3/1`3 Reading Flashcards
1
Q
of bacterial species in subgingival microbiota:
A
300+
2
Q
of specie that can be sampled from a single site:
A
30-1000
3
Q
Have we been able to classify all bacteria as being a member of a specific species?
A
no
4
Q
What can lead to the easy loss of bacteria during characterization?
A
fastidious bacteria
5
Q
These can be substrate sources for bacteria in PDD:
A
substrates released from damaged tissues, deepening of perio pockets
6
Q
Progression pattern of PDD:
A
periods of exacerbation and remission
7
Q
When to take plaque sample from a PDD pt:
A
peak of exacerbation
8
Q
TF? There are multiple PDD s in different subjects
A
T
9
Q
How to differentiate bw the different PDDs:
A
can’t
10
Q
TF? 1 pt may have multiple PDD’s.
A
T
11
Q
What explains the differences in PDD symptoms in different part of the mouth?
A
different levels of pathogens or the stage of the PDD.
12
Q
Can pathogens be carried in low numbers of healthy mouths?
A
yes
13
Q
Define carrier state:
A
pathogen in the mouth of a healthy individual, low numbers free of PDD
14
Q
If a virulent clonal pathogen is detected in an OC, PDD will be present and active.
A
F. could be a healthy OC
15
Q
An inability to distinguish this type of pathogen from this type would impeded understanding:
A
virulent from virulent clonal type
16
Q
More viurlent strains may harbor these:
A
bacteriophages or plasmids
17
Q
Bacterial plasmids code for:
A
virulence factors: invasiveness, adherence, antimicrobial resistance, production of toxins and noxious products
18
Q
Several strains of A.a. from PDD lesion have been found to have identical:
A
profiles consisting of 4 plasmids
19
Q
These can be isolated from recently infected perio sites:
A
phages
20
Q
Criteria for defining pathogens in destructive PDD:
A
isolated from every case, not recovered from cases of other forms of disease or non-pathogenically, induce disease in animals, more freq and higher numbers in cases of infection than wo, elimination of species = remission, host responds to species or antigen via production of antibodies or cellular immune response directed specifically at species, virulence factors, animal studies (induced disease to favor selection of a single or subset of species), risk assessment of PDD progression
21
Q
Discrimination of a pathogen is based on:
A
a weight of evidence
22
Q
Part of pathogen that causes disease:
A
virulence factor
23
Q
Define virulence:
A
cause disease or interfere w a metabolic or physiological function, express pathogenicity, interaction bw microbe and host
24
Q
Interaction bw host and microbe is dependent upon:
A
extrinsic factors of env
25
These distinguish virulent organism from avirulent:
end products of bacterial metabolism, chemical composition of bacterial components, ability to overwhelm host defenses, invasiveness, ability to kill
26
Define virulence factors:
harm host, when absent (ie mutation) impair ability to harm host, but not ability to grow and reproduce
27
Fxns of virulence factors:
induce microbe-host interactions/ attachment, invade host, grow in host cell, evade/interfere w host defenses
28
4 most virulent oral pathogens:
A.a., P.gingivalis, T. forsythia, T. denticola
29
A.a:
small, nonmotile, gram -, saccharolytic, capnophilic, round-ended rod
30
How many serotypes of A.a.?
6 (a-f)
31
Serotype found more frequently and in higher numbers in active PD lesions:
b
32
Serotypes w strong assoc to perio health:
a and c
33
Serotype b, more prevalent in chronic or aggressive PDD?
aggressive
34
Serotype b, more prevalent in those under 18 or over 35?
under 18
35
Is the global distribution of the serotypes homogenous?
no
36
Assoc bw serotype and perio status may depend upon:
geographical location and/or ethnicity
37
LAP sf:
Local aggressive PDD
38
LAP is assoc with this bacteria:
A.a.
39
Prevalence rate of A.a. in early onset/ prepubertal PDD:
40-100%
40
Disease most commonly assic w A.a.:
Localized juvenile PDD (LAP)
41
A.a has been isolated from ___-___% of localized juvenile PDD lesions:
75-100%
42
A.a. is assoc w this syndrome:
Papillon-Lefevre, perio lesions of
43
Papillon-Lefevre syndrome:
dec fxn of monocytes, PMNs, lymphos, may be due to CMV, may be virally mediated host defense lowering setting stage for overgrowth of subgingival A.a.
44
% proportion of adults PDD:
30-40%+
45
Proportion of A.a increases as:
probing depth inc,
46
A.a. is detected __ X more freq in lesions w angular vs horizontal bone loss.
4
47
How many times greater is the breakdown level at sites w A.a. present?
100 times greater
48
Define "active or progressive" disease:
loss of CT attachment of greater than 2mm during a 37d period
49
% of progressing sites that harbored A.a.
90%
50
% of stable or non-progressing sites that harbored A.a.:
44%
51
Prevalence of A.a., progressive lesions vs nonprogreessive:
50% vs 4.8%
52
Lesions where A.a. is particularly frequent:
refractory perio lesions, due to ability to invade gingival tissues and evade removal?
53
Can A.a. be found in ppl w no hx of destructive perio disease?
yes
54
Occurrence of A.a. in perio healthy children under 11yo:
0-26%
55
Occurrence of A.a. in adolescents w healthy periodontium or minimal disease:
less the 15% subgingival A.a.
56
Occurrence of A.a. in young adults w minimal perio disease:
15%+ subgingival A.a.
57
A.a can be isolated from these locations in mouth:
subgingival sites, extracrevicular locations: deep and normal perio sites, pockets and cheek, tongue and saliva, cheek and saliva
58
Bacteria of successful implants:
Gram +, coccoid cells, very few rods, low anaerobe/aerobe ratio
59
Bacteria of infected or failing implants:
inc perio pathogens, Gram = anaerobe rods, motile rods, fusiform bacteria, and spirochetes
60
Colonization can occur secondary to:
antibiotic tx
61
TF? A.a. possess 1 virulence factor.
F. myriad
62
Virulence factors of A.a.:
promote colonization and persistence, interfere w defenses, destroy host tissues, inhibit host repair of tissue
63
Virulence factors of A.a. that promote colonization and persistence:
adhesins, invasins, bacteriocins, antibiotic resistance
64
Virulence factors of A.a that interfere w defenses:
Leukotoxin, Chemotactic inhibitors, Immunosuppressive proteins, Fc-binding proteins
65
Virulence factors of A.a. that destroy host tissues:
cytotoxins, collagenase, bone resorption agents, stimulators of inflammatory mediators
66
Virulence factors of A.a. that inhibit host repair of tissue:
inhibitors of fibroblast proliferation or bone formation
67
TF? Most strains of A.a. do not adhere strongly to epi cells.
F most do
68
How long does it take for binding of A.a to epi cells to reach saturation levels?
1h after infection (very fast)
69
These function in adherence of rough variants:
fimbriae
70
These function in adherence of smooth, highly invasive strains:
nonfimbrial components
71
Ex of nonfimbrial components:
vesicles
72
PGA sf:
poly-N-acetylglucosamine
73
What produces PGA?
A.a.
74
What is PGA?
surface polysaccharide
75
Fxn of PGA:
intercellular adhesion, biofilm formation, detergent resistance
76
What must happen for A.a. to initiate disease in extraoral sites?
must bind ECM
77
Main component of ECM:
collagen
78
What secretes the ECM?
epi and endo cells
79
ECM surrounds:
CT
80
ECM is made of:
proteins and polysaccharides
81
TF? multiple strains of A.a. bind fibroinogen.
F.
82
What do multiple strains of A.a. bind?
several types of CT collagen and fibronectin
83
Collagen types that are substrates for binding of A.a.:
All collagen types
84
A.a. SUNY456 almost completely lacks binding capability to this collagen:
Type 4 collagen
85
Where is Type 4 collagen found?
Basement membrane
86
Binding of A.a. to the insoluble form of proteins that are major structural component of the ECM aids in:
spread and colonization, oral and extraoral
87
___% of A.a. from pt w PDD were resistant to ___:
82%, tetracycline
88
Tetracycline is frequently used as:
an adjunct to mechanical debridemetn in the tx of localized juvenile PDD
89
Pts resistant to tetracycline have this:
Tet B resistance determinant
90
Are trasfrer freq of Tet B resistance higher for Aa. recipient or H.influenza recipient?
A.a.
91
Combo of these 2 drugs led to marked red of subgingival A.a. assoc w the resolution of clinical signs of LJP after 7d course:
systemic metronidazole + amoxicillin
92
Mechs by which A.a. stimulates bone resorption:
LPS, proteolysis-sensitive factor in microvesicles, surface -associated material
93
Molecular chaperone of A.a.:
surface assoc material, GroEL
94
How does GroEL act to promote bone resorption?
acts directly on clasts
95
TF? Collagenase activity is assoc with A.a..
T
96
Most prominent cell type in gingival CT:
fibroblast
97
Major source of collagen in gingival CT:
fibroblasts
98
Fxn of fibroblasts:
structural integrity to tissue
99
These can inhibit fibroblast proliferation:
bacterial toxins
100
Toxin of A.a. that is considered a virulence factor:
heat labile cytotoxin, esp cytotoxic, impact on fibroblast viability
101
Affect of almost all strains of A.a. on membrane vesicles:
extrude vesicles from their surface
102
Vesicles assoc w SUNY 465:
fimbrillar membranous extensions w knob-like ends
103
Vesicles assoc w SUNY 465 often contain:
leukotoxin, endotoxin, bone resorption activity and a bacteriocin, adhesins
104
Why must vesicles assoc w SUNY 465 contain adhesins:
bc their binding to weakly adherent or non-adherent strains inc ability of those strains to attach to epi cells
105
Proteins produced by bacteria that are lethal for other strains and species of bacteria:
bacteriocins
106
Bacteriocins can confer:
colonization advantage by dec ecological pressures assoc w competition for nutrients and space
107
Bacteriocins enhance colonizaiton by:
producing actinobacillin
108
Fxn of actinobacillin:
directly toxic to S.sanguinis and A. viscosus (1' colonizers)
109
TF? Bacteriocins alter cell permeability.
T, leakage of RNA, DNA and other macromolecules and cofactors
110
Virulence factor that belongs to the RTX family of poreforming bacteria, secreted lipoprotein:
Leukotoxin
111
Fxn of leukotoxin:
kills PMN, macs, host cell killing, immune evasion
112
Fc receptors are aka:
Bacterial immunoglobulin-binding proteins
113
Fc receptors bind:
Fc portion of Igs
114
Fxn of Fc-binding proteins:
interfere w complement- or antibody dependent host immune mechs, and immune functions
115
What might inhibit PMN phagocytosis?
binding of other protein to the Fc portion inhibiting binding of the antibody
116
TF? Ig Fc receptors can be found on surface cells of several strains of A.a..
T
117
Ig subclass of monoclonal antibodies of unrelated specificity:
IgG
118
This may help A.a. to persist at extracellular sites during the disease process.
Fc receptor
119
Release of Fc-binding components from bacteria may interfere w:
phagocytic activity (90% red), complement function, dec B-cell proliferation in perio infiltrates
120
What kind of toxin is LPS?
endotoxin
121
TF? LPS can destroy an array of host cells and tissues.
T
122
Low conc of A.a. LPS stimulate:
macs to produce interleukin-1a and 1b, TNF (cytokines involved in inflammation and bone resorption)
123
Mac that migrate to gingival site of A.a. infection will be stimulated to produce:
Interleukin-1a and 1b, TNF
124
Production of this by A.a. down regulates both T and B cell responsiveness though the actions of a subpopulation of B lymphos, induces lympho apoptosis:
cytolethal distending toxin (CDT)
125
CDT sf:
cytolethal distending toxin
126
This suppresses cell proliferation and cytokine production by T cells:
suppressive factor 1
127
Fxn of SF1:
inhibits T cell proliferation and production of Th1 and Th2 cytokines by ConA-stimulated splenic T cells.
128
TH1 produces:
IL-2, IFN
129
TH2 produces:
IL4 and 5
130
SF1 could affect the induction of what type of immune response?
humoral and/or cell-mediated
131
How can SF1 affect the humoral and/or cell-mediated responses?
modulation of T-cell response, including cytokine production
132
Ratio of helper-to-suppressor T-cell ratio of pts w either juvenile or rapidly progressing forms of early onset PDD, inc or dec?
dec
133
Pts w either juvenile or rapidly progressing forms of early onset PDD, dec in these are seen:
dec ratio of helper-to-suppressor T-cell ratio, dec CD4+/CD8+ ratio
134
1st line of defense against invading bac:
recruitment of phagocytes
135
What is made by A.a. that inhibits PMN chemotaxis?
low-molecular weight compound, proteinaseous
136
How can the inhibition of PMN chemotaxis by a compound secreted by A.a. be reversed?
tx w proteinase K
137
Fxn of PMN:
kill bacteria via potent antibacterial agents gained when PMNs fuse w lysosomes
138
How do PMNs gian antibacterial agents that can kill bacteria?
fusion w lysosomes
139
Can A.a. inhibit PMNs from producing antimicrobial compounds?
Yes
140
Is A.a. intrinsically resistant to any of the compounds PMN use as antimicrobial agents?
yes
141
What inhibits the production of hydrogen peroxide by PMNs?
a heat-stable protein.
142
TF? Few strains of A.a. are resistant to high levels of hydrogen peroxide.
F. many strains
143
A.a. is resistant to several of these cationic peptides which are found in PMNs:
defensins
144
TF? CDT can induce apoptosis.
T
145
CDT can induce:
apoptosis, cell cycle block at G2/M phase
146
Active subunit of CDT:
CdtB
147
At which phase of the cell cycle does CDT act?
G2/M phase
148
Can A.a. penetrate the gingival epi?
yes
149
Is the degree of invasion greater or less in KB cells in comparison to cells originating for nonoral sources?
greater
150
A.a. invasion occurred singly in __ of the KB cells:
vacuoles
151
What may be involved in determining the invasive capability of A.a.?
colonial morphology
152
Adv and LJP contain large numbers of bacteria in these areas:
oral epi and adjacent CT
153
Most sections taken from Adv and LJP contain around this number of bacteria in the oral epi:
20+
154
Is there penetration by, or transfer of, bacteria or bacterial antigens into the CT?
yes
155
The numbers of A.a. cultivable from pockets infected w this bacterium correlated w
tissue infiltration by A.a.
156
Organisms of this group are assoc w systemic disease:
HACEK group (Haemophilus, A.a., Cardiobacterium hominis, Eikenella corrodens, Kingella kingae)
157
There is a purported relationship bw PDD and:
CHD, preterm birth, cerebral infarction
158
TF? Systemically compromised have the same risk of becoming ill from dental focal infections as the health systemic pt.
F. higher risk
159
Why are iC pts more likely to get ill from dental focal infection?
OC may be reservoir for serious pathogens
160
Oral issues that inc the likelihood of dissemination of oral microorganisms to nonoral sites:
PDD, odontogenic abscesses, endo infections
161
Can A.a. attach to soft or hard tissue?
both
162
Where does A.a. position itself with attachment?
adjacent to the permeable junctional and pocket epi
163
TF? A.a. has only been isolated for oral sites.
F. from a # of distant organs, can cause serious infection
164
Extraoral infections caused by A.a.:
fascial plane infection, heart infection, pericarditis, lung infection, necrotizing pneumonia, mediastinitis, mediastinal abscess, transdiaphragmatic infection, endopthalmitis, skin infection, vertebral osteomyelitis, cervical lymphadenitis, submandibular space abscess, UTI
165
P. gingivalis:
Gram-, anaerobic, nonmotile, asaccharolytic rods that usuall yexhibit coccal to short rod morphologies
166
P. gingivalis is a member of this group:
black-pigmented Bacteroides
167
Prevalence of P. gingivalis in perio healthy kids and adolescents:
few or none
168
% of LJP pts w P.g.:
37-63%
169
TF? When present, P.g. is seen at the onset of LJP.
F, if present, small portion of microbiota
170
Predominate organism is generalized juvenile PDD:
P.g. (LAP - A.a.)
171
% of P.g. in healthy and minimally diseased adult periodontium:
less than 10%
172
% adult PDD pts w P.g.:
40-100%
173
P.g., more prevalent in deeper or more shallow perio pockets?
deeper
174
P.g., more prevalent in progressive deep perio lesions or in nonprogressive sites?
progressive deep perio lesions
175
Predominate organism in infected and failing implants
Gram- anaerobic rods, motile rods, fusiform bacteria, and spirochetes (F, P.i. A.a., P.m., C.r., C, P.i., P.g,)
176
Outcome of perio tx is better if these pathogens are no longer present:
P.g., A.a.
177
Why are pts that have been treated for PDD more likely to have recurrences?
P.i, P.g., and A.a. are all more likely to reestablishing themselves rapidly, effective plaque control is required
178
Organisms that make LPS:
Gram- prokaryotes, P.g.
179
Layers of cell envelope of Gram- bacteria:
inner (cytoplasmic), outer
180
Where does the outer membrane of Gram - bacteria lay?
external to the peptidoglycan
181
How is the outer membrane of Gram - bacteria attached to peptidoglycan?
via lipoproteins
182
Peptidoglycan, aka:
murein
183
How are lipoproteins attached to A.a.?
covalent and noncovalent bonds to protein units within P.g. and to the outer membrane by their lipid moieties
184
Outer membrane of Gram- bacteria, symmetrical or asymmetrical?
asymmetrical
185
Where is LPS found on Gram - bacteria?
outer leaflet
186
Where is the hydrophilic end of the amphipathic LPS molecule located?
exposed to env on the exterior surface of the outer membrane
187
Location of the core region of LPS:
in outer leaflet
188
Core region connects:
O-antigen to the hydrophobic end of the molecule, lipid A
189
Hydrophobic end of LPS molecule:
Lipid A
190
LPS, large or small?
large 10kDa +
191
What makes up the hydrophilic end of LPS?
polysaccharide or O-specific (somatic)antigen
192
O-specific antigen is aka:
somatic antigen
193
Lipid A is embedded here:
lipid portion of outer membrane leaflet
194
Fxn of LPS:
induce several host derived cyto- and chemokines, cytotoxin
195
TF? The LPS of P.g. is the same as the enteric LPS.
F
196
Does P.g. have higher or lower biological activity than enteric LPS?
lower, very low endotoxicity
197
Why might P.g. be able to colonize and grow in sterile tissue undetected by the host?
low biological activity, very low endotoxicity
198
Outer membrane contains:
LPS, phospholipids, lipoproteins and outer membrane proteins
199
P.g. is capable of:
adhering to a variety of host tissues and cells, and to invade these cells and multiply
200
Define coaggregation:
interaction of pairs of oral bacteria via cognate binding, many species of oral bacteria demonstrate this
201
This may be related to the development of complex biofilms of the OC:
coaggregation
202
This contributes to the characteristics of the complex microbial ecology of biofilms:
intergeneric coaggregation
203
P.g. is capable of coaggregation w:
A.n. two (A.v.), S.gordonii, S. mitis, and fimbriated S.salivarius (n,g,m,s,f)
204
Interaction of P.g w A.n. two (A.v.), S.gordonii, S. mitis, and fimbriated S.salivarius can be altered via:
heat, sugars, AA's, cation chelation, protease tx, (suggesting ligand-receptor interaction)
205
Initial event in pathogenicity of P.g.:
adherence in OC
206
P.g. use these for bacterial adherence:
fimbriae, proteases, hemagglutinins, and LPSD
207
Fimbriae or pili are what type of appendages?
proteinaceous, filamentous
208
How do fimbriae and pili play a role in virulence?
by stimulating bacterial attachment to host cells
209
First fimbriae:
major, long, or FimA fimbriae
210
Second fimbriae:
minor, short, or Mfa1 fimbraie
211
Subunit protein of major fimbriae:
fimbrillin (FimA)
212
How does fimbrilin (FimA) act on bacterial interactions w host tissue?
by mediating bacterial adhesion and colonization in targeted sites
213
Fxn of major fimbriae:
bind and activate various host cells: epi, endo, spleen, peripheral blood monocytes
214
What does the binding and activation of various host cells by major fimbriae result in?
release of cytokines (IL-1, 6, 8, TNF, ICAM-1, VCAM-1, P- and E-selectins
215
Adhesion molecules released by interaction of fimbriae and body cells:
ICAM-1, VCAM-1, P- and E-selectins
216
Which fimbriae are necessary for bacterial invasion to host cells:
major fimbriae
217
appendages in an major fimbriae deficient mutant strain resemble:
minor appendages
218
How do major and minor fimbriae vary?
size, antigenicity
219
fimA mutant, inc or red of adhesive potential to saliva-coated HA, gingival epi cells, and fibroblasts, as well as bone absorption capability
red
220
P.g. can induces:
IL-1a, IL-1B, IL-6, and TNF-a cytokine expression in macs
221
P.g., high or low proteolytic activity?
high
222
1' fxn of proteases and peptidases secreted by assacharoltyic bacteria:
provide nutrients for growth
223
How many secreted proteinases have been described for P.g. and their concerted activity?
at least 8
224
Fxns of secreted proteinases:
provide AA'a, peptides and hemin for growth, processing of essential cell surface components and provision of substrates for bacterial cell adhesion, tissue invasion and destruction by bacteria, evasion and modulation of host immune defenses
225
exs of tissue degradation and attenuation of host defense mechs:
degradation of ECM proteins, activation of MMPs, inactivation of plasma proteinase inhibitors, cleavage of cell-surface receptors, activation or inactivation of complement factors and cytokines, activation of the kellikrien-kinin cascade, stimulation of apoptotic cell death,disruption of PMN function
226
How are the adhesive and enzymatic functions of P.g. proteinases connected?
intrinsically
227
P.g. cells bind to and degrade:
fibronectin, laminin, fibrinogen, collagen
228
Adhesion and degradation process involve:
fimbriae and Arg-X-specific and Lys-X-specific cysteine proteinases
229
The hydrolytic products of these enhance the binding of fimbriae to their substrates:
fibronectin or other matrix poteins such as collagen
230
This hydrolyzes fibronectin or other matrix proteins such as collagen:
P.g. Arg-X proteinases RgpA and RgpB
231
Proteinases can expose sequences that carry:
C-terminal residues
232
What does the exposure of C-terminal residues lead to:o:
adhesion promotion (via fimbrial-arginine interaction)
233
How might initial gingivitis progress to more severe?
exposure of C-terminal residues --> adhesion promotion thru fimbrial-arginine interaction
234
What might expose hidden receptors that would enhance colonization by P.g.?
proteolytic activity assoc w infection of gingival sulcus
235
cysteine proteinases are aka:
gingipains
236
Gingipains cleave:
after
237
Gingipains comprise a group of:
cysteine endopeptidases
238
What % of the general proteolytic activity of P.g. do gingipains account for?
85%
239
% of the expressed "trypsin-like activity" of gingipains of P.g.:
100%
240
Gingipains, soluble or insoluble?
soluble and cell-assoc
241
Gingipains are the products of:
3 genes: rgpA, rgpB, kgp (all encode cysteine proteinases)
242
The product of the kgp gene cleaves:
after lysine
243
Products of rgp! and rgpB genes cleave:
arginine residues
244
How do gingipains contribute to the virulence potential of P.g.?
By influencing bacterium-tissues binding, binding to a cognate receptor, or by exposing cryptitope receptors
245
P.g. strains w high levels of this adhere better to epi cells:
typrsin-like protease activity
246
Mature forms of Arg-gingipain A and Lys-gingipain posses:
a catalytic domain and 3 or 4 hemagglutinin/adhesion (HA) domains linked by noncovalent bonds
247
HA domain sf:
hemagglutinin/adhesion domains
248
Degree of homology shared bw HA domains of gingipain A and Lys-gingipain:
97%
249
HA domains of gingipain A and Lys-gingipain are implicated in:
adherence of P.g. to gingival epi cells
250
Physiological roles of gingipains:
expression of virulence factors, stability and/or processing of extracellular and cell-surface proteins
251
Proteases of P.g. may play a role in:
host destructive events,
252
How does P.g. adhere to and invade epi cells?
targeting specific host receptors, modulating host signalling events and deregulating the host cytokine network
253
P.g and epi interactions lead to:
activation of several cascades that regulate transcription of genes that encode effectors and regulators of the immune response
254
These are upregulated by P.g.-epi interactions:
effectors of the innate immune system, proinflammatory cytokines, chemokines, MMP's and antimicrobial peptides (all may effect disease progression and inflammatory responses, bacterial persistence of chronic manifestation)
255
Members of the red complex:
p.g. T.f., T.d.
256
T.f.:
Gram-, anearobic, fusiform, unique growth req's
257
Growth req's of T.f.:
hemin, menadione, L-cysteine, and N-acetylneuraminic acid
258
T.f., fastidious or not?
fastidious
259
T.f. often isolated form acute or chronic perio pts?
chronic, active
260
PDD that progresses posttherapy:
refractory, aggressive form
261
Refractory PDD is assoc ith this organism:
T.f.
262
T.f. was freq assoc with ___ colonization and elevated in older pts:
P.g.
263
Detection of T.f. is assoc w:
early periodontiits
264
TF? T.f. is a risk factor for periodontitis.
T
265
Presence of T.f. is assoc with:
smokers, positive for aspartate aminotransferase activity, or interleukin-1 genotype (PST test)
266
Test to determine if pt is interleukin-1 genotype:
PST test
267
TF? PDD is assoc w lowered resistance to infection.
T
268
T.f. is assoc w:
viral diseases, HIV, diabetes, Papillon-Lefevre syndrome
269
The robust enzymatic repertoire of T.f. is related to its:
asaccharolytic physiology
270
T.f. produces an enzymatic peptidase activity that degrades:
benzoyl-DL arginine-naphthylamide (BANA)
271
BANA sf:
benzoyl-DL arginine-naphthylamide
272
BANA activity is related to:
sites of perio destruction
273
This, produced by T.f. activates gingival fibroblasts to produce elevated levels of IL-6 and TNF-a
lipoproteins (BfLP)
274
Fxn of IL-6:
inducet acute phase proteins in liver cells involved in cytotoxic T-cell differentiation, growth of myeloma/plasmacytoma cells, induction of B cells,induction of bone resorption by clast formation w soluble IL-6 receptor
275
This is made by T.f. and is thought to be involved in host-cel virulence:
sialidase and a trypsin like enzyme
276
TF? T.f. can induce apoptosis.
T, could be part of progression of periodontitis
277
What may prevent T.f. and P.g from being destroyed by PMNs?
apototic-inducing activity --> elimination of host immune or preimmune cells --> bacterial colonization --> rapid progression of disease
