: biological significance of a biofilmand community life styleP.D.Marsh JCP- 2005

2.Oral biofilms and Calculus text book of Clinicalperiodontology

and Implant dentistry -Jan Lindhe, Lang and Karring 5th Edition

3.Periodontal microbial Ecology Socransky andHaffajee

Periodontology 2000 Volume 38 2005

4.Microbiology of Periodontal diseases: Genetics,Polymicrobialcommunities, selected pathogens and treatment. Haffajee and socransky - Peridontology 2000, Volume 42,


References


126/128


5.Communication among Oral Bacteria Paul E. Kolenbrander,* Roxanna N. Andersen, David S.Blehert,G. Egland,Jamie S. Foster, and Robert J. Palmer Jr.

MICROBIOLOGY AND MOLECULAR BIOLOGY REVIEWS, Sept. 2002

6.Interspecies Interactions within Oral MicrobialCommunities Howard K. Kuramitsu,1 Xuesong He,2 Renate Lux,2Maxwell H.

Anderson,3 and Wenyuan Shi2* MICROBIOLOGY AND MOLECULAR BIOLOGY REVIEWS, Dec. 2007

7.Microbial etiology of periodontitisTatsuji Nishihara & Takeyoshi KosekiPeriodontology 2000 Vol-36


References


127/128


8.Periodontal disease at the Biofilm-Gingivalinterface

Offenbacher et al J.P Oct 2007

9.Impact of 16S rRNA Gene Sequence Analysis forIdentification of

Bacteria on Clinical Microbiology and InfectiousDiseases

Jill E. Clarridge III*` CLINICAL MICROBIOLOGY REVIEWS, Oct. 2004

10.Interspecies interactions within Oral MicrobialCommunities

Howard K.Kuramitsu, Xeusong He, Renate Lux, Maxwell H.Andersonand Wenyuan Shi

Microbiology and Molecular Biology Reviews, Dec.

2007 127DENTAL PAQUE12/27/2011

References


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