Microbiology of Perio diseases 2 Flashcards
Progression of periodontitis vague summary:
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
subgingival innate defences:
- 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.
Microbiota homeostatic balance:
Balance between immunostimulatory and immunosuppressive commensal organisms.
Default state of gingivae thought to be mildly inflamed
Pathogenic synergy
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.
Steps for Microbial Pathogenesis
Entry Attachment Multiplication and consolidation Avoiding host defences Tissue damage Release and spread
Bacterial virulence factors:
- 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
VIRULENCE FACTORS and their functions both CELLULAR & EXTRACELLULAR?
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
Gram positive bacteria Virulence properties:
Teichoic/lipoteichoic acids: adhesion, induction of cytokines, resistance to host defences
Peptidoglycan: Induction of cytokines
Gram Negative bacteria Virulence properties:
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
Toll like receptors
Receptors on/in epithelial cells and immune cells, which detect microbial components MAMPS and initiate cellular response pathways
Enzymes produced by bacteria that are virulence factors:
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
Leukotoxins that are considered virulence factors:
- Specific to 1 type of bact and kill polymorphs (neutrophils)
Cytotoxins that are considered virulence factors:
Specific toxins and metabolic products e.g. butyric and propionic acids =cell death
Keystone concept
Some organisms may have a disproportionate influence on the pathogenicity of the community
e.g.
Porphyromonas gingivalis
Aggregatibacter actinomycetemcomitans
Porphyromonas gingivalis
specific Proteases to this Pg?
Peptidylarginine deiminase (PPAD) Lys-gingipain
How is P gingivalis capable of manipulating host defences?
- 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.
PORPHYROMONAS GINGIVALIS -
affect on virulence generally?
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.
Aggregatibacter actinomycetemcomitans
Keystone pathogen - properties ?
- 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
VIRULENCE FACTORS OF Aa
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
How is AA a keystone pathogen?
A. actinomycetemcomitans leukotoxin and cytolethal distending toxin cause local “immune paralysis” and allow overgrowth of other organisms that increase in prevalence with disease.
What type of virulence factor are Collagenases IgG proteases Capsules Lipopolysaccharides Leukotoxins
Collagenase- aggressin
IgG protease- Impedin and modulin
Capsule- Adhesin and Impedin
Lipopolysaccharide- Adhesin, impedin and modulin
Leukotoxin- Aggressin, impedin and modulin.
