4th Host-microbial Interaction 2013
-
Upload
prince-ahmed -
Category
Documents
-
view
221 -
download
0
Transcript of 4th Host-microbial Interaction 2013
-
8/13/2019 4th Host-microbial Interaction 2013
1/15
1
Microbial interactionwith the host in
periodontal diseases
Malik Hudieb, BDS, PhD
Department of Preventive Dentistry
Faculty of Dentistry
Jordan University of Science and Technology
Pathogenesis.. DefinitionThe development of a disease and the chainof events that led to this disease.
includes the study of the relationship between:
the cause the lesions clinical signs.
Medical dictionary
Gingivitis PeriodontitisHealthy
Gingiva
Gingivitis and Periodontitis
?Plaque
Microbial interaction with the host
Immunesystem
Host response
Inflammation
Clinicalsigns
BacterialPlaque
Periodontal diseases:
Bacterial plaque.. Types of bacteria Immune response.. Inflammation Clinical signs
-
8/13/2019 4th Host-microbial Interaction 2013
2/15
2
Host
tissuesBacterial
Plaque
Periodontal diseases:
HostResponse
Microbial interaction with the host
Host
tissuesBacterial
Plaque
Periodontal diseases:
Protective orDestructive?
Microbial interaction with the host
HostResponse
Clinically healthy gingiva
Copyright 2011WoltersKluwerHealth| Lippincott Williams & Wilkins
Oral Deposits
Acquired Pellicle
Materia alba
Dental Plaque
Calculus
-
8/13/2019 4th Host-microbial Interaction 2013
3/15
3
DENTAL PLAQUEOrganized biofilm..
Adheres to teeth, prostheses, and hard surfaces
Periodontal pockets
(Wilderer and Charaklis 1989)..
DENTAL PLAQUE- Microorganisms: 70%..
- Organic components (influenced by the environment):
polysaccharide-protein matrix, by-products(enzymes..),food debris and desquamated cells.
- Inorganic components such as calcium andphosphate.
Dental Plaque ORGANIC COMPONENTS OF PLAQUE MATRIX
polysaccharides - produced by bacteria
glycoproteins - from saliva/ initially coats theclean tooth (Pellicle)
lipids - membranes of bacterial and host cells
-
8/13/2019 4th Host-microbial Interaction 2013
4/15
-
8/13/2019 4th Host-microbial Interaction 2013
5/15
-
8/13/2019 4th Host-microbial Interaction 2013
6/15
6
Adherence, colonization and survival..
GCF washes the periodontalpocket
Available surfaces:
1. Tooth and root (pellicle,saliva coated).
2. Tissues.
3. Preexisting plaque mass(coaggregation).
Adherence, colonization and survival..
Host tissue invasion
Ulcerations.. (NUG)
Direct penetration..(A.a, P. gingivalis..)
Evasion of host defensemechanisms
Host defensemechanisms???
-
8/13/2019 4th Host-microbial Interaction 2013
7/15
7
The immune system Innate immune systemimmediate, non-specific response
Adaptive immune systemspecific pathogens..
adaptive immune responses faster andstronger attacks at the second exposure..
Defense mechanisms.. (innate)
The intact barriers (junctional epithelium)
The regular shedding of epithelial tissues
Saliva (..)
The gingival crevice fluid (..)
Immune cells: Neutrophils , Macrophages, Complements..
Washing effect..
INFLAMMATION
Inflame to set fire.
Inflammation is A dynamic response of
vascularised tissue to injury.
It is a protective response.
It serves to bring defense & healing
mechanisms to the site of injury.
-
8/13/2019 4th Host-microbial Interaction 2013
8/15
8
Increase blood flow (redness and warmth).
Increase vascular permeability (swelling, pain & loss of
function).
Leukocytic Infiltration.
Inflammation
Injury
Chemical mediators
Leukocyte infiltration..
Mechanism of Inflammation
32
Adaptive immunity
Requires the recognition ofspecific antigens
Antigen presentation
Lag time between exposureand maximal response
Cell-mediated components
Exposure leads toimmunologic memory
-
8/13/2019 4th Host-microbial Interaction 2013
9/15
9
Chemical Mediators:Chemical substances synthesised or released
and mediate the changes in inflammation.
Histamineby mast cells - vasodilatation.
Prostaglandins Cause pain & fever.
Bradykinin- Causes pain.
Microbiota of Disease Gram-negative facultative or anaerobic
bacteria.
P. gingivalis, A.a, T. denticola, B.forsythus, F. nucleatum, P. intermedia, C.rectus, P. micros, E. corrodens.
Bacterial Adherence
Actinomyces viscosus attaches throughfimbriae to proline rich proteins on salivacoated tooth surfaces.
P. gingivalisattaches to other bacteria,epithelial cells, and connective tissuefibrinogen and fibronectin.
Bacterial host tissue invasion
Pathways:
1. Ulcerations in epith. of gingival sulcus orpocket.
2. Direct penetration into host epith. orconnective tissue cells.
Examples: A.a, P.gingivalis,F.nucleatum, T.denticola.
-
8/13/2019 4th Host-microbial Interaction 2013
10/15
10
Bacterial host tissue invasion Clinical significance?
A reservoir for recolonization.
Resistance to mechanical debridement.
Bacterial Host Defense EvasionMechanisms:
Bacterial adherence and tissue invasion.
Production of neutralizing substances.
examples: immunoglobulin-degrading proteases,leukotoxin and cytolethal distending toxin (byA.a), apoptosis of lymphocytes (by
T.forsythus,F.nucleatum), p.gingivalis inhibit theproduction of IL-8 by epithelial cells(evade PMN-killing).
Mechanisms of Host Tissue Damage
Direct degradation of host tissues.
By: metabolic by products (ammonia,
sulfur, fatty acids, peptides and indole)and proteolytic enzymes (trypsin-likedegrading collagen, fibronectin,andimmunoglobulins).
Mechanisms of Host Tissue Damage
Indirect: by release of biologic mediatorsfrom host tissue cells that lead to hosttissue destruction.
Examples: release of IL-1, TNF, PGs bymonocytes,macrophages and PMNs onexposure to bacterial endotoxin. Thesestimulate bone resorption.
-
8/13/2019 4th Host-microbial Interaction 2013
11/15
-
8/13/2019 4th Host-microbial Interaction 2013
12/15
12
Neutrophils Phagocytosis: ingestion of the bacterial
cell.
Bacterial cell killed by oxidative ornonoxidative (lysosomal) mechanisms.
AntibodiesFunctions: facilitate host clearance of
periodontal pathogens.
Essential for opsonization andphagocytosis of A.a and P.gingivalis.
Neutralize bacterial components important
in colonization or host cell interactions.
Host mediators of destruction
Proteinases.
Cytokines.
Prostaglandins.
Proteinases
MMPs:degrade extracellular matrixmolecules(collagen,gelatin,elastin).
expressed by:neutrophils,fibroblasts,macrophages andepithelial cells
secreted in inactive form. Activated bybacterial enzymes and host enzymes.
-
8/13/2019 4th Host-microbial Interaction 2013
13/15
13
Proteinases Neutrophil serine proteinases: elastase
and cathepsin G.
Degrade elastin, collagen and fibronectin.Activate MMPs.
-macrogobulins in plasma and GCFinhibit elastase and cathepsin G.
Cytokines IL-1 and TNF main ones involved in tissue
destruction.
IL-1 and TNF are produced by activatedmacrophages or lymphocytes.
Facilitate recruitment of leukocytes, inducePGE2 production by macrophages and
fibroblasts. Stimulate bone resorption and induce tissue-
degrading proteinases.
Prostaglandins
Are arachidonic acid (found in plasmamembrane of cells) metabolites generatedby cyclooxygenases.
Produced by macrophages and fibroblastsstimulated by IL-1,TNF-, bacterial LPS.
Induces MMPs and bone resorption.
NSAID?
Microbiology and Immunology in health
Predominantly gram-positive facultativeMicroorganisms.
Chronic infl. Cells (lymphocytes),
neutrophils in JE and gingival sulcus. Intact epith., GCF.
BALANCE
-
8/13/2019 4th Host-microbial Interaction 2013
14/15
14
In Gingivitis Increase in proportions of gram-negative
anaerobes.
Infiltration of neutrophils and lymphocytes(mainly T-cells)
Systemic conditions can affect host
susceptibily (ex. Pregnancy)
In Chronic Periodontitis Attachment loss and bone resorption.
Amount of destruction consistent with theamount of local factors.
Specific microorganisms:P.gingivalis,
T.forsythus,T.denticola,P.intermedia,
A.a,F.nucleatum,E.corroens,C. rectus.
serum and GCF antibody specific tothese M.os.
In Chronic Periodontitis
Factors affecting host response such asdiabetes, smoking, stress, and HIVinfection.
Genetics: association between compositegenotype(IL1 genes) and occurrence ofperiodontitis in Caucasians.
In Aggressive Periodontitis
Rapid progression of attachment and boneloss.
Other features indicate a greater influence
of host response in disease process. Primary etiologic role of A.a.
1. leukotoxin production enables it to lysephagocytes.
2. Ability to invade tissues
-
8/13/2019 4th Host-microbial Interaction 2013
15/15
15
Aggressive Periodontitis Problems in host response:
Dysfunctional neutrophils. Problems inchemotaxis.
Elevated levels of proinflammatory cytokines.
Elevated titers of IgG2 (mainly in LAP).
Necrotizing Periodontal Diseases
P. intermedia, F. nucleatum,Spirochetes
Host factors: Immunosuppression, stress,malnutrition, smoking.
NUP and HIV infection.