Mostafa_Microbiology

Question 1

What are the steps of dental plaque formation?

Answer 1

Carranza:
**Pellicle: **Peptides, glycoproteins, phosphoproteins.
**Adhesion: **bacteria attach via Van der Waals & electrostatic forces
**Colonization: **The primary colonizers provide new receptors for co-adhesion and co-aggregation of the secondary colonizers.
Plaque maturation: The plaque reaches maturity

Question 2

What are the attachment modes described by Zander 1953 & Canis ‘79

Answer 2

RISP
1. Cemental Resorption
2. Microscopic irregularities
3.Secondary Cuticle
4. Bacterial penetration
Since then, the cementum penetration has been disproven.

Question 3

What bacteria component mediates adherence to the host cell surface?

Answer 3

Fimbria

Question 4

Which of the following perio pathogens does not invade periodontal tissues?
-add from Mostafa slides-

Question 5

Describe the differences of metabolism and growth speed of the supra- and sub-gingival plaques

Answer 5

Supragingival: Saccharolytic, 4-5 days
Subgingival: Proteolytic, days to weeks

Question 6

What is a key protective function of the biofilm?
1. Spacing
2. Quenching
3. Scaffolding
4. Quorum Sensing

Answer 6

Quorum sensing

Question 7

What are Koch’s postulates?

Answer 7

Koch 1890
1. The microorganism must be found in abundance in the creature with the disease
2. Microorganism can be isolated from the diseased creature and grown in pure culture
3. The cultured microorganism causes disease when introduced to a healthy creature
4. The microorganism is isolated from the newly diseased creature, and is identical to the original microorganism

Question 8

Describe Page & Schroeder ‘76

Answer 8

Stages of periodontal disease progression: Initial, early, established, advanced lesions
* Initial: 2-4 days. Neutrophils predominate. Lesion is localized to the sulcus, JE and part of CT. Perivascular CT starts to disappear.
* Early: 4-7 days. A few neutrophils and over 75% lymphocytes. Lesion localized to the sulcus, JE, and part of CT. About 60-70% CT disappears
* Established: 7-21 days. Mostly Plasma cells. Lesion is localized to the sulcus, JE, and CT. JE starts migrating apically & scarring occurs
* Advanced: Mostly plasma cells, lymphocytes, macrophages. Lesion is no longer localized and affects the bone. Further collagen loss also occurs

Question 9

Describe a famous study (by Kornman) about the pathogenesis of periodontitis.

Answer 9

Page & Kornman ‘97:
Factors influencing the pathogenesis of periodontitis include:
* Microbial challenge
* Host immuno-inflammatory response
* Genetic risk factors
* Environmental & acquired risk factors
* CT and Bone metabolism
* Clinical signs of disease and progression.

Question 10

What study discusses the interleukens associated with TH-2 and TH-1 cells and has the horseshoe diagram?

Answer 10

Gemmel ‘97
TH-2: associated with IL-4, IL-5, IL-6, IL-13
TH-1: associated with IFN-gamma, IL-12, IL-2, IL-10

Question 11

Aggregatibacter Actinomycetemcomitans is in which bacterial complex?

Answer 11

Type a: Green complex
Type b: not associated with any color complexes

Question 12

Name the red complex bacteria

Answer 12

Tannerella forsythia
Porphyromonas gingivalis
Treponema denticola

Question 13

Name the purple complex bacteria

Answer 13

V. parvula
A. odontolyticus

Question 14

What other bacterial types are in the green complex (besides A.A. serotype A)?

Answer 14

various gram(+) Cocci
Eikenella corrodens

Question 15

What bacteria are in the blue complex?

Answer 15

Actinomyces species

Question 16

Besides A.A. serotype b, what other bacteria are in the diagram but not associated with a color group?

Answer 16

Selenomonas noxia : a gram-negative crescent-shaped bacteria. It is associated with periodontal disease.

Question 17

Name several orange complex bacteria

Answer 17

P. intermedia
P. nigrescens
P. micra
C. rectus
C. gracilis
E. nodatum
various F. nucleatum subspecies
S. constellatus
C. showae

Question 18

What are the 4 plaque hypotheses? Describe them briefly

Answer 18

Non-specific: Loesche ‘76, Theilade ‘86. The amount of plaque is what leads to the periodontal disease.
Specific: Loesche ‘76, Socransky ‘98. Loesche originally proposed this for dental caries, and Socransky translated it to periodontal disease. Specific bacteria cause the periodontal disease.
Ecological: Marsh ‘94. The host and the environment contribute to plaque dysbiosis and periodontal disease.
Keystone pathogen: Hajishengallis ‘12. Host immune response, and a few key pathogens, lead to periodontal disease.

Question 19

What is the PSD hypothesis and who proposed it?

Answer 19

Polymicrobial Synergy & Dysbiosis Model - Hajishengallis & Lamont ‘12.
The theory is that a synergistic and dysbiotic biofilm contributes to periodontitis. It questions the red complex hypothesis and instead emphasizes that a combination of genes and microbes lead to a disease state.

Question 20

What 2 studies from the 60’s describe how plaque composition changes over time?

Answer 20

Theilade ‘66: the streptococci are the first colonizers of the plaque, and on days 4-9 the spirochetes appear
Loe ‘65: dental students stopped oral hygiene for 3-4 weeks. At first, the plaque had gram(+) cocci; over time, it moved towards gram(-) bacteria such as fusiform, spirochetes, rods

Question 21

What are the layers of necrotizing periodontitis?

Answer 21

Listgarten ‘65:
1. bacterial zone - bacterial-rich zone with various bacteria
2. neutrophil-rich zone - leukocytes and neutrophils
3. necrotic zone - disintegrating host tissues
4. spirochetal infiltration zone - spirochetes entering the tissues

Question 22

What are the bacteria present in active vs. inactive peri-implantitis lesions?

Answer 22

Hashimoto ‘22
Active lesions - Tanerella spp, Porphyromonas spp, Treponema spp., Fusobacterium spp.. Note that most of these are Red Complex bacteria.

Inactive lesions: lactobacillus and bifidobacterium (common in probiotics)

Question 23

What is the “reservoir theory”?

Answer 23

Quirynen & Listgaarten ‘90; van Winkelhoff ‘00: The theory that periodontal pathogens can spread from teeth to implants, and cause peri-implantitis disease.

However, recent studies seem to refute this theory. Dabdoub ‘13: Within individuals, peri-implant and periodontal biofilms have less than 50% similarity.

Question 24

Which study claims peri-implantitis is similar to a chronic non-healing wound?

Answer 24

Ganesan ‘22:
Pilot study that sampled microbial, crevicular, and tissue samples from healthy & diseased implant sites. Found that the bacterial dysbiosis around implants disrupted the host immune homeostasis, resulting in chronic reprogramming as an unhealing chronic wound.