4th host-microbial interaction 2013

8/13/2019 4th Host-microbial Interaction 2013

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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


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Host

tissuesBacterial

Plaque


HostResponse


Host

tissuesBacterial

Plaque


Protective orDestructive?


HostResponse

Clinically healthy gingiva

Copyright 2011WoltersKluwerHealth| Lippincott Williams & Wilkins

Oral Deposits

Acquired Pellicle

Materia alba

Dental Plaque

Calculus


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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


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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???


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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.


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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

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Adaptive immunity

Requires the recognition ofspecific antigens

Antigen presentation

Lag time between exposureand maximal response

Cell-mediated components

Exposure leads toimmunologic memory


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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.


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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.


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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.


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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


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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


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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.

4th host-microbial interaction 2013

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