Reading 3/27 Flashcards
1
Q
Determine outcome of gingivitis or pdd:
A
Balance of host-microbial interaction and host / bac factors
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
3
Q
Cx man of pdd is modified further via:
A
local and. or systemic factors
4
Q
Define pl biofilm:
A
bac deposits not easily be rinsed away
5
Q
Sites of pl formation:
A
any solid surface, mucosa
6
Q
To visualise pl biofilm:
A
vegetable or synthetic dyes
7
Q
When does biofilm form?
A
When a solid structure is placed in an aqueous env
8
Q
TF? Biofilm can not adhere to restorations.
A
F
9
Q
Difference bw dental biofilm and biofilms on mucosal surfaces:
A
form on non-shedding surface which allows them to form stable communities
10
Q
Formation of biofilm on solid structure vs. shedding surface allows for:
A
formation of stable communities
11
Q
This results in pellicle formation in initial stages of biofilm formation:
A
adsorption of macromolecules
12
Q
Ex’s of macromolecules in initial stage of biofilm formation:
A
salivary mucins and proteins
13
Q
Bac adhere to pellicle via:
A
adhesins (surface receps)
14
Q
How is bac adherence facilitated by the attachment of earlier bac?
A
growth and synthesis of outer membrane component
15
Q
Bac mass on biofilm inc due to:
A
growth of the bac + adherence of new bac
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
17
Q
Synthesis of these allows for attachment of bac that otherwise not be able to attach directly to pellicle:
A
extracellular polymers
18
Q
Superficial layer is bordered by:
A
fluid layer
19
Q
Describe superficial layer:
A
loose, irregular
20
Q
inc in biofilm thickness leads to:
A
dec oxygen and nutrient diffusion
21
Q
Oxygen gradient forms w thickening of bio due to:
A
use by superficial bac, poor diffusion thru bio matrix
22
Q
Source of nutrients for superficial pl:
A
food in saliva
23
Q
Source of nutrients for microbes in deep perio pockets:
A
perio tissues, gcf, blood supply, other microorganisms
24
Q
Major initial colonizers in terms of O2 consumption:
A
aerobic, facultative anaerobes
25
This type of bac grow in proportion after Gram + cocci, esp strep, and eventually outnumber:
Gram + rods
26
Type of bac that may later predominate after Gram+ rods:
Gram + filaments
27
Ex of Gram + filaments that may predominate after Gram+ rods:
Actinomyces spp.
28
These allow for adherence of Gram - bac to biofilm:
Receps on Gram + cocci and rods (not filaments? check)
29
Can Gram - bac adhere directly to pellicle?
no
30
This inc as proportion of Gram - vs. Gram + bac inc:
heterogenicity of microbes
31
Factors that help to establish bac communities:
nutrient exchange bw microbes, bacteriotoxin that kill sp bac
32
How are bac communities established in different sites?
according to local env
33
Bac sites that are more resistant to antibiotics, req much higher doses:
deep pockets, fissures
34
More motile rods, perio health or pdd?
pdd
35
Predominant spp in gi:
Actinomyces (Gram + rods)
36
Bac implicated in pdd progression:
P. gingivalis, Agg actinomycetemcomitans, P. intermedia, F. nucleatum, Eikenella corrodens, T. denticola, Campylobacter rectus, Capnocytophaga, T. fosrythia
37
Major components of GCF in early stages of gi:
complements factors, PMNs Macs
38
Major components of GCF in pdd (adaptive response):
sIgA, IgA, IgM, IgA (supposed to be IgG?), T cell, cytotoxicity
39
Does bac initiate disease specifically or non?
not clear
40
3 main theories of role of bac in pdd:
specific, non, and multiple pathogen
41
What do all 3 theories ignore?
role of host factors
42
Non-specific theory:
no 1 bac is more sig than any other in causing pdd
43
Theory that implies the need for all pts to maintain great OH to prevent pdd:
non-specific
44
Theory that implies you only need to worry about the bac responsible for pdd:
specific
45
Specific plaque hypothesis may explain:
why many pts w considerable pl don't have pdd
46
Theory that implies that we only need to employ procedures that decrease specific bac spp:
Specific
47
Assuming the specific pathogen leading to pdd is a strict anaerobe, how could we prevent disease?
eliminate pathogen or promote community unable to live in (disrupt biofilm)
48
Theory that could explain the success of SRP's in dec pdd:
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.
49
Theory that could allow us to test for at risk pts:
specific, test for only the presence of that bacteria
50
Potential tx for specific theory:
antibiotic chemotherapy directed at species once antibiotic sensitivities are known, vaccination, peptides to prevent adhesion
51
Strongest argument for sp theory:
Inc risk for aggressive pdd in Moroccan youth w Aggregabacter actinomycetencomitans, esp JP2 clone
52
Clone type of Aggregabacter actinomycetencomitans most assoc with aggressive pdd in moroccan youth:
JP2
53
Theory stating that pdd is due to infection w a relatively small # of interacting bac spp:
multiple pathogen theory
54
Major difficulty in multiple pathogen theory:
identifying possible combos of pathogens, whole new list could be made w molecular techniques in future once we can culture those spp
55
TF? The fact that there is a list of predominant bac in pdd sites indicates that they are all involved in tissue damage.
F
56
Why might the predominant bac be at the pdd sites?
more likely to survive in inflammatory conditions of the deep pockets
57
Reasons why determining etiology of pdd is difficult:
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
58
Why aren't spp id'ed via molecular techniques useful in pdd tx?
wo viable microbes antibiotic sensitivities can't be determined
59
initial 1-2d, gi is localized to:
gingival sulcus, subadj perio tissue
60
initial 1-2d, local gi vasodilation brings these:
IgG, complement, fibrin, more PMNs
61
Is there an inc in GCF in initial 1-2d?
yes
62
How do PMN migrate into gingival crevice initial 1-2d?
JE + sulcular epi
63
Where can few lymphos and macs be found in initial 1-2d?
JE
64
How are vascular permeability and inc migration of PMNs accomplished in initial 1-2d?
immune complexes form activating classical complement cascade to prod C3/5
65
Fxns of C3/5
inc vascular permeability, chemotaxins for PMNs
66
There is localized proliferation of these in early 4-7d:
JE and sulcular epi
67
TF? Local vasod brings IgG, complement, fibrin and more PMN all throughout 1st wk.
T
68
When is the max inc in GCF experienced?
2-3wk
69
TF? Loss of attachment begins at 2-3wk
F. advanced stage
70
Proliferation of JE and sulcular epi beings and ends:
4d-3wk
71
Collagen is lost w/in this time frame:
2wk+
72
When does bone loss begin?
Advanced
73
What leads to the change rom successful defense against pdd and pdd?
imbalance in host-microbial interaction
74
New vessel formation begins:
2-3wk
75
These are found adjacent to vessels and gingival lesions in established gingivitis
plasma cells
76
Predominant Ig's in established gi:
IgG + IgA, very little IgM
77
Predominant Ig's in pdd:
IgG + IgA, more IgM than establish gi
78
TF? PMNs are present from day 1 and remain throughout pdd.
T
79
These are prominent in the early stages of gi:
lymphos, mostly T cells
80
What cells dominate in established gi?
T cells
81
There is a dense infiltrate of these in periodontitis:
lymphos, plasma cell, macs
82
What pill allow pl antigens direct access into perio tissues and activate immune cells?
Breakdown of epi barrier (pocket lining)
83
This may lead to bystander damage and further tissue damage in pdd:
Breakdown of pocket lining
84
These antibodies are present in early stage of gi:
serum antibodies to plaque antigens previously encountered
85
Cytokines promote:
further lymphatic infiltration and proliferation
86
These release cytokines in the early stage of gi:
circulating lymphoid cells that have migrated
87
At which stage is lymphocytic proliferative response to pl antigens evident?
established, 2-3wk
88
Cells found in established gi that may seed to the local gingival inflammatory focus, providing source of plasma cells and IgG, IgA, and IgM:
non-specific polyclonal B cell mitogens
89
The presence of IgG/A/M + complement in pdd suggest:
potential for type IV cell mediated and type II and III antibody-antigen reactions that may lead to tissue damage
90
Type II and III reactions are what type?
antibody-antigen reactions
91
Type IV reaction is what type?
cell mediated
92
What reaction types may lead to tissue damage?
I, III, IV
93
Fxn of lympho in pdd:
unknown
94
Imp bac antigens in pdd:
unknown
95
Which is a chronic inflammatory lesion, chronic gi or pdd?
both
96
TF? Attempts to heal do not occur in pdd, this is why we can not regain what is lost.
F
97
Signs that may not be present in order to establish the presence of inflammation:
pain, loss of function
98
Non-specific innate mechs:
barrier effect of intact epi, saliva
99
Bac can be recognized by these receps in innate response:
non-clonal receptors (pattern recognition receps)
100
non-clonal receptors are aka:
pattern recognition receps
101
What do non-clonal receptors recognize?
LPS from Gram - bac, peptidoglycan from Gram +
102
Bac type that produces LPS:
Gram - (only?)
103
Bac type that produces peptidoglycan:
Gram + (only?)
104
Greater pot for tissue damage, innate or adaptive?
innate
105
Diseases that inc in severity w inc in neutropenia:
pdd, agranulocytosis, where cell fxn is impaired: leukocyte adhesion deficiency, lazy leukocyte d, Papillon Lefevre, Chediak-Higashi, Downs, DM
106
Adaptive immunity is characterised by:
specificity, memory, capacity to distinguish self from non-self
107
Flow chart of adaptive immunity:
recognition of antigen via receps on mac or dendritic cells, cytokine release, activate B/T cells, engaging cell-mediated and humoral response
108
TF? Early response is only innate.
F. predominantly, helps focus adaptive response
109
What limits bystander damage in humoral response?
specificity of response
110
How does sIgA protect mucosal surfaces in humoral response?
mainly by preventing bac adherence
111
How is sIgA different from serum IgA
it is dimers held together by J chains and protected from proteolytic breakdown w secretory components
112
From where does GCF originate?
gingival caps
113
Does CF contain immune cells?
some
114
How is the GCF flow interrupted?
It's not
115
Found in GCF:
IgG/A/M, complement components, enzymes (all soluble), polymorphs
116
What does the components of GCF enable?
innate and adaptive responses
117
What marks the transition from a chronic and successful defense to pdd?
the change from established lesion to an advanced lesion
118
How long may an established lesion last?
years
119
Factors that may be responsible for progression from gi to pdd:
host immune reponse, sp microorganisms in pl, change in virulence
120
TF? There is evidence that pdd develops from pre-existing gi.
F. some preceding gingival inflammation may lead to pdd but not always
121
Direction of extension of inflammatory infiltrate:
apically and laterally, w red of collagen contact + dense accum of lymphos, plasma cells, and macs
122
This is occurring in the periphery of pdd:
reparative fibrosis
123
Where is there a breakdown of the epi barrier?
bw pl and perio ct
124
This might be assoc w change in immune response + allowing of direct access of pl antigens and metabolites, leading to pdd:
breakdown of epi barrier bw pl and perio ct
125
Do antibodies protect from disease in pdd?
no, inconsistently invoked
126
Why might antibody titres rise during tx?
instrumentation inoculating antigens
127
Antibody titres may reflect this and not the importance of any one microbial organism in the pathogenesis of pdd:
intrinsic mitogenicity or immunogenicity of pl antigens
128
Effect of IL-1B and TNFa:
bone resorption, pro-inflammatory, fever
129
How do IL-1B and TNFa interact?
synergistically
130
Fxn of IL-6:
B-cell + osteoclast diff, antibody prod
131
Direct mechs of tissue destruction via bac:
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
Bac that damage crevicular epi:
P, ging, Agg actino, T. denticola
133
This can lead to leukocyte killing/ impairment:
leukotoxin (Agg actino)
134
bac that produces leukotoxin:
Agg actino
135
impairment of PMN fxn leads to:
dec in chemotaxis, phago, and intracellular killing
136
These can lead to dysregulation of cytokine network:
p ging, R! proteinase
137
Bac that can lead to degradation of Ig's:
capynocytophaga
138
Fxn of fibrin in pdd prevention:
trap bac, facilitate phagocytosis
139
This can lead to degradation of fibroblastic collagenase:
volatile sulfur compounds from Gram- bac
140
Sulfur, released from Gram + or -?
Gram -
141
Bac that can lead to inc mucosal permeability:
P. ging, P. intermedia, T. forsythia, T. denticola
142
Bac that can breakdown tissues and supply nutrients for Gram- bac via collagenase:
P.ging, Agg Actino, spirochetes
143
Bac that can breakdown perio tissues via trysin-like proteinases:
P ging, T. forsythia
144
What activates complement and bone resorption:
LPS
145
Bone resorption is stimulated by lipoteichoic acid from
Gram + bac cell wall
146
lipoteichoic acid, from Gram - or + cell walls:
+
147
Indirect mechs of tissue destruction via bac:
Trigger of humoral immunity, polyclonal activation of B cells, cellular immunity activated T cells, PMNs
148
How does triggering humoral immunity lead to tissue damage?
acitvaton of complement, mroe inflammation, recruitment of inflammatory cells, release of tissue destructive enzymes
149
How does polyclonal activation of B cells lead to tissue damage?
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
Example of a B cell mitogen that leads to stimulation o polyclonal activation of B cells:
LPS
151
How does cellular immunity activated T cells lead to tissue damage?
activates antigen presenting cells and macs, they release cytokines: IL-1/6, TNFa, autoreactive/cytotoxic response to perio tissue
152
Cytokines released by antigen presenting cells and macs:
IL-1/6, TNFa, autoreactive/cytotoxic response to perio tissue
153
How do PMNs lead to tissue damage?
release enzymes: MMPs incl collagenases, elastases, stromelysins
154
MMPs that cans destroy tissue:
collagenases, elastases, stromelysins
155
Mechs involved in mediating tissue damage:
hypersensitivy-like responses and incl antibody-mediated, cellular cytotoxicity, and IgE mediated hypersensitivity-like rxn
156
Cytotoxic cellular immune response to self and pro-infalmmatory responses involve release of:
IL-1B, TNFa, IL-6 (all cause tissue destruction
157
Th1/2 paradigm now incl:
Other T cell subsets:Th17, Treg cellls,
158
Fxn of TH17 cells:
make pro-inflammatory IL-17, TH17 + other cytokines like IL-12, cells can develop into TH1 cells
159
These cells acn swith to Th17 cells:
Tregs
160
What is req for Treg cells to change to TH17 cells?
cytokines: IL-6 and 21
161
I did not make cards for 95% of potential tx
ok
