Microbiology Of Disease

Question 1

What study provided evidence for microbial ethology of perio disease

Answer 1

Experimental gingivitis in man love et al 1965

Aimed to produce gingivitis in subjects with healthy gingiva by withdrawing all effort at oral hygiene and study changes in microbial flora

With gingivitis, gram positive bacteria reduced from >80 to 45-60%. Dysbiosis. Shift of flora ad bacterial plaque matures. Resumption of oral hygiene resulted in resolution of gingivitis

Question 2

What is the non specific plaque hypothesis

Answer 2

Theilade 1986

Increase in biomass important in chronic periodontitis

Question 3

What is the specific plaque hypothesis

Answer 3

Loesche 1987

Specific pathogens responsible for periodontal disease. Some pathogens more pathogenic than others eg late colonisers produce toxins

Question 4

What is the ecological plaque hypothesis

Answer 4

Marsh 1994

Microbial balance and homeostasis exists in periodontal health. Localised environmental change in gingivitis eg lower oxygen tension results in ecological shift to predominantly gram negative microflora and obligate anaerobes

Question 5

Why are obligate anaerobes not able to grow in presence of oxygen

Answer 5

Lack or have low levels of superoxide dismutase that converts superoxide into oxygen and hydrogen peroxide

Question 6

What is the pH in a deep periodontal pocket

Answer 6

There is mostly proteolytic bacteria in the perio pocket which break down protein and produce ammonia, raising pH to alkaline levels pH 7.4-7.8. This promotes growth of bacteria

Question 7

What are the main bacterial species associated with chronic periodontal disease

Answer 7

Red complex:
Porphyromonas gingivalis
Treponema denticola
Tannerella forsythia

Red complex shows increased bacteria count with increased probing depthj

Question 8

Criteria for defining perio pathogens

Answer 8

Association
Host response
Virulence factors
Animal studies
Elimination

Question 9

Microbiology of aggressive periodontal disease

Answer 9

Microflora is more sparse and less diverse, mostly capnophilic organisms

Presence of leukotoxin producing a actinomycetemcomitans

Question 10

What is an exotoxin

Answer 10

Toxic soluble bacterial protein. It is strongly antigenic and can work without bacteria around

Question 11

What is an endotoxins

Answer 11

It is lipid a of lipopolysaccharide. In the membrane of gram negative bacteria. Causes septic shock

Question 12

JP2 strain bacteria are

Answer 12

High leukotoxin producers. Have 530 bp deletion at 3’ end of promoter region

Question 13

What is the effect of cytolethal distending toxin

Answer 13

Causes a G2/m arrest in the cell cycle

Question 14

What is direct pathogenicity

Answer 14

Pathogens produce virulence factors

Question 15

What is indirect pathogenicity

Answer 15

Induce host inflammatory response contributing to tissue damage. Eg prostaglandins stimulate bone resorption, cytokines eg tnf a contribute to bone resorption and tissue damage

Question 16

Pros and cons of using culture

Answer 16

Costly and laborious. Sample require immediate processing

Allow determination of antimicrobial susceptibility. Allow quantification of viable microorganisms in sample

Question 17

What is the benefit of PCR based detection

Answer 17

Specific and sensitive, does not require preservation of viable organisms

Question 18

How long to blow air at fgm for to visualise subg calculus

Answer 18

1-2s

Question 19

What instruments can you use to check for calculus free

Answer 19

Perio probe
Sharp explorer
Perio explorer 11/12

Question 20

What study suggests non linear model to periodontitis

Answer 20

Minnesota twin studies by michalowicz revealed genetic influence in progression to severe periodontitis. It found that there was a 50% chance of periodontal disease being hereditary. If one twin has severe perio, the other twin is also likely to have severe perio

Question 21

What was the main finding in chapple 2015

Answer 21

Host immune response is responsible for 80% of tissue damage. Bacteria itself is insufficient to cause progression of disease, though necessary for initiation. Requires host response for progression. Exaggerated non resolving inflammation leads to tissue destruction

Question 22

Describe incipient dysbiosis in gingivitis

Answer 22

Imbalance in bacterial flora. The biofilm accumulates and thickens, reduction in oxygen in the layer, favouring microbial shift from aerobic to anaerobic. This results in stronger host response, leading to gingival inflammation and haem which encourages proliferation of periopathogens

Question 23

How does periodontitis develop from incipient dysbiosis in gingivitis

Answer 23

In a susceptible patient eg impaired neutrophil function, incipient dysbiosis triggers excessive inappropriate host response.

Excessive inflammatory response results in collateral periodontal tissue damage

Failure to control bacterial challenge results in chronic inflammation

Question 24

What are the host defence mechanisms

Answer 24

Saliva which flushes oral cavity continuously to prevent accumulation of food debris and plaque. Contains antibodies to kill bacteria

GCF ie exudate from ecm flushes the sulcus and contains specific antibodies

Resident natural surveillance team eg macrophages phagocytose bacteria in the pocket

Epithelial cells have high turn over rate to replace cells damaged by bacterial challenge

Question 25

``` What immune cell predominant in: Initial phase (0-4 days) of gingivitis Early phase (4-8 days) of gingivitis ```

Answer 25

Initial: PMN leukocytes Early: lymphocytes

Question 26

What is the linear model of disease progression

Answer 26

In 76% of the population. Jeffcoat et al 1991, loe et al 1986 Linear attachment loss. Studies showed that populations with no access to oh had periodontal disease that occured at a relatively constant pace

Question 27

What is the random burst model

Answer 27

In 12% of population Disease may occur in periods of peak activity in individual's life. Rapid breakdown, then slow down and become stagnant (socransky)

Question 28

Asynchronous burst vs random burst model

Answer 28

Socransky et al 1984 jeffcoat et al 1991 Asynchronous happen in a shorter period of time with longer periods of remission