Subgingival Plaque and Periodontitis

Question 1

What are key findings of the Loe et al. Study (1965) Experimental Gingivitis in Man?

Answer 1

1. After participants stopped oral hygiene, plaque increased and gingivitis followed.
2. After oral health resumed, gingivitis resolved.
3. Demonstrated a temporal relationship between plaque and gingivitis.

Question 2

Order of microorganism occurance

Answer 2

1. Cocci & small rods (actinomyces naeslundii)
2. Filamentous flora (fusobacterium nucleatum)
3. Vibrios & Spirochetes (tanerella forsythia)

Question 3

What are the bacteria most strongly associated with disease and tissue damage (proteolytic & induce host response & are anaerobic)?

Answer 3

p. gingivalis
b. forsythus
t. denticola.

Question 4

Which 2 bacteria are found in higher numbers in deep perio pockets?

Answer 4

t.forsythus & p.gingivalis

Question 5

waht are the core species found in subgingival plaque?

Answer 5

Campylobactergracilis
Fusobacterium nucleatum ss. vencentii

Question 6

What are the 4 Koch Postulates?

Answer 6

A set of rules to link specific bacteria with specific diseases.

1. The microorganism must be present in every case of the disease and not in healthy individuals
2. The microorganism must be isolated from the diseased individual and grown in a pure culture
3. The isolated microorganism should reproduce the specific disease when inoculated into a healthy individual
4. The same microorganism must be reisolated from the experimental infection

Question 7

Sokransky’s Modifications to Koch’s postulates

Answer 7

• Be present in high numbers in disease
• Be absent, or in low numbers in health
• Mimic human disease in animal models
• Produce virulence factors correlating with the tissue damage seen
• Result in high levels of antibody in patients with the disease
• Removal of the microorganism results in clinical improvement

Question 8

Specific Plaque Hypothesis (1976)

Answer 8

P.gingivalis, b.forsythus, t.denticola
are associated with disease and tissue damage (proteolytic, induce host response and are anaerobic).

Question 9

Non-Specific Plaque Hypothesis

Answer 9

All plaque is equally pathogenic.

Question 10

Ecological Plaque Hypothesis (1994)

Answer 10

Plaque accumulation = inflammatory host response which favors growth of proteolytic, anaerobic and often gram negative bacteria.

Problem: doesnt talk about genetic factors.

Question 11

Keystone Pathogen Hypothesis (2012)

Answer 11

Certain microbial pathogens (in low abundance) cause inflammatory disease by decreasing the quantity of the normal microbiota and changing its composition.

Problem: p.gingivalis is found in abundance in diseased areas.

Question 12

Polymicrobial Synergy and Dysbiosis (2014)

Answer 12

Combo of Keystone + Ecological Plaque

Dysbiotic community = inflammation.

Health = symbiotic community.

Question 13

Immune-mediated polymicrobial-emergence and dysbiotic exacerbation model (IMPEDE) 2020

Answer 13

Inflammation induces a feeforward loop of uncontrolled inflammation and tissue destruction.

Question 14

Metagenomics

Answer 14

the study of the genetic material from an environment

Question 15

Metatranscriptomics

Answer 15

Looking at the gene expression of microorganisms from an environment is enabling researchers to investigate the functions and virulence properties of entire microbial communities.

Question 16

What are the virulence factors of p. gingivalis?

Answer 16

1. Lipopolysaccharides: found on the outer membrane that can manipulate host response and stimulate bone resorption and inflammation.
2. Gingipains: extracellular proteases and adhesins that disrupt the host response by degrading immunoglobulins and compliment proteins, destroy tissue and activate matrix metalloproteinases.
3. Fimbriae: cell-surface protrusions that facilitate the adhesion of p-gingivalis to various things and enable colonization.
4. Outer Membrane Vesicles (OMV’s): bud off of the outer membrane and carry LPS, fimbriae and gingipains to penetrate other tissues.

Question 17

Define pathobiont

Answer 17

a harmless (normally) symbiont part of the normal commensal microbiota that can be disease-causing.