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periodontal microbiology Flashcards

1
Q

Oral bacterial microbiome of adults encompasses approximately ______ commonly occurring species

A

700

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2
Q

Dental Plaque as a Biofilm

A

Organized communities of microorganisms
Bound to a surface
Non-random distribution of microorganisms within a matrix
Exchange of nutrients and metabolic substances amongst microorganisms

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3
Q

Why are biofilms less susceptible to host defense systems (immune responses)?

A

protected by their matrix and altered phenotypes

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4
Q

Why is biofilm 1000-1500 times more resistant to antibiotics compared to single cells?

A

Penetration is delayed by matrix
Cell growth rate is delayed
Enzymes produced inhibit antibiotics
DNA exchange

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5
Q

What are the three phases of plaque maturation?

A

1.Formation of dental pellicle

2.Initial colonization by bacteria

3.Secondary colonization by bacteria

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6
Q

What is the dental pellicle composed of?

A

Glycoproteins derived from:
saliva
GCF
bacterial and host tissue cells.

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7
Q

How quickly can the dental pellicle form on clean enamel surfaces?

A

Within 1 minute.

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8
Q

What are the functions of the dental pellicle?

A

Provides protection, lubrication, and a substrate to which bacteria can attach (mattress)

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9
Q

What type of microorganisms are the initial colonizers in plaque maturation?

A

Gram-positive facultative aerobic microorganisms.

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10
Q

What structures facilitate colonization in the host pellicle during the initial phase?

A

Adhesins and fimbriae.

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11
Q

Which bacteria are prominent in the initial colonization phase?

A

Streptococcus: >20%
Actinomyces

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12
Q

How do microbes adhere to existing bacterial cells during secondary colonization?

A

coaggregation

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13
Q

When do secondary colonizers establish themselves?

A

After the initial colonizers have formed the plaque mass.

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14
Q

Name some microbes that participate in secondary colonization. PPFC

A

Prevotella, Capnocytophaga, Fusobacterium, Porphyromonas.

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15
Q

Which bacteria colonize last in plaque maturation? FPT

A

Fusobacterium nucleatum
Porphyromonas gingivalis
Treponema denticola (a spirochete).

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16
Q

What type of bacteria are found at the tooth surface in supragingival biofilm?

A

Gram-positive facultative bacteria.

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17
Q

Where are Gram-negative (G-) bacteria located in supragingival biofilm?

A

At the soft tissue interface/gingival margin

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18
Q

What is the primary nutrient source for supragingival biofilm?

A

Sugars from saliva.

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19
Q

What increases during the host’s inflammatory response to biofilm?

A

Migration of polymorphonuclear leukocytes (PMNs).

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20
Q

What allows the initial migration of Gram-positive (G+) bacteria in subgingival biofilm formation?

A

Weakening of attachment between the tooth and junctional epithelium (JE).

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21
Q

What follows the migration of G+ bacteria during subgingival biofilm expansion?

A

Gram-negative (G−) bacterial mass.

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22
Q

What host-bacteria interaction occurs during subgingival and supragingival biofilm expansion?

A

A plaque-induced inflammatory response.

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23
Q

What increases in response to subgingival biofilm expansion?

A

Migration of polymorphonuclear leukocytes (PMNs), plasma cells, and gingival crevicular fluid (GCF).

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24
Q

What happens to host tissue during subgingival biofilm expansion?

A

breakdown

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25
What physical change occurs in the gingiva due to subgingival biofilm expansion?
A physical shift in gingival position
26
What type of bacteria dominate in subgingival pocket flora?
Gram-negative aerobic bacteria.
27
What nutrients support subgingival pocket flora?
Peptides, amino acids, and gingival crevicular fluid (GCF).
28
What contributes to nutrient availability in subgingival pockets?
Host tissue breakdown and interbacterial feeding.
29
What happens to the epithelium in subgingival pockets?
becomes ulcerated
30
How do microbes in subgingival pocket flora interact with host tissue?
They invade host tissue and evade host defense mechanisms.
31
What is the primary idea of the Nonspecific Plaque Hypothesis?
Plaque accumulation (the entire biofilm) on the tooth surface and in the gingival crevice contributes to pathological changes.
32
T or F: According to the Nonspecific Plaque Hypothesis, Small amounts of plaque can be “handled” by host defenses.
True
33
What happens when plaque accumulation becomes large, according to the Nonspecific Plaque Hypothesis?
“overwhelm” the host defenses
34
In the Nonspecific Plaque Hypothesis, what factor is most important in contributing to pathological changes?
The quantity of plaque accumulation
35
What is the main idea of the Specific Plaque Hypothesis?
Only certain bacteria whose levels increase during periodontal disease are causative.
36
How many species are typically found in increased proportions in periodontally diseased sites according to the Specific Plaque Hypothesis?
Less than 20 species
37
According to the Specific Plaque Hypothesis, what factor is most important in causing periodontal disease?
The quality of bacteria, not just the quantity, is the key factor.
38
What distinguishes the Specific Plaque Hypothesis from the Nonspecific Plaque Hypothesis?
The Specific Plaque Hypothesis focuses on certain bacteria being causative, while the Nonspecific Plaque Hypothesis emphasizes the quantity of plaque accumulation.
39
What two factors are emphasized in the Ecological Plaque Hypothesis?
The quantity and quality of plaque.
40
What is "Dysbiosis" in the context of the Ecological Plaque Hypothesis?
shifts in the resident microbiota that can contribute to periodontal disease.
41
According to the Ecological Plaque Hypothesis, what factors can affect the balance of the microbiota?
interaction between microbes and the host
42
What is the goal of therapy in the Ecological Plaque Hypothesis?
eliminate disease-inducing factors to restore balance in the microbiota.
43
What is the main idea of the Keystone Pathogen Hypothesis?
Certain low-abundance microbial pathogens, like Porphyromonas gingivalis, trigger a shift from a benign microbiota to a dysbiotic one, leading to periodontitis.
44
What evidence supports the Keystone Pathogen Hypothesis?
Exposure to a low amount of P. gingivalis (<0.1% of total microbiota) led to periodontal bone loss in specific pathogen-free mice but not in germ-free mice or mice lacking C3a or C5a complement receptors.
45
What are the mechanisms by which keystone pathogens contribute to periodontitis?
manipulate the host immune response by regulating Toll-like receptors, cytokine expression, the complement system, and other immune factors.
46
What type of bacteria are commonly found in healthy oral environments?
Gram-positive facultative microbes, such as Actinomyces and Streptococcus.
47
What bacteria are commonly associated with plaque-induced gingivitis?
Gram-positive facultative microbes: Actinomyces, Streptococcus Gram-negative microorganisms: Fusobacterium, Capnocytophaga, Prevotella, Proph
48
What are some Gram-negative microorganisms associated with chronic periodontitis? (Aunt Polly Plays Chess Everyday To Teach Friends
Aggregatibacter actinomycetemcomitans Porphyromonas gingivalis Prevotella intermedia Campylobacter rectus Eikenella corrodens Tannerella forsythensis Treponema denticola Fusobacterium nucleatum
49
What are the Gram-negative microorganisms associated with aggressive periodontitis? CAP
Campylobacter rectus Aggregatibacter actinomycetemcomitans Prevotella intermedia
50
Which viruses may be involved in aggressive periodontitis?
Herpes Simplex Virus (HSV) Epstein-Barr Virus (EBV)
51
What is the typical microbial composition of a periodontal abscess? PPPTF
Porphyromonas gingivalis - 14% Prevotella intermedia - 9% Peptostreptococcus micros - 9% Tannerella forsythensis (formerly Bacteroides forsythus) - 3% Fusobacterium nucleatum - 3%
52
What type of infection is a periodontal abscess?
mixed infection.
53
What is important about antibiotic coverage for periodontal abscesses?
needs to cover both Gram-positive and Gram-negative microbes.
54
What are the main functions of virulence factors?
Facilitate colonization and invasion, adherence, host tissue damage, and evasion of host defense mechanisms.
55
To what does P. gingivalis adhere in connective tissue?
Fibrinogen and fibronectin.
56
What does LPS stimulate the release of from monocytes, macrophages, and PMNs?
IL-1, TNF, and prostaglandins.
57
What processes are activated by LPS?
Cytokine production, inflammatory response, and bone resorption.
58
Which periodontal pathogen is associated with collagenase, which degrades collagen?
P. gingivalis
59
Which bacteria directly invade host tissue in periodontal infections? APFT
Aggregatibacter actinomycetemcomitans Porphyromonas gingivalis Fusobacterium nucleatum Treponema denticola
60
What condition in the tissue facilitates host tissue invasion?
Ulcerations
61
T or F: Studies have shown that some strains of microbes are more pathogenic than others
True
62
What type of bacteria is Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans?
Gram-negative, nonmotile anaerobic rod.
63
Where is Porphyromonas gingivalis increased?
In periodontitis lesions.
64
What is the significance of Porphyromonas gingivalis in chronic periodontitis?
It is considered the “keystone” pathogen.
65
What are the virulence factors of Porphyromonas gingivalis?
Cell adherence and tissue invasion Collagenase Endotoxin (LPS)
66
What immune response is associated with Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans in periodontitis?
Increased antibody levels.
67
In which periodontal conditions is A. actinomycetemcomitans increased?
Aggressive periodontitis and sometimes chronic periodontitis lesions.
68
What are the virulence factors of A. actinomycetemcomitans?
Tissue invasion Collagenase Endotoxin Leukotoxin (lyses human neutrophils)
69
Biofilm is __________ and _________ for the development of plaque-induced gingivitis
necessary, sufficient
70
What study provided experimental evidence for biofilm-induced gingivitis?
Experimental Gingivitis Studies in Man by Loe and Theilade, 1967.
71
Biofilm is necessary but __ _____________ for the development of periodontitis
not sufficient
72
T or F: Not all plaque-induced gingivitis progresses to periodontitis
True
73
48
Why is it difficult to determine which gingivitis sites will progress to periodontitis?
74
Why is it difficult to determine which gingivitis sites will progress to periodontitis?
Because periodontitis is multifactorial and has variable progression, making it unpredictable. So treat all sites
75
What are the goals of periodontal therapy regarding biofilm?
Reduce the organization and mass of the biofilm Create shallow gingival crevices, which are inhospitable to anaerobic microbes

periodontics II (22 decks)

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