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					Microbial interactions
   with the host in
 periodontal disease
     Dr. Reem Abdel-Hafez
    BDSc, MFDS, DCD(perio),
           FRACDS
Periodontal disease

 Initiating factor: Bacterial Plaque
 Mechanism:
     Directly: tissue destruction
     Indirectly: stimulating and modulating host
     response.
Host Response

 Protective?

 Destructive?
Microbiologic Aspects of the
interaction
Virulence factors:
   enable the bacterium to colonize the
  host tissue and to evade the host
  defense mechanisms.
  Factors that enable a bacterium to
  directly or indirectly cause
  destruction.
Bacterial Adherence
   GCF constantly washes the
   periodontal pocket→need for
   bacterial adherence.
   Available surfaces for attachment:
1. Tooth and root (pellicle, saliva
   coated).
2. Tissues.
3. Preexisting plaque mass
   (coaggregation).
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
 through fimbriae to proline rich
 proteins on saliva coated tooth
 surfaces.
 P. gingivalis attaches to other
 bacteria, epithelial cells, and
 connective tissue fibrinogen and
 fibronectin.
Bacterial host tissue invasion
   Bacteria detected in host periodontal
   tissues on histological exam.
   Pathways:
1. Through ulcerations in epith. of
   gingival sulcus or pocket.
2. Direct penetration into host epith. or
   connective tissue cells.
   Examples: A.a, P.gingivalis,
   F.nucleatum, T.denticola.
Bacterial host tissue invasion

 Clinical significance?

   A reservoir for recolonization.

   Resistance to mechanical debridement.
Bacterial Host Defense Evasion
Mechanisms:
 Bacterial adherence and tissue
 invasion.
 Production of neutralizing substances.
 examples: immunoglobulin-degrading
 proteases, leukotoxin and cytolethal
 distending toxin (by A.a), apoptosis of
 lymphocytes (by T.forsythus,F.nucleatum),
 p.gingivalis inhibit the production 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-like degrading collagen,
 fibronectin,and immunoglobulins).
Mechanisms of Host Tissue
Damage
 Indirect: by release of biologic
 mediators from host tissue cells that
 lead to host tissue destruction.
Examples: release of IL-1, TNF, PGs by
 monocytes,macrophages and PMNs
 on exposure to bacterial endotoxin.
 These stimulate bone resorption.
Immunologic aspects of the
interaction
 Innate factors and the initiation of
 inflammation. Complement system

 Neutrophils (acute infl. response)

 Macrophages and lymphocytes
 (chronic infl. response).
Innate factors

 Responsible for signs of vascular
 changes (erythema and edema).
 Complement derived anaphylatoxins
 lead to degranulation of mast cells.
 A cascade of events that result in
 production of inflammatory cytokines
 and chemotaxis of leukocytes into
 local tissues.
Neutrophils
 First leukocytes to arrive at the site of
 inflammation. Dominant in JE and gingival
 crevice.
 Functions: transendothelial migration,
 chemotaxis, transepithelial migration,
 opsonization, phagocytosis and
 intraphagolysosomal killing.
 Disorders→aggressive periodontitis.
 P.gingivalis impedes transepithelial
 migration.
Neutrophils

 Opsonization: coating of particles
 (bacteria) with host proteins to
 facilitate phagocytosis.
 Examples: molecules derived from
 complement component, specific
 antibodies (mainly IgG).
Neutrophils

 Phagocytosis: ingestion of the
 bacterial cell.

 Bacterial cell killed by oxidative or
 nonoxidative (lysosomal)
 mechanisms.
Antibodies

Functions: facilitate host clearance of
 periodontal pathogens.
 Essential for opsonization and
 phagocytosis 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 matrix
 molecules(collagen,gelatin,elastin).

 expressed by:
 neutrophils,fibroblasts,macrophages
 and epithelial cells
 secreted in inactive form. Activated by
 bacterial enzymes and host enzymes.
Proteinases

 Neutrophil serine proteinases:
 elastase and cathepsin G.

 Degrade elastin, collagen and
 fibronectin. Activate MMPs.

 α-macrogobulins in plasma and GCF
 inhibit elastase and cathepsin G.
Cytokines
 IL-1 and TNF main ones involved in tissue
 destruction.
 IL-1 and TNF are produced by activated
 macrophages or lymphocytes.
 Facilitate recruitment of leukocytes, induce
 PGE2 production by macrophages and
 fibroblasts.
 Stimulate bone resorption and induce
 tissue-degrading proteinases.
Prostaglandins

 Are arachidonic acid (found in plasma
 membrane of cells) metabolites
 generated by cyclooxygenases.
 Produced by macrophages and
 fibroblasts stimulated by IL-1ß,TNF-α,
 bacterial LPS.
 Induces MMPs and bone resorption.
 NSAID?
Microbiology and Immunology in
health
 Predominantly gram-positive
 facultative Microorganisms.
 Chronic infl. Cells (lymphocytes),
 neutrophils in JE and gingival sulcus.
 Intact epith., GCF.

              BALANCE
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
  the amount 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 to
  these M.os.
In Chronic Periodontitis

 Factors affecting host response such
 as diabetes, smoking, stress, and HIV
 infection.
 Genetics: association between
 composite genotype(IL1 genes) and
 occurrence of periodontitis in
 Caucasians.
In Aggressive Periodontitis
 Rapid progression of attachment and
 bone loss.
 Other features indicate a greater
 influence of host response in disease
 process.
 Primary etiologic role of A.a.
 1. leukotoxin production enables it to
 lyse phagocytes.
 2. Ability to invade tissues
Aggressive Periodontitis

 Problems in host response:
   Dysfunctional neutrophils. Problems in
   chemotaxis.
   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.
Conclusion

 Specific plaque hypothesis.
 Host defense mechanisms contribute
 to protection and destruction.
 Complex interactions between
 microorganisms and the host. Not
 fully understood!!
Thank You

				
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posted:7/16/2011
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