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Oral Sciences > Reading 3/27 > Flashcards

Reading 3/27 Flashcards

1
Q

Determine outcome of gingivitis or pdd:

A

Balance of host-microbial interaction and host / bac factors

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2
Q

How to change balance bw host and bacterial factors leading to gingivitis or pdd:

A

red host resistance, inc pl biofilm, inc bac virulence

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3
Q

Cx man of pdd is modified further via:

A

local and. or systemic factors

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4
Q

Define pl biofilm:

A

bac deposits not easily be rinsed away

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5
Q

Sites of pl formation:

A

any solid surface, mucosa

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6
Q

To visualise pl biofilm:

A

vegetable or synthetic dyes

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7
Q

When does biofilm form?

A

When a solid structure is placed in an aqueous env

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8
Q

TF? Biofilm can not adhere to restorations.

A

F

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9
Q

Difference bw dental biofilm and biofilms on mucosal surfaces:

A

form on non-shedding surface which allows them to form stable communities

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10
Q

Formation of biofilm on solid structure vs. shedding surface allows for:

A

formation of stable communities

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11
Q

This results in pellicle formation in initial stages of biofilm formation:

A

adsorption of macromolecules

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12
Q

Ex’s of macromolecules in initial stage of biofilm formation:

A

salivary mucins and proteins

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13
Q

Bac adhere to pellicle via:

A

adhesins (surface receps)

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14
Q

How is bac adherence facilitated by the attachment of earlier bac?

A

growth and synthesis of outer membrane component

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15
Q

Bac mass on biofilm inc due to:

A

growth of the bac + adherence of new bac

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16
Q

Another factor that inc adherence of additional bac to biofilm:

A

synthesis of extracellular polymers, attachment for bac that would otherwise not ba able to

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17
Q

Synthesis of these allows for attachment of bac that otherwise not be able to attach directly to pellicle:

A

extracellular polymers

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18
Q

Superficial layer is bordered by:

A

fluid layer

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19
Q

Describe superficial layer:

A

loose, irregular

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20
Q

inc in biofilm thickness leads to:

A

dec oxygen and nutrient diffusion

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21
Q

Oxygen gradient forms w thickening of bio due to:

A

use by superficial bac, poor diffusion thru bio matrix

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22
Q

Source of nutrients for superficial pl:

A

food in saliva

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23
Q

Source of nutrients for microbes in deep perio pockets:

A

perio tissues, gcf, blood supply, other microorganisms

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24
Q

Major initial colonizers in terms of O2 consumption:

A

aerobic, facultative anaerobes

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25
Q

This type of bac grow in proportion after Gram + cocci, esp strep, and eventually outnumber:

A

Gram + rods

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26
Q

Type of bac that may later predominate after Gram+ rods:

A

Gram + filaments

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27
Q

Ex of Gram + filaments that may predominate after Gram+ rods:

A

Actinomyces spp.

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28
Q

These allow for adherence of Gram - bac to biofilm:

A

Receps on Gram + cocci and rods (not filaments? check)

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29
Q

Can Gram - bac adhere directly to pellicle?

A

no

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30
Q

This inc as proportion of Gram - vs. Gram + bac inc:

A

heterogenicity of microbes

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31
Q

Factors that help to establish bac communities:

A

nutrient exchange bw microbes, bacteriotoxin that kill sp bac

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32
Q

How are bac communities established in different sites?

A

according to local env

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33
Q

Bac sites that are more resistant to antibiotics, req much higher doses:

A

deep pockets, fissures

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34
Q

More motile rods, perio health or pdd?

A

pdd

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35
Q

Predominant spp in gi:

A

Actinomyces (Gram + rods)

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36
Q

Bac implicated in pdd progression:

A

P. gingivalis, Agg actinomycetemcomitans, P. intermedia, F. nucleatum, Eikenella corrodens, T. denticola, Campylobacter rectus, Capnocytophaga, T. fosrythia

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37
Q

Major components of GCF in early stages of gi:

A

complements factors, PMNs Macs

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38
Q

Major components of GCF in pdd (adaptive response):

A

sIgA, IgA, IgM, IgA (supposed to be IgG?), T cell, cytotoxicity

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39
Q

Does bac initiate disease specifically or non?

A

not clear

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40
Q

3 main theories of role of bac in pdd:

A

specific, non, and multiple pathogen

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41
Q

What do all 3 theories ignore?

A

role of host factors

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42
Q

Non-specific theory:

A

no 1 bac is more sig than any other in causing pdd

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43
Q

Theory that implies the need for all pts to maintain great OH to prevent pdd:

A

non-specific

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44
Q

Theory that implies you only need to worry about the bac responsible for pdd:

A

specific

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45
Q

Specific plaque hypothesis may explain:

A

why many pts w considerable pl don’t have pdd

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46
Q

Theory that implies that we only need to employ procedures that decrease specific bac spp:

A

Specific

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47
Q

Assuming the specific pathogen leading to pdd is a strict anaerobe, how could we prevent disease?

A

eliminate pathogen or promote community unable to live in (disrupt biofilm)

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48
Q

Theory that could explain the success of SRP’s in dec pdd:

A

specific theory: disrupt biofilm, prevent bacteria responsible from attaching (ask? Why SRP disruption of biofilm only implicate one species? Multiple species could be attached that are virulent, non virulent could be the one attaching and virulent attaching to it, etc.

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49
Q

Theory that could allow us to test for at risk pts:

A

specific, test for only the presence of that bacteria

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50
Q

Potential tx for specific theory:

A

antibiotic chemotherapy directed at species once antibiotic sensitivities are known, vaccination, peptides to prevent adhesion

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51
Q

Strongest argument for sp theory:

A

Inc risk for aggressive pdd in Moroccan youth w Aggregabacter actinomycetencomitans, esp JP2 clone

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52
Q

Clone type of Aggregabacter actinomycetencomitans most assoc with aggressive pdd in moroccan youth:

A

JP2

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53
Q

Theory stating that pdd is due to infection w a relatively small # of interacting bac spp:

A

multiple pathogen theory

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54
Q

Major difficulty in multiple pathogen theory:

A

identifying possible combos of pathogens, whole new list could be made w molecular techniques in future once we can culture those spp

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55
Q

TF? The fact that there is a list of predominant bac in pdd sites indicates that they are all involved in tissue damage.

A

F

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56
Q

Why might the predominant bac be at the pdd sites?

A

more likely to survive in inflammatory conditions of the deep pockets

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57
Q

Reasons why determining etiology of pdd is difficult:

A

600+ spp in different ppl, 30-100/ site, habitat determines which can grow, many fastidious or can’t be grown, trouble getting representative spp from a site, contaminating spp may be present + complicate analysis and interpretation, if spp shift during active phase time of sampling is important, current classification of pdd may not be good enough to distinguish bw different types of pdd, each grouping may represent a highly heterogenous group, different sites may break down due to different pathogens, sites may show activity due to one pathogen at one time and bc of another at a later time, difficult to distinguish bw opportunistic spp 2’ to disease vs. causing the disease, difficult to eval possible pairs of spp (P. gingivalis may be present in pts w no disease), different strains of 1 spp may be virulent vs. avirulent, individual variation in immune response

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58
Q

Why aren’t spp id’ed via molecular techniques useful in pdd tx?

A

wo viable microbes antibiotic sensitivities can’t be determined

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59
Q

initial 1-2d, gi is localized to:

A

gingival sulcus, subadj perio tissue

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60
Q

initial 1-2d, local gi vasodilation brings these:

A

IgG, complement, fibrin, more PMNs

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61
Q

Is there an inc in GCF in initial 1-2d?

A

yes

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62
Q

How do PMN migrate into gingival crevice initial 1-2d?

A

JE + sulcular epi

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63
Q

Where can few lymphos and macs be found in initial 1-2d?

A

JE

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64
Q

How are vascular permeability and inc migration of PMNs accomplished in initial 1-2d?

A

immune complexes form activating classical complement cascade to prod C3/5

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65
Q

Fxns of C3/5

A

inc vascular permeability, chemotaxins for PMNs

66
Q

There is localized proliferation of these in early 4-7d:

A

JE and sulcular epi

67
Q

TF? Local vasod brings IgG, complement, fibrin and more PMN all throughout 1st wk.

A

T

68
Q

When is the max inc in GCF experienced?

A

2-3wk

69
Q

TF? Loss of attachment begins at 2-3wk

A

F. advanced stage

70
Q

Proliferation of JE and sulcular epi beings and ends:

A

4d-3wk

71
Q

Collagen is lost w/in this time frame:

A

2wk+

72
Q

When does bone loss begin?

A

Advanced

73
Q

What leads to the change rom successful defense against pdd and pdd?

A

imbalance in host-microbial interaction

74
Q

New vessel formation begins:

A

2-3wk

75
Q

These are found adjacent to vessels and gingival lesions in established gingivitis

A

plasma cells

76
Q

Predominant Ig’s in established gi:

A

IgG + IgA, very little IgM

77
Q

Predominant Ig’s in pdd:

A

IgG + IgA, more IgM than establish gi

78
Q

TF? PMNs are present from day 1 and remain throughout pdd.

A

T

79
Q

These are prominent in the early stages of gi:

A

lymphos, mostly T cells

80
Q

What cells dominate in established gi?

A

T cells

81
Q

There is a dense infiltrate of these in periodontitis:

A

lymphos, plasma cell, macs

82
Q

What pill allow pl antigens direct access into perio tissues and activate immune cells?

A

Breakdown of epi barrier (pocket lining)

83
Q

This may lead to bystander damage and further tissue damage in pdd:

A

Breakdown of pocket lining

84
Q

These antibodies are present in early stage of gi:

A

serum antibodies to plaque antigens previously encountered

85
Q

Cytokines promote:

A

further lymphatic infiltration and proliferation

86
Q

These release cytokines in the early stage of gi:

A

circulating lymphoid cells that have migrated

87
Q

At which stage is lymphocytic proliferative response to pl antigens evident?

A

established, 2-3wk

88
Q

Cells found in established gi that may seed to the local gingival inflammatory focus, providing source of plasma cells and IgG, IgA, and IgM:

A

non-specific polyclonal B cell mitogens

89
Q

The presence of IgG/A/M + complement in pdd suggest:

A

potential for type IV cell mediated and type II and III antibody-antigen reactions that may lead to tissue damage

90
Q

Type II and III reactions are what type?

A

antibody-antigen reactions

91
Q

Type IV reaction is what type?

A

cell mediated

92
Q

What reaction types may lead to tissue damage?

A

I, III, IV

93
Q

Fxn of lympho in pdd:

A

unknown

94
Q

Imp bac antigens in pdd:

A

unknown

95
Q

Which is a chronic inflammatory lesion, chronic gi or pdd?

A

both

96
Q

TF? Attempts to heal do not occur in pdd, this is why we can not regain what is lost.

A

F

97
Q

Signs that may not be present in order to establish the presence of inflammation:

A

pain, loss of function

98
Q

Non-specific innate mechs:

A

barrier effect of intact epi, saliva

99
Q

Bac can be recognized by these receps in innate response:

A

non-clonal receptors (pattern recognition receps)

100
Q

non-clonal receptors are aka:

A

pattern recognition receps

101
Q

What do non-clonal receptors recognize?

A

LPS from Gram - bac, peptidoglycan from Gram +

102
Q

Bac type that produces LPS:

A

Gram - (only?)

103
Q

Bac type that produces peptidoglycan:

A

Gram + (only?)

104
Q

Greater pot for tissue damage, innate or adaptive?

A

innate

105
Q

Diseases that inc in severity w inc in neutropenia:

A

pdd, agranulocytosis, where cell fxn is impaired: leukocyte adhesion deficiency, lazy leukocyte d, Papillon Lefevre, Chediak-Higashi, Downs, DM

106
Q

Adaptive immunity is characterised by:

A

specificity, memory, capacity to distinguish self from non-self

107
Q

Flow chart of adaptive immunity:

A

recognition of antigen via receps on mac or dendritic cells, cytokine release, activate B/T cells, engaging cell-mediated and humoral response

108
Q

TF? Early response is only innate.

A

F. predominantly, helps focus adaptive response

109
Q

What limits bystander damage in humoral response?

A

specificity of response

110
Q

How does sIgA protect mucosal surfaces in humoral response?

A

mainly by preventing bac adherence

111
Q

How is sIgA different from serum IgA

A

it is dimers held together by J chains and protected from proteolytic breakdown w secretory components

112
Q

From where does GCF originate?

A

gingival caps

113
Q

Does CF contain immune cells?

A

some

114
Q

How is the GCF flow interrupted?

A

It’s not

115
Q

Found in GCF:

A

IgG/A/M, complement components, enzymes (all soluble), polymorphs

116
Q

What does the components of GCF enable?

A

innate and adaptive responses

117
Q

What marks the transition from a chronic and successful defense to pdd?

A

the change from established lesion to an advanced lesion

118
Q

How long may an established lesion last?

A

years

119
Q

Factors that may be responsible for progression from gi to pdd:

A

host immune reponse, sp microorganisms in pl, change in virulence

120
Q

TF? There is evidence that pdd develops from pre-existing gi.

A

F. some preceding gingival inflammation may lead to pdd but not always

121
Q

Direction of extension of inflammatory infiltrate:

A

apically and laterally, w red of collagen contact + dense accum of lymphos, plasma cells, and macs

122
Q

This is occurring in the periphery of pdd:

A

reparative fibrosis

123
Q

Where is there a breakdown of the epi barrier?

A

bw pl and perio ct

124
Q

This might be assoc w change in immune response + allowing of direct access of pl antigens and metabolites, leading to pdd:

A

breakdown of epi barrier bw pl and perio ct

125
Q

Do antibodies protect from disease in pdd?

A

no, inconsistently invoked

126
Q

Why might antibody titres rise during tx?

A

instrumentation inoculating antigens

127
Q

Antibody titres may reflect this and not the importance of any one microbial organism in the pathogenesis of pdd:

A

intrinsic mitogenicity or immunogenicity of pl antigens

128
Q

Effect of IL-1B and TNFa:

A

bone resorption, pro-inflammatory, fever

129
Q

How do IL-1B and TNFa interact?

A

synergistically

130
Q

Fxn of IL-6:

A

B-cell + osteoclast diff, antibody prod

131
Q

Direct mechs of tissue destruction via bac:

A

damage crevicular epi, leukoctye killing/impairment via leukotoxin, PN impairment, dysregulation of cytokine networks, degradation of Ig’s, degradation of fibrin, inc mucosal permeability and disaggregate proteogglycans via disruption of SH bonds, impaired host cell fxn, degradation of collagen breakdown of perio tissue, activation of complement and bone resorption via LPS, bone resorption via lipoteichoid acid from Gram + bac cell walls

132
Q

Bac that damage crevicular epi:

A

P, ging, Agg actino, T. denticola

133
Q

This can lead to leukocyte killing/ impairment:

A

leukotoxin (Agg actino)

134
Q

bac that produces leukotoxin:

A

Agg actino

135
Q

impairment of PMN fxn leads to:

A

dec in chemotaxis, phago, and intracellular killing

136
Q

These can lead to dysregulation of cytokine network:

A

p ging, R! proteinase

137
Q

Bac that can lead to degradation of Ig’s:

A

capynocytophaga

138
Q

Fxn of fibrin in pdd prevention:

A

trap bac, facilitate phagocytosis

139
Q

This can lead to degradation of fibroblastic collagenase:

A

volatile sulfur compounds from Gram- bac

140
Q

Sulfur, released from Gram + or -?

A

Gram -

141
Q

Bac that can lead to inc mucosal permeability:

A

P. ging, P. intermedia, T. forsythia, T. denticola

142
Q

Bac that can breakdown tissues and supply nutrients for Gram- bac via collagenase:

A

P.ging, Agg Actino, spirochetes

143
Q

Bac that can breakdown perio tissues via trysin-like proteinases:

A

P ging, T. forsythia

144
Q

What activates complement and bone resorption:

A

LPS

145
Q

Bone resorption is stimulated by lipoteichoic acid from

A

Gram + bac cell wall

146
Q

lipoteichoic acid, from Gram - or + cell walls:

A

+

147
Q

Indirect mechs of tissue destruction via bac:

A

Trigger of humoral immunity, polyclonal activation of B cells, cellular immunity activated T cells, PMNs

148
Q

How does triggering humoral immunity lead to tissue damage?

A

acitvaton of complement, mroe inflammation, recruitment of inflammatory cells, release of tissue destructive enzymes

149
Q

How does polyclonal activation of B cells lead to tissue damage?

A

prevents useful specific antibody production, nonspec is produced preventing adaptive responses from focusing on those antigens that would lead to protection, LPS is a B cell antigen hat stimulates polyclonal activation of B cells

150
Q

Example of a B cell mitogen that leads to stimulation o polyclonal activation of B cells:

A

LPS

151
Q

How does cellular immunity activated T cells lead to tissue damage?

A

activates antigen presenting cells and macs, they release cytokines: IL-1/6, TNFa, autoreactive/cytotoxic response to perio tissue

152
Q

Cytokines released by antigen presenting cells and macs:

A

IL-1/6, TNFa, autoreactive/cytotoxic response to perio tissue

153
Q

How do PMNs lead to tissue damage?

A

release enzymes: MMPs incl collagenases, elastases, stromelysins

154
Q

MMPs that cans destroy tissue:

A

collagenases, elastases, stromelysins

155
Q

Mechs involved in mediating tissue damage:

A

hypersensitivy-like responses and incl antibody-mediated, cellular cytotoxicity, and IgE mediated hypersensitivity-like rxn

156
Q

Cytotoxic cellular immune response to self and pro-infalmmatory responses involve release of:

A

IL-1B, TNFa, IL-6 (all cause tissue destruction

157
Q

Th1/2 paradigm now incl:

A

Other T cell subsets:Th17, Treg cellls,

158
Q

Fxn of TH17 cells:

A

make pro-inflammatory IL-17, TH17 + other cytokines like IL-12, cells can develop into TH1 cells

159
Q

These cells acn swith to Th17 cells:

A

Tregs

160
Q

What is req for Treg cells to change to TH17 cells?

A

cytokines: IL-6 and 21

161
Q

I did not make cards for 95% of potential tx

A

ok

Oral Sciences (16 decks)

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