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GOOD MORNING

DENTAL PLAQUE

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DR. ANUJ SINGH PARIHARSenior Lecturer

Dept. of Periodontics

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CONTENTS• INTRODUCTION • HISTORY• DEFINITION OF TERMS• CLASSIFICATION OF DENTAL PLAQUE• COMPOSITION OF DENTAL PLAQUE• FORMATION OF DENTAL PLAQUE• MICROBIAL COMPLEXES• DENTAL PLAQUE AS BIOFILM• MICROBIAL SPECIFICITY OF PERIODONTAL DISEASE• CRITERIAS OF IDENTIFICATION OF PATHOGENS• PLAQUE CONTROL• CONCLUSION

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DENTAL PLAQUE

A

BIOFILM

MICRO-ORGANISMS

PERIODONTITIS

DENTAL CARIES

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DEFINITIONS

• Dental Plaque Soft deposits that form the biofilm adhering to the tooth surface or

other hard surfaces in the oral cavity, including removable & fixed restorations”

Bowen , 1976

• Bacterial aggregations on the teeth or other solid oral structures Lindhe, 2003

DEFINITIONS

DENTAL PLAQUE “is a specific but highly variable

structural entity, resulting from sequential colonization of microorganisms on tooth surfaces, restorations & other parts of oral cavity, composed of salivary components like mucin, desquamated epithelial cells, debris & microorganisms, all embedded in extracellular gelatinous matrix.”

WHO-1961

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Dental Calculus is a an adherent calcified or calcifying mass that forms on the

surface of natural teeth & prosthesis.

MATERIA ALBA is a deposit composed of aggregate of microorganisms,

leucocytes & dead exfoliated epithelial cells , randomly organized & loosely adherent to the surfaces of the teeth, plaque & gingiva.

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HISTORY

J Leon Williams (1897) – described dental plaque

GV Black (1899) – coined term “gelatinous dental plaque”

Waerhaug (1950) described the importance of bacterial plaque in the etiology of periodontal disease

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HISTORY

Schei (1959), Russel (1967) Epidemiological studies- positive correlation between the amount of bacterial plaque

and the severity of gingivitis

Loe et al (1965), landmark study on plaque , saying that plaque is main etiological agent in periodontal diseaes.

W.Loesche (1976) Modern theories of specificity

PD Marsh (1994) Ecological plaque hypothesis

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CLASSIFICATION

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SUPRA- GINGIVAL PLAQUE• Supragingival plaque is found at or above the gingival

margin.

• Supragingival plaque in direct contact with the gingival margin is referred to as marginal plaque

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SUBGINGIVAL PLAQUE

• Sub gingival plaque is found below the gingival margin, between the tooth and gingival sulcular tissue.

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Tooth attached Unattached Tissue Attached

Gram positive – rods and cocci,

Gram negative rods, filaments,

spirochetes

Gram variable

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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COMPOSITION OF DENTAL PLAQUE

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COMPOSITION OF DENTAL PLAQUE

• Dental plaque is composed primarily of microorganisms. • These organisms exist within an intercellular matrix.

INTER-CELLULA

R MATRIX

MICRO-

ORGANIS

MS

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BIOFILM

The term biofilm describes the relatively indefinable microbial community associated with a tooth surface or any other hard, non-shedding material.

(Wilderer & Charaklis 1989)

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• Biofilm consists of one or more communities of micro-organisms embedded in glycocalyx , that are attached to solid surfaces.

(Costerton et al 1994)

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INTERCELLULAR MATRIX

• This contains a few host cells such as epithelial cells , macrophages & leukocytes.

• Forms 20%-30 % of plaque mass.

ORGANIC

MATERIAL

INORGANIC

MATERIAL

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ORGANIC MATERIAL

• Polysaccharides ( 30% ) produced by bacteria. Dextran

• Protein (30%) –Albumin (originating from GCF)

• Glycoproteins from saliva.

• Lipid (15%) consists of debris from disrupted bacteria, host cells & food debris

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INORGANIC MATERIAL

• Predominantly – calcium, sodium, phosphorous, potassium & fluorides (in traces)

• Source of inorganic material in supragingival plaque is primarily saliva

• source of inorganic material in sub gingival plaque is

GCF

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EXOPOLYSACCHARIDES – the backbone of the biofilm

The bulk of the biofilm consists of the matrix, composed predominantly of water and aqueous solutes.

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Maintaining the integrity & protecting microbial cells within the biofilm by preventing desiccation and attack by harmful agents.

They bind essential nutrients such as cations to create a nutritionally rich environment favouring specific micro- organisms.

Act as a buffer and assist in retaining extracellular enzymes (and their substrates), enhancing substrate utilization by bacterial cells.

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•

One gram of plaque contains approximately

2 X 1011 bacteria. (Socransky SS,1953), (Schroeder,

De Boever-1970)

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NON BACTERIAL ORGANISMS IN PLAQUE

MYCOPLASMASPECIES

YEAST

PROTOZOA

VIRUSES

NON BACTERIAL

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FORMATION OF DENTAL PLAQUE

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Dental plaque may be readily visualized on teeth after 1-2 days of no oral hygiene.

FORMATION OF DENTAL PELLICL

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INITIAL ADHESI

ON & ATTACH

MENT

COLONIZATION

& PLAQUE MATURATION

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I. FORMATION OF DENTAL PELLICLE

• Acquired pellicle may be defined as 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 is found within 30 min. Within 24 hr, the pellicle is around 0.1-0.8 µm in diameter.

• Derived from components of saliva and crevicular fluid as well as bacterial and host tissue cell products and food debris.

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• Consists of numerous components, including glycoprotein (mucins), proline-rich proteins, phosphoproteins (e.g., statherin), histidine-rich proteins, enzymes (e.g., α-amylase), and other molecules that can function as adhesion sites for bacterial receptors.

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FUNCTIONS OF DENTAL PELLICLE

Protective barrier

Lubrication

Preventing tissue

desiccation

Substrate to which bacteria

attaches

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II. INITIAL ADHESION & ATTACHMENTOF BACTERIA

• We cannot conclude a single mechanism that dictates the adhesiveness of micro-organisms .

TRANSPORT

TO SURFA

CE

INITIAL ADHESI

ON

ATTACHMENT

COLONIZATION OF

SURFACE &

BIOFILM

FORMATION

SCHEIE ( 1994)

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A) TRANSPORT TO SURFACE • The first stage involves the initial transport of the bacterium to

the tooth surface.

• Random contacts may occur

o Brownian motion (average displacement of 40 µm/hour)

o Sedimentation of microorganisms,

o Liquid flow

o Active bacterial movement (chemotactic activity).

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B) INITIAL ADHESION

• There is an initial, reversible adhesion of the bacterium. • It is initiated by the interaction between the bacterium and the

surface, from a certain distance (50 nm), through long-range and short-range forces, including van der Waals attractive forces and electrostatic repulsive forces.

• The total interaction energy, also called the total Gibbs energy (GTOT).

• (GTOT = GA + GE)

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INITIAL ADHESION

• For most bacteria, GTOT consists of a

o Secondary minimum (where a reversible binding takes place: 5-20 nm from the surface)

o A positive maximum (an energy barrier B) to adhesion

o A steep primary minimum (located at <2 nm away from the surface), where an irreversible adhesion is established.

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C) ATTACHMENT

• After initial adhesion, a firm anchorage between bacterium and surface will be established by specific interactions (covalent, ionic, or hydrogen bonding).

• The bonding between the bacteria & pellicle is mediated by specific extracellular components of organisms & complementary receptors on pellicle surface.

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ATTACHMENT OF BACTERIA

• The attachment to tooth surface is the essential first step in the development of a biofilm.

• Many bacterial species possess surface structures such as FIMBRIAE and FIBRILS that aid in their attachment to different surfaces.

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• The fimbriae of A. naeslundii are the best characterized of the gram-positive oral bacteria.

Type I fimbrae

• Associated with adhesion of A. naeslundii to salivary acidic proline- rich proteins and to statherin deposited within the salivary pellicle.

Type II fimbrae• Associated with attachment of A.

naeslundii to glycosidic receptors on epithelial cells, polymorphonuclear leukocytes and oral streptococci .

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FORMATION OF DENTAL PELLICLE

INITIAL ADHESION &

ATTACHMENT

• TRANSPORT• INITIAL ADHESION• ATTACHMENT• COLONIZATION

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III. COLONIZATION &

PLAQUE MATURATION

• 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 are the microorganisms that do not initially colonize clean tooth surfaces, including Prevotella intermedia, Prevotella loescheii, Capnocytophaga spp., Fusobacterium nucleatum, and Porphyromonas gingivalis.

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COAGGREGATION

• Coaggregation is referred to as cell-to cell recognition of genetically distinct partner cell types.

• Occurs primarily through the highly specific stereo chemical interaction of protein and carbohydrate molecules located on the bacterial cell surfaces.

• Also by the less specific interactions resulting from hydrophobic, electrostatic, and van der Waals forces.

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COAGGREGATION

• 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

• A co-aggregation bridge is formed when the common partner bears two or more types of coaggregation mediators.

• These mediators can be various types of polysaccharides or various adhesin or combination of two

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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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CORN COB formation – streptococci adhere to filaments of Bacterionema.matruchotti or F.nucleatum.

CORNCOB STRUCTURE TEST TUBE BRUSH

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MICROBIAL COMPLEXES

Socransky et al. in 1998 examined over 13,000 subgingival plaque samples from 185 adult subjects and DNA hybridization methodology described the presence of specific complexes of periodontal microorganisms.

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ACTINOMYCESSPECIES

V. ParvulaA.odontolyticus

S.MitisS.Oralis

S.Sanguis

Streptococcus sp.S.gordonii

S.intermedius

PRIMARY COLONIZERS

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P.IntermediaP.Nigrescens

P.MicrosF.nucleatum

C.rectus

E.nodatum

C.showae

E.CorrodensCapnocyptophaga spp

A.actinomycetemcomitans

P.GingivalisB.ForsythusT.denticola

SECONDARYCOLONIZERS

ACTINOBACILLUS ACTINOMYCETEMCOMITANS

• It is non motile & gram negative.• This bacteria is small, short ,straight or curved with rounded

ends.

AGGREGAGIBACTER. ACTINOMYCETUMCOMITANS (LAURITSON & KILION,2006)

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VIRULENCE FACTORS OF A. ACTINOMYCETEMCOMITANS

FACTOR EFFECTLIPOPOLYSACCHARIDE Release of endotoxin

LEUKOTOXIN • forms pores in the membranes of Pmns, monocytes and lymphocytes causing osmotic imbalance leading to cell death

COLLAGENASE reduce collagen density

PROTEASE Able to cleave Ig G

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PORPHYROMONAS GINGIVALIS

• It is a gram negative , non-motile & obligate anaerobe.

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VIRULENCE FACTORS OFPORPHYROMONAS GINGIVALIS

FACTOR EFFECTFIMBRIAE attach to epithelial cells, fibroblasts,

hemoglobin

PROTEINASES provide nutrients for bacterial growth

degrade type I and IV collagen and extracellular matrix proteins

FIMBRILLIN bind to proline rich proteins

PROTEASE Able to cleave Ig G

HAEMOLYSIN & COLLAGENASE

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GINGIPAIN

• Trypsine like protinases

ARGININE

LYSINE

GINGIPAINS

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BACTERIODS FORSYTHUS

• It is a non-motile , spindle shaped & gram negative obligate anaerobe.

TANNERELLA.FORSYTHENSIS (SAKA MOTO et al ,2002)

TANNERELLA.FORSYTHIA (MAIDEN et al,2003)

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VIRULENCE FACTORS OFTANNERELLA FORSYTHIA

FACTOR EFFECTLIPOPROTEINS bind to other bacteria and host cells

PROTEINASES degrades benzoyl arginine naphthylamide, activity of which appears related to sites of periodontal infection

ENVELOPELIPOPROTEIN

activate gingival fibroblaststo produce elevated levels of IL-6 and TNF α

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TREPONEMA.DENTICOLA

• This is a classified species of SPIROCHAETES.• These organisms are gram negative spiral , motile organisms• It is difficult to grow these organisms on culture media , as

these require strict anaerobic conditions.

PATHOGENIC CHARACTER

• Ability to travel in viscous environment & penetrate both epithelium and connective tissue.

• These can degrade collagen & dentine.• Produce proteolytic enzymes that destroys immunoglobulins.

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CHARACTERSTICS OF BIOFILM

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1) PHYSIOLOGICAL HETEROGENECITY WITHIN BIOFILM

• Cells of same microbial species can exhibit extremely different physiological states in a biofilm though separated by little distance of 10 micrometer.

• pH can vary quite remarkably over short distances within a biofilm .

• Bacteria in biofilm several enzymes Beta- lactamase, Superoxide dismutase, Elastases, Cellulases.

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2) QUORUM SENSING

• Quorum sensing in bacteria , ‘‘involves the regulation of expression of specific genes through the accumulation of signaling compounds that mediate intercellular communication.”

(Prosser 1999)

• This is a method of intercellular communication. Quorum sensing depends on cell density.

• Once signaling compounds reach a threshold level, gene expression is activated.

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Quorum sensing may give biofilms their distinct properties:

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3) ANTIBIOTIC RESISTANCE:

• Resistance of bacteria to antibiotics, or preservatives is affected by their

- position of bacteria - growth rate - temperature & PH

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PROPERTIES OF BIOFILM

• Cooperating community of various types of micro-organisms.

• Micro-organisms are arranged in microcolonies.

• Micro-organisms are surrounded by protective matrix.

• There is differing environment within micro-colonies which impact the property of PHYSIOLOGICAL HETEROGENICITY.

• Micro-organisms have antibiotic resistance mainly due to phenomenon of QUORUM SENSING.

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EXPERIMENTAL GINGIVITIS MODEL ( SAYED, LOESCHE, 1978)

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TOPOGRAPHY OF SUPRA GINGIVAL PLAQUE

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PLAQUE RETENTIVE FACTORS

Surface irregularities

Restorative materials

Removable partial dentureCalculus

Abnormal tooth position

Erupting teeth

Carious lesion

Orthodontic therapy

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VARIATIONS IN DENTITION

Molar

>

front

region

Buccal surfaces more especially in the upper jaw

Interdental areas compared to strict buccal or oral surfaces

Plaque growth rate

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MICROBIAL SPECIFICITY OF PERIODONTAL DISEASES

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NON-SPECIFIC PLAQUE HYPOTHESIS

SPECIFIC PLAQUE HYPOTHESIS

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NON SPECIFIC PLAQUE HYPOTHESIS

• Non specific plaque hypothesis was proposed by

WALTER LOESCHE(1976).

• In the mid-1900s, periodontal disease was believed to result from an accumulation of plaque over time in conjunction with a diminished host response and increased host susceptibility with age.

• This thinking is referred as “NON-SPECIFIC PLAQUE HYPOTHESIS”

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• The nonspecific plaque hypothesis maintains that periodontal disease results from the “elaboration of noxious products by the entire plaque flora.”

• Thus it lead to concept that control of periodontal disease depends on control of the amount of plaque accumulation.

• Treatment of periodontitis by debridement (nonsurgical or surgical) and oral hygiene measures focuses on the removal of plaque and its products

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SPECIFIC PLAQUE HYPOTHESIS

• Specific plaque hypothesis states that only certain plaque is pathogenic, and its pathogenicity depends on the presence of or increase in specific microorganisms.

NEWMAN MG , SOCRANSKY SS (1977),ADI et al ,(1978)

• Plaque harboring specific bacterial pathogens results in periodontal disease.

• A. actinomycetemcomitans as a pathogen in localized aggressive periodontitis.

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TISSUE INVASIVE PROPERTY

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ECOLOGICAL PLAQUE HYPOTHESIS

• A change in a key environmental factor (or factors) will trigger a shift in the balance of the resident plaque microflora, and this might predispose a site to disease.

( PD Marsh 1994)

• This hypothesis is based on the theory that the unique local microenvironment influences the composition of the oral microflora.

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• This hypothesis postulated dynamic relationship between environmental cause & ecological shifts within the biofilm.

• It also introduced the concept that the disease can be prevented not only by inhibiting the putative pathogens, but also interfering with the environmental factors driving the selection & enrichment of these bacteria.

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CRITERIA FOR IDENTIFICATION OF PERIODONTAL PATHOGENS

In the 1870s, Robert Koch postulated the criteria by which an organism can be judged to be causative agent in human infections

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Pathogen must be routinely isolated from the diseased individuals.

Must be grown in pure culture in the laboratory.

Must produce a similar disease when inoculated into susceptible lab animals.

Must be recovered from lesions in a diseased laboratory animals.

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SIGMUND SOCRANSKY (1992) proposed criteria

by which periodontal microorganisms may be judged to be potential pathogens.

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• Must be associated with disease, as evident by increases in the number of organisms at diseased site.

• Must be eliminated or decreased in sites that demonstrate clinical resolution of disease with treatment.

• Must demonstrate host response, in form of alteration in host cellular or humoral immune reaction.• Must be capable of causing disease in experimental animal models.

• Must demonstrate virulence factors responsible for enabling the microorganisms to cause destruction of the periodontal tissues.

PLAQUE CONTROL

DETECTION OF PLAQUE DISCLOSING AGENTS

It is a preparation in liquid , tablet or lozenge which contains a dye or other colouring agent. A disclosing agent is used for identification of dental plaque which is otherwise not visible to naked eye .

THE AGENTS THAT ARE USED AS DISCLOSING AGENTS ARE:

• Iodine preparation• Bismark brown• Erythrosine• Fast green• Basic fuschin

PLAQUE CONTROL• It is defined as the removal of microbial plaque &

prevention of its accumulation on the teeth & adjacent gingival tissue. It also deals with prevention of calculus formation.

MECHANICALCHEMICAL

MANUAL TOOTH BRUSH

IONIC TOOTH BRUSH

SONIC TOOTHBRUSH

POWERED TOOTH BRUSH

INTER DENTAL AIDS

DENTAL FLOSS

INTER DENTAL AIDSINTER DENTAL

BRUSH

INTER DENTAL AIDSUNITUFTED

BRUSHED

CHLORHEXIDINE GLUCONATE

• ADVANTAGE• 1. anti plaque & anti bacterial • properties• 2. property of SUBSTANTIVITY• • DISADVANTAGE• brownish staining of teeth

• MECHANISM 1. prevent pellicle formation. 2. prevent plaque maturation

POVIDONE IODINE

• ADVANTAGE• 1. no staining of teeth seen• 2. reduces inflammation• • DISADVANTAGE• reduced substantivity

DELMOPINOL

This is a morpholinoethanol derivative.

Inhibits plaque growth & reduces inflammation.

But has less substantivity in

comparison to others

CONCLUSION

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REFERENCES• Clinical Periodontology - Carranza (9th & 10th edn)

• Clinical Periodontology- Jan Lindhe, Thorklid Karring , Niklaus P Lang

• Clinical Periodontology : Listgarten • Periodontal microbial ecology - Perio 2000,Vol. 38, 2005, 135–

187

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• Are dental diseases examples of ecological catastrophes? - P. D. Marsh - Microbiology (2003), 149, 279–294

• Dental biofilms: difficult therapeutic targets - Periodontology 2000, Vol. 28, 2002, 12–55

• Dental biofilms: difficult therapeutic targets - Periodontology 2000, Vol. 28, 2002, 12–55

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