perio slide #5

8/13/2019 Perio Slide #5

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Pathogenesis..

Immunesystem

Host response

Inflammation

Clinical

signs

BacterialPlaque

Periodontal diseases:


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Pathogenesis..

Host

tissuesBacterial

Plaque


Host

Response


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Pathogenesis..

Host

tissuesBacterial

Plaque


Host

ResponseProtective or

Destructive?


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The presence of periodontal pathogens alone is

insufficient to cause the tissue destruction

seen in periodontitis.

It is the bodys response to the periodontal

pathogens that is the cause of nearly all the

destruction seen in periodontitis.

So..


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Bacterial Virulence Factors

Virulence factorsmechanisms that

enable the bacteria to colonize and invade

the tissues of the periodontium

Minor causeof periodontal destruction


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Bacterial Virulence Factors:

Characteristics of the bacteria,

themselves

Products produced by the bacteria


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Bacterial Characteristics

Bacterial invasion factorsallow

bacterium to actively penetrate the

epithelium lining of the pocket wall and

enter the gingival connective tissue

Peptidesfound in the bacterial cell

membrane


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Bacterial Products

Exotoxinsharmful proteins (potent

toxin) released from the bacterial cell

Enzymesproteins that catalyze

chemical reactions that are harmful to the

bodys cells


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Bacterial Colonization

(biofilm)


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Bacterial Colonization


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Coaggregation of Bacteria

Coaggregationthe cell-to-cell

adherence of one oral bacterium to

another.

Coaggregation is NOT random, each

bacterial strain only has a limited set of

bacteria to which they are able to adhere.


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Coaggregation of Bacteria

Early

Intermediate

Late


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Early Colonizers

The first bacteria to colonize the tooth

surface are nonpathogenic.

Periodontal pathogens are UNABLE to

colonizethe biofilm alone.

Non-

Pathogenic

PathogenicTooth/ or

hard tissue


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Colonization of the Pellicle

Early Gram-positive: Act inomyces v iscosus

Attaches to fimbriae to proline rich proteins on saliva coated

tooth surfaces.

Streptococcus sanguis


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Streptococcal SpeciesEarly

Colonizers

Many streptococcal species have the

ability to attach to the tooth pellicle

Other early colonizers coaggregate with

the streptococcal species.


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The Importance of Early

Colonizers

Free-floating periodontal pathogens

cannot cause disease.

Every time the biofilm is disrupted, the

process must start all over again with

the early colonizers.


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Intermediate and Late

Colonizers

Like the early colonizers, the intermediate

and late bacterial colonizers must join the

biofilm in the proper sequence.

Many of the periodontal pathogens are

late colonizersof the biofilm.


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Intermediate Coaggregation

Bacteria begin to multiply.


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Gram-Negative Organisms

Gram-negative bacteria join:

Fusobacterium nucleatum

Prevotella intermedia


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Gram-negative bacteria colonize

Porphyromonas gingivalis

Capnocytophaga gingivalis

Gram-Negative Organisms


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Socranskys

Microbial Complexes


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Biochemical Mediators


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Biochemical mediatorsare biologically

active compounds secreted by the immune

cells that activate the bodys inflammatory

response.


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Biochemical Mediators

Released by the immune cells to activate the

inflammatory response.

Inflammatory mediators of importance in

periodontal disease are

Cytokines

Prostaglandins

Matrix metalloproteinases (MMPs)


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CytokinesCell signalling protein molecules

Powerful mediators produced by immune

cells

Influence the behavior of other cells

Signalto the immune system to send morephagocytes to site of infection


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Cytokines (cont.)Produced by many different cellsPMNs,

macrophages, B lymphocytes, epithelialcells, gingival fibroblasts, and osteoblasts

Produced in response to tissue injury

Cytokines important in periodontal disease

include IL-1, IL-6, IL-8, and TNF-alpha.


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Functions of Cytokines

Recruit cells (PMNs and macrophages) to

infection site

Increase vascular permeability that increases

movement of immune cells into the tissues

Can initiate tissue destruction and bone

lossin chronic infections, such as

periodontal disease


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ProstaglandinsPotent inflammatory mediators

Series of prostaglandinsD, E, F, G, H, IMost cells can produce prostaglandins

(arachidonic acid in the cell membrane)

Macrophages and fibroblasts


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Functions of Prostaglandins

Increase permeability and dilatation of blood

vessels to promote increased movement ofimmune cells and complement to the

infection site

Trigger osteoclastsbone-consuming

cellsto destroy the alveolar bone


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Functions of Prostaglandins

Promote the overproduction of destructive

MMP enzymes

Prostaglandins of the E series (PGE)

initiate most of the alveolar bone

destruction in periodontitis.


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Matrix Metalloproteinases

(MMPs)

Family of at least 12 different enzymes

Produced by various cells of the body

PMNs, macrophages, fibroblasts, JE cells

Enzymes act together to breakdown

connective tissue matrix (collagen,gelatin,elastin)


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Function of MMPs in Health

In health, MMPs facilitate normal turnover of

the periodontal connective tissue matrix.


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MMPsChronic Bacterial

InfectionMMPs are released

Overproduction of MMPs results in

breakdown of connective tissue of the

periodontium.


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High MMP levels result in extensive collagen

destruction in the periodontal tissues.

Gingival recession, pocket formation, and

tooth mobility.

MMPsChronic Bacterial

Infection


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Host Response in

Periodontal Disease


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Initial


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Bacteria colonize the tooth near the

gingival margin.

Bacteria initiate host response.

PMNs pass from bloodstream into

the gingival connective tissue.

PMNs release cytokines that

destroy gingival connective tissue,

allowing PMNs to move quickly

through the tissue.

PMNs migrate into the sulcus andphagocytize bacteria.


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Early


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Bacteria penetrate into the

connective tissue.

PMNs release cytokinescausing more localized

destruction of the

connective tissue.

Macrophages release

cytokines, PGE2, and

MMPs.


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Established


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Plaque biofilm extends

subgingivally

Host cells produce more toxic

chemicalscytokines, PGE2,

and MMPs.

Increase in proportions of

gram-negative anaerobes.


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Advanced


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Cytokines destroy the connective

tissue and PDL fibers.

Cytokines, PGE2, and MMPs

destroy the connective tissue and

bone.

PGE2 initiates bone destruction.

Specific microorganisms:

P.gingivalis, T.forsythus,

T.denticola, P.intermedia,A.a,F.nucleatum, E.corroens,

C. rectus


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Mechanisms ofAlveolar Bone Destruction


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Macrophagesproduce cytokines,

PGE2, and MMPs.

This will stimulate

fibroblasts to secrete

PGE2 and MMP.

Destruction of the

connective tissue.

PGE2 stimulates

osteoclasts to resorb

the alveolar bone.


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Let us remember that..

For the periodontium to remain healthy,

the bacterial infection must be controlled

so as not to trigger a chronic,

exaggerated host immune response.

The bodys immune response to the

bacteria causes most of the tissue

perio slide #5

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