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Microbiology of Microbiology of

periodontal diseaseperiodontal disease

DefinitionsDefinitions

Materia Alba is the soft accumulation of bacteria and tissue Materia Alba is the soft accumulation of bacteria and tissue cells that lack the organized structure of dental plaque, and is cells that lack the organized structure of dental plaque, and is easily displaced with a water Spray.easily displaced with a water Spray.

Dental Pellicle is a glycoprotein (prolineDental Pellicle is a glycoprotein (proline--rich protein) coat rich protein) coat derived from components of saliva and crevicular fluid as well derived from components of saliva and crevicular fluid as well as from bacterial and host tissue cell products and debris. as from bacterial and host tissue cell products and debris. Dental pellicle is initially coats a clean tooth surface.Dental pellicle is initially coats a clean tooth surface.

Dental Plaque is the soft deposits that form the bioflim Dental Plaque is the soft deposits that form the bioflim adhering to the tooth surface or other hard surfaces In the oral adhering to the tooth surface or other hard surfaces In the oral cavity. Dental plaque is a hostcavity. Dental plaque is a host--associated biofl which is associated biofl which is important for the microorganisms.important for the microorganisms.

Calculus Is a hard deposit that forms by mineralization of Calculus Is a hard deposit that forms by mineralization of dental plaque and is generally covered by a layer of dental plaque and is generally covered by a layer of unmineralized plaque.unmineralized plaque.

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Materia AlbaMateria Alba

Is a yellow or grayish white, soft, sticky, deposit, and less adherent then Is a yellow or grayish white, soft, sticky, deposit, and less adherent then dental plaque.dental plaque.

It Is a concentration of microorganisms, desquamated epithellal cells, It Is a concentration of microorganisms, desquamated epithellal cells, leukocytes, and a mixture of salivary proteins and lipids with few or no leukocytes, and a mixture of salivary proteins and lipids with few or no food particles.food particles.

It Is clearly visible and forms on tooth surfaces, restorations, calculus and It Is clearly visible and forms on tooth surfaces, restorations, calculus and gingiva.gingiva.

It accumulates on the gingival third of the teeth and on malposed teeth.It accumulates on the gingival third of the teeth and on malposed teeth.

It could be formed within a few hours on cleaned teeth when no food is It could be formed within a few hours on cleaned teeth when no food is ingested.ingested.

It can be flushed with water spray and mechanical cleansing is required.It can be flushed with water spray and mechanical cleansing is required.

It has an Irritating effect on gingiva which is caused by bacteria and their It has an Irritating effect on gingiva which is caused by bacteria and their products. It could be toxic.products. It could be toxic.

Formation of Dental PellicleFormation of Dental Pellicle

The pellicle forms by selective adsorption of the The pellicle forms by selective adsorption of the environmental macromolecules. This is indicated by environmental macromolecules. This is indicated by early early 22--hour enamel pellicle study which revealed hour enamel pellicle study which revealed that Its amino acid composition differs from that of that Its amino acid composition differs from that of saliva. This enamel (dental) pellicle is derived from saliva. This enamel (dental) pellicle is derived from components of saliva and crevicular fluid and host components of saliva and crevicular fluid and host tissue cell products and debris.tissue cell products and debris.

Pellicies function as a protective barrier, providing Pellicies function as a protective barrier, providing lubrication for the surfaces and preventing tissue lubrication for the surfaces and preventing tissue desiccation. It also provides a substrate to which desiccation. It also provides a substrate to which bacteria attach.bacteria attach.

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Classification of Dental PlaqueClassification of Dental Plaque::

Dental plaque is classified asDental plaque is classified as

11) Supraciingival Plague is found at or above the gingival margin, ) Supraciingival Plague is found at or above the gingival margin, in direct contact with the gingival margin and referred to as in direct contact with the gingival margin and referred to as marginal plaquemarginal plaque..

22) Suboinqival Plaque is found below the gingival margin, ) Suboinqival Plaque is found below the gingival margin, between the tooth and the gingival sulcular tissue. It could be between the tooth and the gingival sulcular tissue. It could be toothtooth--associated plaque and/or tissueassociated plaque and/or tissue--associated plaque.associated plaque.

Marginal plaque is important in the development of gingivitis.Marginal plaque is important in the development of gingivitis.

Supragingival and toothSupragingival and tooth--associated subginglval plaque are associated subginglval plaque are critical in calculus and root caries.critical in calculus and root caries.

TissueTissue--assodated subgingivai plaque Is Important in different assodated subgingivai plaque Is Important in different forms of periodontitis. forms of periodontitis.

Composition of Dental PlaqueComposition of Dental Plaque

It is composed primarily of microorganisms. One gram of wet It is composed primarily of microorganisms. One gram of wet weight plaque contains weight plaque contains 2 2 x x 1011 1011 bacteria. Bacterial and nonbacteria. Bacterial and non--bacterial microorganisms are the components of the dental bacterial microorganisms are the components of the dental plaque.plaque.

Bacterial account for almost all of the plaque weight. More Bacterial account for almost all of the plaque weight. More than than 325 325 different bacterial species may be found in plaque, different bacterial species may be found in plaque, e.g. Porphyromonas gingivalis, Porphyromonas endodontalis, e.g. Porphyromonas gingivalis, Porphyromonas endodontalis, Prevotella lntermedia, Prevotella melaninogenica, Prevotella Prevotella lntermedia, Prevotella melaninogenica, Prevotella denticola, Prevoteila loescheil, Campylobacter rectus and denticola, Prevoteila loescheil, Campylobacter rectus and Campylobacter curvus.Campylobacter curvus.

NonNon--Bacterial microorganisms include Myocplasma species, Bacterial microorganisms include Myocplasma species, yeasts, protozoa, and viruses.yeasts, protozoa, and viruses.

Microorganisms exist in an intercellular matrix which also Microorganisms exist in an intercellular matrix which also contains a few host cells, such as epithelial cells, macrophages contains a few host cells, such as epithelial cells, macrophages and leukocytes.and leukocytes.

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The interce matrix is The interce matrix is 20 20 to to 3030% of the plaque mass. It % of the plaque mass. It forms a hydrated gel in which the embedded bacteria forms a hydrated gel in which the embedded bacteria exist and proliferate. Intercellular matrix consists of exist and proliferate. Intercellular matrix consists of organic and Inorganic materials derived from saliva, organic and Inorganic materials derived from saliva, gingival crevicular fluid, and bacterial products.gingival crevicular fluid, and bacterial products.

Organic materials include polysaccharides, proteins, Organic materials include polysaccharides, proteins, glycoproteins, and lipids.glycoproteins, and lipids.

Inorganic materials are calcium and phosphorus, with Inorganic materials are calcium and phosphorus, with traces of sodium, potassium, and fluoride.traces of sodium, potassium, and fluoride.

The source of inorganic supragingival plaque is salivaThe source of inorganic supragingival plaque is saliva

The inorganic component of subgingival plaque is The inorganic component of subgingival plaque is derived from crevicular fluidderived from crevicular fluid

The fluoride of the plaque is derived from fluoridated The fluoride of the plaque is derived from fluoridated toothpastes and rinses.toothpastes and rinses.

The Intercellular matrix functions as a barrier, and The Intercellular matrix functions as a barrier, and protects the bacteria from antimicrobial agents. protects the bacteria from antimicrobial agents.

Formation of Dental PlaqueFormation of Dental Plaque

It Is visualized after It Is visualized after 1 1 to to 2 2 days with no oral hygiene. days with no oral hygiene.

Plaque Is white, grayish or yellow and has a globular Plaque Is white, grayish or yellow and has a globular

appearance. It accumulates on the gingival third of appearance. It accumulates on the gingival third of

the tooth surface, in cracks, pits, fissures, under the tooth surface, in cracks, pits, fissures, under

overhanging restorations, and around malanigned overhanging restorations, and around malanigned

teeth.teeth.

Detection of plaque is done by a periodontal probe or Detection of plaque is done by a periodontal probe or

explorer along the gingival third of the tooth. It is explorer along the gingival third of the tooth. It is

also done by the use of also done by the use of disclosing solutionsdisclosing solutions..

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Phases of Plaque FormationPhases of Plaque Formation

11)) Formation of the dental pellicle.Formation of the dental pellicle.

22)) Initial colonization by bacteria.Initial colonization by bacteria.

33)) Secondary colonization and plaqueSecondary colonization and plaque

maturation.maturation.

1.1. Formation of the Dental Pellicle:Formation of the Dental Pellicle: All surfaces of the All surfaces of the oral cavity as well as surfaces of teeth and fixed and oral cavity as well as surfaces of teeth and fixed and removable restorations are coated with the pellicle. Pellicles removable restorations are coated with the pellicle. Pellicles provide a substance to which bacteria attach. Pellicle on the provide a substance to which bacteria attach. Pellicle on the nonnon--shedding hard surfaces provides a substrate on which shedding hard surfaces provides a substrate on which bacteria progressively accumulate to form dental plaque.bacteria progressively accumulate to form dental plaque.

2.2. Initial Colonization of the Tooth SurfaceInitial Colonization of the Tooth Surface:: Within a Within a few hours, bacteria are found on the dental pellicle. The initial few hours, bacteria are found on the dental pellicle. The initial bacteria which colonize the pellicle are Grambacteria which colonize the pellicle are Gram--positive positive facultative microorganisms, e.g. Actinomyces viscosus and facultative microorganisms, e.g. Actinomyces viscosus and Streptococcus sanguis. These bacteria adhere to the pellicle. Streptococcus sanguis. These bacteria adhere to the pellicle. The plaque mass then matures through the growth of attached The plaque mass then matures through the growth of attached species as well as additional species. There is a transition species as well as additional species. There is a transition from aerobic Gramfrom aerobic Gram--positive species to a highly Opositive species to a highly O2 2 environment in which Gramenvironment in which Gram--negative anaerobic negative anaerobic microorganisms predominate.microorganisms predominate.

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3)3) Secondary Colonization and Plaque MaturationSecondary Colonization and Plaque Maturation: : Secondary colonizers are microorganisms that do not Secondary colonizers are microorganisms that do not colonize clean tooth surfaces,colonize clean tooth surfaces, e.g. Prevotella intermedia, Prevotella loescheii, e.g. Prevotella intermedia, Prevotella loescheii,

Capnocytophaga species, fysobacterium nucleatum and Capnocytophaga species, fysobacterium nucleatum and Porphyromonas gingivalis. These microorganisms adhere Porphyromonas gingivalis. These microorganisms adhere to cells of bacteria in the dental plaque mass.to cells of bacteria in the dental plaque mass.

CoaggregationCoaggregation is the ability of different species of is the ability of different species of plaque microorganisms to adhere to one another. plaque microorganisms to adhere to one another. WellWell--characterized interactions of secondary characterized interactions of secondary colonizers with early colonizers include the colonizers with early colonizers include the coaggregation of F. nucleatum with S. sanguis, coaggregation of F. nucleatum with S. sanguis, P.loescheii with A. viscosus, and Capnocytophaga P.loescheii with A. viscosus, and Capnocytophaga ochracea with A. viscosus. In the later stages of ochracea with A. viscosus. In the later stages of plaque formation, coaggregation between different plaque formation, coaggregation between different GramGram--negative species predominate, e.g. F. negative species predominate, e.g. F. nucleatum with P. gingivalisnucleatum with P. gingivalis

Structure of Dental PlaqueStructure of Dental Plaque

Supragingival plaque demonstrates GramSupragingival plaque demonstrates Gram--positive positive cocci and short rods at the tooth surface.cocci and short rods at the tooth surface.

GramGram--negative rods, filaments, and spirochetes negative rods, filaments, and spirochetes predominate in the outer surface of the mature plaque predominate in the outer surface of the mature plaque mass.mass.

LongLong--standing supragingival plaque near the gingival standing supragingival plaque near the gingival margin demonstrates "corncob" arrangement. The margin demonstrates "corncob" arrangement. The central (inner) core of the "corncob" arrangement is central (inner) core of the "corncob" arrangement is formed of rodformed of rod--shaped bacterial cells (bacterionoma shaped bacterial cells (bacterionoma mantruchotii , or F.neucletum) coccal cells (e.g. mantruchotii , or F.neucletum) coccal cells (e.g. Streptococci or . P.gingivalis) attach along the surface Streptococci or . P.gingivalis) attach along the surface of the rodof the rod--shaped cell.shaped cell.

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Subgingival plaque the toothSubgingival plaque the tooth--associated (attached) associated (attached) plaque is characterized by Gramplaque is characterized by Gram--positive rods and positive rods and cocci including Streotococcus mitis, S. sanguis, A. cocci including Streotococcus mitis, S. sanguis, A. viscosus , actinomyces naesluldii and Eubacterium viscosus , actinomyces naesluldii and Eubacterium speciesspecies

The apical border of the plaque is separated from the The apical border of the plaque is separated from the junctional epithelium by a layer of host leukocytes. junctional epithelium by a layer of host leukocytes. This apical toothThis apical tooth--associated plaque contains increased associated plaque contains increased concentration of Gramconcentration of Gram--negative rods.negative rods.

TissueTissue--associated plaque is loosely organized than the associated plaque is loosely organized than the very dense toothvery dense tooth-- associated region. It contains Gramassociated region. It contains Gram--negative rods and cocci, as well as filaments, negative rods and cocci, as well as filaments, flagellated rods, and spirochetes. Host tissue cells flagellated rods, and spirochetes. Host tissue cells (WBCs, and epithelium cells) may be found in this (WBCs, and epithelium cells) may be found in this plaque. P. gingivalis, P. intermedia, and C. ochracea plaque. P. gingivalis, P. intermedia, and C. ochracea are found in this tissueare found in this tissue--associated plaque.associated plaque.

Plaque HypothesisPlaque Hypothesis

Recognition of the differences in plaque at Recognition of the differences in plaque at

sites of different clinical status (i.e. disease sites of different clinical status (i.e. disease

versus health) led to new plaque hypothesis.versus health) led to new plaque hypothesis.

The renewed search showed a conceptual The renewed search showed a conceptual

transition from the non specific to the specific transition from the non specific to the specific

plaque hypothesis.plaque hypothesis.

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A.A. NonNon--Specific Plaque Hypothesis:Specific Plaque Hypothesis: This states This states that periodontal disease results from the elaboration that periodontal disease results from the elaboration

of noxious products by the entire plaque flora. of noxious products by the entire plaque flora.

According to this, small amounts of plaque that According to this, small amounts of plaque that

produce small noxious products, are neutralized by produce small noxious products, are neutralized by

the host. Similarly, large amounts of plaque the host. Similarly, large amounts of plaque

produce large amounts of noxious products which produce large amounts of noxious products which

overwhelm the hostoverwhelm the hosts defense. This hypothesis s defense. This hypothesis

brought the concept of controlled periodontal brought the concept of controlled periodontal

disease which depends on removal of the dental disease which depends on removal of the dental

plaque by debridement (nonplaque by debridement (non--surgical or surgical) surgical or surgical)

and oral hygiene measures. Much clinical treatment and oral hygiene measures. Much clinical treatment

Is still based on the nonIs still based on the non--specific plaque hypothesis.specific plaque hypothesis.

B.B. Specific Plaque Hypothesis :Specific Plaque Hypothesis : This This hypothesis states that only certain plaque is hypothesis states that only certain plaque is pathogenic, and its pathogenicity depends on pathogenic, and its pathogenicity depends on the presence of, or increase in specific the presence of, or increase in specific microorganisms. Example that helped in microorganisms. Example that helped in accepting this specific hypothesis is the accepting this specific hypothesis is the recognition of Actinobacillus recognition of Actinobacillus actinomycetemcomitans as a pathogen in L. actinomycetemcomitans as a pathogen in L. juvenile periodontitis.juvenile periodontitis.

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Criteria That Determine the Relationship of Bacteria Criteria That Determine the Relationship of Bacteria

to Diseaseto Disease

1.1. High numbers of organisms should be at sites of disease High numbers of organisms should be at sites of disease

and absent or infrequently found at healthy sites.and absent or infrequently found at healthy sites.

2.2. Elimination or suppression of the organism by treatment Elimination or suppression of the organism by treatment

should have a positive influence.should have a positive influence.

3.3. Elevated immune response to the organism should be Elevated immune response to the organism should be

present. This may be an elevated antibody response or a present. This may be an elevated antibody response or a

cellular response.cellular response.

4.4. The organism should cause some of the characteristics of The organism should cause some of the characteristics of

the disease in experimental animals (i.e. inflammation, the disease in experimental animals (i.e. inflammation,

connective tissue destruction and bone loss).connective tissue destruction and bone loss).

5.5. The putative pathogen should possess pathogenic or The putative pathogen should possess pathogenic or

virulent potential.virulent potential.

Each disease is associated with different Each disease is associated with different

groups of microorganisms, resulting in clinical groups of microorganisms, resulting in clinical

signs and symptoms that can be similar or signs and symptoms that can be similar or

unique.unique.

The mechanisms by which subgingival The mechanisms by which subgingival

bacteria contribute to pathogenesis of bacteria contribute to pathogenesis of

periodontal disease are varied.periodontal disease are varied.

The periodontal pathogens possess numerous The periodontal pathogens possess numerous

(actors that permit them to damage the (actors that permit them to damage the

periodontium directly or to trigger a pathologic periodontium directly or to trigger a pathologic

host response indirectly. host response indirectly.

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Pathogenic Bacterial Mechanisms in Pathogenic Bacterial Mechanisms in

Periodontal DiseasePeriodontal Disease

Pathogenic microorganisms may influence the Pathogenic microorganisms may influence the

course of the disease process by producing course of the disease process by producing

tissuetissue--toxic substances, by directly invading toxic substances, by directly invading

host tissues, and by stimulating a host responsehost tissues, and by stimulating a host response

The pathogenic process happens when a The pathogenic process happens when a

bacterium colonizes the appropriate host bacterium colonizes the appropriate host

tissue site, then causes destruction of the host tissue site, then causes destruction of the host

tissues.tissues.

Pathogenic mechanismsPathogenic mechanisms are:are:

1.1. Invasion.Invasion.

2.2. Production of exotoxins.Production of exotoxins.

3.3. Role of cell constituents (endotoxins, surface Role of cell constituents (endotoxins, surface

components, capsular components, etc ..components, capsular components, etc ..

4.4. Production of enzymes.Production of enzymes.

5.5. Evasion of immunologic host responses.Evasion of immunologic host responses.

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In periodontitis, the Initial step is the In periodontitis, the Initial step is the

colonization of the periodontal tissues by colonization of the periodontal tissues by

pathogenic species. Entry of the bacterium, pathogenic species. Entry of the bacterium,

itself, (invasion) or bacterial products into the itself, (invasion) or bacterial products into the

periodontal tissues Is essential for disease periodontal tissues Is essential for disease

process.process.

Virulence products are two groups:Virulence products are two groups:

1.1. Factors that enable a bacterial species to colonize Factors that enable a bacterial species to colonize and Invade host tissues.and Invade host tissues.

2.2. Factors that enable a bacterial species to directly or Factors that enable a bacterial species to directly or Indirectly cause host tissue damage.Indirectly cause host tissue damage.

3.3. Bacterial species colonize the region of the gingival Bacterial species colonize the region of the gingival sulcus and periodontal pocket. These bacterial must sulcus and periodontal pocket. These bacterial must attach to available surfaces (tooth or mot tissue) to attach to available surfaces (tooth or mot tissue) to avoid displacement by gingival crevicular fluid avoid displacement by gingival crevicular fluid (GCF) flow. So, adherence represents a virulence (GCF) flow. So, adherence represents a virulence factor for periodontal pathogens.factor for periodontal pathogens.

Bacteria which colonize periodontal tissues attach Bacteria which colonize periodontal tissues attach to the pelliclesto the pellicles-- or salivaor saliva--coated tooth surfaces.coated tooth surfaces.

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Host Tissue InvasionHost Tissue Invasion

Bacteria may enter host tissues through ulcerations in the Bacteria may enter host tissues through ulcerations in the epithelium of the gingival sulcus or pocket, microorganisms epithelium of the gingival sulcus or pocket, microorganisms have been observed In intercellular spaces of the gingival have been observed In intercellular spaces of the gingival tissues. Tissue invasion may also involve the direct penetration tissues. Tissue invasion may also involve the direct penetration of bacteria into host epithellal or connective tissue cells, e.g. of bacteria into host epithellal or connective tissue cells, e.g. A. actinomyceterncomilans p. gingivals and Trepanema cola A. actinomyceterncomilans p. gingivals and Trepanema cola have the ability to invade host tissue cells. This ability to have the ability to invade host tissue cells. This ability to invade is a key factor that distinguish pathogenic from invade is a key factor that distinguish pathogenic from nonpathogenic Gramnonpathogenic Gram--negative species.negative species.

Bursts of disease activity in perlodontitis may be related to Bursts of disease activity in perlodontitis may be related to phases of bacterial invasion of the tissue. An additional phases of bacterial invasion of the tissue. An additional possibility Is that bacteria In tissue may enable persistence of possibility Is that bacteria In tissue may enable persistence of that species In the periodontal pocket by providing a reservoir that species In the periodontal pocket by providing a reservoir for refor re--colonization.colonization.

Bacterial Evasion of Host Defense Bacterial Evasion of Host Defense

MechanismMechanism

For bacteria to survive in tissues, they must For bacteria to survive in tissues, they must

neutralize or evade the host mechanisms Induced neutralize or evade the host mechanisms Induced

involved in bacterial clearance and killing. Bacterial involved in bacterial clearance and killing. Bacterial

Factors that help in evasion of host defenses are:Factors that help in evasion of host defenses are:

1.1. Inhibition of PMNS : Leukotaxia, chemotaxis inhibitors Inhibition of PMNS : Leukotaxia, chemotaxis inhibitors

decreased phagocytosis and intracellular killing.decreased phagocytosis and intracellular killing.

2.2. Lymphocytes alterations.Lymphocytes alterations.

3.3. Endotoxicity.Endotoxicity.

4.4. IgA, IgG proteases.IgA, IgG proteases.

5.5. Catalase Catalase

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Adherence of bacteria allows it to avoid displacement Adherence of bacteria allows it to avoid displacement

by host secretions. Eukaryotic cells invasion disrupts by host secretions. Eukaryotic cells invasion disrupts

the natural bafflers formed by host tissue cells. the natural bafflers formed by host tissue cells.

Production of immunoglobulinProduction of immunoglobulin--degrading proteases degrading proteases

by specific microorganisms may counteract host by specific microorganisms may counteract host

defenses. Bacteria also produce substances that defenses. Bacteria also produce substances that

suppress the activity of, or kill polymorphonuclear suppress the activity of, or kill polymorphonuclear

leukocytes (PMNs) and lymphocytes that are leukocytes (PMNs) and lymphocytes that are

normally involved in host defenses.normally involved in host defenses.

Mechanisms of Host Tissue DamageMechanisms of Host Tissue Damage

Bacterial properties can be categorized Into (a) those Bacterial properties can be categorized Into (a) those that cause the release of biologicallythat cause the release of biologically--active active substances from host tissue cells and (b) those substances from host tissue cells and (b) those resulting directly in degradation of host tissues.resulting directly in degradation of host tissues.

Some bacterial products inhibit the growth or alter the Some bacterial products inhibit the growth or alter the metabolism of host tissue cells; (e.g. a number of metabolism of host tissue cells; (e.g. a number of metabolic byproducts such as ammon volatile sulfur metabolic byproducts such as ammon volatile sulfur compounds; and may adds, peptides, and indole).compounds; and may adds, peptides, and indole).

Exotoxins produced by some plaque microorganism Exotoxins produced by some plaque microorganism are responsible of that tissue damage. A. are responsible of that tissue damage. A. actinomycete,ncomitans produces an exotoxin that actinomycete,ncomitans produces an exotoxin that evade the host defense of phagocytosls. This exotoxin evade the host defense of phagocytosls. This exotoxin is known as is known as because of Its toxic effect on human because of Its toxic effect on human PMNs.PMNs.

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Cell constituents of both GramCell constituents of both Gram--positive and positive and GramGram--negative bacteria may also play a role in negative bacteria may also play a role in periodontal disease. These include endotoxins, periodontal disease. These include endotoxins, bacterial surface components and capsular bacterial surface components and capsular components.components.

Endotoxins, or lipoollgosaccharlde (= Endotoxins, or lipoollgosaccharlde (= lipopolysaccharlde) is found In the outer lipopolysaccharlde) is found In the outer membrane of all Grammembrane of all Gram--negative bacteria.negative bacteria.

Endotoxins are highly toxic substances, Endotoxins are highly toxic substances, affecting tissues directly and through affecting tissues directly and through activation of host responses. They penetrate activation of host responses. They penetrate gingival epithelium.gingival epithelium.

Role of Endotoxins in Periodontal Role of Endotoxins in Periodontal

DiseasesDiseases1.1. Production of leukopenia.Production of leukopenia.

2.2. Activation of factor X (or HagemanActivation of factor X (or Hagemans factor), which s factor), which affects the clotting system leading to intravascular affects the clotting system leading to intravascular coagulation.coagulation.

3.3. Activation of the complement by the alternative Activation of the complement by the alternative pathway.pathway.

4.4. Localization of Shwartzman phenomenon, with Localization of Shwartzman phenomenon, with tissue necrosis after two or more exposures to tissue necrosis after two or more exposures to endotoxins.endotoxins.

5.5. Endotoxins have cytotoxic effects on cells such as Endotoxins have cytotoxic effects on cells such as fibroblasts.fibroblasts.

6.6. Endotoxins also induce bone resorption in organ Endotoxins also induce bone resorption in organ culture.culture.

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GramGram--positive and Grampositive and Gram--negative subgingival negative subgingival bacteria produce toxic endproducts (e.g. fatty acids, bacteria produce toxic endproducts (e.g. fatty acids, amines, volatile sulpher compounds, ammonia end amines, volatile sulpher compounds, ammonia end products, and glycans), which are capable of tissue products, and glycans), which are capable of tissue destruction.destruction.

Peptidoglycan, a cellPeptidoglycan, a cell--wall component of Gramwall component of Gram--positive and Grampositive and Gram-- negative species, activates negative species, activates complement system, causes immunosuppressive complement system, causes immunosuppressive activity, stimulates the reticuloendothelial system, activity, stimulates the reticuloendothelial system, and produces Immunopotentiating properties.and produces Immunopotentiating properties.

Peptidoglycan also can stimulate bone resorption and Peptidoglycan also can stimulate bone resorption and macrophages to produce prostaglandin and macrophages to produce prostaglandin and coliagenase.coliagenase.

Enzymes produced by periodontal microorganisms Enzymes produced by periodontal microorganisms are capable of degrading all the host tissue and are capable of degrading all the host tissue and intercellular matrix molecules. intercellular matrix molecules.

Examples:Examples:

p gingivalis produces collagenases, proteases, p gingivalis produces collagenases, proteases,

including a trypsinincluding a trypsin--like enzyme, enzymes that like enzyme, enzymes that

degrade collagen, fibronectin, and Igs.degrade collagen, fibronectin, and Igs.

A.A. actinomvcetemcomitans produce collagenase.actinomvcetemcomitans produce collagenase.

B.B. Gingivalis and T. denticola produce keratinase.Gingivalis and T. denticola produce keratinase.

C.C. Ginaivalis and B. forsytlius produce neuraminase.Ginaivalis and B. forsytlius produce neuraminase.

Other enzymes are hyaluronidase, gelatinase, Other enzymes are hyaluronidase, gelatinase,

phospholipase, and alkaline and acid phospholipase, and alkaline and acid

phosphatases.phosphatases.

Bacterial enzymes facilitate tissue destruction and Bacterial enzymes facilitate tissue destruction and

invasion of bacteria into host tissue.invasion of bacteria into host tissue.

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Host Immune system involves a complex interactions Host Immune system involves a complex interactions

between cells and regulatory molecules. Bacterial between cells and regulatory molecules. Bacterial

products may perturb the system, resulting tissue products may perturb the system, resulting tissue

destruction. Example the interaction between destruction. Example the interaction between

interleukininterleukin--1 1 (IL(IL-- tumor necrosis factor, and tumor necrosis factor, and

prostaglandins (from macrophages and monocytes), prostaglandins (from macrophages and monocytes),

and bacterial endotoxin (lipopolysaccaride). These and bacterial endotoxin (lipopolysaccaride). These

hosthost--derived cytokines stimulate bone resorption and derived cytokines stimulate bone resorption and

activate or inhibit other host immune cells.activate or inhibit other host immune cells.

Periodontal destruction means the degradation of Periodontal destruction means the degradation of

collagen. The primary source of collagenase is host collagen. The primary source of collagenase is host

tissue cells, but bacterial collagenases may also tissue cells, but bacterial collagenases may also

contribute to collagen degradation.contribute to collagen degradation.

Bacterial hyaluronidase alters gingival Bacterial hyaluronidase alters gingival

permeability by allowing apical proliferation permeability by allowing apical proliferation

of the junctional epithelium along the root of the junctional epithelium along the root

surface.surface.

Hvaluronidase is higher in concentration in Hvaluronidase is higher in concentration in

periodontal pocket than in normal sulcl. It periodontal pocket than in normal sulcl. It

leads to widening of the intercellular spaces leads to widening of the intercellular spaces

and increased permeability.and increased permeability.

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Microorganisms in Periodontal HealthMicroorganisms in Periodontal Health

The gingival crevice is not sterile. In healthy The gingival crevice is not sterile. In healthy

sulci from young adults, Gramsulci from young adults, Gram--positive positive

microorganisms form microorganisms form 22//3 3 of the total flora.of the total flora.

The total number of bacteria per gram of The total number of bacteria per gram of

plaque Is twice as high in periodontally disease plaque Is twice as high in periodontally disease

sites than in healthy sitessites than in healthy sites

GramGram--positive facultative rods and cocci positive facultative rods and cocci 7575% [ of % [ of Streatococus Actinomyces (e.g. S. sanguis S. mitis Streatococus Actinomyces (e.g. S. sanguis S. mitis A. viscosus A. naeslundii)]A. viscosus A. naeslundii)]

GramGram--negativenegative 1313% (e.g. P. intermedia, F. % (e.g. P. intermedia, F. nudeatum and Capnocytophaga, Neisseria, and nudeatum and Capnocytophaga, Neisseria, and Veillonella species).Veillonella species).

Spirochetes and motile rods are found.Spirochetes and motile rods are found.

Certain bacterial species may be protective or Certain bacterial species may be protective or beneficial to the host (e.g. S. sanaulis, Velionella beneficial to the host (e.g. S. sanaulis, Velionella parvula and C. odvara) These are present at parvula and C. odvara) These are present at periodontal sites In high numbers but do not cause periodontal sites In high numbers but do not cause attachment loss (inactive sites). They are found in less attachment loss (inactive sites). They are found in less numbers at sites with active destruction. These numbers at sites with active destruction. These species function in preventing the colonization or species function in preventing the colonization or proliferation of pathogenic microorganisms (e.g. proliferation of pathogenic microorganisms (e.g. 55. . sanauls produce l which is lethal to sanauls produce l which is lethal to 44. . actinomvceterncormtans)actinomvceterncormtans)

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Microorganisms Associated with Microorganisms Associated with

GingivitisGingivitis

In chronic gingivitis, bacteria consist of In chronic gingivitis, bacteria consist of 5656% %

GramGram--positive species and positive species and 4444% Gram% Gram--

negative species. negative species. 5959% of facultative and % of facultative and 4141% %

of anaerobic microorganisms . of anaerobic microorganisms .

1.1. GramGram--positive are S. sanpuis S. mitis A. viscasus positive are S. sanpuis S. mitis A. viscasus

A. naeslundii, and Paptostmptococcus microsA. naeslundii, and Paptostmptococcus micros

2.2. GramGram--negative are nudealum P. intermedia V. negative are nudealum P. intermedia V.

parvula and Haemophllus and Campylobacter parvula and Haemophllus and Campylobacter

species.species.

In pregnancy gingivitis, dramatic Increases in In pregnancy gingivitis, dramatic Increases in P. intermedia which use the steroid (hormone) P. intermedia which use the steroid (hormone) as growth factor are evident.as growth factor are evident.

In acute necrotizing ulcerative gingivitis In acute necrotizing ulcerative gingivitis (ANUG), high levels of a intermedia and (ANUG), high levels of a intermedia and spirochetes. Spirochetes penetrate necrotic spirochetes. Spirochetes penetrate necrotic tissue as well as unaffected connective tissues.tissue as well as unaffected connective tissues.

Gingivitis is associated with alterations In the Gingivitis is associated with alterations In the microbial composition of dental plaque and is microbial composition of dental plaque and is not due to an accumulation of plaque.not due to an accumulation of plaque.

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Microorganisms Associated with Adult Microorganisms Associated with Adult

PeriodontitisPeriodontitis

Elevated proportions of spirochetes.Elevated proportions of spirochetes.

High anaerobic (High anaerobic (9090%) Gram%) Gram--negative (negative (7575%) species.%) species.

In chronic adult periodontitis, high levels of In chronic adult periodontitis, high levels of

gingivalis, Bacteriodes forsythus P. intermedia, C. gingivalis, Bacteriodes forsythus P. intermedia, C.

rectus, Eikenella convdens F., nudeaturn A. rectus, Eikenella convdens F., nudeaturn A.

actinomvcetemcomitans treponema and Eubacterium actinomvcetemcomitans treponema and Eubacterium

species.species.

In active sites (I.e. with recent attachment loss), .C. In active sites (I.e. with recent attachment loss), .C.

rectus . P., gingivalis, B. Intermedia if nudeatum B., rectus . P., gingivalis, B. Intermedia if nudeatum B.,

forsythas are elevated than at inactive sites (I.e. no forsythas are elevated than at inactive sites (I.e. no

recent attachment loss).recent attachment loss).

Rapidly Progressive PeriodontitisRapidly Progressive Periodontitis

P. gingivalis, B. intermedia A. P. gingivalis, B. intermedia A.

actinomycetemcormtans E. corrodens, actinomycetemcormtans E. corrodens,

C rectus and B. acteriodes capilus.C rectus and B. acteriodes capilus.

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Juvenile PeriodontitisJuvenile Periodontitis

Microorganisms are GramMicroorganisms are Gram--negative, negative,

Capnophilic and anaerobic rods.Capnophilic and anaerobic rods.

Almost all L. juvenile periodontitis sites Almost all L. juvenile periodontitis sites

harbor A. actinomycetemcormtans which harbor A. actinomycetemcormtans which

make up make up 9090% of the total microbiota.% of the total microbiota.

Other organisms include Other organisms include . gingivalis E. . gingivalis E.

corrodens C. rectus nucleatum B. capilus, corrodens C. rectus nucleatum B. capilus,

Eubacterium brachy Capnocytophaga Eubacterium brachy Capnocytophaga

subspecies (ssp) and Spirochetes.subspecies (ssp) and Spirochetes.

Prepubertal PeriodontitisPrepubertal Periodontitis

Microorganisms are P. gingivalis, P. Microorganisms are P. gingivalis, P.

intermedia,. A. actinomycetemcomtans and F. intermedia,. A. actinomycetemcomtans and F.

nucleatum.nucleatum.