Periodontal Microbiology

Question 1

Describe the Non-specific plaque hypothesis.

Answer 1

It doesn’t matter what bacteria are in plaque, all plaque is bad.

Question 2

What was the fall through of the non-specific plaque hypothesis?

Answer 2

aggressive periodontitis. Have deep pockets, but teeth are ok so all plaque are not affecting all tisssues

Question 3

Describe the specific plaque hypothesis.

Answer 3

Specific organisms in dental plaque are the etiological agents.

Question 4

What was used to control localized aggressive periodontitis during the time the specific plaque hypothesis was accepted?

Answer 4

local debridement and systemic antibiotics

Question 5

Describe ecological plaque hypothesis.

Answer 5

Plaque will be around regardless. When levels of bacteria are normal, the biofilm will live in equilibrium/homeostasis.
If you change the ecosystem by not brushing, smoking, hyperglycemia, stress, etc. you will predispose yourself to more inflammation

Question 6

As you progress from a healthy mouth to gingivitis to periodontitis, what type of bacteria are present?

Answer 6

anaerobic

Question 7

Describe the Keystone Pathogen Hypothesis.

Answer 7

specific bacteria within plaque do not have to be high in number, but are community activists. No damage is caused, but those specific bacteria gather surrounding bacteria to become rebellious and shift the community by activating them. (oral dysbiosis)

Question 8

What is required for a pathogen to be a considered a pathogen?

Answer 8

virulence
nutrients
host susceptibility

Question 9

What are different mechanisms pathogens colonize?

Answer 9

Adhesins (fimbriae, receptors on host cells)
coaggregation
nutrient utilization
competitive inhibition (bacteriocins, H2O2)

Question 10

Where does veillonella gain its nutrients in the oral cavity?

Answer 10

It utilizes lactate made by streptococci

Question 11

Where does campylobacter gain its nutrients?

Answer 11

formate made by Selenomonas

Question 12

Where does Porphyromonas get its nutrients?

Answer 12

It utilizes hemin from blood in the sulcus

Question 13

How do pathogens overcome host defenses?

Answer 13

desquamation of epithelium
antibody prevent binding
phagocytic cells

Question 14

What specifically produces leukotoxin?

Answer 14

Aa

Question 15

Where on the host do adhesions from bacteria bind?

Answer 15

host receptors

Question 16

What are different virulence factors bacteria possess?

Answer 16

fimbriae or pili
adhesion
Major sheath protein

Question 17

What are fimbriae/pili?

Answer 17

polymeric fibrils extending from bacterial cell membrane

Question 18

Aa bacteria uses adhesions as a virulence factor. What structure is important in producing the ECM for the adhesions?

Answer 18

pili

Question 19

What characteristics of a major sheath protein make it virulent?

Answer 19

it is highly immunogenic and mediates coaggregation with other bacteria

Question 20

Which bacteria is known for producing a major sheath protein?

Answer 20

T. denticola

Question 21

What ways do bacteria initiate and succeed at tissue destruction? Ie: What are tissue destruction promoting factors?

Answer 21

trypsin-like proteases
gingipains
leukotoxin of Aa

Question 22

What bacteria produce trypsin like proteases?

Answer 22

P. gingivalis
T. denticola
T. forsythia

Question 23

What tissue destruction promoting factor is responsible for 85% of the total proteolytic activity of P. gingivalis?

Answer 23

gingipains

Question 24

How do gingipains work?

Answer 24

They degrade cytokines. Therefore, reducing the host response.

Question 25

How do leukotoxins affect the body?

Answer 25

• Delivers adenylate cyclase domain to cells

* catalyzes uncontrolled conversion of ATP to cAMP

Question 26

When would you see effects hyperleukotoxic strains of bacteria?

Answer 26

aggressive periodontitis

Question 27

What are different strategies for evading host immunity?

Answer 27

extracellular capsule
proteolytic degradation of host immune components
modulation of host responses
invasion of gingival epithelial cells

Question 28

What type of bacteria form localized abscesses?

Answer 28

acapsular bacteria

Question 29

What cytokines do gingipains specifically degrade?

Answer 29

C3, C4, C5 and factor B

Question 30

What does interpain A degrade?

Answer 30

C3

Question 31

What mediates adhesion to and the invasion of host cells?

Answer 31

ApiA

Question 32

What bacteria components bind factor H and prevent the complement cascade?

Answer 32

Omp 100 or ApiA

Question 33

Has current knowledge changed the way we treat patients/plaque?

Answer 33

We still remove all plaque, but we know antibiotics affect the oral microbiome and can cause negative effects if used incorrectly. We also know better strategies to remove biofilm (brushing).