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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
Periodontal diseases:
Host
Response
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Pathogenesis..
Host
tissuesBacterial
Plaque
Periodontal diseases:
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