Lecture 11-12 Periodontitis

Question 1

Define Periodontitis

Answer 1

Plaque-induced inflammation of gingival tissues that results in destruction of the periodontal ligament, loss of alveolar bone, and migration of the junctional epithelium.

Question 2

Is periodontitis reversible?

Answer 2

No, it is irreversible damage which distinguishes it from gingivitis

Question 3

Active periodontal disease causes destruction of tooth attachment leading to what?

Answer 3

Periodontal pocket formation; loss of collagen attachment fibers and loss of alveolar bone that persists after the active disease process has stopped.

Question 4

T or F, Attachment loss indicates if disease is ongoing or occurred earlier

Answer 4

False, it does not indicate

Question 5

Severe periodontitis occurs in what population of people

Answer 5

More commonly in older individuals. However msot periodontitis is largely due to loss over a lifetime becoming more obvious and easier to measure in older individuals.

Question 6

Do genetic factors play a role in periodontitis

Answer 6

Yes a major role. Up to 18x over ‘normal’ patients

Question 7

What causes periodontitis

Answer 7

It could be the result of a variety of disease mechanisms. Multiple factors may have to work in synergy to bring about attachment loss. It is not clear what specifically causes active periodontal disease.

Question 8

3 Major hypotheses to what causes periodontitis

Answer 8

1. A specific bacterium
2. Specific mechanism, multiple bacteria
3. Multiple mechanism, multiple bacteria ***

Question 9

3 major hypotheses to periodontal cause can be restated into what two hypothesis?

Answer 9

1. Nonspecific Plaque hypothesis

2. Specific Plaque Hypothesis

Question 10

What is the nonspecific plaque hypothesis

Answer 10

• All plaque is bad (forget a specific bacterium). Small amounts of plaque are neutralized by host. Large amounts of plaque produce disease. Plaque control is treatment. Much clinical treatment is still based on this theory

Question 11

What is the Specific plaque hypothesis

Answer 11

Only certain plaque is pathogenic. Certain bacteria within the plaque produce more substances that cause the destruction of periodontal tissues.

Question 12

Major suspected periodontal pathogens include: (5)

Answer 12

1. Prophyromonas gingivalis
2. Tannerella forsythia
3. Treponema denticola
4. Prevotella intermedia
5. Aggregatibacter actinomycetemcomitans

Question 13

5 Socransky’s postualtes for oral lesion

Answer 13

1. Association with disease
2. Elimination: decrease disease
3. Consistant correlation with disease
4. Is animal pathogen
5. Possesses virulence factors for man

Question 14

T or F, Few active disease sites in a mouth full of inactive sites usually exemplify Periodontitis

Answer 14

True

Question 15

Make up of bacteria when healthy

Answer 15

Mainly G+ cocci with few spirochaetes or motile G- rods

Question 16

Make up of bacteria with chronic gingivitis

Answer 16

About 55% G+ with occasional spirochetes and G- motile rods

Question 17

Make up of bacteria with Chronic periodontitis

Answer 17

About 75% G- (>90% anaerobes). Motile rods and spirochetes are prominant

Question 18

Make up of bacteria with Aggressive periodontitis

Answer 18

About 70% G- rods. Few spirochetes or mobile rods present. Associated with immune or genetic defects

Question 19

What are the “Perio Pathogens”

Answer 19

A. actinomycetemcomitans

P. gingivalis

Question 20

A. Actinomycetemcomitans

• G+ or G-
• Capnophilic or Aerobic
• Microaerophilic or Facultative
• Optimum pH
• Saccharolytic or Asaccharolytic

Answer 20

• G-
• Capnophilic (Like’s CO2)
• Facultative
• pH 7-8, 7.5 optimum (inflammed pocket = 8!)
• Saccharolytic (odd)

Question 21

T or F, A. actinomycetemcomitans increase growth with steroid hormones but do not have catalase activity

Answer 21

False, It does increase growth with steroid hormones and also has catalase activity (H2O2 - detoxify)

Question 22

A. actinomycetemcomitans major virulence factors:

Answer 22

1. Fimbrae bind:
   - epithelial cells
   - matrix protein
   - salivary proteins
   - F. nucleatum
2. LPS vesicles (Blebs)
   - LPS activates Macrophages
   - Bone resorp.
   - **Filled with Leukotoxin = pore protein (Cytotoxic for PMNs and Macrophages)

Question 23

How much of aggressive adult periodontitis is associated with A. a.

Answer 23

30-50%

Question 24

P. gingivalis

• G+ or G-
• Capnophilic, Anaerobic or Anarobic
• Motile or non-motile
• Optimum pH
• Saccarolytic or Asaccharolytic

Answer 24

• G- Rod
• Anaerobic
• Non-motile
• pH 7.5-8.5
• Asaccharolytic

Question 25

T or f, P. gingivalis needs Hemin - forms pigment

Answer 25

True

Question 26

Major Virulence factors for P. gingivalis

Answer 26

1. CHO Capsule
2. Fimbrae
3. Toxic Products
4. LPS (Not very inflammatory!!)***
5. LPS Blebs
6. Secretes many enzymes (proteases)

Question 27

T or F, P. gingivalis and a. actinomycetemcomitans are found in very small numbers in a healthy mouth

Answer 27

True, (<.05%)

Question 28

T or F, A.A is associated with localized aggressive periodontitis and P.G. with generalized chronic periodontitis

Answer 28

True

• A.A. is found at few sites
• P.G., if present, found at most sites

Question 29

What causes sulcular ecology to be an anaerobic environment

Answer 29

Whatever oxygen makes it to this area is rapidly removed by reaction with organic molecules

Question 30

What causes sulcular ecology to have bacteria use protein as substrate?

Answer 30

Low levels of saliva and food residue to these areas require that most of the bacteria here use protein as substrate rather than sugars

Question 31

Is bacterial adhesion an important colonization factor in gingival pockets

Answer 31

No, the slow flow of fluid and absence of salivary washing decrease the role of bacterial adhesion as an important colonization factor and may of the organisms here are highly motile

Question 32

What is the major function of PMNs in the gingival pockets and sulcular ecology

Answer 32

Remove LPS, detoxifying this potent bacteriallyy-derived inflammatory endotoxin

Question 33

Will the LPS concentration be high or low in gingival pockets

Answer 33

High, since most of the subgingival flora are G-

Question 34

What controls the mechanism of attachment loss?

Answer 34

Under gingival Th cell direction. The slow maintenance, replacement, and repair gives way to the final strategy of removing the inflammatory site. Keep the infection from going systemic at all costs!