Microbiology of Perio diseases 2

Question 1

Progression of periodontitis vague summary:

Answer 1

Accumulation of plaque in the subgingival crevices induces an inflammatory host response which causes environmental change where increased inflammation is characterised by high gcf flow, bleeding and high temp.
This selects for particular bacterial species- the species’ metabolic activities drives further changes to the local environment by slightly increasing the pH and decreasing the redox pot
Changes lead to an ecological shift from a health associated to a disease associated community

Question 2

subgingival innate defences:

Answer 2

• GCF -
• — exudate composed of immunoglobulins and components of the complement system, Lymphocytes, Polymorphs (neutrophils) and host defense peptides such as Defensins.
• Epithelial defences
• — Produce chemokines and cytokines after a bacterial insult.
• Neutrophils
• — Form part of the host defense system and are there to regulate the proportions of bacteria.

Question 3

Microbiota homeostatic balance:

Answer 3

Balance between immunostimulatory and immunosuppressive commensal organisms.
Default state of gingivae thought to be mildly inflamed

Question 4

Pathogenic synergy

Answer 4

Bacteria that are able to cause tissue damage may be dependant on other species to survive by obtaining nutrients or by attachment
Synergy refers to cooperation and bacteria that support the growth of pathogens may be called accessory pathogens even if they are not themselves capable of causing damage.

Question 5

Steps for Microbial Pathogenesis

Answer 5

Entry
Attachment
Multiplication and consolidation
Avoiding host defences
Tissue damage
Release and spread

Question 6

Bacterial virulence factors:

Answer 6

• Adhesin: Adherence - enables binding to host tissue
• Invasin: enables invasion of host cell/tissue
• Impedin: enables avoidance of host defence mechanism(s)
• Aggressin: causes direct damage to host
• Modulin: induces indirect damage by perturbing regulation of host defences

Question 7

VIRULENCE FACTORS and their functions both CELLULAR & EXTRACELLULAR?

Answer 7

Capsule - for K-antigens, adhesion, resistance to phagocytosis and complement
Fimbriae/pili/fibrils- Adhesion, gene transfer (conjugation: pili), receptors (e.g. virus)
Extracellular products - Nutrition, host damage, interaction with host cells
Flagellum- Motility, H-antigens, inter- action with host cells

Question 8

Gram positive bacteria Virulence properties:

Answer 8

Teichoic/lipoteichoic acids: adhesion, induction of cytokines, resistance to host defences

Peptidoglycan: Induction of cytokines

Question 9

Gram Negative bacteria Virulence properties:

Answer 9

Peptidoglycan: Induction of cytokines
Lipopolysaccharide: O-antigen; induction of cytokines and inflammatory response; resistance to host defences; adhesion; mediation of bone resorption, killing of macrophages

Question 10

Toll like receptors

Answer 10

Receptors on/in epithelial cells and immune cells, which detect microbial components MAMPS and initiate cellular response pathways

Question 11

Enzymes produced by bacteria that are virulence factors:

Answer 11

Proteases — breakdown of host proteins, deregulation of host defences
Collagenases — destruction of periodontal ligaments
Fibrinolysin, hyaluronidase, heparinase — breakdown of specific host proteins
IgA and IgG proteases — breakdown of immunoglobulins

Question 12

Leukotoxins that are considered virulence factors:

Answer 12

• Specific to 1 type of bact and kill polymorphs (neutrophils)

Question 13

Cytotoxins that are considered virulence factors:

Answer 13

Specific toxins and metabolic products e.g. butyric and propionic acids =cell death

Question 14

Keystone concept

Answer 14

Some organisms may have a disproportionate influence on the pathogenicity of the community
e.g.
Porphyromonas gingivalis
Aggregatibacter actinomycetemcomitans

Question 15

Porphyromonas gingivalis

specific Proteases to this Pg?

Answer 15

Peptidylarginine deiminase (PPAD) 
Lys-gingipain

Question 16

How is P gingivalis capable of manipulating host defences?

Answer 16

• Invasion of epithelial cells and local chemokine paralysis
• affecting neutrophil migration and adhesion
• Inhibition of complement activation - produces a degrading C3 and C4inhibitor
• Disruption of immune regulation – by degrading host protease
• Disrupts TLR2 and TLR4 responses
• Direct cytotoxicity
• Produces PPAD enzyme which modifies host proteins and initiates autoimmune diseases.

Question 17

PORPHYROMONAS GINGIVALIS -

affect on virulence generally?

Answer 17

Porphyromonas gingivalis elevates the virulence of the entire community
Host immune surveillance is impaired and the dysbiotic community increases in number eventually disrupting tissue homeostasis and causing destruction of periodontal tissues.

Question 18

Aggregatibacter actinomycetemcomitans

Keystone pathogen - properties ?

Answer 18

• Gram-negative coccobacillus, anaerobic
• Associated with localised aggressive periodontitis (LAP)
• Aggressive periodontitis associated with functional abnormalities of neutrophils , e.g. signal transduction pathways, decr chemotaxis, incr superoxide radical
• 6 serotypes: serotype b more common in aggressive periodontitis patients

Question 19

VIRULENCE FACTORS OF Aa

Answer 19

Potent leukotoxin (toxic for neutrophils) – overproduced by serotype b
Cytolethal distending toxin – lymphocytes
Adhesins – adhere to epithelial cells and proliferate, biofilm formation, coaggregation
LPS – stimulates bone resorption
Cell-associated materials – induces bone resorption
Collagenase
Invasive – gingival connective tissue

Question 20

How is AA a keystone pathogen?

Answer 20

A. actinomycetemcomitans leukotoxin and cytolethal distending toxin cause local “immune paralysis” and allow overgrowth of other organisms that increase in prevalence with disease.

Question 21

What type of virulence factor are 
Collagenases 
IgG proteases 
Capsules
Lipopolysaccharides 
Leukotoxins

Answer 21

Collagenase- aggressin
IgG protease- Impedin and modulin
Capsule- Adhesin and Impedin
Lipopolysaccharide- Adhesin, impedin and modulin
Leukotoxin- Aggressin, impedin and modulin.