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DENTAL PLAQUE
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PRESENTED BY; DR. POOJA BHASALE

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INTRODUCTION
Dental caries and periodontal diseases are the two most common diseases of the oral cavity. Their prevalence is recorded along with history of man after his appearance on earth. Experimental and epidemiologic studies have demonstrated that these diseases are dependant on the microorganisms present in plaque. It is the build up of plaque that serves as an irritant to the gingiva.

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Dental plaque is defined clinically as a

structured resilient, yellow-grayish substance that adheres tenaciously to the intra oral hard surfaces, including removable and fixed restorations. Bowen WH 1976
Dental plaque- highly complex structural

entity which comprises of large species of microorganisms embedded in a mucinous matrix-American Academy of Periodontology 1986

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COMPOSITION OF DENTAL PLAQUE

Composed of bacteria in a matrix of salivary

glycoproteins and extra cellular polysaccharides

One gram of plaque - 1011 bacteria.(Schroeder

etal 1970)

Number of bacteria in supragingival plaque on a

single tooth surface - > 109

In a periodontal pocket - 103 to 108

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TEETH AS PORT OF ENTRY OF PERIOPATHOGENS

l

The unusual anatomic feature, that a mineralized structure, the tooth, passes through the integument, so that part of it is exposed to the external environment while part is within the connective tissues. The tooth provides a surface for the colonization of a diverse array of bacterial species. In contrast to the outer surfaces of most parts of the body,the outer layers of the tooth do not shed, and thus microbial colonization is facilitated. In addition the tooth provides sanctuaries in which organisms can hide,persist at low levels during treatment and the re-emerge to cause

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CLASSIFICATION
l

Dental plaque is classified as SUPRAGINGIVAL or SUBGINGIVAL SUPRAGINGIVAL- found at or above the gingival margin, when in direct contact with the gingival margin it is referred as marginal plaque SUBINGIVAL- below the gingival margin, between the tooth and the gingival pocket epithelium.

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STRUCTURE OF SUPRAGINGIVAL PLAQUE

Stratified organization of a multilayered accumulation of bacterial morphocytes

Gram positive cocci and short rods predominate at the tooth surface, where as gram negative rods and filaments as well as spirochetes predominate in the outer surface of the mature plaque mass

1st bacteria to colonize are streptococci species and Actinomyces. Veillonella is also an early colonizer

Plaque grows by cell division of adherent bacteria

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Clinical photo of 10 day old supragingival plaque. The first symptoms of gingival inflammation (arrows) are becoming visible.

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STRUCTURE OF SUPRAGINGIVAL PLAQUE

The material present between the bacterial cells- Intermicrobial matrix 3 sources contribute to it- the plaque microorganisms, the saliva, gingival exudate Intermicrobial matrix varies in regions - fibrillar component between gram +ve cocci - granular or homogenous in other regions - in the presence of gram ve organisms, vesicles seen. These vesicles contain endotoxins and proteolytic enzymes and are

Long standing supragingival plaque near the gingival margin demonstrates corncob arrangement

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STRUCTURE OF SUBGINGIVAL PLAQUE

l

Subgingival microbiata differs in compostion from the supragingival plaque primarily because: a) Local availability of blood products. b) Low oxidation-reduction (redox) potential which characterizes the anaerobic environment. c) Gingival crevice or pocket is bathed by the flow of crevicular fluid.
SUBGINGIVAL PLAQE

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STRUCTURE OF SUBGINGIVAL PLAQUE

A relatively thin layer of adherent bacteria covers the tooth surface. Rods and filaments tend to be arranged in a palisading pattern, with the long

axis of the cells perpendicular to the tooth surface.

Unique bacterial aggregates, resembling test-tube brushes, can be found

attached to the adhering plaque and extending into the space between the bacterial layer and the adjacent soft tissue wall.
The bristles of these test-tube brush formations are gram-negative

filamentous bacteria, some of which may be flagellated.

The axial portion of the test-tube brush consists of a single or several long

filaments held together by an amorphous extracellular matrix.

The bulk of the subgingival microbiota consists of a complex mixture of

predominantly anaerobic bacteria that surround and cover the test- tube brush formations.
The structure of Dental plaque- Max. Listgarten,

Periodontology 2000,

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STRUCTURE OF SUBGINGIVAL PLAQUE

The subgingival plaque has two regions1). Tooth associated region of subgingival plaque and 2). Tissue associated region of subgingval plaque Both morphologic and microbiologic studies reveal distinction between the tooth associated and tissue associated regions of subgingival plaque. (Listgarten etal 1970)

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TOOTH ASSOCIATED PLAQUE

l l l

Filamentous microorganisms dominate Increased number of gram positive rods and cocci are seen. In the deeper parts - filamentous organisms are fewer and in the apical region - absent. The apical border of the plaque mass is separated from the junctional epithelium by a layer of host leukocytes, and the bacteria of this apical tooth associated region show an increased number of gram-negative rods.

Tooth associated plaque- S.mitis, S.sanguis, A.viscosus, A.naeslundii, Eubacterium species seen predominatly
Carranzas Clinical Periodontology 10th edition

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TISSUE ASSOCIATED PLAQUE

Primarily contain gram-negative rods and cocci, large numbers of filaments, flagellated rods, and spirochetes. motile bacteria and there is no intermicrobial matrix between them. This outer part of the microbial accumulation in the periodontal pocket adheres loosely to the soft-tissue pocket wall. (Listgarten1976). Host tissue cells e.g. white blood cells and epithelial cells are also found. Soft tissue plaque- S.oralis, S.intermedius, P.gingivalis, P.intermedia, T.forsythia and Fusobacterium Nucleatum. (Dzink etal 1989)

The multitude of spirochetes and flagellated organisms are

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PERIIMPLANT PLAQUE
Plaque forms on oral implants as well Similarities between peri-implant and subgingival microbial deposits have been demonstrated in cross sectional studies (Mombelli et al. 1987,1995) and longitudinal studies (Mombelli et al. 1988; Pontoriero et al. 1994)

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SITE SPECIFICITY OF PLAQUE

Marginal plaque

Gingivitis

Supragingival plaque and tooth associated subgingival

plaque

Calculus and root caries

Tissue associated sub gingival plaque

tissue

destruction

Periodontitis

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FORMATION OF DENTAL PLAQUE

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FORMATION OF PELLICLE
All surfaces of the oral cavity, hard and soft get coated with a pellicle Within nanoseconds after prophylaxis, saliva derived acquired pellicle formed

Composition- Glycoproteins, proline-rich proteins, phosphoproteins, histidine-rich proteins, enzymes

Studies indicate that bacteria can be part of the early deposit (Ronstrom A, Edwardsson S, Atistrom R, 1977)

Composition of pellicle differs from saliva indicating it forms by selective adsorption of environmental macromolecules

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INITIAL COLONIZATION OF TOOTH SURFACE

The dental pellicle that is formed, alters the charge and free

energy of the surface which in turn increase the efficiency of bacterial adhesion. with in 5min. 106 bacteria colonize per cm2 the tooth surface.

Within few hrs. bacteria are found on the dental surface. In fact Initial bacteria that colonize the tooth surface are predominantly

gram +ve facultative micro organisms such as A. viscosus and S. sangius. physio-chemical surface properties of the bacterium and the substratum.

Adhesion of bacteria is determined by the enviroment and the

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MECHANISM OF ADHESION
Electrostatic forces

Hydrophobic forces

Short range forces(<1nm from the surface)

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SECONDARY COLONIZATION AND PLAQUE MATURATION

These include micro organisms that do not initially

colonize tooth surface and includes P.intermedia, P.loesheii, Capnocytophaga, F. nucleatum and P. gingivalis .

The micro organism may interact with pellicle, bacterial

polysaccharide or there may be direct interaction between bacterial cell surfaces.

This last bacterial cell to cell interaction is termed as co-

aggregation and was first described by Gibbons and Nygaard in 1970.

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Mc Intire, et al in 1978 described co-aggregation between A.

naeslundii and S. oralis. This interaction was between proteinaceous molecule which acted as a lectin on A. naeslundii and a carbohydrate receptor on S. oralis.

Direct cell to cell interaction were also noticed in early electron

microscopic studies of dental plaque. Clearly observed in these studies were morphologic forms arising from the direct association of different cell types.
The interaction of filamentous cells with coccal cells were

particularly noticeable and these co-aggregated cells were labeled corncobsor test tube brushes or bristle brush due to their appearance.

corncobs

The name corncobs was coined by Jones in 1971. Vincentini in 1897 and thought that the structures were composed of a single microbial species and named them Letotrix racemosa.

It was first described by

It is now known that

corncob unit consists of a central filamentous

Electron micrographs of

cross section of corncobs indicated that that attachment of cocci to the filament occurred via hair like appendages that are commonly found on some species of oral streptococci.(coaggregation)

These fimbrae were

found to be located on one pole rather than uniformly distributed over the cell surface as found in other oral streptococci.

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Another feature of corncobs was the firmness of

attachment between component micro organism.

Attempt to separate component micro organism by

sonification failed.

In 1997 Mouton, et al used a combination of

micromanipulation and culture to isolate both filamentous organism and the attached streptococci.

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Lancy, et al 1980 developed a quantitative assay for

corncob formation.

Using this assay and electron microscope it was

subsequently found that F. nucleatum also formed corncobs with S.cristae. This was a very important finding since F. nucleatum is a major inhabitant of sub gingival plaque

Thus formation of Fusobacterial corncobs could provided

a connective link between supra and sub gingival plaque

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Multi generic co-aggregation

Another important feature during secondary colonization

and plaque maturation includes the concept of multi generic co-aggregation.

Kolenbrander and Andersen 1986 showed that multi

generic aggregates are a composite of independent inter generic co-aggregates.

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Bridging is also the property of co aggregating cells and

have important ecological implication. Bridging refers to observation that two non-aggregating strains may participate together in a multi generic if they recognize a common partner by distinct mechanism.

E.g :- A. israelii does not co-aggregate with S. oralis.

However P. loescheii co-aggregates with both strain by means of different adhesins. When the three were mixed, all three cell types were found in aggregated form. Kolenbrander 1985 .

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Another concept put forward by Kolenbrander, et al

in1990 that play a role in plaque formation is the possibility that intra generic co-aggregation between different streptococci.

Of all the bacteria that participated in intra generic co-

aggregation only Fusobacteria and streptococci were capable of intra generic co-aggregation.

. F. nucleatum acts as a bridge between early and late

colonizers, which may partially explain why fusobacteria are so numerous in samples from both healthy and diseased sites

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In addition to interactions with oral bacteria and host

cells, F. nucleatum interacts with and binds hostderived molecules, such as plasminogen.

F. nucleatum is generally nonproteolytic, but

organisms that coexist with it, such as P.gingivalis, are highly proteolytic and can activate fusobacterium- bound plasminogen to form fusobacterium-bound plasmin,a plasma serine
protease .

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MICROBIAL COMPLEXES
The association of bacteria within mixed biofilms is not

random, rather there are specific associations among bacterial species

Socransky et al.(1998) examined over 13,000 subgingival

plaque samples from 185 adult subjects and used cluster analysis and community ordination techniques to demonstrate the presence of specific microbial groups within dental plaque
Six closely associated groups of bacterial species were

recognized
Clinical Periodontology & Implant Dentistry 5th edition Jan Lindhe

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These included the Actinomyces,

A yellow complex consisting of members of genus

Streptococcus
A green complex consisting of Capnocytophaga species,

A.actinomycetemcomitans serotype a, E. corrodens and Campylobacter concisus

A purple complex consisting of V.parvula and Actinomyces

odontolyticus
These groups of species are early colonizers of the tooth surface

whose growth usually precedes the multiplication of the

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The red complex consists

of B.forsythus, P. gingivalis and T.denticola (and sometimes Eubacterium nodatum)

The "red complex" was

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DENTAL PLAQUE AS BIOFILM

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The term biofilm describes the relatively undefinable

microbial community associated with tooth surface or any other hard, non-shedding material (Wilderer and Charaklis 1989).

A biofilm is a well organized community of bacteria

that adheres to surfaces and is embedded in an extracellular slime layer(Jill S.Nield-Gehrig).

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BIOFILM: ANALOGY TO A CITY

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NATURE OF BIOFILM
Preferred method of growth for microorganisms

Provides advantages for colonizing species

Protection from Competing microorganisms Environmental factors, host defense Toxic substances, such as lethal chemicals, antibiotics Facilitate processing and uptake of nutrients, cross-

feeding,removal of harmful metabolic products

Development of an appropriate physico-chemical environment.

Clinical Periodontology & Implant Dentistry 5th edition

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COMPOSITION OF BIOFILM
Composed of micro colonies (15-20% by volume) distributed in

a shaped matrix or glycocalyx (75-80% volume)

Presence of voids or water channels o Permit the passage of nutrients and other agents, acting as

circulatory

system

Organic constituents include: o Polysaccharides o Proteins

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Exopolysaccharides-backbone of the biofilm

DRY material-exopolysaccharides,proteins,salts,cell material

Exopolysaccharides-major component(50-95%)

Plays major role in maintaining the integrity of biofilm

Several different polysaccharides

Some are neutral(mutans),some highly charged polyanionic

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Protects microbial cells from dessication & attack by harmful

agents

Creates a local nutritionally rich enviorment by binding to

essential nutrients

Acts as a buffer

Maintain biofilm structure-formation of networked cross linked

linear macromolecules

Type and not the quantity of exopolysaccharide has an effect

on biofilm.

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DEVELOPMENT OF DENTAL PLAQUE BIOFILM

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Stages of biofilm maturation

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Attachment

Begins with pellicle formation Pellicle- thin coating of salivary proteins Acts as a double-sided adhesive tape

Adhering to tooth surface on one side and providing a sticky surface for bacterial attachment on the other side

Bacteria connect to each other and pellicle by fimbrae, fibrils

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Once they stick,bacteria produce substances that stimulate other free flowing bacteria to get attached

2 days of no tooth cleaning tooth surface colonized by gram +ve cocci(streptococci species)

Attachment to a solid surface stimulates bacteria to secrete extracellular slime layer that helps in anchoring and protection for attached bacteria.

FACTORS AFFECTING ATTACHMENT OF BIOFILMS

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I-physical properties
Increased surface roughness>increased surface

area>increase colonisation

II-chemical properties
Chemical composition of surface;eg-brass,polyvinyl

chloride
Cohesiveness of conditioning film(Bos R 1999) Surronding saliva and its flow rate

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Formation of microcolonies

Begins after tooth surface is covered with attached bacteria

Biofilm grows primarily through cell division of adherent bacteria

Bacteria begin to grow away from the tooth

Plaque grows quickly in early development and slower in more mature biofilms

Bacterial blooms- specific species grow at rapid accelerated rates

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Secondary colonization and biofilm maturation

Prevotella intermedia, Prevotella loescheii, Capnocytophaga, Fusobacterium nucleatum ,Porphyromonas gingivalis Secondary colonizers

Adhere to cells of bacteria already attached Adhere to one another by coaggregation

Bacteria cluster together to form sessile,mushroom-shaped micro colonies that are attached to tooth surface at a narrow base

Results in formation of a complex array of different bacteria linked to another

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Detachment

Essential to allow colonization of new habitats

Cells detach in different fashions-Erosion-detachment of single cells in a continuous fashion -Sloughing-sporadic detachment of large group of cells -intermediate process where large pieces of biofilm are shed

Rate of detachment not clear (Watnick P, Kolter R, 2000)

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Rate of growth in many biofilms is slow and detachment is an uncommon event

Cells in such biofilms are metabolically active and capable of growth once released from the biofilm

Detachment is active ongoing process

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Factors affecting biofilm development and behaviour

Shear stress-high shear-thinner and denser biofilms,colonies are elongated and capable of rapid oscillation -low shear-roughly circular cluster of cells separated by voids,colonies are tower/mushroom shaped

Hydrodynamics-Biofilms under laminar flow(low shear) and turbulent flow(high shear) are different

Changes in nutrient concentration -addition of nutrients to a biofilm increased both mass and structure

Stoodley et al 1999

Bacterial behavior within the biofilm

Bacteria growing in microbial communities do not behave the same as those growing in a planktonic state

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E.g. the resistance of bacteria to antibiotics is increased in the biofilm about 1000-1500 times compared to those in their planktonic state (Costerton JW 1999)

Mechanism of increased resistance in biofilms differs from species to species, antibiotic to antibiotic and biofilms growing in different habitats

Resistance of bacteria to antibiotics is affected by their nutritional status, growth rate, temperature, pH and previous exposure to sub effective concentrations of antimicrobials (Brown MRW, Collier PJ,

Gilbert P,1990)

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Slower rate of growth of bacteria within the biofilm also makes them less susceptible to some antibiotics (Brooun A, Liu S, Lewis K,

2000)

Matrix performs a homeostatic function

-cells deep in the film and that at the periphery experience different growing conditions or cells growing planktonically -growth rates of the cells also differ -slow growing cells(deeper cells)express non-specific defense mechanisms i.e shock proteins and multi drug efflux mechanisms and so increased exopolymer synthesis -this exopolymer has certain properties that retards diffusion
Clinical Periodontology & Implant Dentistry 5th edition Jan Lindhe

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Eg-strongly charged or chemically highly reactive agents fail to

reach the deeper zones of biofilm as the biofilm acts as an ion exchange resin removing such molecules from solution
Extracellular enzymes get trapped and concentrated in the

extracellular matrix ,thus inactivating positively charged hydrophilic antibiotics charged are unaffected

Hydrophobic antibiotics like macrolides though positively ability of extracellular matrix to act as a barrier depends on the

type of antibiotic,its binding to the matrix,levels of antibiotic agent,a biofilm of greater bulk will deplete the agent more

As reaction between agent and matrix will reduce the level of Alteration in genotype and phenotype of bacteria is also

important

Clinical Periodontology & Implant Dentistry 5th edition Jan Lindhe

 Recently a subpopulation of cells within a biofilm that are

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super-resistent was proposed

Such cells explained the elevated levels of resistance to ceratin

antibiotic
Brooun et al 2000 examined multi drug resistant pumps to

antibiotic resistance of organisms grown in biofilms

These pumps extruded the chemically antimicrobial agents from

the cell

Extrusion placed the antibiotics outside the cell

membrane,hence offering protection to the biofilm from the antibiotics targeting the cell wall synthesis

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Quorum sensing

Comes from the same term used in a committee when enough members are present to legally take some action

It was first observed in the marine bacterium Vibrio fischeri, which can produce light after a sufficient population of this bacterium has developed

Is the ability of the bacteria and microcolonies to communicate with each other in the biofilm

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Involves the regulation of expression of specific

genes through the accumulation of signaling compounds that mediate inter cellular communication(Prosser 1999)
depends on cell density At threshold level, (quorum cell density) gene

expression is activated
Cell signaling appears to be mediated by an N-acyl

homoserine lactone encoded by a lux1 gene

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Though planktonic cells secrete chemical signals (HSLs, for homoserine lactones), the low concentration of signal molecules does not change genetic expression. Biofilm cells are held together in dense populations, so the secreted HSLs attain higher concentrations. HSL molecules then re-cross the cell membranes and trigger changes in genetic activity

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Plays a role in - antibiotic resistance at high cell densities -encourages growth of beneficial species -discourages growth of competitors

Physiological properties of bacteria in a community may be altered(Cooper et al 1995)

Autoinducer-2 a universal signal molecule is recently discovered in mixed species communities(Kolenbrander et al 2006)

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QUORUM SENSING
Quorum sensing systems bacteria have been generally

divided into at least three classes:

(1) LuxI/LuxRtype quorum sensing in Gram-negative

bacteria, which use acyl-homoserine lactones (AHL) as signal molecules. ( Lux- bacterial luciferase gene).
(2) Oligopeptide-two-component-type quorum sensing in

Gram-positive bacteria, which use small peptides as signal molecules.

(3) luxS-encoded autoinducer 2 (AI-2) quorum sensing in

both Gram-negative and Gram-positive bacteria.

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Autoinducer-2 a universal signal molecule is recently

discovered in mixed species communities(Kolenbrander et al 2006)

AI-2 allows for inter-species communication, so it is called a

universal languageused for cross-species communication.

AI-2 is produced from S-adenosylmethionine through several

steps, including the required enzymatic conversion of the intermediate S-ribosylhomocysteine by LuxS to 4,5-dihydroxy2,3-pentanedione, which is unstable and is predicted to cyclize spontaneously (133, 134) into a variety of molecules called proAI-2 before forming a mature AI-2LuxP complex.

The luxS gene, encoding S-adenosylhomocysteinase (LuxS) is

DE NOVO SUPRAGINGIVAL PLAQUE FORMATION: CLINICAL ASPECTSfollows an exponential growth curve Plaque formation
(Quirynen et al 1989)
Negligible in the 1st 24 hours . Increases rapidly in the next 3

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days and then slows down

There is a shift toward anaerobic and gram-negative flora Follows a typical topographic pattern. Initial growth along the

gingival margin and interdental space (areas protected by shear stress)

Can also start from grooves, cracks, perikymata or pits Rough intra oral surfaces accumulate and retain more plaque

(Quirynen and Bollen)

Plaque formation occurs much faster in the lower jaw, molar

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DE NOVO SUBGINGIVAL PLAQUE FORMATION

Technically impossible to record the dynamics of subgingival

plaque formation

Studies show that tooth surfaces harbor plaque and calculus

after scaling. These remain the primary source for subgingival recolonization

Leknes et al in 1994 did a study on beagle dogs. Studied the

extent of colonization in 6mm pockets. Observed that smooth surfaces harbored significantly less plaque

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PHYSIOLOGIC PROPERTIES OF DENTAL PLAQUE

Transition from gram positive to gram negative is accompanied

by physiologic transition in the developing plaque

Early colonizers lower the redox potential of the environment

and favour the growth of anaerobic species

Lactate and formate, by products of metabolism of streptococci

and actinomycetes maybe used in the metabolism of other plaque microorganisms

Host is also an important source of nutrients

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Nutritional interdependencies are critical for growth and

survival of the microorganism in dental plaque and partly explains the highly specific structural interactions among bacteria in plaque

Some researchers say the pathologic flora is due to ecological

plaque hypothesis

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Mid 1900s- periodontal disease was thought to be due to:

NONSPECIFIC PLAQUE HYPOTHESIS (Theilade 1986)

- accumulation of plaque over time - decreased host response - increased host susceptibility

This hypothesis maintains that periodontal disease results from the

elaboration of noxious products by the entire plaque flora.

The theory maintains that control of periodontal disease depends on control of

the amount of plaque accumulation.

Although discarded in favor of the Specific plaque hypothesis, clinical

treatment is still based on this theory.

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NONSPECIFIC PLAQUE HYPOTHESIS

Contradictions of theory: Individuals with considerable amounts

of plaque, calculus and gingivitis did not develop destructive periodontitis.

Individuals with periodontitis

demonstrated site-specificity in the disease pattern.

Some sites were unaffected whereas

SPECIFIC PLAQUE HYPOTHESIS

Sir Walter Loesche 1979 States that only certain plaque is pathogenic Pathogenecity depends on presence or increase in specific microorganisms Plaque which has specific bacterial pathogens results in periodontal disease- these organisms destroy host tissues Association of specific bacterial species with disease originated in 1960

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 Proposed by PD Marsh in 1991

ECOLOGICAL PLAQUE HYPOTHESIS

shift in the balance of the resident plaque microflora which might predispose a site to disease

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Says that a change in a key environmental factor will trigger a

In health, these organisms are only weakly competitive and not

significant clinically. Microbial specificity in disease is because only certain species are competitive under the new environmental conditions

It is a basic tenet of microbial ecology that a major change to an

ecosystem produces a corresponding disturbance to the stability of the resident microbial community (Brock 1966; Alexander

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ECOLOGICAL PLAQUE HYPOTHESIS

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CRITERIA FOR IDENTIFICATION OF PERIODONTAL PATHOGENS

In the 1870s Robert Koch developed classic criteria by which

a microorganism can be judged to be a causative agent in human infections

These criteria, known as KOCHS POSTULATES, stipulate the

following for the causative agents:

Must be routinely isolated from diseased individuals

Must be grown in pure culture in the laboratory

Must produce a similar disease when inoculated into susceptible

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Difficulties exist in the application of these criteria in the case

of periodontitis as:

1. 2. 3.

The inability to culture all the microorganisms that have been associated with the disease.(spirochetes). Difficulties inherent in defining and culturing sites of active disease Lack of good animal model system for study of periodontitis.

Carranzas Clinical Periodontology 10th edition

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In 1992, Sigmund Socransky , a researcher at Forsyth Dental Institute at Boston proposed criteria by which periodontal microorganisms maybe judged to be potential pathogens

These criteria are:

Must be increase in the number of organisms at diseased sites

Must be decreased at sites that show improvement with treatment

Must demonstrate a host response

Capable of causing disease in experimental animals

2/15/13 Association of plaque microorganisms with Periodontal disease

3 factors determine occurrence of active periodontitis:

Susceptible host

Presence of pathogenic species

Absence or a small proportion of beneficial bacteria

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SUSCEPTIBILITY OF HOST
Partially hereditary. Maybe influenced by smoking, diabetes

stress

Genetic mutations have been identified that alter host response

to bacteria and are associated with periodontal disease

Grossi et al. 1998 found a direct relation between periodontitis

and the level of smoking

Diabetics are at higher risk for periodontal destruction

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Marsh PD, Devine DA. How is the development of dental biofilms influenced by the host? J Clin Periodontol 2011;

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PRESENCE OF PATHOGENS
Presence of pathogens in sufficient numbers is essential

Key pathogens- Aggregetibacter actinomycetemcomitans,

Tannerella Forsythia and Porphyromonas gingivalis

Moderate evidence for etiology- Prevotella intermedia,

Prevotella nigrescens, Campylobacter rectus, Peptostreptococcus micros, Fusobacterium nucleatum, Eubacterium nodatum (past a certain threshold level)

Evidence based on epidemiologic data and results of animal

innoculation

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ROLE OF BENEFICIAL SPECIES

Affect disease progression in the following ways:

- occupying a niche that might otherwise have pathogens - limiting pathogens ability to adhere to appropriate tissue surfaces - affecting the growth of the pathogen - affecting the ability to produce virulence factors - degrading virulence factors produced by the pathogen
e.g. S. Sanguis produces hydrogen peroxide that kills A.

actinomycetemcomitans. (Hillman etal 1985)

Carranzas Clinical Periodontology 10th edition

2/15/13

MICROBIAL SHIFT DURING DISEASE

Gram positive to gram negative

From cocci to rods (later to spirochetes)

Non motile to motile organisms

Facultative to obligate anaerobes

Microbial shifts during dental biofilm redevelopment in the absence of oral hygiene in periodontal health and disease
Naciye G. Uzel1,, Flavia R. Teles1,2, Ricardo P. Teles1,2, Xiaoging Q. Song1, Gay Torresyap1,, Sigmund S. Socransky1, Anne D. Haffajee1 Journal of Clinical Periodontology Volume 38, Issue 7, pages 612620, July 2011

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Abstract Aim: To monitor microbial shifts during

dental biofilm re-development.

Materials and methods: Supra- and

subgingival plaque samples were taken separately from 28 teeth in 38 healthy and 17 periodontitis subjects at

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STRATEGIES TO PREVENT PERIODONTAL DISEASES

Conventional methods involve mechanical removal of

subgingival plaque along with antimicrobial therapy

Ecologic approach- alter the environment of the pocket to

prevent growth of pathogens

Can be done by: - Antimicrobial and anti-inflammatory agents - Oxygenating and redox agents

Novel drugs that specifically target quorum sensing systems are

1) Q uorumSensing (Y ung -H L 1,2,* is ua i capableiaolin Tian )and Bacterial Social Interactions ininfections in a manner that and of attenuating bacterial Biofilms A X nd less Sensors 2012 ,12 likely to result in the development of resistant mutants.(eg

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OMNIGENE
These are DNA probe systems for a

number of known periodontopathogen subgingival bacteria.

A paper point sample of sub-gingival

plaque is placed in the container provided and mailed off to the company for assay.

Probes are available for the detection of

A. actinomycetemcomitans, P. gingivalis, P. intermedia, F. nucleatum, C. rectus, T. denticola and E. corrodens.

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EVALUSITE
Evalusite is a kit that employs a novel membrane-based enzyme immunoassay for the detection of three putative periodontopathogens: Aa, Pg and Pi. A sub-gingival sample is collected using paper points and added to a sample tube. The eluent is then added to the kit, which employs a sandwich-type ELISA (enzyme-linked immunosorbent assay); a pink spot is displayed if the test organism is present. The main weaknesses of this test kit reside in
1) 2) 3)

the assumption that the three detected organisms are causing disease; (2) it is a multistage test; (3) it has a subjective calorimetric end point and

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PERIOSCAN
Perioscan is a diagnostic test kit that utilizes the BANA (N-

benzoyl-DL-arginine-2-naphthylamide)-hydrolysis reaction, developed to detect bacterial trypsin-like proteases in the dental plaque . gingivalis, T. denticola, T. forsythia and some Capnocytophagia strains. BANA is an example of a substrate-conjugated betanepthylamine (p-NA), which is hydrolyzed by this trypsin-like enzyme to release free p-NA. The latter is a chromophore and reacts with a variety of dyes (e.g. Fast-Garnet GBC) to produce colored products. Subgingival plaque is collected and placed on a BANAcontaining strip, which is then folded to contact a second strip containing the Fast-Black dye reagent.

A trypsin-like activity has been identified in strains of P.

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CONCLUSION
Dental plaque biofilm cannot be eliminated. However, the

pathogenic nature of the dental plaque biofilm can be reduced by reducing the bioburden (total microbial load and different pathogenic isolates within that dental plaque biofilm) and maintaining a normal flora with appropriate oral hygiene methods that include daily brushing, flossing and rinsing with antimicrobial mouthrinses. This can result in the prevention or management of the associated sequelae, including the development of periodontal diseases and possibly the impact of periodontal diseases on specific systemic disorder

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REFERENCES
Carranzas Clinical Periodontology- 9th , 10th Edition Clinical Periodontology and Implant Dentistry- Lindhe, 4th,5th Edition

The structure of Dental plaque- Max. Listgarten, Periodontology 2000, Vol 5. 1994

Microbial ecology of dental plaque and its significance in health and diseaseP.D. Marsh

Dental biofilms:difficult therapeutic targets- Sigmund Socransky and Anne D Haffajee, Periodontology 2000, Vol 28. 2002

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