plaque - nitika
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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
12/27/2011 DENTAL PAQUE 2020
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
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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
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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.
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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.
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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
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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
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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
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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
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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.
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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
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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
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Physiologic properties of
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Physiologic properties ofdental plaque
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Host as important source
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Host as important sourceof nutrients
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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
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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.
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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.
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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
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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
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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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Click to edit Master subtitle style
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.
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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:
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Microbial Specificity of
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p yPeriodontal Diseases
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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.
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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.
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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.
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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 )
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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.
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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.
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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.
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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.
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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.
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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.
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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)
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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.
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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)
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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).
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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)
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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.
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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
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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.
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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,
125DENTAL PAQUE12/27/2011
References
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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
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References
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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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