Risk factors for periodontitis - specific bacteria Flashcards
Define periodontal diseases.
Bacterially-induced, immune mediated inflammatory diseases of the tissues supporting the teeth.
Describe healthy sites compared to diseased sites.
Healthy sites: well-defined, precisely orchestrated, effective immune response.
Diseases sites: exacerbated, detrimental immune response.
What are the 3 prerequisites for periodontal disease initiaiton and progression?
- The virulent periodontal pathogens: Adhesins, co-aggregation, invasion, factors that cause tissue damage.
- The local environment.
- Host susceptibility ( Gene polymorphism, PMN defects, smoking , diabetes, immunosuppression.)
What is the role of fusobacterium nucleatum in dental biofilm?
It is a BRIDGING species, which means it has a lot of ADHESINS, which attatch to primary and late colonisers in the biofilm
What are the differences in between supragingival and subginival biofilm?
supragingival:
Nutrients: diet, saliva Carbohydrates- principal energy source
Firmly adherent m.o
Higher oxygen tension- Aerobes
Subgingival:
Nutrients: GCF
Proteins as source of energy
Many motile forms
Reduced redox potential
Anaerobes
What is the role of symbiotic microbiota?
This is good bacteria that protects the periodontium.
Explain what happens in the bacteria biofilm to cause periodontal disease?
slide 10
What is the role of the keystone pathogen and give an example of one.
an example is P. Gingivalis.
These keystone pathogens may inhibit phagocytosis, leading to overgrowth of dental biofilm and dysbiosis:
What are the 2 paths of periodontal tissue destruction and their percentages?
- Direct action of the microorganisms (20%)
- De-regulated inflammatory (immune) response to dental plaque i.e disruption of protective innate immunity or unresolved inflammation (80%)
What are the 4 stages of periodontal disease?
- Specific pathogenic bacteria produce antigens, LPS and other virulence factors.
- This causes a host immuno-inflammatory response - This releases cytokines (IL-1B), prostaglandins (PGE2) and matrixmatelloproteinases.
- This leads to the degradation of connective tissue and causes bone metabolism.
4.Periodontitis.
What are the 5 different functions of bacterial virulence factors?
Attachment
invasion
survival
direct damage and indirect damage
Give 5 examples of bacterial components which can be used for attachment.
adhesin
exopolysaccharides
lipoterichoic acid
outer membrance proteins
outer membrane vesicles
Give 3 examples of bacterial components which can be used for invasion.
flagella
enzymes
sulfatase
Give 7 examples of bacterial components which can be used for survival and evasion of the host immune response.
exotoxins
flagella
lipopolysaccahrides
exoploysaccharides
Give 3 examples of bacterial components which can be used for direct damage to the host.
exotoxins
enzymes
sulfatase
Give 5 examples of bacterial components which can be used for indirect damage.
lipopolysacharides
peptidoglycan
fimbriae
What do Toll-Like Receptors do?
Recognise different bacterial antigens
Why does P. gingivalis appear red?
Uses iron in haem as a growth factor.
What are gingipains?
Trypsin-like cysteine proteinases produced by P. gingivalis - these inhibit acute inflammation and allow dysbiosis to occur. (More on the process in another flashcard)
What is the mechanism of action for gingipains?
It promotes inflammation, but this inflammation that it causes is inneffective in clearing the P. Gingivalis. This is by cleaving C5 to C5a which then acts on C5aR, therefore produving inflammation.
However, overproduction of C5a uncouples inflammation from phagocytosis, and therefore causes dysbiosis as acute inflammation is a protective mechanism.
This overproduction of C5a causes PREVENTION of actin polymerisation, and therefore inhibiting phagocytosis.
P. gingivalis has a LPS chain which is recognised by TLRs. What is one of the properties of the LPS of P. Gingivalis?
It has many different types of LPS which are associated with both health and dysbiosis
The LPS from P. Gongivalis is recognised by which TLR?
TLR4
How does dental plaque bacteria cause direct damage?
Direct tissue damage - Hyaluronidase, Collagenase, Cytotoxins.
Direct bone resorption - Surface associated material, Lipoteichoic acid, Lipopolysaccharide
How does dental plaque bacteria cause indirect damage?
Indirect tissue damage - Leukotoxins trigger phagocytic cells to release lysosomal enzymes and free radicals causing tissue damage.
Indirect bone resorption - Prostaglandins cause this - they are also triggered by humoral immunity with antigens from plaque bacteria.
