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Oral Sciences > Unit 3 > Flashcards

Unit 3 Flashcards

1
Q

TF? Mature plaque is composed of gram-negative and not gram+ bacteria.

A

F. Both, greater proportion of gram -, also fungi and other organism

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2
Q

How do the # of bac spp vary?

A

site to site, P2P

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3
Q

Late colonizers:

A

T. denticola, P. gingivalis, A. actino… , P. intermedia, Eubacteria, S. flueggel, C. sputigena, fusobacterium nucleatum (bridge bw early and late)

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4
Q

Affect bac colonization:

A

genes, age, indegenous flora/ competition, host response, food, environment

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5
Q

4 habitats in mouth:

A

tongue, buccal mucosa, tooth plaque (sub and supragingival), saliva

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6
Q

Cheeks, lips, palate:

A

low diversity of microflora, fac anaerobes, Strept spp mainly, some perio pathogens persists by invading the buccal CELLS

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7
Q

Tongue:

A

diverse microflora, fac and obligate anaerobes, (StRAN) Strep, Rothia, Actinomyces, Neisseria, some gram - anaerobes, some anaerobic sites

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8
Q

Teeth:

A

diverse microflora, many obligate anaerobes, (STAF VP) Strep, Treponema, Actinomyces, Fusobacterium, Veillonella, Prevotella, unculturable organisms, influenced by saliva and GCF

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9
Q

2 most prominent cultivatable bac spp pop in saliva, buccal mucosa, tongue dorsum, and supragingival plaque

A

S oralis and S. mitis

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10
Q

5 most prominent cultivatable bac pop in tongue dorsum:

A

S. oralis/ mitis/ salivarus, A. naeslundi, Haemophius spp.

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11
Q

4 most prominent cultivatable bac pop in supragingival plaque:

A

A. naeslundii, A. odontolyticus, S. mutans, S. sanguinis,

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12
Q

bacterial like this temp range:

A

33’-37’C, sulci: 33’-36’C, perio: 39’C

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13
Q

Effect of inc temp on bac expression:

A

inc expression of some proteins

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14
Q

palatal, buccal mucosa, healthy gingival crevice, & diseased gingival crevice pH

A

7.34, 6.3, 6.9, 7.4+

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15
Q

critical pH:

A

5.5

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16
Q

3 bac to that can survive at the highest pH

A

S. mutans, Lactobacilus, P. gingivalis,

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17
Q

5 bac that can survive at the lowest pH:

A

S. mutans/ sobrinus/ sanguinis, Lactobacilus, Actinomyces (root caries)

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18
Q

Most oral organisms are:

A

most anaerobic, fac or obligate anaerobes, early O2 rich, mature anaerobic

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19
Q

This flow is increased in pd:

A

GCF, from circulatory system, nutrients, proteins, inflammatory cells, host defense

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20
Q

Endogenous nutrient availability:

A

Saliva, GCF, bac products

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21
Q

nutrients from saliva:

A

protein, glycoprotein, AA’s, peptides

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22
Q

Nutrients from GCF:

A

protein, glycoprotein, albumin

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23
Q

How are exogenous nutrients used in the oc?

A

up to EC polysacs or down to lactic acid

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24
Q

extrapolysaccharides used for glucan and fructan synthesis:

A

glucose or fructose

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25
Q

Why are glucans/ fructans built and what are they built from?

A

extra food source in times of famine, extra food source, sucrose

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26
Q

Glucans, soluble or in-?

A

either

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27
Q

How are intracellular ps’s used?

A

energy

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28
Q

How are extracellular ps’s used?

A

biofilm, adhesion via S. mutans and other bac

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29
Q

Type of glucan S. mutans makes from sucrose, soluble or insoluble?

A

both water-soluble and water-insolube glucans

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30
Q

Uses of water-soluble glucans:

A

energy, lactic acid formation

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31
Q

Uses of water-insoluble glucans:

A

plaque accumulation (sticky, hard, cement-like)

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32
Q

Why older pts have different bac in oc:

A

other diseases, meds, esp. antibiotics, weak IS, dec saliva, dentures

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33
Q

Why are dentures prone to fungus accumulation?

A

differences bw the 2 surfaces

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34
Q

3 bac, not detectable at 3mo, detectable at 32mo:

A

(SPF 32) Selenomonas, P. denticola, Fusobacterium nucleatum

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35
Q

4 bac that were found in 100% of 32mo old kids:

A

(F*** PCP) Fusobacterium nucleatum, P. melaninogenica, Capnocytophaga, non-pigmented Prevotella

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36
Q

Bac w largest inc after tooth eruption, highest first:

A

(F*** PCP) Fusobacterium/ P. denticola, Capnocytophaga, P. loescheii,

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37
Q

Bac found in just after birth:

A

S. mitis/ S. salivarius, a. naeslundii (?)

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38
Q

Commensal bac’s:

A

S. sanguinis, gordonii, oralis, mitis (That bloody at bitch can commence giving me head bc it’s mighty good))

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39
Q

Structural formation of initial microcolonies:

A

columnar

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40
Q

TF? All pioneer spp. are rod shaped.

A

F. cocci, layer on pellicle.. Strep..COCCI

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41
Q

TF? Later plaque is comprised mainly of rod shaped bac.

A

T

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42
Q

Which adhere more tightly, early or late colonizers.

A

Late, denser, break off, disease in distant sites (harder for a pt, with the same amt of effort, to clear mature plaque than early plaque?)

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43
Q

More anaerobic bac:

A

P. gingivalis, T. forsythia, spirochetes like T. denticola

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44
Q

TF? In ppd, plaque is deeper in crevice, and invade INTO epi cells

A

T.

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45
Q

Are gram - bac capable of invading the CT and collagen?

A

yes

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46
Q

Define calculus:

A

calcium phosphate on tartar, rough surface, colonizing spot

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47
Q

After how many days of not brushing will gram - rods appear in the oral bac?

A

~5d

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48
Q

After how many days of not brushing will spirochettes appear in the oral bac?

A

~10d

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49
Q

How many days did it take to get rid of gram - bac once a person began brushing?

A

~5d

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50
Q

This is used as a measure of gingivitis:

A

gingival index

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51
Q

How many days after not brushing did gingivitis begin?

A

~10, same time as appearance of spirochetes

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52
Q

This bac initially inc in the 1st wk of not brushing, then dec:

A

S. sanguis

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53
Q

These 2 bac both inc weekly w not brushing:

A

A. viscosus, F. nucleatum

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54
Q

Bac found in fissures:

A

Strep, actinomyces, Gram +, fac anaerobes

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55
Q

Bac found in approximal areas:

A

Gram + & -, fac and obligate anaerobes: (SPANV-span the V shaped embrasure from tooth to tooth) Strep, Prevotella, Actinomyces, Neisseria, Veilonella

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56
Q

Bac found in gingival crevice:

A

Gram + & -, fac and obligate anaerobes, (SAFE TP) Strep, Actinomyces, Fusobacterium, Eubacterium, Treponema, Prevotella

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57
Q

Are cariogenic plaque bac more acid producing or acid tolerating?

A

both

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58
Q

TF? The proportion of S. mutans inc w caries progression.

A

F. dec

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59
Q

Most oral bacteria, motile or non-motile?

A

non-motile, no flagella, carried by salivary flow

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60
Q

Causes of expulsion or death of bac:

A

agglutination, mechanical shearing, antimicrobial saliva, antagonistic bac

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61
Q

Promote colonization:

A

adherence properties, synergistic bac, nutritional substrates, temp and moisture

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62
Q

Proteins & glycoproteins in pellicle formation:

A

mucins, agglutinin, PRP’s, amylase, sialic acid

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63
Q

Bacterial components of pellicle:

A

glucan (sugar chains), glucosyltransferase (Gtf)

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64
Q

1st 3 steps in bac colonization:

A

assoc, adhesion, invasion

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65
Q

This is a weak, reversible attachment:

A

associaton

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66
Q

Is bac assoc reversible or ir-? Type of bond?

A

reversible, electrostatic

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67
Q

Is adhesion reversible or -ir?

A

irreversible

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68
Q

These are responsible for adhesion:

A

adhesins, complementary molecule on host surface

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69
Q

beginning of complex biofilm formation:

A

coaggregation

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70
Q

Adhesion is interaction bw:

A

bac adhesin & pellicle or cell receptor

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71
Q

Host surface receptors to which bac can attach:

A

glycan, glycolipid, glycoprotein, ECM glycoprotein, surface integrin, fibronectin

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72
Q

Pili or fimbriae attachment is to:

A

glycolipid or glycoprotein

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73
Q

Afimbrial adhesin attachment is to:

A

glycan, ECM glycoprotein, surface integrin, fibronectin

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74
Q

bac attach to pellicle via:

A

PRP’s, a-amylase, sialic acid, statherin (PASS)

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75
Q

bacterial/ metabolic food chains:

A

complex substrates —> 1’ feeder –> product –> 2’ feeder –> simpler product

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76
Q

aerobic early/ secondary colonizers:

A

capnophilic, facultative anaerobes

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77
Q

Autoinducer-2:

A

universal interspecies signal, luxS, in both gram + and - bac

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78
Q

Competence stimulating peptide (CSP):

A

Strep quorum sensing signal, induces genetic competence enabling exchange of free DNA to transformation-competent cells

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79
Q

Carriage of this can prevent against S. areus carriage:

A

S. pneumoniae

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80
Q

pneumococcal conjugate vaccine inc rate of:

A

Staph areus and related diseases

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81
Q

S. pneumoniae protection against S. areus can be disrupted by

A

vaccinating kids w pneumoccocal conjugate vaccines (red carriage of vaccine-type S. pneumoniae in nasopharynx)

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82
Q

P. gingivalis bind this weakly in suspension and tightly on surface:

A

S. gordonii

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83
Q

oxygen req for P. gingivalis:

A

obligate anaerobe, redox pot must be low, O2 scarce

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84
Q

Site of P. gingivalis attachment to plaque:

A

S gordonii

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85
Q

Types of viral infections that inc susceptabilty to bac infection

A

measles, retroviruses

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86
Q

Diseases caused by combo of 2 or more nonpathogenics

A

abdominal/ lung/ brain abscess or subdural empyema, 2’ peritonitis, odontogenic infection, chronic otitis media or mastoiditis, liver infection, soft-tissue infection, fasciitis, bacteremia

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87
Q

TF? All polymicrobial infections depend on biofilm for resulting infection.

A

F. Most

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88
Q

Can single spp result in alv bone loss?

A

yes

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89
Q

symbiosis gone awry:

A

dysbiosis

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90
Q

Causes of altered commensal bac composition:

A

inc total commensal bac load, inc sp oral bac

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91
Q

These can be found in subgingival samples from aggressive periodontitis:

A

EBV, CMV, herpes, (ech…)

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92
Q

Proposed mech of interaction bw Herpes and perio bac:

A

Herpes lowers local defense, increasing aggressiveness of pd causing bac, bac inc virulence of herpes

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93
Q

Virus found in highest number in pd:

A

EBV, CMV, Herpes-1, 7, 8, 6

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94
Q

VIruses found w ANUG + malnutrition:

A

coinfection > CMV > EBV-1

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95
Q

Lesions S. mutans induces in animal models:

A

smooth, fissure and root lesions

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96
Q

Dominant bac spp. in rampant caries:

A

Lactobacillus spp, inc sig from initial to deep lesion

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97
Q

Is Lactobacillus found in healthy pts?

A

no

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98
Q

Is there a sig assoc bw S mutans and caries progression?

A

no

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99
Q

Bac assoc w caries progression but not found at high levels:

A

Propionibacterium

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100
Q

Additional candidates for progression of caries:

A

S. mitis, Selenomonas, Neisseria (MSN)

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101
Q

Periapical osteitis is aka:

A

apical peiodontitis

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102
Q

TF? Chronic endo infections are always of polymicrobial etiology.

A

F. Almost always

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103
Q

Routes of endo infection:

A

dentinal tubules, open cavity, perio sulcus via lateral canal or apical foramen, defective restoration, bacteremia

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104
Q

Cause of inflammation in apical periodontitis:

A

irritants seeping out of inflamed or necrotic pulp

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105
Q

Irritants that can cause inflammation:

A

bac, their toxins, trauma, debris added during endo

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106
Q

Apical periodontitis is aka:

A

granulomas (check)

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107
Q

Central zone cells of apical periodontitis:

A

plasma cells and lympho

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108
Q

Area beyond the central zone:

A

fibrous capsule (circular layer), outer margin limits bone regeneration

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109
Q

Duration for complete necrosis of pulp w granulomas and abscesses due to pulp exposure in rats:

A

9d+

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110
Q

This occurred 14-28d after pulp exposure in germ free rats:

A

dentinal bridging (?what is this?)

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111
Q

PA reaction of strep:

A

weak

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112
Q

Can enteroccoci survive when introduced as a single strain in apical periodontitis?

A

Yes

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113
Q

Result of adding single strains to apical periodontitis:

A

reestablishment of “8 Strain collection”

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114
Q

Root lesion bac composition, highest to lowest %:

A

S. anginosus, fusobacterium nucleatum, bacteroides forsythus

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115
Q

Bac NOT found in pus samples:

A

Actinomyces israelii, actinobacillus actinomycetemcomitans or fungal spp.

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116
Q

Bac found in endo infections:

A

red complex, Prevotella intermedia, Porphyromonas endodontalis, Fusobacteria, G+ anaerobic rods: filifactor alocis, actinomyces, G+ cocci: strep, enterococcus faecalis

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117
Q

Bac often found in failed root canals:

A

Enterococcus faecalis

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118
Q

Enterococcus faecalis:

A

failed root canals, in poor nutrient supply, resist meds (Ca2+ hydroxide, Na+ hypochlorite), pH, salinity & antibiotics, forms biofilm in canal

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119
Q

ANUG is aka:

A

Trench mouth, Vincent’s gingivitis

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120
Q

These predispose to ANUG:

A

stress, malnutrition, smoking, immnodeficiency

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121
Q

ANUG:

A

necrosis of gingival margin and interdentinal papilla, pain, swelling, odor, NUP also possible

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122
Q

Bac in NUG:

A

fusobacterial and spirochetal forms, wide range of spp, many anaerobes

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123
Q

Potentially life-threatening cellulitis of floor of mouth, usually in adults w dental infections, can restrict airway:

A

Ludwig’s angina

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124
Q

Ludwig’s angina is aka:

A

Angina ludovici

125
Q

NOMA is aka:

A

cancrum oris

126
Q

NOMA:

A

orofacial gangrene, malnourished kids, POH, debilitating concurrent illness, begins as ulcer of mucous mem w edema of face extending out, rapidly destroys soft tissue and bone, almost always fatal wo tx

127
Q

NOMA is attributable primarily to:

A

intrauterine growth retardation (check)

128
Q

Is NOMA a primary disease?

A

No

129
Q

Illnesses that predispose to NOMA:

A

malnutrition, measles (viral predisposing to bac infection), TB, leukemia, AIDS

130
Q

Initial lesion of NOMA could appear as:

A

common cellulitis

131
Q

Role of malnutrition in NOMA:

A

alters cell-mediated immune function, breaks down epi tissues, then invasion by pathogens

132
Q

Microbial etiology of NOMA:

A

probably Borrelia vincentii and Fusobacterium, esp F. necrophorum, mixed w others

133
Q

Possible role of F. necrophorum in NOMA:

A

rapid spread thru soft tissue bc it produces dermatotoxins

134
Q

This creates a staging period of NOMA:

A

infection w endemic viruses

135
Q

Cytokine profile shift seen in NOMA:

A

inflammatory to anti-inflammatory cytokines

136
Q

Factors involved in NOMA path:

A

malnutrition, impaired oral mucosal immunity, immune dysfunction, infection w endemic viruses, effective structural integrity of oral mucosa, selective overgrowth of pathogenic microorganisms, inc oxidative stress, shift from inflammatory to anti-inflammatory cytokine profile

137
Q

NOMA tx:

A

might be resistant to penicillin, use amoxicillin-metronidazole (last 2 letters of NOMA backwards)

138
Q

Tx of polymicrobial infections:

A

debridement, incision, drainage, SRP, RCT, antibiotics, improved OH and regular visits

139
Q

difficulty in articulating words due to disease of the central nervous system

A

dysarthria

140
Q

Case: sudden dysarthria, L-sided hemiparesis, multilobar hemorrhagic lesion involving R thalamus w edema extending to brainstem, lots of periapical radiolucencies:

A

Brain abscess, G+, Strep intermedius, no issue in blood or Xray

141
Q

Most common dental bac that leads to brain abscess:

A

Polymicrobial, then Fusobacterium spp (Gram -), Peptostreptococcus spp, Strep intermedius

142
Q

Systemic infections w dental etiology:

A

Liver, brain, bone, lung, soft tissue infections, infective endocardiits

143
Q

Bone infection is aka:

A

osteomyelitus

144
Q

Soft tissue infections occur:

A

in muscle

145
Q

Pts must likely to get thrush:

A

infants, IC, older, tumors, burns, oral prosthesis, catheters, hemodialysis, antibiotics, corticosteroids, antineoplastic or psycho-active drugs

146
Q

% of pop that are carriers for OC:

A

35%

147
Q

1st question if patients presents w oral can:

A

are you on antibiotics?

148
Q

Why psycho-active drugs predispose to OC:

A

decrease saliva flow, predispose to oral can

149
Q

OC:

A

Can really only colonize mouth, not found anywhere else, no other animals, not in soil, etc. HUMANS ONLY, been w us for a long time

150
Q

Are neonates or infants more likely to get OC?

A

infants, 1-18mo (44%)

151
Q

Why are neonates at lower risk for OC than infants?

A

maternal immunity

152
Q

Where can the yeast be found in mouth?

A

tongue, palate, buccal mucosa, max denture, saliva, NOT man denture

153
Q

Are candida spp normally found on the skin?

A

yes

154
Q

C. albicans most to least prevalent locations in body:

A

mouth, vagina, resp tract, urine/pus, blood

155
Q

2 most common Candida spp in oral cavity after albicans:

A

glabrata, then tropicalis

156
Q

Projections from candida that extend into deeper layer:

A

hypha

157
Q

Cationic antifungal peptides:

A

calprotectins, histatins

158
Q

histatins are anti:

A

fungal

159
Q

Th1 response to candidiasis:

A

IL12, IFNy, protective

160
Q

Th2 response to candidiasis:

A

IL4, 5, 10, non-protective

161
Q

protective response to candidiasis:

A

Th1 and 17 response, IL12, IFNy, IL-17, 23

162
Q

non-protective response to candidiasis:

A

Th2 response, IL4, 5, 10

163
Q

Th17 response to candidiasis:

A

Protective, IL-17, 23

164
Q

Primary response to candidiasis:

A

TH17, protective Il-17, 23

165
Q

Cells involved in innate immune response:

A

PMNs, macs

166
Q

Localized candidiasis can focus here:

A

kindey, liver, spleen, endocarditis

167
Q

Localized candidiasis w high mortality rate, difficult to treat:

A

spleen

168
Q

Disseminated candidiasis is aka:

A

candidal septicemia

169
Q

TF? Biopsy is an easy, effective method to dx candidiasis.

A

F, bc it is normally there in mouth, T if it is in another organ

170
Q

Why have deaths due to systemic candidiasis risen since the 60s?

A

more ppl living w immune suppression

171
Q

Cause of chronic mucocutaneous candidiasis:

A

immune dysfunction

172
Q

Cx ind of chronic mucocutaneous candidiasis:

A

persistent superficial lesions

173
Q

TF? chronic mucocutaneous candidiasis responds well to antimycotic agents.

A

F. poor response

174
Q

If a person has persistent superficial lesions, what is the % likelihood that there is an oral manifestation of the disease?

A

90%

175
Q

Tx for chronic mucocutaneous candidiasis:

A

antifungal

176
Q

Cutaneous candidiasis can be on these body parts:

A

under/ around finger nails, crease of elbow, groin, moist, hidden areas

177
Q

Acute pseudomembranous OC is aka:

A

thrush

178
Q

Underlying disease assoc w OC:

A

leukemia, diabetes, xerostomia (radiation, drug induced), AIDS

179
Q

OC is often diagnosed before this underlying disease is found:

A

leukemia

180
Q

Tx for OC in infants:

A

time, antifungals

181
Q

About __% of HIV patients will have oral Candidiasis at some point.

A

90

182
Q

Cell count assoc with initial dx and severity of HIV:

A

CD4

183
Q

Prevalence of candidiasis in HIV infected individuals:

A

9-90%

184
Q

Dx of acute pseudomembranous candidiasis:

A

circumscribed white plaques, microbial smears, leaves red underlying tissue when wiped away, classic hyphae form under microscope

185
Q

Are the colonies of acute pseudomembranous candidiasis confluent?

A

no

186
Q

TF? OC can be on both the hard and soft palate.

A

T

187
Q

Why is denture induced stomatitis rarely under lower denture?

A

attached KERATINIZED tissue

188
Q

Which is more inflammatory, denture induced stomatitis or OC?

A

DIS

189
Q

TF? There is invasion of the palatal epi in DIS.

A

F.

190
Q

Type of inflammation in DIS:

A

diffuse sub-epi

191
Q

Cause of inflammatory reaction in DIS:

A

yeast proteases, secreted

192
Q

IR to DIS:

A

innate immunity, no cell mediated IR (it doesn’t enter the cell!)

193
Q

Candida spp isolated from DIS in greatest proportion:

A

C. albicans

194
Q

3 Candida spp isolated from DIS:

A

C. albicans, C. tropicalis, C. glabrata

195
Q

How is DIS classified?

A

severity of inflammation

196
Q

Cx signs of DIS:

A

usually asymptomatic, itching, burning, dryness, usually not assoc w infection

197
Q

What infection is DIS usually associated with?

A

None.

198
Q

Newton Type 1 DIS:

A

pinpoint erythema, enlargement of palatal minor duct orifices, small localized areas of inflammation

199
Q

Newton Type 2 DIS:

A

diffuse hyperemia & erythema, inflammation of denture bearing area only

200
Q

How to know if erythema under a denture is DIS or simple irritation?

A

of candida present

201
Q

Inflammation in Newton Type 2 DIS is localized here:

A

under max denture

202
Q

Newton Type 3 DIS:

A

epi hyperplasia, granular or nodular lesion, diffuse erythema, entire palate, ground hamburger meat appearance, spongey, soft feel

203
Q

Etiology of DIS:

A

yeast AND bac, prosthesis overuse/misfit, lack of saliva to affected area, (salivary antifungal histatins, re-infection from denture)

204
Q

TF? mechanical inflammation can lead to DIS.

A

T. ill-fitting dentures

205
Q

How to determine if OC is DIS or APC:

A

past border of denture - acute pseudomembranous candidiasis

206
Q

Can we clean dentures with chlorhexidine?

A

No, it will stain them

207
Q

Candida leukoplakia (CL) is aka:

A

chronic hyperplastic candidiasis

208
Q

CL:

A

discrete areas, can’t be removed, on buccal mucosa, assoc w tobacco use and atypia

209
Q

candida is always:

A

superficial and removable w gauze

210
Q

Angular cheilitis (AC):

A

fissuring, soreness, redness, may be white, may be assoc w other forms of OC

211
Q

Tx for AC:

A

Nystatin, 5 X day (pid?)

212
Q

Pts prone to AC:

A

overclosed pts

213
Q

Midline glossitis (MG): is aka:

A

Median rhomboid glossitis, antibiotic sore tongue, papillary atrophy

214
Q

MG:

A

deep red midline of tongue, not actually candida

215
Q

2 major classes of antifungal drugs:

A

polyene, azole

216
Q

MOA of polyenes:

A

mem disruption, perforation

217
Q

MOA of azoles:

A

inhibit ergosterol synthesis, main fungal sterol

218
Q

Toxic polyene when delivered systemically:

A

Amphotericin B, last resort when pt will die wo, causes kidney damage

219
Q

Topical polyene:

A

Nystatin (Mycostatin) (AC)

220
Q

Topical azole:

A

Clotrimazole (Mycelex, e.g. Mycelex 7- yeast infection)

221
Q

2 systemic azoles:

A

Ketoconazole (Nizoral), Fluconazole (Difflucan)

222
Q

Give this as a prophylactic to AIDS pts:

A

Diflucan

223
Q

2 drugs for vaginal candidiasis:

A

Ketoconazole (Nizoral) (check), Fluconazole (Diflucan)

224
Q

Issue w topical tx:

A

Pt must dissolve 1 tablet 5 times daily for 10d, poor compliance, vs. systemic: 1 daily for 3k

225
Q

Adjunct therapies for candidiasis:

A

chlorhexidine rinse, neutral NaF

226
Q

When to Rx chlorhexidine as prophylactic:

A

IC, irradiated, leukemic pts

227
Q

When to use neutral NaF as an adjunct therapy:

A

while using Nystatin topical agents (AC)

228
Q

Does chlorhexidine (0.2%) target bac or yeast more?

A

bac

229
Q

Prescribe this w Nistatin/ Mycostatin for pt w teeth:

A

NaF (1%)

230
Q

2 forms of topical treatment for DIS:

A

troche, pastilles

231
Q

2 topical drugs to treat DIS:

A

Mycelex, Mycostatin

232
Q

Which tx is a pt more likely to comply w for DIS?

A

mycelex, 3/d vs. 5/d

233
Q

Overall tx for DIS:

A

topical, disinfect dentures, chlorhexidine rinse

234
Q

When to prescribe prophylactic fluconazole to HIV pts:

A

CD4 count under 100, 1 episode of candidiasis

235
Q

What type or candidiasis are HIV pts likely to get?

A

oropharyngeal candidiasis, emergence of resistant spp

236
Q

Antifungal that is ineffective in tx of oropharyngeal candidiasis in HIV pts:

A

topical antifungals

237
Q

Are pts likely to comply w Difflucan tx for OC or HIV pts?

A

yes, 1/d or 1 every other day

238
Q

Key point in the treatment of any OC:

A

address underlying cause, prevent recurrence

239
Q

OC arises in:

A

commensalism

240
Q

Can cross infection occur w OC?

A

yes

241
Q

Human cells are about __ X larger than bac and the adult human body has __ X more microbial cells than the human cell:

A

10, 10

242
Q

TF? Humans are wo any microorganisms in the placenta.

A

T

243
Q

First exposure to microorganisms:

A

vaginal canal, sterile until rupture of amniotic membrane

244
Q

Most microbial cells inhabit:

A

mucosal surfaces

245
Q

Largest microbial community in body:

A

colon (up to 100 trillion bac)

246
Q

A person’s microbial community is established by this age:

A

2

247
Q

Strongest (?) influencing factor in a person’s microbial community:

A

genetics, twins very similar

248
Q

Lager health effects of gut microbial flora on body:

A

fat storage, obesity

249
Q

2 lifestyles commensals can have:

A

commensalism, mutualism

250
Q

Commensalism:

A

unidirectional, 1 benefits, other unharmed

251
Q

Mutualism:

A

Synergistic, both benefit

252
Q

Bifidobacterium longum, commensal or pathogen?

A

commensal, in gut, promotes health, possible role in digestion & processing of “non-digestible” plant polymers

253
Q

Bacillus anthracis, commensal or pathogen?

A

pathogen, resp and skin infection

254
Q

What type of pathogen is S. aureus?

A

opportunistic, multiple infections, 100,000+/yr, 30% have w no effect

255
Q

Bacterium causing disease depends upon:

A

inherent virulence, host response, bac count

256
Q

These inc inherent virulence of an organism:

A

virulence factors, enterotoxins

257
Q

TF? Bac is always required in high numbers to cause disease.

A

F. depends on the virulence of the bac

258
Q

prototypical biofilm:

A

plaque

259
Q

factors affecting bacterial composition:

A

pH, O2, temp, redox potential, nutrients

260
Q

Cause endo infection:

A

caries, exposure through trauma, bloodstream bac (not common), resto tooth interface, perio attachment loss, radicular dentin (?)

261
Q

1st to discover bac:

A

Leeuwenhoek

262
Q

Bac assoc with pain:

A

B. melaninogenicus

263
Q

Most common bac in mouth:

A

actinomyces and fusobacterium naeslundii

264
Q

Oxygen requirement of most bac in mouth:

A

anaerobic

265
Q

to id Antigens sp to a bacteria

A

Immmunofluorescnce

266
Q

Tolerate acidic condition and inc susceptibility to caries:

A

s. mutans and sobrinus

267
Q

Red complex, new periodontal paradigm to include:

A

Filofactor alocis, Gram + bacilus

268
Q

Filofactor alocis:

A

Gram + bacilus

269
Q

Problems w id’ing all oral bac:

A

inability to cultivate, inadequate media, metabolic interdependencies

270
Q

Strep produces ___, which is a nutrient for____

A

lactate, Veillonella

271
Q

List all taxonomical groups for S. gordonii:

A

Bacteria, Frimuicutes, Bacilli, Lactobacilus, Streptococcacae, Streptococcus, gordonii

272
Q

Term used instead of species to refer to a novel cluster of sequences:

A

phylotype, usually >2% difference in 16 sRNA sequences = distinct phenotype

273
Q

Form the 50s subunit of rDNA:

A

23s and 5s (31 proteins)

274
Q

Form the 30s subunit of rDNA:

A

16s (21 proteins)

275
Q

50s and 30s subunit combine to form:

A

70s

276
Q

Most evolutionarily conserved macromolecule:

A

16s rDNA, ued to determine relatedness

277
Q

Which yields a more diverse view ot he oral flora, direct amplification or cultivation?

A

direct amlificaiton of 16s rDNA

278
Q

Bac w a high level of genetic variation or diversity w/in individuals:

A

S. mitis

279
Q

Methanobrevibacter smithii:

A

in gut, assoc w sever pd in mouth, health in clon, consumes end products of bacterial fermentation, combines H w CO2 to form methane

280
Q

Non-albicans candida is most often found:

A

in blood

281
Q

TF? The Th1 response will prevent candidiasis infection if the Th17 response is inhibited.

A

need Th17

282
Q

Places to which candidiasis disseminates:

A

lungs, meninges, GI tract, dx these via culture

283
Q

Where in mouth can candidal leukoplakia be found?

A

buccal mucosa only

284
Q

Kids using asthma inhalers may get:

A

midline glossitis

285
Q

pastille drug:

A

mycostatin (nistatin)

286
Q

troche drug:

A

mycelex

287
Q

What not to Rx for HIV pts with OC:

A

topicals

288
Q

Are spirochetes free-living or symbiotic?

A

both

289
Q

Only bac group w periplasmic flagella:

A

spirochetes

290
Q

Ex of spirochete commensalism:

A

clam and termite digestive tracts

291
Q

Causes relapsing fever:

A

Borrelia hermsii

292
Q

Causes Leptospirosis:

A

Leptospira interrogans

293
Q

Causes of Lyme d. and Syphillis:

A

Borrelia burgdorferi, T. palladium

294
Q

Spatial distribution of P. gingivalis and T. denticola in plaque:

A

co-localized

295
Q

Assoc of spirochetes w oral diseases, highest to lowest:

A

early onset, adult, localized juvenille periodontitis

296
Q

TF? There are fewer spirochetes after tx than in health.

A

F. more

297
Q

Most common bac in endo infection:

A

T. socaranskii, T. denticola, T. amylovorum, T. medium, T. maltophilum (T. madms)

298
Q

Trep that can be cultivated:

A

T. denticola

299
Q

Virulence factors of spirochetes:

A

cytotoxicity, tissue invasion and destruction, immnomodulation

300
Q

Facilitates tisseu invasion by spirochetes:

A

chymotrypsin like protease, degrade laminin, fibronectin

301
Q

These are being resisted in immunomodulation:

A

complement, neutrophils

302
Q

T. denticola affects on fibrolasts:

A

degranulation, actin rearrangement, detachment

303
Q

T. denticola affects on epi cells:

A

degranulation, membrane blebs, cytoskeleton, disruption and death

304
Q

Macs, when activated by T. denticola, acitvate:

A

IL-1, TNF-a

305
Q

Fxn of metalloproteinases:

A

disrupt gingival tissues

306
Q

How does T. denticola avoid PMNs?

A

O2 production inhibition, release of enzymes like metalloproteinases

307
Q

Fxn of cystalysin:

A

break cystein glutathione down to pyruvate, NH3, and H2S, which then are used for energy, to break RBCs and, promote perio lesions, anti-acid, inc oral mucosa permeability, and hydrolyze disulfide bonds of IgG, cytokines and chemokines

308
Q

coincubation of Tmac w complement:

A

R chain of c3 & a-chain of C4 degrade

309
Q

How does T. denticola inhibit neutrophil activation and migration?

A

MSP

Oral Sciences (16 decks)

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