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DEN1SKB > week 5 > Flashcards

week 5 Flashcards

1
Q

What colour is gram positive and why?

A

Purple because there is lots of peptidoglycan in the cell wall

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2
Q

What is an example of a gram positive bacteria?

A

Lipotechnoic acid

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3
Q

What colour is gram negative and why?

A

Pink, thin layer of peptidoglycan

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4
Q

What is an example of gram negative?

A

Lipopolysaccharide

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5
Q

What is saccharolytic metabolism?

A

resides in supragingivial plaque and sugars promote acid production.

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6
Q

What does it mean that saccharolytic metabolism forms fructans

A

its food storage for biofilm bacteria and it aids in bacterial attachment.

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7
Q

What is Asaccharolytic metabolism?

A

breaks down proteins into amino acids and nitrogen in periodontal pockets

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8
Q

What are obligate anaerobes?

A

O2 is toxic because they lack the enzymes to break it down. Eg P Gingivalis

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9
Q

What are facultative anaerobes

A

grow in or without oxygen, supragingival species such as streptococcus mutans

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10
Q

what are microaerophilic bacterias?

A

require little O2 for growth

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11
Q

Capnophilic bacteria

A

requires CO2

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12
Q

Is the development of the oral biofilm in toddlers influenced by the eruption of teeth?

A

Yes

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13
Q

At what age does the oral microbiome become complex?

A

3 yrs

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14
Q

Does the oral microbiome continue to develop in complexity over time?

A

Yes

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15
Q

Is an edentulous patient’s oral microbiome as complex as that of a fully dentate adult?

A

No

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16
Q

List three main components of the oral microbiome:

A

Shedding surfaces, non-shedding surfaces, secretions

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17
Q

Can plaque biofilms form on shedding surfaces?

A

Yes

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18
Q

Are shedding surfaces self-cleansing?

A

Yes

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19
Q

What are aerobic shedding surfaces?

A

gum tissues, soft and hard palate

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20
Q

What are anaerobic shedding surfaces?

A

Interproximal areas, subgingival areas, back of tongue

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21
Q

Give 4 examples of non-shedding surfaces in the oral cavity

A

Hard surfaces such as restorations, dentures, ortho, implants, and teeth. supra and subgingival

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22
Q

What is the source of saliva?

A

salivary glands

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23
Q

What is the source of gingival crevicular fluid (GCF)

A

blood plasma

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24
Q

What is the habitat provision for saliva and GCF?

A

Moist, aqueous, nutrient-rich environment beneficial for biofilms. Flushing action eliminates planktonic bacteria and poorly adhered cells

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25
Q

What are the nutrients in saliva?

A

Water, carbs, protein, vitamin

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26
Q

What are the nutrients in GCF

A

protein, Haem containing nutrients, erythrocytes

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27
Q

What are the antibacterial properties of saliva?

A

flushing action, antibodies, mucins, agglutinins

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28
Q

What are the antibacterial properties of GCF

A

Cytokines, antibodies, Compliment neutrophils

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29
Q

What are the habitat and growth requirements of bacteria

A

oxygen, pH, temp, nutrients, food webs, carb metabolism, protein metabolism

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30
Q

What is the normal pH of the gingival sulcus in health?

A

6.75-7.25

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31
Q

what change in pH occurs in gingival plaque during periodontal disease?

A

increase

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32
Q

What effect does an increase in pH in gingival sulcus have on the growth of periodontal pathogens?

A

improves it

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33
Q

what is the normal temp of gingival sulcus in health?

A

36.8 degrees

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34
Q

What change in temperature occurs in active periodontal pockets?

A

increase

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35
Q

What effect does an increase in temp have on enzyme activity and gene expression (eg protease production by P. gingivalis

A

increase

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36
Q

Why are bacterial adhesion to the pellicle and coaggregation important bacterial interactions in biofilms?

A

oral bacteria can get washed away quickly by saliva

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37
Q

What cell surface features facilitate surface binding by early colonising bacteria?

A

pili, flagella, receptors

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38
Q

What is a foodweb?

A

interdependent relationships between different bacteria occur when the metabolic byproducts of one bacteria can be used for another species

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39
Q

Give an example of a food web

A

streptococci produce bacteria which is used by veillonella spp

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40
Q

List the three innate host defenses present in the periodontal tissues.

A

saliva - lubricates, digests, nutrition, antibodies
Junctional and Sulcular Epithelial Barriers - attachment to tooth, antimicrobial defense, GCF flow

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41
Q

Does the junctional epithelium have an active role in host defense

A

yes

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42
Q

List the elements of the non-specific plaque hypothesis

A

all plaque is equally pathogenic, it is the bulk that causes the disease

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43
Q

what is the supporting evidence for the NSPT

A

plaque growth resulted in gingival inflammation within 10-20 days, after reinstituting oral hygiene it resolved back to health

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44
Q

What were the deficiencies or limitations of the NSPT?

A

not all patients progressed from gingivitis to periodontitis

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45
Q

of those patients with gingivitis who progressed to periodontitis, what happened

A

there was a spectrum of disease progression, some patients had rapid attachment loss with little plaque, not all sites within the patient behaved the same way

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46
Q

During the 1950’s and 1960’s, the progression of periodontitis was thought to be slow, linear and continuous.
Given contemporary knowledge, are the linear pathogenesis and continuous disease progression models valid?

A

No

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47
Q

The advent of which two microbiological techniques greatly expanded our knowledge of periodontal
microbiology?

A

postulates for “putative periodontopathogens” and DNA-DNA hybridisation

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48
Q

in health, there is little

A

bacterial load, and saccharolytic plaque.

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49
Q

In health, there is predominantly

A

aerobic gram positive organisms

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50
Q

In health, the species are

A

cocci

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51
Q

In gingivitis the species are

A

gram positive rods

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52
Q

In periodontitis there is high

A

bacterial load and subgingival plaque, asaccharolytic bacteria, motile rods

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53
Q

In periodontitis the species are

A

gram negative rods

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54
Q

What is the Specific Plaque Theory?

A

A few specific pathogens within the biofilm that causes periodontisis. The remaining microbiome doesn’t influence the disease process

55
Q

If the SPT explained the aetiology of periodontitis, how does this knowledge shift the approach to periodontal
treatment?

A

continued use of antibiotics resulted in antibiotic resistance and sensitivity. putative periodontopathogens returned after sessation of antibiotic use

56
Q

The aetiology of which two periodontal conditions are explained by the SPT? List the applicable bacteria.

A

periodontitis - opportunistic endogenous bacteria
gingivitis - treporema denticola and fusiforms

57
Q

List the main limitations of the SPT.

A

disease is caused by resident microflora, the bacteria associated with active periodontitis are found in low proportions of the dental plaque in health and gingivitis states

58
Q

List four significant contributions Haffajee and Socransky made to periodontal microbiology.

A

identified purative periodontal pathogen
used DNA to study complex microbial ecosystems
associated red complex bacteria with periodontal disease parameters such as probing depth

59
Q

List the five postulates or conditions a bacterium must achieve before being described as a “putative
periodontopathogen”

A

association, elimination, host response, animal studies, virulence factors

60
Q

describe “association” as a requirement for something being putative periodontopathogen

A

in higher numbers in disease

61
Q

describe “elimination” as a requirement for something being putative periodontopathogen

A

reduced numbers in health

62
Q

describe “Host Response” as a requirement for something being putative periodontopathogen

A

higher antibody levels against the putative periodontal pathogen in periodontitis patients

63
Q

describe “animal studies” as a requirement for something being putative periodontopathogen

A

the putative pathogen isolated from periodontal pockets must cause periodontitis in animals

64
Q

describe “virulence factors” as a requirement for something being putative periodontopathogen

A

the putative pathogen must demonstrate virulence factors that cause periodontal disease

65
Q

Name the three bacteria that make up the red complex

A

P gingivalis, T forsythia, T Denticola

66
Q

What is the cell morphology of P gingivalis, T Forsythia, T Denticola

A

Red Complex

67
Q

What are the characteristics of P Gingivalis

A

non-motile, gram-negative, requires haemin for growth

68
Q

What are the characteristics of T Forsythia

A

gram negative, difficult to culture, grows on blood agarplate

69
Q

what are the characteristics of T Denticola

A

gram negative, difficult to culture only possible through DNA analysis

70
Q

what are the virulence factors of P Gingivalis

A

Trypsin-like proteases, gingipains, invade epithelial cells

71
Q

What are the virulence factors of T Forsythia

A

trypsin like proteases, invades epithelial cells

72
Q

What are the virulence factors for T Denticola

A

adherence, motility, trypsin, invades epithelial cells

73
Q

Summarise the conclusions from Socransky, Haffajee, Goodson, Lindhe’s (1984) Random burst theory paper.

A

Sites enter a state of disease activity for short periods of time followed by longer periods of remission and no activity

74
Q

Does periodontitis progress on a site-level or at a patient (or dentition) level?

A

site level

75
Q

What is a biofilm?

A

an arranged community of microorganisms that are 3-D, located in an aqueous environment, embedded in a protective slime/sticky matrix called extracellular polymeric substance

76
Q

Are conditions the same throughout a biofilm?

A

no

77
Q

Are conditions the same throughout a biofilm?

A

no

78
Q

Does this property of biofilms increase or decrease the biodiversity of plaque?

A

increase

79
Q

What is “extracellular polymeric substance” (EPS)?

A

consists or organic and inorganic material derived from bacteria, saliva, and GCF

80
Q

List three main functions of EPS.

A
  1. helps bacteria stay together
  2. protects against phagocytosis
  3. provides a source of energy and nutrients to bacteria
81
Q

What is the purpose of “fluid channels” in a biofilm”?

A

allows movement of nutrients and O2 for bacteria and removes waste products and enzymes. communicates with other genetic materials and increases metabolic diversity.

82
Q

what are the main stages of biofilm formation

A
  1. formation of pellicle
  2. passive transport of salivary microorganisms
  3. reversible attachment of bacteria to pellicle
  4. irreversible attachment of early colonisers
  5. secondary colonisers bind, maturation, detachment
83
Q

describe pellicle formation

A

adsorption of salivary proteins onto a tooth surface. electrostatic attachment with hydroxyapatite onto enamel

84
Q

describe irreversible attachment of early colonisers

A

adhesins to pellicle receptors (streptococci) attach to glycoproteins by their fimbriae/pilli

85
Q

describe secondary colonisers bind

A

co-aggregation - receptor binding driven by bacterial cells, aerobic bacyeria consume oxygen, inflammation

86
Q

describe maturation of biofilm formation

A

stable, mature plaque, diverse ecology, motiles covered by EPS

87
Q

what is the purpose of detachment in biofilm formation?

A

allows colonization elsewhere

88
Q

which bacteria are early colonising species?

A

blue, purple, green, yellow

89
Q

which bacteria are orange

A

secondary colonisers

90
Q

which bacteria are red

A

late/tertiary colonisers

91
Q

Does saliva influence the binding of the biofilm layers and constituents?

A

yes

92
Q

Do biofilms protect resident bacteria from antimicrobial agents?

A

yes

93
Q

Can biofilms become resistant to antimicrobials through horizontal gene transfer?

A

yes

94
Q

Give two examples of bacterial communication throughout a biofilm.

A

when an antibody dies, they lyse and eDNA is released and easily transferred to another bacterium. Horizontal gene transfer, free uptake of DNA

95
Q

Can bacteria actively suppress neighbouring species?

A

yes

96
Q

where does supragingival plaque form?

A

interproximal surfaces, enamel pits and fissures

97
Q

where does subgingival plaque form?

A

epithelium, tooth and root surfaces in a periodontal pocket

98
Q

what are the oxygen conditions of supragingival plaque

A

aerobic and anaerobic

99
Q

what are the oxygen conditions of subgingival plaque?

A

anaerobic

100
Q

what is the nutrient source for supragingival plaque?

A

Saliva

101
Q

what is the nutrient source for subgingival plaque?

A

GFC

102
Q

what are the typical bacteria properties of supragingival plaque

A

sacchorolytic gram positive

103
Q

what are the typical bacterial properties of subgingival plaque

A

motile, gram negative

104
Q

what is an example of a supragingival bacteria

A

streptococcus mutans

105
Q

what is an example of a subgingival bacteria

A

spirochaetes

106
Q

How does calculus form?

A

by mineralising plaque, precipitation of phosphate salts within

107
Q

what are the differences in colour between supra and subgingival plaque?

A

sub is darker because it is stained with haemin from blood

108
Q

Bacteria are required to trigger and propagate the host response in periodontitis. True or False

A

True

109
Q

Is the host response responsible for most of the tissue damage in periodontitis?

A

Yes

110
Q

What innate host defenses are present in the periodontium?

A

Resident flora, secretions, epithelial barriers, inflammation, compliment proteins

111
Q

What triggers gingival inflammation?

A

plaque bacteria and plaque antigens

112
Q

What is the speed of inflammatory response to plaque bacteria?

A

rapid

113
Q

What is the speed of immune response to plaque antigens?

A

slow

114
Q

what is involved in inflammatory response to plaque bacteria?

A

epithelial barrier, compliment cascade, cytokines, adhesion molecules

115
Q

what is involved in immune response to plaque antigens?

A

Helper Ts, cytotoxics, B cells, antibodies, macrophages, compliment cascade

116
Q

which response to plaque bacteria triggers chronic inflammation?

A

immune response

117
Q

what happens when inflammatory response and immune response happen together?

A

chronic stimulation because plaque is not removed by host responses

118
Q

Why are neutrophils the “first line of defense” against the plaque front?

A

phagocytose foreign bacteria, create extracellular nets, degranulate lysosomal enzymes

119
Q

How do activated cytotoxic T cells cause tissue damage in periodontitis?

A

compliment system forming membrane attack complex, stimulates B cells, creates pores that disrupts bacterial cell wall integrity and cell lysis occurs.

120
Q

How does antibody release by plasma cells cause tissue destruction in
periodontitis?

A

targets soluble antigens in extracellular material leading to tissue destruction

121
Q

What is bystander damage?

A

host destruction of its own tissue. Involves alveolar reabsorption, connective tissue breakdown and apoptosis of epithelial cells

122
Q

How does periodontal tissue destruction of collagen occur?

A

14-21 days of plaque formation, anoxia in capillaries causing RBC to escape breaking down collagen

123
Q

How does periodontal tissue destruction of bone occur?

A

extensive number of T cells and plasma cells

124
Q

For “Initial lesion” of biofilm induced gingivitis how many days has the plaque been there and what it is the state of the gingiva?

A

2-4 days, healthy

125
Q

For “Early Lesion” of biofilm induced gingivitis how many days has the plaque been there and what it is the state of the gingiva and what immune cell type is working?

A

1 week, supragingival plaque, gram positive microbes, some destroyed collagen fibres, T cells and macrophages activated

126
Q

For “Established Lesion”/chronic of biofilm induced gingivitis how many days has the plaque been there and what it is the state of the gingiva and what immune cell type is working?

A

1-2 weeks, pocket formation, chronic gingivitis, damaged fibroblasts and collagen fibres, plasma cells derived from B

127
Q

For “Advanced Lesion” of biofilm induced gingivitis how many days has the plaque been there and what it is the state of the gingiva and what immune cell type is working?

A

over 2 weeks, periodontitis, coronal detachment, damaged fibroblasts collagen fibres and alveolar bone reabsorption, plasma cells

128
Q

Do all established lesions progress to advanced lesions?

A

No

129
Q

The red complex bacteria are implicated in periodontal tissue breakdown,
however the host response to these bacteria (i.e. inflammation and immune
responses) is responsible for how much of the tissue destruction in
periodontitis?

A

80%

130
Q

what are the main concepts of symbiosis

A

a mutual relationship of oral flora and host. nutrient competition, barrier function, protection

131
Q

what are the main concepts of dysbiosis

A

the shift from gram positive to gram negative, altered pH or diet, smoking causing a pathogen enriched microflora

132
Q

summarize ecological plaque theory

A

both the quantity and quality of bacteria can trigger the dease condition and the host risk factors contribute to the severity and extent of the resulting gingivitis and periodontitis

133
Q

summarize keystone pathogen theory

A

host defenses can’t effectively clear the pathogen

134
Q

summarize the IMPEDE Model

A

no RX - dysbiosis and tissue damage can be exacerbated

DEN1SKB (12 decks)

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