11-12. Opportunist Oral Pathogens & The Immunobiology of Periodontitis

Question 1

What is Periodontitis?

Answer 1

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

Question 2

True/False: Periodontitis is reversible like gingivitits

Answer 2

FALSE, Periodontitis is NOT reversible (aka, it is ireversible), while gingivitis is reversible

Question 3

Periodontitis has a combination of “____ _______” loss and/or burst of “______” loss. Therefore, “___________” doe not indicate if disease is ongoing or has occurred.

Answer 3

Periodontitis has a combination of “SLOW GRADUAL” loss and/or burst of “RAPID” loss. Therefore, “ATTACHMENT” doe not indicate if disease is ongoing or has occurred.

Question 4

What are 9 risk factors for Perio?

Answer 4

smoking
systemic disease
drugs/medication
crooked teeth
pregnancy
genes
age
poverty
amount of pathogenic bacteria present

Question 5

What are the 3 major hypotheses that are thought to cause perio?

Answer 5

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

Question 6

What is the most popular idea/mechanism thought to cause perio?

Answer 6

Multiple mechanisms, multiple bacteria. A unique combinatino of organisms along with a malfunctions host immunity, may lead to disease

Question 7

What is Nonspecific Plaque Hypothesis?

Answer 7

All plaque is bad.Large amounts of plaque produce disease (the more you have the worse you are). Plaque control is treatment. (This is what many clinical treatment is based off of)

Question 8

Specific Plaque hypothesis states: Only “_______” plaque is pathogenic.

Answer 8

Specific Plaque hypothesis states: Only “certain” plaque is pathogenic.

Question 9

What are the 5 major ‘suspected’ periodontal pathogens?

Answer 9

Prophyromonas gingivalis 
Tannerella forsythia
Treponema denticola
Prevotella intermedia 
Aggregatibacter actinomycetemcomitans (A.a.)

Question 10

Of the 5 major ‘suspected’ periodontal pathogens, which 3 have the red complex?

Answer 10

Prophyromonas gingivalis
Tannerella forsythia
Treponema denticola

Question 11

A patient with a ‘healthy’ gingival condition mainly has “____-______” cocci with “___” spirochaetes or motile gram-negative rods.

Answer 11

A patient with a ‘healthy’ gingival condition mainly has “GRAM-POSITIVE” cocci with “FEW” spirochaetes or motile gram-negative rods.

Question 12

What is the bacterial status of a patient with chronic gingivitis?

Answer 12

About 55% gram positive

occasional spirochaetes and gram-negative motile rods

Question 13

What percent of bacteria gram-negative and are anaerobes in a patient with chronic periodontitis?

Answer 13

~75% gram-negative

>90% anaerobes

Question 14

Which morphological type of bacteria exist in a chronic perio condition? (e.g. rod, cocci, spirochaetes)

Answer 14

Motile rods and spirochaetes are prominant

Question 15

What signs and bacteria would a patient with aggressive perio show?

Answer 15

~70% gram negative rods.
Few motile spirochaetes
Mobile rods present
Associated with immune or genetic defect

Question 16

What is the general/big picture in terms of healthy and diseased gingiva?

Answer 16

Healthy = more gram-positive cocci and rods with few gram-negative.
Diseased = more gram negative, few gram-positive

Question 17

Of the 5 major suspected perio pathogens, which 2 are thought to be more associated with perio?

Answer 17

A.a (Aggregatibacter actinomycetemcomitans)

P. ginigivalis (Porphyromonas gingivalis)

Question 18

List the characteristics of A.a
gram +/-
Capnophilic?
aerobic/anaerobic/faculative etc.
catalase?
pH levels?
Asaccharolytic vs Saccharolytic 
effect of steriod hormone?

Answer 18

A.a. is
gram - Rod
Capnophilic - love CO2
Faculative
Catalase - breaks H2O2 -> H2O & O2
pH 7-8, optimum = 7.5 (inflamed pocket = 8)
Saccharolytic
Increased growth with steriod hormone

Question 19

What are the major virulence factors of A.a.?

Answer 19

Fimbriae

***LPS Vessicles (Blebs)

Question 20

What are the effects of the LPS released by A.a.?

Answer 20

Activates macrophage
Stimulate osteoclast for bone resoption
Release leukotoxin = pore protein
Huge inflammation response in host

Question 21

What is leukotoxin?

Answer 21

a cytolytic toxin that creates pores in it’s targets membranes. cytotoxic for PMN & macrophage

Question 22

What are the characteristics of P. gingivalis?
gram +/-
aerobic/anaerobic/faculative etc.
Hemin?
pH levels?
Asaccharolytic vs Saccharolytic

Answer 22

Gram - Rod
Anaerobic
Needs Hemin (contains iron)
pH 7.5-8.5
Asaccharolytic

Question 23

Major virulence factors of P. gingivalis

Answer 23

Fimbriae
Invade tissues (happens in NUG)
Secretion of enzymes /proteases (for food)
LPS (LPS BLEBS)

Question 24

How does LPS released by P. gingivalis act on the host?

Answer 24

100-1000x less inflammation

Can ‘shut down’ PMNS or inflammation

Question 25

96. A.A. vs P.G. - Periodontitis
    - Which is found in younger individuals?
    - Which is distributed over the whole mouth, while the other is found in significant numbers in only a few sites?

Answer 25

Younger: A.A.

Distributed over whole mouth: P.G.

Found in only a few sites at sig. numbers: A.A.

Question 26

96. A.A. vs P.G. - Periodontitis
    - What form of periodontitis is A.A. associated with?
    - What form of periodontitis is P.G. associated with?

Answer 26

A.A. - Localized aggressive periodontitis (LAP)

P.G. - Generalized chronic periodontitis (GCP)

Question 27

98. What are four virulence factors for A.A.?

Answer 27

1. Possesses CAT to combat H2O2
2. Leukotoxin Porins
3. LPS (strong form)
4. Anti-phagocytic capsule

Question 28

98. What are four virulence factors for P.G.?

Answer 28

1. Production of toxic Indole, NH3, H2S
2. Enzyme proteases
3. LPS (weak form) - blocks chemotaxis
4. Anti-phagocytic capsule

Question 29

98. What are four protective mechanisms employed by PMN’s to defend against A.A. and P.G.?

Answer 29

Oral PMNs (10^10 / day)

1. Resistant to LPS toxicity
2. Can function anaerobically and
3. Detoxify areas
4. Opsonization of protective capsules

Question 30

99. Gingival pockets and perio disease - Sulcular ecology
    - Anaerobic or aerobic environment?
    - What’s the primary food source for bacteria?
    - Is bacterial adhesion an important colonization factor?

Answer 30

1. Anaerobic
2. Protein (instead of sugar)
3. No, because there is less fluid and no salivary washing

Question 31

99. Gingival pockets and perio disease - Sulcular ecology
    - Why is this environment’s surfaces considered more “complex”?
    - What’s the major function of PMN’s here?
    - What is a downside of having a steady stream of plasma containing complement, IgG, and various cytokines?

Answer 31

1. Considered more complex because of the different surfaces available (tooth pellicle, gingival epithelium, and the “wall of neutrophils”
2. PMN’s can remove LPS, detoxifying this inflammatory endotoxin
3. All of these mechanisms can lead to both immunity and host collateral damage

Question 32

99. Gingival pockets and perio disease - Sulcular ecology

- Why is the concentration of LPS high here?

Answer 32

[LPS] high because most of the subgingival flora are gram-negative
- Results in massive cytokine production by macrophages leading to osteoclasts (bone loss) and fibroblasts (collagen degradation)

Question 33

100. What are some signs that the body is attempting the “final solution” towards resolving an inflammatory site in a tooth?

Answer 33

1. Bacteria deeply penetrate junctional epithelium (leukotoxins and reduced strength LPS)
2. Massive B-cell buildup (no one knows why)
3. Fibroblast switches from production of collagen to collagenase and PGE2
4. Osteoclast activation and loss of bone (due to IL-1, TNF-α, PGE2