Risk Factors: Specific Bacteria Flashcards
What are the two main microbiological differences between healthy and diseased sites?
- Types of bacteria
- More gram negative, anaerobic bacteria - Host immune response
- Inflammation is uncontrolled leading to tissue destruction
What are the 3 prerequisites for PDD?
- Virulent Pathogens
- Virulence factors: adhesins, invasion factors, co-aggregation - Local Environment
- Lower oxygen tension - Host Susceptibility
- Gene polymorphism, smoking, diabetes, immunosuppression
Summarise how the dental biofilm forms
- Formation of acquired pellicle formed of adhesion to saliva glycoproteins, proteoglycans onto the tooth surface
- Adhesion of the pioneer species such as Streptococci attaching to pellice and produce extra-cellular polysaccharide
- Bridging species allowing late colonisers to attach
What are the main differences between the supra and sub gingival biofilm?
Supra:
- Nutrients from saliva and diet
- Carbohydrates are main energy source
- Firmy attached
- Higher oxygen tension: aerobes
Sub:
- Nutrients from GCF
- Motile forms
- Anaerobic bacteria
- Reduced oxygen tension
What is the key stone theory to PDD?
Acquired pellicle starts on the tooth surface and ecological growth promotes the growth of key stone species. These species induce impairment of the host protective mechanisms. This leads to overgrowth of dental biofilm and exacerbated inflammation and periodontal tissue damage.
Name some examples of virulence factors that bacteria may have
Adhesins to attach to tooth tissue.
Invasion factors - flagella, enzymes (collagenase, fibrinolysin).
Survival enhancement - producing different immunoglobulin proteases, cytotoxin production
Direct damage - exotoxins, enzymes, metabolic end products
Indirect damage (caused by host response) - lipopolysaccharides, lipoproteins, DNA, peptidoglycan)
Name some examples of virulence factors that bacteria may have
Adhesins to attach to tooth tissue.
Invasion factors - flagella, enzymes (collagenase, fibrinolysin).
Survival enhancement - producing different immunoglobulin proteases, cytotoxin production
Direct damage - exotoxins, enzymes, metabolic end products
Indirect damage (caused by host response) - lipopolysaccharides, lipoproteins, DNA, peptidoglycan)
How does the immune system recognise all these pathogens?
Toll-like receptors. Each of these recognise different bacterial antigens such as LPS, flagella, membrane types and raw components.
P.Gingivalis:
1. Gram + or -?
2. Aerobic or anaerobic?
3. What is the main virulence factor?
- -
- Anaerobic
P.Gingivalis:
1. Gram + or -?
2. Aerobic or anaerobic?
3. What is the main virulence factor?
- -
- Anaerobic
- LPS (component of outer membrane in gram - bacteria)
Once toll receptors recognise LPS in gram - bacteria, what happens inside the immune cells?
Production of different pro-inflammatory mediators, prostaglandins and cytokines.
Why does our body become inflamed as a protective response?
To clear the damaging pathogen or any invading pathogens
How does P.Gingivalis overcome the host inflammatory response?
- It uncouples inflammation from phagocytosis to promote dysbiosis
- Inhibition of phagocytic cells promotes dysbiosis in the sub-gingival dental biofilm
- Other bacteria can then grow and cause further inflammation
What are the 3 main pro-inflammatory cytokines produced by macrophages, fibroblasts and epithelial cells?
IL1, IL6, IL8
What are some of the characteristics of necrotising periodontal disease?
- Gingival necrosis
- Punched out papillae
- Gingival bleeding
- Pain
- Bad breath
- Pseudomembranes