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
Q

What physical change occurs in the gingiva due to subgingival biofilm expansion?

A

A physical shift in gingival position

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26
Q

What type of bacteria dominate in subgingival pocket flora?

A

Gram-negative aerobic bacteria.

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27
Q

What nutrients support subgingival pocket flora?

A

Peptides, amino acids, and gingival crevicular fluid (GCF).

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28
Q

What contributes to nutrient availability in subgingival pockets?

A

Host tissue breakdown and interbacterial feeding.

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29
Q

What happens to the epithelium in subgingival pockets?

A

becomes ulcerated

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30
Q

How do microbes in subgingival pocket flora interact with host tissue?

A

They invade host tissue and evade host defense mechanisms.

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31
Q

What is the primary idea of the Nonspecific Plaque Hypothesis?

A

Plaque accumulation (the entire biofilm) on the tooth surface and in the gingival crevice contributes to pathological changes.

32
Q

T or F: According to the Nonspecific Plaque Hypothesis, Small amounts of plaque can be “handled” by host defenses.

33
Q

What happens when plaque accumulation becomes large, according to the Nonspecific Plaque Hypothesis?

A

“overwhelm” the host defenses

34
Q

In the Nonspecific Plaque Hypothesis, what factor is most important in contributing to pathological changes?

A

The quantity of plaque accumulation

35
Q

What is the main idea of the Specific Plaque Hypothesis?

A

Only certain bacteria whose levels increase during periodontal disease are causative.

36
Q

How many species are typically found in increased proportions in periodontally diseased sites according to the Specific Plaque Hypothesis?

A

Less than 20 species

37
Q

According to the Specific Plaque Hypothesis, what factor is most important in causing periodontal disease?

A

The quality of bacteria, not just the quantity, is the key factor.

38
Q

What distinguishes the Specific Plaque Hypothesis from the Nonspecific Plaque Hypothesis?

A

The Specific Plaque Hypothesis focuses on certain bacteria being causative, while the Nonspecific Plaque Hypothesis emphasizes the quantity of plaque accumulation.

39
Q

What two factors are emphasized in the Ecological Plaque Hypothesis?

A

The quantity and quality of plaque.

40
Q

What is “Dysbiosis” in the context of the Ecological Plaque Hypothesis?

A

shifts in the resident microbiota that can contribute to periodontal disease.

41
Q

According to the Ecological Plaque Hypothesis, what factors can affect the balance of the microbiota?

A

interaction between microbes and the host

42
Q

What is the goal of therapy in the Ecological Plaque Hypothesis?

A

eliminate disease-inducing factors to restore balance in the microbiota.

43
Q

What is the main idea of the Keystone Pathogen Hypothesis?

A

Certain low-abundance microbial pathogens, like Porphyromonas gingivalis, trigger a shift from a benign microbiota to a dysbiotic one, leading to periodontitis.

44
Q

What evidence supports the Keystone Pathogen Hypothesis?

A

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
Q

What are the mechanisms by which keystone pathogens contribute to periodontitis?

A

manipulate the host immune response by regulating Toll-like receptors, cytokine expression, the complement system, and other immune factors.

46
Q

What type of bacteria are commonly found in healthy oral environments?

A

Gram-positive facultative microbes, such as Actinomyces and Streptococcus.

47
Q

What bacteria are commonly associated with plaque-induced gingivitis?

A

Gram-positive facultative microbes: Actinomyces, Streptococcus
Gram-negative microorganisms: Fusobacterium, Capnocytophaga, Prevotella, Proph

48
Q

What are some Gram-negative microorganisms associated with chronic periodontitis? (Aunt Polly Plays Chess Everyday To Teach Friends

A

Aggregatibacter actinomycetemcomitans
Porphyromonas gingivalis
Prevotella intermedia
Campylobacter rectus
Eikenella corrodens
Tannerella forsythensis
Treponema denticola
Fusobacterium nucleatum

49
Q

What are the Gram-negative microorganisms associated with aggressive periodontitis? CAP

A

Campylobacter rectus
Aggregatibacter actinomycetemcomitans
Prevotella intermedia

50
Q

Which viruses may be involved in aggressive periodontitis?

A

Herpes Simplex Virus (HSV)
Epstein-Barr Virus (EBV)

51
Q

What is the typical microbial composition of a periodontal abscess? PPPTF

A

Porphyromonas gingivalis - 14%
Prevotella intermedia - 9%
Peptostreptococcus micros - 9%
Tannerella forsythensis (formerly Bacteroides forsythus) - 3%
Fusobacterium nucleatum - 3%

52
Q

What type of infection is a periodontal abscess?

A

mixed infection.

53
Q

What is important about antibiotic coverage for periodontal abscesses?

A

needs to cover both Gram-positive and Gram-negative microbes.

54
Q

What are the main functions of virulence factors?

A

Facilitate colonization and invasion, adherence, host tissue damage, and evasion of host defense mechanisms.

55
Q

To what does P. gingivalis adhere in connective tissue?

A

Fibrinogen and fibronectin.

56
Q

What does LPS stimulate the release of from monocytes, macrophages, and PMNs?

A

IL-1, TNF, and prostaglandins.

57
Q

What processes are activated by LPS?

A

Cytokine production, inflammatory response, and bone resorption.

58
Q

Which periodontal pathogen is associated with collagenase, which degrades collagen?

A

P. gingivalis

59
Q

Which bacteria directly invade host tissue in periodontal infections? APFT

A

Aggregatibacter actinomycetemcomitans
Porphyromonas gingivalis
Fusobacterium nucleatum
Treponema denticola

60
Q

What condition in the tissue facilitates host tissue invasion?

A

Ulcerations

61
Q

T or F: Studies have shown that some strains of microbes are more pathogenic than others

62
Q

What type of bacteria is Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans?

A

Gram-negative, nonmotile anaerobic rod.

63
Q

Where is Porphyromonas gingivalis increased?

A

In periodontitis lesions.

64
Q

What is the significance of Porphyromonas gingivalis in chronic periodontitis?

A

It is considered the “keystone” pathogen.

65
Q

What are the virulence factors of Porphyromonas gingivalis?

A

Cell adherence and tissue invasion
Collagenase
Endotoxin (LPS)

66
Q

What immune response is associated with Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans in periodontitis?

A

Increased antibody levels.

67
Q

In which periodontal conditions is A. actinomycetemcomitans increased?

A

Aggressive periodontitis and sometimes chronic periodontitis lesions.

68
Q

What are the virulence factors of A. actinomycetemcomitans?

A

Tissue invasion
Collagenase
Endotoxin
Leukotoxin (lyses human neutrophils)

69
Q

Biofilm is __________ and _________ for the development of plaque-induced gingivitis

A

necessary, sufficient

70
Q

What study provided experimental evidence for biofilm-induced gingivitis?

A

Experimental Gingivitis Studies in Man by Loe and Theilade, 1967.

71
Q

Biofilm is necessary but __ _____________ for the development of periodontitis

A

not sufficient

72
Q

T or F: Not all plaque-induced gingivitis progresses to periodontitis

73
Q

48

A

Why is it difficult to determine which gingivitis sites will progress to periodontitis?

74
Q

Why is it difficult to determine which gingivitis sites will progress to periodontitis?

A

Because periodontitis is multifactorial and has variable progression, making it unpredictable.
So treat all sites

75
Q

What are the goals of periodontal therapy regarding biofilm?

A

Reduce the organization and mass of the biofilm
Create shallow gingival crevices, which are inhospitable to anaerobic microbes