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Introduction to Periodontics and Prevention > Lecture 11 & 12 > Flashcards

Lecture 11 & 12 Flashcards

1
Q

Biofilm is made of a ___ matrix

A

polymeric

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2
Q

TF? Biofilm can adhere to both inert or living surfaces.

A

T

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3
Q

TF? All bacteria live in biofilm.

A

F. most

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4
Q

premedication is important for:

A

arificial heart valve, prosthetic limb, etc., , bacteria attach and grow, leading to failure and death

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5
Q

Why not just medicate IF colonization happens, instead of premedicating?

A

Much harder to break down after colonization

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6
Q

TF? Bacteria are methanogenic.

A

T

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7
Q

Benefit to bacteria of living in biofilm:

A

provides protection against environmental stressors

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8
Q

Bacteria found in biofilm is __ times more resistant to antibiotics than free bacteria.

A

1000

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9
Q

Biofilm growth sites:

A

hot tubs, ships, cooling pipes of power plant, oil pipelines

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10
Q

Biofilms on heart valves cause:

A

Endocarditis

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11
Q

Site of pseudomonas biofilm growth in IC people?

A

Alveoli

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12
Q

This bacteria can grow on tampons:

A

Strep

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13
Q

What bacteria grows in the biofilm of IC ppl?

A

pseudomonas

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14
Q

This bacteria can cause toxic shock:

A

Streptococci

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15
Q

___% of all infections in developed countries caused by biofilms:

A

65

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16
Q

Most common forms of oral disease:

A

Dental Caries and Periodontal Disease

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17
Q

The most common forms of oral disease are caused by:

A

Oral Biofilms

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18
Q

Steps in biofilm formation:

A

attachment, EPS and “irreversible” attachment, growth and maturation, dispersion of planktonic bacteria

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19
Q

Which is more similar to oral biofilm, coral reef or yogurt?

A

yogurt

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20
Q

TF Biofilms are homogenous.

A

F

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21
Q

How does water flow through biofilms?

A

channels

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22
Q

Fxn of water in biofilm:

A

Clear waste, bring nutrients, bacterial growth

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23
Q

bacteria in biofilm talk to each other via:

A

quorum sensing

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24
Q

This is a type of decision making process in bioilm:

A

quorum sensing

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25
Q

Quorum sensing:

A

decision-making process in biofilms, work together, more virulent, coordinate gene expression, form a multicellular organism, send signals and produce pathogenic molecules

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26
Q

TF? Biofilm is hard to kill with chlorhexidine.

A

T

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27
Q

What prevents the rinse from entering the biofilm to get to bacteria?

A

Matrix

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28
Q

Biofilms protect bacteria from both:

A

antiseptics and antimicrobials

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29
Q

Biofilm matrix:

A

restricts penetration of, and binds antimicrobials, reduces effective concentration, impairs phagocytic cells

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30
Q

TF? Free-living bacteria are harder to kill than bacteria in biofilm.

A

F. Bacteria in biofilm are harder to kill (100-1000 times harder)

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31
Q

How are bacteria id’ed in plaque and how many have been found?

A

nucleic acid technology, about 1000

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32
Q

Oral Biofilm is aka:

A

Dental plaque, sessile microbial communities, structured, yellow-grayish

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33
Q

All free-floating bacteria are:

A

planktonic

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34
Q

Does plaque develop on hard or soft tissue?

A

either

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35
Q

What is dental plaque made of?

A

Living and non living bacteria, their products, and salivary compounds

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36
Q

Dental plaque adheres stronger to (hard/soft) tissues

A

hard

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37
Q

TF? All bacteria in dental plaque are alive.

A

F. some alive, some dead

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38
Q

Primary colonizer of heart valve:

A

strep

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39
Q

Composition of dental plaque:

A

Microorganisms in bacterial polysaccharide matrix and salivary glycoproteins, sticky, impossible to remove by rinsing

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40
Q

There are more than ___ different bacterial species

in dental plaque.

A

800

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41
Q

How many bacteria are there per milligram wet weight in dental plaque?

A

> 10^10 (10 billion)

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42
Q

What, besides bacteria, is in dental plaque?

A

viruses, protozoa, yeast, and ameobas

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43
Q

Plaque Dry Weight:

A

70-80 % bacteria, 20-30 % intercellular matrix

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44
Q

The intercellular matrix of plaque is mainly:

A

bacterial products (glucans)

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45
Q

What are bacterial products?

A

glucans

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46
Q

TF? The composition of dental plaque is the same, whether it is sub- or supragingival.

A

F.

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47
Q

How does dental plaque differ in the mouth?

A

surpragingival vs. subgingival, healthy (ask, healthy plaque? Aerobic bacteria?) vs. diseased, different types of diseased tissues

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48
Q

What is the matrix of plaque composed of?

A

extracellular polysaccharide

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49
Q

TF? Materia alba is easily rinsed or sprayed away.

A

T

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50
Q

What is materia alba?

A

soft accumulations of bacteria and other material

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51
Q

What is calculus?

A

hard deposits

mineralized, plaque covered by plaque

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52
Q

Materia alba is (soft/hard), whereas calculus is (soft/hard).

A

soft, hard

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53
Q

TF? Supragingval plaque is associated with caries, but not gingivitis.

A

F. both

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54
Q

Different Kinds of Supragingival Plaque:

A

fissure, smooth surface, approximal

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55
Q

Where is fissure plaque found?

A

mainly in molar fissures

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56
Q

Where is msooth surface plaque found?

A

buccal and palatal surfaces

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57
Q

Where is approximal plaque found?

A

contact points of teeth

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58
Q

TF? All supragingival plaque produce acid and can lead to decalicification.

A

T

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59
Q

TF? Caries cause more plaque to accumulate.

A

T

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60
Q

When will improving OH alone not be sufficient to reduce the severity of gingivitis?

A

Many caries along the crevice

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61
Q

How long does the initial colonization take in the formation of dental plaque?

A

1-2 hours

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62
Q

What type of organisms are involved in the initial colonization in the formation of dental plaque?

A

aerobes, generally non-pathogenic, gram positive cocci and rods

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63
Q

List 3 early colonizeres:

A

S. sanguis, S. mutans, Act. viscosus

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64
Q

Is the attachment in the initial colonization reversible or irreversible?

A

reversible

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65
Q

Which attachment is irreversible.

A

the secondary, strong attachment

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66
Q

Which is stronger, the intial or the secondary attachement?

A

secondary

67
Q

What increases the strength of the attachment in the formation of dental plaque over time?

A

Initial, weak attachement gets stronger as it produces extracellular matrix that binds them together

68
Q

What type of bacteria are the pioneer species in the formation of dental plaque?

A

planktonic bacteria, within an hour

69
Q

Are the primary colonizers GENERALLY pathogenic or non-pathogenic.

A

non-pathogenic

70
Q

TF? Plaque can attach to tooth, epitelial tissue and ct, but not bone.

A

F. can attach to all of these surfaces or remain unattached

71
Q

Subgingival plaque is associated with:

A

gingivitis and periodontitis

72
Q

Subgingival plaque lays between the:

A

tooth and the sulcular / pocket epithelium

73
Q

Plaque against tooth surface has different _____ than that along the epithelial surface.

A

receptors

74
Q

TF? The bacteria found in deeper pockets is different than bacteria found in shallow pockets.

A

T

75
Q

Why is supragingival plaque bacteria different than subgingival?

A

exposed to different nutrients and saliva, subgingival: more blood, less oxygen, more anaerobic

76
Q

Serous fluid leaks out of ______.

A

crevicular lining

77
Q

What part of hemin does P. gingivalis use?

A

protoporhorin, reduced oxygen tension, more anaeroebic the deeper the pocket

78
Q

Supragingival plaque mainly thrives on:

A

polysaccharides, sacchrolytic

79
Q

Will the presence of sugar help P. gingivalis to grow?

A

No

80
Q

What are produced in deep pockets?

A

Proteolytic enzymes, immunoglobins cleave via proteases and use peptides for growth

81
Q

Where does plaque formation start?

A

gingival margin and interdental spaces, areas protected against shear forces

82
Q

In which direction does plaque formation extend?

A

coronally (ask, why do we specify coronally? It extends into the sulcus (apically) as well, right?)

83
Q

Stages of Dental Plaque Formation:

A

deposition of pellicle, initial bacterial colonization, late bacterial colonization, maturation (DILM)

84
Q

Via what structures do bacteria bind to other bacteria?

A

Pili, fibria (receptors), or lipopolysaccharide sugars

85
Q

What is the first step in the formation of dental plaque?

A

deposition of pellicle

86
Q

What is pellicle?

A

salivary glycoproteins, thin, microscopic coating of (ask, only the first, thin layer of plaque?)

87
Q

How long does it take for pellicle to absorb to enamel?

A

seconds (we always have a pellicle layer on our teeth, R?)

88
Q

What type of film is the pellicle?

A

conditioning film, amorphous, acellular

89
Q

What is the second step in the formation of dental plaque?

A

initial colonization

90
Q

Mechanisms of bacterial attachment:

A

hydrophobic interaction, calcium bridging (divalent ion), extracellular polysaccharide, surface appendages (Fimbria will bind sugars on proteins via adhesins)

91
Q

calcium + bacteria may lead to:

A

clumping

92
Q

To which portion of the tooth will bacterial attachment take place?

A

mineralized portion (? because Ca or P is required?) is this always via divalent calcium interaction?) ask

93
Q

What is the third step in the formation of dental plaque?

A

late bacterial colonization

94
Q

Late Bacterial Colonization:

A

Gram-positives multiply, secondary colonizers (ask, are all secondary colonoizers gram negative? yes) attach and multiply, subgingival colonization starts

95
Q

When do secondary colonizers attach?

A

1-3 days later

96
Q

To what do the secondary colonizers attach?

A

gram-positive species

97
Q

TF? Secondary colonizers can also be primary colonizers.

A

F.

98
Q

What type of bacteria are secondary colonizers?

A

Gram-negative cocci and rods, facultative and obligate anaerobes (pattern to attachment? Facultative first, closer to oxygen? Ask)

99
Q

3 examples of secondary colonizers:

A

Fusobacterium nucleatum, Prevotella intermedia, Capnocytophaga species

100
Q

What is the primary etiology for periodontal diseases?

A

subgingival colonization of dental plaque

101
Q

What is the fourth step in the formation of dental plaque?

A

maturation

102
Q

Maturation step in the formation of dental plaque:

A

increased plaque, tertiary colonizers, complex structure (i.e. Corn cob)

103
Q

What type of bacteria are tertiary colonizers?

A

Gram negative bacteria

104
Q

5 examples of tertiary colonizers in the formation of dental plaque:

A

Porphyromonas gingivalis, Campylobacter rectus, Eikenella corrodens, Aggregatibacter, actinomycetemcomitans, Oral spirochetes (should this include the red complex? denticola, forsythus, P. gingivalis?)

105
Q

spirochetes are:

A

mobile bacteria

106
Q

In which step of dental plaque formation do corn cob bacteria appear?

A

Step 4: maturation, “test-tube brushes” or “corn-cob” adherence of cocci to filaments

107
Q

Timeline for dental plaque development:

A

0-2 days: thin biofilm, easily disrupted, 2-4 days: increase mass, 4-7 days: goes subgingivally, 7-11 days: increase diversity, 21+ days: biofilm mass - relative stability

108
Q

Bacterial shifts in dental plaque formation:

A

Gram-positive cocci and rods –> Gram-negative cocci and rods –>
Filaments, fusobacteria, spirils and spirochaetes

109
Q

What surrounds fluid channels of plaque?

A

bacterial microcolonies, intermicrobial matrix, and pellicle

110
Q

Bacteria are surrounded by:

A

intercellular matrix

111
Q

What is the intercellular matrix composed of?

A

Polysaccharides from bacterial metabolism

112
Q

Minor components of intercellular matrix:

A

Salivary and serum proteins/glycoproteins

113
Q

TF? The type of food consumed affects the type of bacteria present in the oral cavity.

A

T

114
Q

Bacterial metabolism leads to the formation of:

A

polysaccharides

115
Q

What complexes are mainly associated with peio disease?

A

Red and Orange Complex

116
Q

Red complex bacteria:

A

P. gingivalis, T. forsythensis, T. denticola

117
Q

Orange complex bacteria:

A

P. intermedia, nigrescens, and micros, F nuc. vincentii, nucleatum, polymorphum, and periodonticum, Outer: C. gracilis, C. rectus, E. nodatum, C. showae, S. consellatus

118
Q

TF? Bacteria act as individual species

A

F. as microbial complexes

119
Q

TF? Bacteria act as microbial complexes.

A

T

120
Q

TF? Plaque causes gingivitis.

A

T

121
Q

3 hypotheses related to plaque and oral disease:

A

non-specific, specific, and ecological plaque hypotheses

122
Q

non-specific plaque hypothesis:

A

disease results from masses of plaque bacteria, “dirty mouth”

123
Q

“Specific plaque hypothesis”:

A

disease results from certain species of plaque bacteria

124
Q

“Ecological plaque hypothesis”:

A

changes in the environment “turn on” plaque bacteria to become ‘pathogenic’, no specific etiology, dynamic relationship between host and microbiota, increase biofilm, increase inflammatory response, alters local environment, selecting for more proteolytic microbes that lead to greater inflammation

125
Q

Theories as to why stress can lead to more PD:

A

more steroids in body, not brushing as well due to stress

126
Q

Tx for ecological plaque hypothesis:

A

remove biofilm and interfere with selective pressures

127
Q

Effects of Metronidozol:

A

kills more anaerobic, gram negative than aerobic, gram positive

128
Q

TF? Listerine and chlorhexidine kill bacteria non-selectively.

A

T

129
Q

Therapeutic Implications for Plaque Hypotheses:

A

“Non-specific plaque hypothesis”: oral hygiene, “Specific plaque hypothesis”: antibiotics, vaccines, “Ecological plaque hypothesis”: diet, buffers, chelators, oxygen (environmental approaches)

130
Q

Host defenses that influence oral microbiota:

A

temp, atmosphere, pH, genetics, health, lifestyle, receptors, nutrients, host defenses, microbial interactions

131
Q

What does high crevicular fluid result in?

A

more food for proteolytic bacteria

132
Q

Is there more or less tissue turnover with strong inflammation?

A

more

133
Q

Will there be more bleeding with low or high gingival crevicular fluid (GCF) flow?

A

high

134
Q

Will there be a low Eh, a raised pH and C with low or high gingival crevicular fluid (GCF) flow?

A

low

135
Q

TF? The obligatory anaerobic biofilm is saccharolytic.

A

F. proteolytic

136
Q

Most common biofilm diseases are:

A

periodontal disease and dental caries

137
Q

How to reduce periodontal disease and dental caries

A

Daily removal of biofilm, periodic professional cleaning, frequency of recalls, determined by professional

138
Q

Name of the explorer:

A

EXD: 11-12

139
Q

Type of perio probe we use:

A

Michigan O (University of Michigan probe)

140
Q

What type of calculus is the sickle scaler designed to remove?

A

supragingival calculus

141
Q

How many straight cutting edges does the sickle scaler have?

A

2

142
Q

The pointed tip of a sickle scaler:

A

toe

143
Q

Use this primarily for mesial surfaces:

A

11/12

144
Q

This can be used for BL and distal surfaces:

A

13/14

145
Q

These tend to be more angled, 60-70 degree:

A

Graceys’ (single cutting edge)

146
Q

These have two parallel cutting edges that converge:

A

curettes

147
Q

Shape of scaler and curette in crossection

A

triangle, semicircle

148
Q

Shape of the toe of a curette:

A

rounded

149
Q

Angle of face for the universal curette:

A

90d to terminal shank

150
Q

TF? The universal curette adapts to all four tooth surfaces

A

T

151
Q

Angle of face for the area specific curette:

A

60- to 70-d to terminal shank, 1 cutting edge

152
Q

How many surfaces can be cleaned with an area specific curette?

A

one

153
Q

Which is is the cutting edge used in instrumentation for a curette?

A

the lower edge (i.e., the longer outer curved edge)

154
Q

most versatile periodontal instrument:

A

curette

155
Q

Curettes are designed for:

A

subgingival areas

156
Q

Area-specific curettes are aka:

A

Gracey curettes

157
Q

Angle fo the blade for Gracey curettes:

A

60-70d to the shank

158
Q

Angle of shank in relation to blade for universal curettes:

A

90d

159
Q

Chisel scaler is used for:

A

tenacious calculus- cutting edge beveled at 45d

160
Q

Primary objective in sharpening a tool:

A

70-80 d internal angle of blade

161
Q

Benefits of sharp instruments:

A

Better calculus removal with fewer strokes, smoother root surfaces, improved tactile sensitivity, requires less lateral pressure, increase control of strokes, and reduce clinician fatigue

162
Q

Proper angle for sharpening:

A

100 to 110d angle,stone and face of blade

163
Q

True or False? All primary colonized are non pathogenic.

A

F. Most

164
Q

EPS stands for:

A

Extracellular polymeric substances

Introduction to Periodontics and Prevention (8 decks)

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