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Flashcards in Oral Micro II Deck (142)
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1
Q

Bacterial populations adherent to each other and to the surrounding environment (surfaces or interfaces), and enclosed in a Matrix are called what?

A

Biofilms

2
Q

T/F

Maintained bacterial biofilms in the mouth generally cause problems.

A

False

*Normal flora

3
Q

T/F

Biofilms are a complex, cooperating, and competing community

A

True

4
Q

What is the protective matrix made of that surrounds microcolonies of biofilm?

A

CHO

*also secreted ECM

5
Q

The primitive/simple communication system used by microorganisms can be thought of as…

A

Quorum sensing

6
Q

Once a quorum is sensed, a colony turns certain genes on and the biofilm can become _____ to antibiotics.

A

More resistant

7
Q

What is the most conspicuous biofilm in the mouth?

A

Plaque

8
Q

What 2 things happen as plaque increases in thickness?

A

Becomes less permeable to oxygen and saliva

higher conc. of toxic products, acids, inflammatory bacterial components

9
Q

T/F

Plaque alters the environment to promote growth of different species

A

True

10
Q

T/F

Too much plaque can lead to dental caries, which leads to consistent loss of periodontal ligament

A

False

*Intermittent loss

11
Q

Three types of flora:

A

Normal

Supplemental (minority of pop., generally act like normal flora)

Transient (brought in)

***also, there are Opportunists (part of normal flora that become bad actors when things go wrong)

12
Q

T/F

Most Transient Flora causes problems

A

False

*difficult time colonizing

13
Q

T/F

Some Transient Flora contain true pathogens and will cause overt disease.

A

True

14
Q

T/F

The indigenous flora is often site specific and tend to recolonize, and aren’t usually pathogenic at that site

A

True

15
Q

What role of Normal Flora leads to Innate Immunity?

A

Competition

16
Q

The fact that some women carry Staph aureus in their vaginal flora that is benign for them would be an example of…

A

Supplemental flora

*flora that exists in some individuals

17
Q

What is a major bacterial species important for seeding the epithelium (and mouth) at birth?

A

Lactobacillus

candida, etc also colonizes

18
Q

Actinomyces israelii is transmitted _______.

A

Orally

19
Q

When the teeth erupt, new ______ develop.

A

Niches

*4 new niches

20
Q

Initial plaque colonizers must be able to do what?

A

Adhere to teeth

21
Q

Dental plaque ecology becomes relatively stable with the eruption of what teeth?

A

Primary 2nd Molars (around 2 yrs)

22
Q

What bacteria can’t hold onto the hard surface of the teeth?

A

Salivarius

23
Q

Why is competition for a foothold in the mouth fierce for bacteria?

A

Most surfaces have high turnover or are flushed with saliva.

24
Q

What teeth pioneer species (2 species) provide binding sites that other bacteria can secondarily grow on (increasing plaque)?

A

S. sanguinis

S. mitis

25
Q

T/F

There is a direct link between the mother’s S. mutans and the baby’s

A

True

26
Q

What is generally the 1st pioneer species of the tooth?

What is the second (appearing in pits/fissures around 2 years)?

A

S. sanguinis

S. mutans

27
Q

Why doesn’t S. mutans appear on the teeth until around 2 years?

A

Doesn’t adhere well to smooth surfaces of teeth erupted up until that time

28
Q

What bacteria doesn’t appear in the mouth until later in life?

A

A. viscosus

29
Q

Supragingival plaque contains what 2 G+ bacteria?

Subgingival plaque contains what 2 G- bacteria?

(obviously more are present, these are good examples)

A

Streptococcus and Actinomyces

Treponema and Fusobacterium

30
Q

T/F

Subgingival bacteria contain mobile forms

A

True

31
Q

Supragingival metabolic byproducts tend to be _____

Subgingival bacteria always use what as a food source.

A

Acidic

Protein

**caries caused by acidic environment in supragingival

32
Q

What class of molecules allow Streptococci to be one of the major bacteria in the oral cavity?

A

Adhesion

*allows Strep to colonize most niches

33
Q

Bacteria tend to grow what direction from the tooth surface?

these multispecies complexes are held together by linking polymers = Biofilms

A

Perpendicular

34
Q

If a biofilm becomes large enough, what no longer works to combat them?

A

Saliva buffers

35
Q

A complex grouping of various bacteria species that adhere to one another, bacteria products, and salivary proteins.

A

Plaque Biofilm

36
Q

What did a classic study of poor oral hygiene find correlated with gingivitis?
(general type of bacteria)

A

Anaerobic forms and rods

*Reversible after 21 days

37
Q

If brushing stops, what increases?

What decreases?

A

Gram- anaerobes

Gram+ aerobes

38
Q

What occurs as plaque increases in complexity and density?

A

Food Chains develop

39
Q

What glucose polymers make up a good amount of matrix?

A

Dextrans

40
Q

What vitamin is associated with periodontal disease?

What does it do?

A

Vitamin K

Fertilizes G-

41
Q

T/F

Many forms of subgingival bacteria stink

A

True

42
Q

What is the inflammation of gingival tissues, typically due to plaque build-up?

A

Gingivitis

43
Q

What 3 things differentiate Gingivitis from Periodontitis?

A

No irreversible destruction of perio ligament

No bone loss

No apical migration of junctional epithelium

44
Q

T/F

Healthy to Acute to Chronic gingivitis is all reversible

A

True

45
Q

T/F

Chronic gingivitis to Periodontal disease is reversible

A

False

46
Q

T/F
Fluctuations in host defense capabilities brought on by stress, drugs, disease, etc, contributes to gingival disease outcome

A

True

47
Q

T/F

The factors enabling the progression of Gingivitis to Periodontal disease are largely known

A

False

48
Q

What are the 2 major categories of Periodontal disease?

A

Chronic

Aggressive

  • a third one is associated with Systemic Disease
49
Q

Most periodontis pockets display what?

A

Climax Community Flora

50
Q

Why do most of us develop chronic gingivitis?

A

Gingival inflammatory response ensures Bacteria don’t invade tissues

*and this is ongoing

51
Q

The key to inducing a bleeding gingivitis is the introduction of what?

A

One or more G- anaerobic bacteria

*also leads to Periodontitis

52
Q

Initially (before gingivitis), what two species are dominant on supragingival plaque?

What species increases as plaque load grows?
Why?

A

Strep. and Actino.

Actino.

Actino. is Microaerophilic

53
Q

What organisms need the heme that inflammation provides?

What does this organism produce once it has heme?

A

Bacteroides

LPS (highly inflammatory type)

***this leads to Bleeding Gingivitis

54
Q

In a very basic sense, the Loe experiment demonstrated what?

A

When Good bacteria decrease Bad increase

55
Q

Chronic marginal gingivitis is a ________ inflammatory response to supra-gingival plaque

A

non-specific

56
Q

Who did the experiments that definitively laid out the relationship between oral hygiene, plaque, and progression of gingivitis?

A

Loe

*also found gingivitis reversible after 21 days

57
Q

What might initiate gingival disease progression?

A

Interruption of “balance” of normal bacteria/host defense

58
Q

Name 5 factors that influence Gingivitis

A

Hormonal changes (pregnancy)

Drugs (cyclosporin, Ca channel blockers)

Disease (diabetes)

Stress

Oral Habits (chewing, smoking, mouth breathing, etc)

59
Q

The severity of gingivitis depends on the balance between what?

A

Plaque bacteria and Immune response to it

60
Q

What is characterized by painful gingival lesion with gray pseudo-membrane that readily sloughs revealing bleeding and necrosis?

A

NUG - Necrotizing Ulcerative Gingivitis

aka Vincent’s Infection

61
Q

What is the onset time of NUG?

Diagnostic shortcut?

Where are the lesions usually found?

A

Quick

Bad breath

Interdental gingival tips (papillae)

62
Q

What population is NUG found in and why?

A

Homeless

Stress

***elevated corticosteroids suppress immunity

63
Q

What was a classic case of NUG in history?

A

Trench Mouth

64
Q

How is NUG different from most bacterial invasions in gingivitis?

What causes the bad breath?
(2 species)

A

True infection

Treponema spp (G- spirochete)

Prevotella intermedia (G- rod)

(they produce noxious sulfur)

65
Q

T/F
NUG is most often seen in young adults from 16-30 years.
The more severe sub-saharan disease (90% mortality) is called NOMA and causes massive facial damage.
NUG is 70% Gram- Rod

A

True

66
Q

What are the 3 main zones of a NUG lesion?

A

Grayish pseudomembrane

Red bleeding necrotic zone

Deeper tissue of tissue being invaded by G-

67
Q

NUG is associated with decreased host immunity, especially in regard to _____.

One of the major causes may be increased levels of ______ in response to stress.

A

PMN’s

Corticosteroids

68
Q

What % of americans have periodontal disease?

What is the most predictive factor?

A

50%

Age

69
Q

Name 4 factors in Periodontal disease pathology

A

Microbes

Host Genetics

Oral Environment

Immunology

70
Q

Age, Poverty, Tobacco, Systemic diseases (diabetes), medications, crooked teeth, pregnancy, Red complex bacteria, Heredity, and oral hygiene are all factors in Periodontal disease.

A

True

71
Q

Two defining results of Periodontal disease.

A

Periodontal ligament destruction

Irreversible damage

72
Q

T/F

Loss of collagen attachment persists after the active periodontal disease process has ceased

A

True

73
Q

Can attachment loss indicate if perio disease is ongoing or a result of previous manifestation?

A

NO

74
Q

Most periodontis is due to what?

A

Loss over a lifetime

75
Q

T/F

Periodontitis is a polygenetically influenced disease

A

True

76
Q

Periodontitis could be due to multiple _____ or multiple ______.

A

disease mechanisms

synergistic factors in susceptible hosts

77
Q

Why is it not clear what specifically causes active periodontal disease?

A

Bacterial products damage tissue

Inflammatory factors damage tissue

*Imbalance may cause perio disease

78
Q

T/F

An as yet unknown oral organism may be the causative agent in perio disease.

A

True

*but unlikely

79
Q

T/F

Unique combinations of organisms along with impaired host immunity may cause perio disease

A

True

80
Q

What are the 3 major hypotheses of Perio Disease?

A

Specific bacteria

Specific mechanisms, multiple bacteria

Multiple mechanisms, multiple bacteria

81
Q

As far as treatment is concerned, what are the 3 Hypotheses of Perio Disease?

A

Nonspecific Plaque Hypothesis - all plaque bad (mow lawn)

Specific Plaque Hypothesis - Certain plaque pathogenic

Dysbiosis - Ecological imbalance causes biofilm and disease

82
Q

What does Dysbiosis involve that disproportionally effects environment?

A

Keystone Pathogens

**may be part of Dysbiosis theory

83
Q

List the 5 major suspected Periodontal pathogens, starting with the 3 that make up the Red Complex.

A

Porphyromonas gingivalis

Tannerella forsythia

Treponema denticola

Prevotella intermedia

Agregatibacter actinomycetemcomitans

84
Q

Which bacteria is most associated with Chronic perio?

Which bacteria is most associated with Aggressive perio?

A

Porphyrymonas gingivalis (chronic)

Aggregatibacter a. (aggressive)

85
Q

3 damaging microbe products:

A

Exoenzymes

Exotoxins

Toxic metabolites (ammonia)

86
Q

Name 2 defense inhibitors deployed by microbes causing Perio disease?

A

decrease PMN migration

decrease T/B-cell function

87
Q

Type I-IV immune hypersensitivity is kicked off by an unknown antigen in Perio disease. (?)

What is also bad?

A

True

Hyposensitivity

88
Q

Koch’s postulates generally don’t work with Periodontitis. What replaced these?

A

Socransky’s postulates

89
Q

What gram stain tends to be good for Perio disease and bad for caries?

A

G+

90
Q

7 features of Aggregatibacter actinomycetemcomitans:

A

G- Rod

Caphophilic (loves CO2)

Facultative

Catalase+

pH 7-8, slightly alkaline

Saccharolytic

Increased growth with Steroid Hormones

91
Q

Pound for Pound, A.a. makes what?

A

More LPS

92
Q

The LPS vesicles (blebs) of A.a. do what 3 things?

A

LPS activates Macrophage

releases Leukotoxin (cytotoxic exotoxin for PMN’s, Macrophage)

Stimulates osteoclasts (via protein)

93
Q

A.a. is found in ___% of ___ in adult periodontitis

A.a. is found in 90% of _______

A

30-50%, Agressive

Aggressive juvenile Perio (localized)

94
Q

5 features of Porphymonas gingivalis (P.g.)

A

G- rod

Anaerobic

Needs Hemin

pH 7.5-8.5

Asaccharolytic (protein major food source for G-)

95
Q

Name 5 virulence factors for P.g.

A

CHO capsule

Toxic products

LPS (much much less inflammatory)

Proteases

Invades/quorum sensing

96
Q

What is a major difference between A.a. and P.g.?

A

LPS is very stealthy in P.g.

97
Q

In terms of A.a. and P.g., how does Periodontitis change with age?

A

A.a. dominant when young

P.g. dominant when old

98
Q

Where are A.a. and P.g. found in the mouth?

A

A.a. - specific sites

P.g. - everywhere

99
Q

P.g. and A.a. are found in what numbers in a healthy mouth?

A

Small numbers - .005%

100
Q

A.a. is associated with what type of periodontitis?

P.g.?

A

LAP (localized aggressive perio)

GCP (generalized chronic perio)

101
Q

LAP shows what ethnic bias?

There is a ____ fold difference between European population and African in the US of LAP

A

(north) African

(and African American in the US)

20 fold

102
Q

T/F

P.g. dodges Antibody complement

A

True

103
Q

T/F

Oxygen is removed from the sulcus by organic molecules, creating an anaerobic environment.

A

True

104
Q

The low levels of saliva/food in the sulcus means most bacteria will dine on what?

A

Protein

105
Q

Because salivary washing isn’t much of a factor in the sulcus, what virulence factor is no longer very important?

A

Adhesion

106
Q

The different surfaces of the gingival sulcus create what?

A

More complex environment

107
Q

The major function of PMN’s in the gingival sulcus is what?

A

LPS removal

108
Q

What controls the mechanisms of attachment loss in perio?

A

Th cell direction

109
Q

Why is tooth loss not a bad thing systemically?

A

Removes the insult

110
Q

What is damaged with increased bacterial penetration into the sulcus?

A

Junctional epithelium

111
Q

T/F

The role of the large B cell buildup upon bacterial invasion of the junctional epithelium isn’t well understood

A

True

112
Q

IL-1 switches fibroblast function from collagen production to production of what 2 things?
(this is upon bacterial invasion of the junctional epithelium)

A

Collagenase

PGE2

113
Q

IL-1, TNF-alpha, and PGE2 switches bone repair to what?

upon bacterial invasion of jct. epi

A

Osteoclast activation

114
Q

North Africans have a higher rate of LAP that other populations due to what clone (bp deletion) in what species?

A

JP2

A.a.

115
Q

The JP2 clone in A.a. is more pathogenic why?

A

Leukotoxin production maxed

116
Q

T/F

JP2 clone doesn’t spread easily to Europeans.

A

True

117
Q

What is the term for inflammation of the pulp?

A

Pulpitis

118
Q

Pulp tissue responds to insults with what process?

A

Inflammatory

119
Q

Why will pulp become quickly necrotic?

A

Poor collateral circulation

120
Q

What is the most common way for pulp to become infected?

Another way?

A

Caries

“leaky” restorations

121
Q

What are the initial bugs that make it through the dentin into the pulp?

A

Lactobacillus

*then taken over by Perio bugs like Pg and Aa

122
Q

In a carious lesion, ______ chops at enamel and ______ is the first to hit the pulp.

A

Mutans

Lactobacillus

123
Q

Two forms of pulpitis:

A

Reversible (insult removed)

Irreversible

124
Q

PMN:

Name 3 mononuclear cells:

A

Neutrophils

Macrophage, T-cells, B-cells (also NK cells)

125
Q

Look for ____ in acute pulp infection and _____ in chronic infection.

*both these cells cause significant damage themselves

A

PMN’s

Macrophage

126
Q

What is the term for microbial leakage out of the root apex and destroying surrounding bone tissue in pulp infection?

A

Periapical Granuloma

127
Q

Dental pulp is generally free of viruses. What is one exception?

A

HSV

128
Q

How was the bacterial damage in pulpitis definitively shown?

A

Germ free animals didn’t develop

129
Q

At what point in penetration of the tooth does bacteria reach the pulp?

A

Once Dentin reached, bacteria can travel down tubules

Infection precedes carie in this way

130
Q

What type of inflammation usually occurs as infection precedes the carie reaching the pulp?

What occurs in Dentin during this process?

A

Chronic - mononuclear dominated (Macrophage, T/B cells)

Bacteria induce reactionary/reparative dentin

131
Q

The type of pulpal inflammation tissue is capable of recovering from (once noxious stimuli removed) is called?

A

Reversible pulpitis

*during which time a tooth may be saved

132
Q

Once ______ reaches the pulp, irreversible inflammation sets in.

This defines?

A

Plaque Bacteria

Irreversible pulpitis

133
Q

T/F

Pulp infections are almost always polymicrobial

A

True

134
Q

What type of microorganisms dominate infected pulp?

3

A

Subgingival, G-, facultative/anaerobic

135
Q

The G- facultative/anaerobic bacteria infecting pulp is made up of how many species?

A

10-30

136
Q

What is a G+ bacteria commonly associated with Pulpitis?

A

Lactobacillus

137
Q

Name 5 G- bacteria commonly associated with Pulpitis

A
Fusobacterium 
Porphyromonas
Prevotella
Tannerella
Treponema
138
Q

The bacteria infecting the root canal mirrors bacteria infecting _____

A

Periodontal disease

139
Q

What identification problem is the same in Periodontal disease and Root pulp infections?

A

Instigator bacteria vs. follower bacteria

140
Q

Describe the 2 step treatment course for Infected Dental Pulp.

A

Mechanical/chemical elimination of Agents

Restoration (unleaky)

141
Q

Bacteria in biofilms can be up to _______ less sensitive to anti-microbial agents.

How is this often achieved?

A

1000x

Communication (quorum sensing)

*latter may explain the smoldering effect followed by explosion in many infections

142
Q

T/F

Bacteria at the biofilm suggest a periapical tissue lesion is a biofilm disease.

A

True

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