DENTAL PLAQUE
GUIDED BY:DR. RUPINDER KAURDR. DIVYA JAGGI
PRESENTED BY:
DR.MALVIKA THAKUR
PG II YEAR
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CONTENTS
1. Introduction2. Classification of soft deposits3. Definitions of dental plaque4. History of dental plaque5. Classification of dental
plaque6. Composition & Structure of
dental plaque7. Formation of dental plaque
8. Dental plaque as a biofilm
9. Physiological properties
10. Microbial specificity of
periodontal disease
11. Detection of dental plaque
12. Conclusion
13. References
PART - I PART - II
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INTRODUCTIONHuman fetus is sterile.Colonization starts at birth.Within hours – facultative & aerobic bacteria.2nd day – anaerobic bacteria.Within 2 weeks – mature microbiota estd in gut.After weaning - 1014 microorganisms with 400 different type
of bacteria.There are 10 times more bacteria than human cells.
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Establishing microbiota - harmony with the host. Constant renewal - prevents the accumulation of
microorganisms.Teeth provide hard, non-shedding surfaces - accumulation &
metabolism of bacteria on hard oral surfaces is considered the primary cause of dental caries, gingivitis, periodontitis and peri-implant infections.
In the oral cavity, the bacterial deposits have been termed dental plaque or bacterial plaque.
In 1 mm3 of dental plaque weighing approximately 1mg, approx 1011 bacteria are present. [Socransky et al ,1953]
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Classification of soft deposits
MATERIAL ALBA
FOOD DEBRIS
A non-cellular thin film
An organized transparent deposit which is primarily composed of bacteria and their
products
Soft, whitish deposit with no specific architecture, which can be removed by
water spray.
Retained food which is usually removed by saliva and oral muscular action.
Schwartz et al 1969
ACQUIRED PELLICLE
DENTAL PLAQUE
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Bowen W.H. (1976) defined dental plaque clinically as a structured, resilient,yellow-grayish substance that adheres tenaciously to the intraoral hard surfaces, including removable and fixed restorations.
According to Schwartz & Massler (1969) – Plaque is a dense microbial Layer consisting of coherent mass of filamentous, rod like and coccoidalmicroorganisms embedded in an inter microbial matrix which accumulates on tooth surface.
Davies et al (1963) defined plaque as a soft concentrated mass containing mainly of large variety of bacteria together with certain amount of cellular debris which develops within a short time after tooth brushing.
DEFINITIONS
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According to WHO (1978) Plaque is a specific but highly variable structural entity resulting from colonization and growth of microorganisms on surfaces of teeth and consisting of numerous microbial species and stains embedded in a extracellular matrix.
According to the GPT, 4th Edition An organized mass, consisting mainly of microorganisms, that adheres to teeth, prostheses, and oral surfaces and is found in the gingival crevice and periodontal pockets. Other components include an organic, polysaccharide-protein matrix consisting of bacterial by-products such as enzymes, food debris, desquamated cells, and inorganic components such as calcium and phosphate
According to Carranza, 11th Edition Dental plaque is defined clinically as a structured, resilient yellow-grayish substance that adheres tenaciously to the intraoral hard surfaces, including removable and fixed restorations.
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HISTORY J Leon Williams (1897) – Described dental plaque
GV Black (1899) – Coined term “gelatinous dental plaque”
W D Miller (1902) - Bacterial plaque
Wild (1941) - Shortened Black’s terminology to the term ‘Plaque’
Waerhaug (1950) Described the importance of bacterial plaque in the etiology of periodontal disease
Loe et al (1965), Landmark study on plaque , saying that plaque is main etiological agent in periodontal disease.
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Schei (1959), Russel (1967) - Epidemiological studies- Positive correlation between the amount of bacterial plaque and the
severity of gingivitis
W.Loesche (1976) - Modern theories of specificity – “Specific plaque hypothesis”
Socransky 1979 - Modern Version of Specific Plaque Hypothesis
Thelaide 1986 - Unified Theory
PD Marsh & Martin (1999) - Ecological plaque hypothesis
Costerton (1999) - Evolved Biofilm
Hajishengallis et al 2012 - Keystone Pathogenic Hpothesis
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I. GRANTS CLASSIFICATION- ACCORDING TO LOCATION
A. Coronal plaque- Coronal to the gingival margin
B. Gingival plaque- forms on the external surface of the oral
epithelium and attached gingiva
C. Sub gingival plaque- located between the periodontal
attachment and the gingival margin, within the sulcus or
pocket.
D. Fissure plaque- develops in pits and fissures
E. Peri-implant plaque.
CLASSIFICATION
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II. GLICKMAN’S CLASSIFICATION- ACCORDING TO LOCATION
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SUPRAGINGIVAL PLAQUE SUBGINGIVAL PLAQUE
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TOOTH ATTACHED
UNATTACHED TISSUE ATTACHED
Gram +ve,Few Gram –ve rods and cocci,
Gram negative rods, filaments,
spirochetes
Gram negative rods, filaments,
spirochetes
Does not extend to JE
Extend to JE Extend to JE
Calculus formation, root
caries
Gingivitis Gingivitis, periodontitis
May penetrate cementum
- May penetrate epithelium and
connective tissue
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Pavel Godoroja and Olga Dulghieru 2004 The dental plaque is differentiated into two categories by
Supra‑gingival plaque
Gingival third of the crown of the tooth
Inter‑proximal areas
Pits and fissures and also on other such surface with
irregularities.
Sub‑gingival plaque
Tooth adherent zone
Epithelial adherent zone
Non adherent zone
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Composition of dental plaque
Micro-organisms
70%
•Bacterial•Non-bacterial
Intercellular Matrix20%-30%
•Organic material•Inorganic materials
MICROORGANISM
INTERCELLULAR MATRIX
PLAQUE
SOLIDS 20-30%
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BACTERIAL PORTION 70 to 80 % of total solid plaque volume. 1 gm of plaque contains approximately 2 X 1011 bacteria. (Socransky SS,1953), (Schroeder, De Boever-1970)
Bacteria Facultative Anaerobic
Gram +ve Strep.mutansStrep.sanguisA.viscosus
Gram -ve A.actinomycetemcomitansCapnocytophypa sp.Ekinella corrodens
P.GingivalisF.nucleatumP.intermediaB.forsythusC.rectus
Spirochetes T.denticola
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VIRUSESYEAST
PROTOZOA MYCOPLASMA
NON BACTERIAL
NON BACTERIAL PORTION
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ORGANIC CONTENT
CARBOHYDRATES30%
PROTEINS30%
LIPIDS15%
INTERCELLULAR MATRIX
Accounts for 20% to 30% of the plaque mass Organic and inorganic material.. Derived from – Saliva , Gingival crevicular fluid and Bacterial products.
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CALCIUM
PHOSPHO
RUS
OTHER MINERALS
INORGANIC CONTENT
SODIUMPOTASSIUMFLOURIDE
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MICROSCOPIC STRUCTURESUPRAGINGIVAL PLAQUE Typically demonstrates a stratified organization of the bacterial
morphotypes. Gram-positive cocci and short rods predominate at the tooth
surface Gram-negative rods and filaments ,spirochetes predominate in
the outer surface of the mature plaque mass. Supra gingival plaque can have a structured architecture
polymer containing channel or pores have been observed that link the plaque/oral environment interface to the tooth surface ( Wood et al 2000,Auschillet al 2001,Zaura Arite et al 2001)
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Thin section of supragingival plaque
GRAM POSITIVE BACTERIA IN
PALISADING ARRANGEMENT
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SUBGINGIVAL PLAQUEBetween sub gingival plaque and the tooth an electron dense
organic material is interposed , termed as cuticle.Gingival crevicular fluid, -contains many substances that the
bacteria may use as nutrients Host inflammatory cells and mediators have influence on the
establishment and growth of bacteria in this region.
DENTA PLAQUE UNDER X 400 MAGNIFICATION
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Thin section of plaque in a deep pocket
FILAMENTS
RODS
COCCI
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DEVELOPMENT OF DENTAL PLAQUE
The formation of the pellicle on the tooth
surface
Initial adhesion and attachment of
bacteria
Colonization and plaque maturation
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I. Formation of the pellicleVigorous tooth brushing – nanoseconds – acquired pellicle .Acquired pellicle - a homogenous, membranous, acellular film that
covers the tooth surface and frequently form the interface between the tooth ,the dental plaque and calculus. (Schluger)
`A fully established pellicle - 30 min, within 24 hr- 0.8 µm in diameter.
Derived from components of saliva and crevicular fluid as well as bacterial and host tissue cell products and food debris.
12/27/2011Transmission electron micrograph (TEM) of the acquired pellicle on an enamel surface
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ULTRA STRUCTURE OF DENTAL PELLICLE Salivary pellicle can be detected on clean enamel surfaces
within 1 minute. By 2 hours, the pellicle is essentially in equilibrium. 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
(Panacea for Periodontology: Basic Tissue, Etiology and PathogenesisBy Dr. Priyam Mishra)
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Studies shows ( 2 hours) enamel pellicle, its amino acids composition differs from that of saliva, indicating that the pellicle forms by selective adsorption of the environmental macromolecules. (Scannapieo FA et al , “ saliva and dental pellicles’” contemporary periodontics, 1990)
Mechanism involved are: Electrostatic forces Van der waals Hydrophobic forces
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CHEMICAL COMPOSITION OF ACQUIRED PELLICLE (Mayhell & Butller 1976, Sonju 1975)
Amino acids - 4.6%
Pellicle contains more hydrophobic and less neutral amino acids than whole saliva (ie more leucine, alamine, tyrosine and sereine than saliva)
Hexosamines - 2.7%
Glucosamine - 18%, Galactosamine -18%
Carbohydrates - 14%
Glucose - 20%, Galactose - 27%Mannose - 9% Fructose - 18%
Salivary Molecules Mucins
Proline rich proteins - statherinsCystatins, AmylasesDuctal & stromal productsLactoferrin & Lysozyme
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SIGNIFICANCE OF PELLICLEPROTECTIVE provide barrier against acids thus may reduce dental caries attack.
LUBRICATIONkeep surface moist prevent drying.
NIDUS FOR BACTERIA: Plaque formation by adherence of microorganisms.
ATTACHEMENT OF CALCULUS: A mode of calculus attachment.
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II. Initial Adhesion and Attachment of Bacteria
TRANSPORT TO SURFACE
INITIAL ADHESION
ATTACHMENT
COLONIZATION OF SURFACE & BIOFILM FORMATION
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PHASE I. Transport to the surface
RANDOM CONTACTS
OCCUR THROUGH
:
Brownian motion ( 40 µm/hour)
Sedimentation of organisms
Liquid flow
Active bacterial
movement (chemotactic
activity)
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PHASE II. INITIAL ADHESION
Transport to surface
Initial adhesion
Attachment
Colonization of the surface and biofilm formation
Reversible adhesion of the bacterium and the surface.
Physical phase
Initiated by interactions b/w bacterium and surface through long range and short range forces, including Van der Waals attractive forces Electrostatic repulsive forces
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DLVO theory
Derjaguin, Landau, Verwey & Overbeek (DLVO) have postulated that above a separation distance of 1nm, the summation of previous two forces describes total range interaction also called as Total Gibbs Energy (GTOT).
The result of summation (GTOT= GA+GE) is function of a separation distance between negatively charged particle and a negatively charged surface in a medium ionic strength suspension medium.
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Three stages
1. Secondary minimum (reversible attraction)2. Positive maximum (energy barrier)3. Primary minimum (irreversible attraction)
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PHASE III. AttachmentA firm anchorage between bacterium and surface will be
established by specific interactions ( ionic, covalent, or hydrogen bonding)
This follows direct contact or bridging true extra cellular filamentous appendages (with length up to 10nm).
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On a rough surface, bacteria are better protected against shear forces so that a change from reversible to irreversible bonding occurs more easily and more frequently.
The bonding between bacteria and pellicle is mediated by specific extracellular proteinaceous components (adhesions) of the organism and complementary receptors (proteins, glycoproteins, polysaccharides) on the surface (pellicle) and is species specific.
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Streptococci (mainly S. sanguis) – Primary colonizer - binds to acidic proline-rich-proteins
α-amylase sialic acid.Actinomyces - Primary colonizers, eg A. viscosus possesses
fimbrae - adhesins - specifically bind to proline-rich proteins of dental pellicle.
A. viscosus - reognises cryptic segments [cryptiotopes] of proline rich proteins, which are only available in adsorbed molecules. ( with lock &key mech.)
( Mergenhagen et al 1987)
Receptors in pellicle
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Selected Bacterial Adhesins & Target SubstratesATTACHMENT SURFACE
SUBSTRATE BACTERIAL SPECIES
ADHESIN SUBSTRATE RECEPTOR
Tooth Saliva coated surfaces
A.ViscsusS.MitisF.Nucleatum
FimbriaeProline rich proteins.Saliva treated hydroxyapatite
Tissue Epithelial cells
FibroblastsPMN`S
Connective tissue
P.GingivalisA.ViscosusT.DenticolaA.ViscosusA.NaeslundiiP.GingivalisP.intermedia
FimbriaeFimbriaeSurface proteinFimbriae
Membrane protein
Galactosyl residuesGalactosyl / Mannose residuesFibrinogen/ fibronectin
Pre existing plaque mass
S.SanguisA.NaeslundiiA.IsraeliiS.SanguisA.IsraeliiP.Gingivalis
C.Ochracea
P.Loescheii
F.Nucleatum
Heat sensitive protein
Fimbrial protein
Outer membrane protein
Rhamnose/ fucose/ N-acetyl neura acidGalactosyl residues
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III. Colonization and plaque maturation
Mainly by 2 mechanisms COAGREGGATION. COADHESION
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Transport to surface
Initial adhesion
Attachment
Colonization of the surface and biofilm formation
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PRIMARY COLONIZERS
They provide new binding sites for adhesion by other oral bacteria. The early colonizers (e.g., streptococci and Actinomyces species) use
oxygen and lower the reduction-oxidation potential of the environment, which then favors the growth of anaerobic species.
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SECONDARY COLONIZERS
They do not initially colonize the clean tooth surface but adhere to bacteria already in the plaque mass.
Including Prevotella intermedia, Prevotella loescheii, Capnocytophaga spp., Fusobacterium nucleatum, and Porphyromonas gingivalis.
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Co-aggregation is the interaction
between planktonic micro-organisms
of a different strain or species
Co-adhesion is the interaction
between a sessile, already adhering
organism and planktonic micro-
oganisms of a different strain or
species
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Co- Aggregation
It was described by Gibbsons & NygaardCell to cell recognition of a genetically distinct partner cell type.Occurs primarily through 1. Highly specific interaction of
protiens and carbohydrate molecules located on the bacterial cell surfaces.
2. Less specific interaction resulting from hydrophobic electrostatic & van der waals forces.
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Well characterized interaction include the coaggregation of:
• Fusobacterium nucleatum S. sanguis,• Prevotella loescheii A. viscosus• Capnocytophaga ochraceus A. viscosus
• Streptococci show intrageneric co-aggregation bind to the nascent monolayer of already bound streptococci.
Later stages – coaggregation between different Gram negative species seen – F. nucleatum & P. gingivalis or T. denticola.
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Coaggregation Bridges: Formed when the common partner bears two or more types of
coaggregation mediators. Mediators can be various types of receptor polysaccharides, or various types
of adhesins, or a mixture of the two. Bridging is usually considered to be a cooperative event that brings three or
more cell types into close proximity and fosters symbiotic relationships. Bridging can also be an antagonistic event which brings together organisms
that compete with each other for nutrient or other needs.
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Thus most coaggregation among strains of different genera are mediated by lectin-like adhesin & can be inhibited by lactose & other glycosides.
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• F.nucleatum is central to the mechanism - since this organism can co aggregate with numerous other species.
• Examples
F.nucleatum: S.sanguis P. loescheii A.viscous Capnocytophaga P.gingivalis B.forsythus T.denticola
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COAGGREGATION COMPETITION: Competition occurs when multiple cell types recognize the same
coaggregation mediator on the common coaggregation partner.
Model depicting competition for binding sites on Streptococcus oralis .
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Test tube brush: Composed of a central axis of a filamentous
bacterium with perpendicularly associated short filaments.
Commonly seen in the subgingival plaque of teeth associated with periodontitis
Detected between filaments of bacteria to which gram –ve rods adhere.
Corncob formation: Feature of plaque present on teeth
associated with gingivitis . Rod-shaped bacterial cells eg.
Bacterionema matruchotii or Actinomyces sp. that forms inner core of the structure and coccal cells eg. Streptococci or P. gingivalis that attach along the surface of the rod shaped cells.
Described by Gibbsons and Nygaard
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S.mitisS.oralis
S.sanguis
Streptococcus spsS.gorondi,S.intermedius
EARLY
COLONIZERS
V.parvulaA.odontolyticus
P.intermediaP.nigrescensP.microsF.nucleatum
C.rectus
E.nodatum
C.showae
E.corrodens Capnocytophaga spsA.actinomycetocomitans
P.gingivalisT.forsythusT.denticola
CLOSELY ASSOCIATEDCOMPLEXES IN THE ORAL CAVITY
LATE COLONIZERS
12/27/2011 Socransky et al (1998)
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Distribution of different complexes in subgingival plaque sample
Kigure et al (1995)
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CO-ADHESION
• Some bacteria are unable to bind directly to the conditioning film, but are able to interact with molecules on bacteria that are already attached (co-adhesion), also by adhesin-receptor interactions.
• One bacterium, Fusobacterium nucleatum, can co-adhere with almost all other bacteria found in dental plaque, and is considered to be a key bridging organism between early and later colonisers.
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Development of dental plaque on a clean enamel surface. Coccal bacteria attach to the enamel pellicle as pioneer species (A) and multiply to form microcolonies (B), eventually resulting in confluent growth (biofilm formation) embedded in a matrix of extracellular polymers of bacterial and salivary origin (C). With time, the diversity of the microflora increases, and rod and filament-shaped bacteria colonize (D and E). In the climax community, many unusual associations between different bacterial populations can be seen, including ‘corn-cob’ formations (F). (Magnification approx. × 1150)
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