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Oral Sciences > 3/1`3 Reading > Flashcards

3/1`3 Reading Flashcards

1
Q

of bacterial species in subgingival microbiota:

A

300+

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2
Q

of specie that can be sampled from a single site:

A

30-1000

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3
Q

Have we been able to classify all bacteria as being a member of a specific species?

A

no

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4
Q

What can lead to the easy loss of bacteria during characterization?

A

fastidious bacteria

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5
Q

These can be substrate sources for bacteria in PDD:

A

substrates released from damaged tissues, deepening of perio pockets

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6
Q

Progression pattern of PDD:

A

periods of exacerbation and remission

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7
Q

When to take plaque sample from a PDD pt:

A

peak of exacerbation

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8
Q

TF? There are multiple PDD s in different subjects

A

T

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9
Q

How to differentiate bw the different PDDs:

A

can’t

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10
Q

TF? 1 pt may have multiple PDD’s.

A

T

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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.

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12
Q

Can pathogens be carried in low numbers of healthy mouths?

A

yes

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13
Q

Define carrier state:

A

pathogen in the mouth of a healthy individual, low numbers free of PDD

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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

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15
Q

An inability to distinguish this type of pathogen from this type would impeded understanding:

A

virulent from virulent clonal type

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16
Q

More viurlent strains may harbor these:

A

bacteriophages or plasmids

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17
Q

Bacterial plasmids code for:

A

virulence factors: invasiveness, adherence, antimicrobial resistance, production of toxins and noxious products

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18
Q

Several strains of A.a. from PDD lesion have been found to have identical:

A

profiles consisting of 4 plasmids

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19
Q

These can be isolated from recently infected perio sites:

A

phages

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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

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21
Q

Discrimination of a pathogen is based on:

A

a weight of evidence

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22
Q

Part of pathogen that causes disease:

A

virulence factor

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23
Q

Define virulence:

A

cause disease or interfere w a metabolic or physiological function, express pathogenicity, interaction bw microbe and host

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24
Q

Interaction bw host and microbe is dependent upon:

A

extrinsic factors of env

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25
Q

These distinguish virulent organism from avirulent:

A

end products of bacterial metabolism, chemical composition of bacterial components, ability to overwhelm host defenses, invasiveness, ability to kill

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26
Q

Define virulence factors:

A

harm host, when absent (ie mutation) impair ability to harm host, but not ability to grow and reproduce

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27
Q

Fxns of virulence factors:

A

induce microbe-host interactions/ attachment, invade host, grow in host cell, evade/interfere w host defenses

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28
Q

4 most virulent oral pathogens:

A

A.a., P.gingivalis, T. forsythia, T. denticola

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29
Q

A.a:

A

small, nonmotile, gram -, saccharolytic, capnophilic, round-ended rod

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30
Q

How many serotypes of A.a.?

A

6 (a-f)

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31
Q

Serotype found more frequently and in higher numbers in active PD lesions:

A

b

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32
Q

Serotypes w strong assoc to perio health:

A

a and c

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33
Q

Serotype b, more prevalent in chronic or aggressive PDD?

A

aggressive

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34
Q

Serotype b, more prevalent in those under 18 or over 35?

A

under 18

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35
Q

Is the global distribution of the serotypes homogenous?

A

no

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36
Q

Assoc bw serotype and perio status may depend upon:

A

geographical location and/or ethnicity

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37
Q

LAP sf:

A

Local aggressive PDD

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38
Q

LAP is assoc with this bacteria:

A

A.a.

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39
Q

Prevalence rate of A.a. in early onset/ prepubertal PDD:

A

40-100%

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40
Q

Disease most commonly assic w A.a.:

A

Localized juvenile PDD (LAP)

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41
Q

A.a has been isolated from ___-___% of localized juvenile PDD lesions:

A

75-100%

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42
Q

A.a. is assoc w this syndrome:

A

Papillon-Lefevre, perio lesions of

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43
Q

Papillon-Lefevre syndrome:

A

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.

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44
Q

% proportion of adults PDD:

A

30-40%+

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45
Q

Proportion of A.a increases as:

A

probing depth inc,

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46
Q

A.a. is detected __ X more freq in lesions w angular vs horizontal bone loss.

A

4

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47
Q

How many times greater is the breakdown level at sites w A.a. present?

A

100 times greater

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48
Q

Define “active or progressive” disease:

A

loss of CT attachment of greater than 2mm during a 37d period

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49
Q

% of progressing sites that harbored A.a.

A

90%

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50
Q

% of stable or non-progressing sites that harbored A.a.:

A

44%

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51
Q

Prevalence of A.a., progressive lesions vs nonprogreessive:

A

50% vs 4.8%

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52
Q

Lesions where A.a. is particularly frequent:

A

refractory perio lesions, due to ability to invade gingival tissues and evade removal?

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53
Q

Can A.a. be found in ppl w no hx of destructive perio disease?

A

yes

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54
Q

Occurrence of A.a. in perio healthy children under 11yo:

A

0-26%

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55
Q

Occurrence of A.a. in adolescents w healthy periodontium or minimal disease:

A

less the 15% subgingival A.a.

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56
Q

Occurrence of A.a. in young adults w minimal perio disease:

A

15%+ subgingival A.a.

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57
Q

A.a can be isolated from these locations in mouth:

A

subgingival sites, extracrevicular locations: deep and normal perio sites, pockets and cheek, tongue and saliva, cheek and saliva

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58
Q

Bacteria of successful implants:

A

Gram +, coccoid cells, very few rods, low anaerobe/aerobe ratio

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59
Q

Bacteria of infected or failing implants:

A

inc perio pathogens, Gram = anaerobe rods, motile rods, fusiform bacteria, and spirochetes

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60
Q

Colonization can occur secondary to:

A

antibiotic tx

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61
Q

TF? A.a. possess 1 virulence factor.

A

F. myriad

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62
Q

Virulence factors of A.a.:

A

promote colonization and persistence, interfere w defenses, destroy host tissues, inhibit host repair of tissue

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63
Q

Virulence factors of A.a. that promote colonization and persistence:

A

adhesins, invasins, bacteriocins, antibiotic resistance

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64
Q

Virulence factors of A.a that interfere w defenses:

A

Leukotoxin, Chemotactic inhibitors, Immunosuppressive proteins, Fc-binding proteins

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65
Q

Virulence factors of A.a. that destroy host tissues:

A

cytotoxins, collagenase, bone resorption agents, stimulators of inflammatory mediators

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66
Q

Virulence factors of A.a. that inhibit host repair of tissue:

A

inhibitors of fibroblast proliferation or bone formation

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67
Q

TF? Most strains of A.a. do not adhere strongly to epi cells.

A

F most do

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68
Q

How long does it take for binding of A.a to epi cells to reach saturation levels?

A

1h after infection (very fast)

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69
Q

These function in adherence of rough variants:

A

fimbriae

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70
Q

These function in adherence of smooth, highly invasive strains:

A

nonfimbrial components

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71
Q

Ex of nonfimbrial components:

A

vesicles

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72
Q

PGA sf:

A

poly-N-acetylglucosamine

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73
Q

What produces PGA?

A

A.a.

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74
Q

What is PGA?

A

surface polysaccharide

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75
Q

Fxn of PGA:

A

intercellular adhesion, biofilm formation, detergent resistance

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76
Q

What must happen for A.a. to initiate disease in extraoral sites?

A

must bind ECM

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77
Q

Main component of ECM:

A

collagen

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78
Q

What secretes the ECM?

A

epi and endo cells

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79
Q

ECM surrounds:

A

CT

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80
Q

ECM is made of:

A

proteins and polysaccharides

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81
Q

TF? multiple strains of A.a. bind fibroinogen.

A

F.

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82
Q

What do multiple strains of A.a. bind?

A

several types of CT collagen and fibronectin

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83
Q

Collagen types that are substrates for binding of A.a.:

A

All collagen types

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84
Q

A.a. SUNY456 almost completely lacks binding capability to this collagen:

A

Type 4 collagen

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85
Q

Where is Type 4 collagen found?

A

Basement membrane

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86
Q

Binding of A.a. to the insoluble form of proteins that are major structural component of the ECM aids in:

A

spread and colonization, oral and extraoral

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87
Q

___% of A.a. from pt w PDD were resistant to ___:

A

82%, tetracycline

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88
Q

Tetracycline is frequently used as:

A

an adjunct to mechanical debridemetn in the tx of localized juvenile PDD

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89
Q

Pts resistant to tetracycline have this:

A

Tet B resistance determinant

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90
Q

Are trasfrer freq of Tet B resistance higher for Aa. recipient or H.influenza recipient?

A

A.a.

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91
Q

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:

A

systemic metronidazole + amoxicillin

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92
Q

Mechs by which A.a. stimulates bone resorption:

A

LPS, proteolysis-sensitive factor in microvesicles, surface -associated material

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93
Q

Molecular chaperone of A.a.:

A

surface assoc material, GroEL

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94
Q

How does GroEL act to promote bone resorption?

A

acts directly on clasts

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95
Q

TF? Collagenase activity is assoc with A.a..

A

T

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96
Q

Most prominent cell type in gingival CT:

A

fibroblast

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97
Q

Major source of collagen in gingival CT:

A

fibroblasts

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98
Q

Fxn of fibroblasts:

A

structural integrity to tissue

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99
Q

These can inhibit fibroblast proliferation:

A

bacterial toxins

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100
Q

Toxin of A.a. that is considered a virulence factor:

A

heat labile cytotoxin, esp cytotoxic, impact on fibroblast viability

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101
Q

Affect of almost all strains of A.a. on membrane vesicles:

A

extrude vesicles from their surface

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102
Q

Vesicles assoc w SUNY 465:

A

fimbrillar membranous extensions w knob-like ends

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103
Q

Vesicles assoc w SUNY 465 often contain:

A

leukotoxin, endotoxin, bone resorption activity and a bacteriocin, adhesins

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104
Q

Why must vesicles assoc w SUNY 465 contain adhesins:

A

bc their binding to weakly adherent or non-adherent strains inc ability of those strains to attach to epi cells

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105
Q

Proteins produced by bacteria that are lethal for other strains and species of bacteria:

A

bacteriocins

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106
Q

Bacteriocins can confer:

A

colonization advantage by dec ecological pressures assoc w competition for nutrients and space

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107
Q

Bacteriocins enhance colonizaiton by:

A

producing actinobacillin

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108
Q

Fxn of actinobacillin:

A

directly toxic to S.sanguinis and A. viscosus (1’ colonizers)

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109
Q

TF? Bacteriocins alter cell permeability.

A

T, leakage of RNA, DNA and other macromolecules and cofactors

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110
Q

Virulence factor that belongs to the RTX family of poreforming bacteria, secreted lipoprotein:

A

Leukotoxin

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111
Q

Fxn of leukotoxin:

A

kills PMN, macs, host cell killing, immune evasion

112
Q

Fc receptors are aka:

A

Bacterial immunoglobulin-binding proteins

113
Q

Fc receptors bind:

A

Fc portion of Igs

114
Q

Fxn of Fc-binding proteins:

A

interfere w complement- or antibody dependent host immune mechs, and immune functions

115
Q

What might inhibit PMN phagocytosis?

A

binding of other protein to the Fc portion inhibiting binding of the antibody

116
Q

TF? Ig Fc receptors can be found on surface cells of several strains of A.a..

A

T

117
Q

Ig subclass of monoclonal antibodies of unrelated specificity:

A

IgG

118
Q

This may help A.a. to persist at extracellular sites during the disease process.

A

Fc receptor

119
Q

Release of Fc-binding components from bacteria may interfere w:

A

phagocytic activity (90% red), complement function, dec B-cell proliferation in perio infiltrates

120
Q

What kind of toxin is LPS?

A

endotoxin

121
Q

TF? LPS can destroy an array of host cells and tissues.

A

T

122
Q

Low conc of A.a. LPS stimulate:

A

macs to produce interleukin-1a and 1b, TNF (cytokines involved in inflammation and bone resorption)

123
Q

Mac that migrate to gingival site of A.a. infection will be stimulated to produce:

A

Interleukin-1a and 1b, TNF

124
Q

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:

A

cytolethal distending toxin (CDT)

125
Q

CDT sf:

A

cytolethal distending toxin

126
Q

This suppresses cell proliferation and cytokine production by T cells:

A

suppressive factor 1

127
Q

Fxn of SF1:

A

inhibits T cell proliferation and production of Th1 and Th2 cytokines by ConA-stimulated splenic T cells.

128
Q

TH1 produces:

A

IL-2, IFN

129
Q

TH2 produces:

A

IL4 and 5

130
Q

SF1 could affect the induction of what type of immune response?

A

humoral and/or cell-mediated

131
Q

How can SF1 affect the humoral and/or cell-mediated responses?

A

modulation of T-cell response, including cytokine production

132
Q

Ratio of helper-to-suppressor T-cell ratio of pts w either juvenile or rapidly progressing forms of early onset PDD, inc or dec?

A

dec

133
Q

Pts w either juvenile or rapidly progressing forms of early onset PDD, dec in these are seen:

A

dec ratio of helper-to-suppressor T-cell ratio, dec CD4+/CD8+ ratio

134
Q

1st line of defense against invading bac:

A

recruitment of phagocytes

135
Q

What is made by A.a. that inhibits PMN chemotaxis?

A

low-molecular weight compound, proteinaseous

136
Q

How can the inhibition of PMN chemotaxis by a compound secreted by A.a. be reversed?

A

tx w proteinase K

137
Q

Fxn of PMN:

A

kill bacteria via potent antibacterial agents gained when PMNs fuse w lysosomes

138
Q

How do PMNs gian antibacterial agents that can kill bacteria?

A

fusion w lysosomes

139
Q

Can A.a. inhibit PMNs from producing antimicrobial compounds?

A

Yes

140
Q

Is A.a. intrinsically resistant to any of the compounds PMN use as antimicrobial agents?

A

yes

141
Q

What inhibits the production of hydrogen peroxide by PMNs?

A

a heat-stable protein.

142
Q

TF? Few strains of A.a. are resistant to high levels of hydrogen peroxide.

A

F. many strains

143
Q

A.a. is resistant to several of these cationic peptides which are found in PMNs:

A

defensins

144
Q

TF? CDT can induce apoptosis.

A

T

145
Q

CDT can induce:

A

apoptosis, cell cycle block at G2/M phase

146
Q

Active subunit of CDT:

A

CdtB

147
Q

At which phase of the cell cycle does CDT act?

A

G2/M phase

148
Q

Can A.a. penetrate the gingival epi?

A

yes

149
Q

Is the degree of invasion greater or less in KB cells in comparison to cells originating for nonoral sources?

A

greater

150
Q

A.a. invasion occurred singly in __ of the KB cells:

A

vacuoles

151
Q

What may be involved in determining the invasive capability of A.a.?

A

colonial morphology

152
Q

Adv and LJP contain large numbers of bacteria in these areas:

A

oral epi and adjacent CT

153
Q

Most sections taken from Adv and LJP contain around this number of bacteria in the oral epi:

A

20+

154
Q

Is there penetration by, or transfer of, bacteria or bacterial antigens into the CT?

A

yes

155
Q

The numbers of A.a. cultivable from pockets infected w this bacterium correlated w

A

tissue infiltration by A.a.

156
Q

Organisms of this group are assoc w systemic disease:

A

HACEK group (Haemophilus, A.a., Cardiobacterium hominis, Eikenella corrodens, Kingella kingae)

157
Q

There is a purported relationship bw PDD and:

A

CHD, preterm birth, cerebral infarction

158
Q

TF? Systemically compromised have the same risk of becoming ill from dental focal infections as the health systemic pt.

A

F. higher risk

159
Q

Why are iC pts more likely to get ill from dental focal infection?

A

OC may be reservoir for serious pathogens

160
Q

Oral issues that inc the likelihood of dissemination of oral microorganisms to nonoral sites:

A

PDD, odontogenic abscesses, endo infections

161
Q

Can A.a. attach to soft or hard tissue?

A

both

162
Q

Where does A.a. position itself with attachment?

A

adjacent to the permeable junctional and pocket epi

163
Q

TF? A.a. has only been isolated for oral sites.

A

F. from a # of distant organs, can cause serious infection

164
Q

Extraoral infections caused by A.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
Q

P. gingivalis:

A

Gram-, anaerobic, nonmotile, asaccharolytic rods that usuall yexhibit coccal to short rod morphologies

166
Q

P. gingivalis is a member of this group:

A

black-pigmented Bacteroides

167
Q

Prevalence of P. gingivalis in perio healthy kids and adolescents:

A

few or none

168
Q

% of LJP pts w P.g.:

A

37-63%

169
Q

TF? When present, P.g. is seen at the onset of LJP.

A

F, if present, small portion of microbiota

170
Q

Predominate organism is generalized juvenile PDD:

A

P.g. (LAP - A.a.)

171
Q

% of P.g. in healthy and minimally diseased adult periodontium:

A

less than 10%

172
Q

% adult PDD pts w P.g.:

A

40-100%

173
Q

P.g., more prevalent in deeper or more shallow perio pockets?

A

deeper

174
Q

P.g., more prevalent in progressive deep perio lesions or in nonprogressive sites?

A

progressive deep perio lesions

175
Q

Predominate organism in infected and failing implants

A

Gram- anaerobic rods, motile rods, fusiform bacteria, and spirochetes (F, P.i. A.a., P.m., C.r., C, P.i., P.g,)

176
Q

Outcome of perio tx is better if these pathogens are no longer present:

A

P.g., A.a.

177
Q

Why are pts that have been treated for PDD more likely to have recurrences?

A

P.i, P.g., and A.a. are all more likely to reestablishing themselves rapidly, effective plaque control is required

178
Q

Organisms that make LPS:

A

Gram- prokaryotes, P.g.

179
Q

Layers of cell envelope of Gram- bacteria:

A

inner (cytoplasmic), outer

180
Q

Where does the outer membrane of Gram - bacteria lay?

A

external to the peptidoglycan

181
Q

How is the outer membrane of Gram - bacteria attached to peptidoglycan?

A

via lipoproteins

182
Q

Peptidoglycan, aka:

A

murein

183
Q

How are lipoproteins attached to A.a.?

A

covalent and noncovalent bonds to protein units within P.g. and to the outer membrane by their lipid moieties

184
Q

Outer membrane of Gram- bacteria, symmetrical or asymmetrical?

A

asymmetrical

185
Q

Where is LPS found on Gram - bacteria?

A

outer leaflet

186
Q

Where is the hydrophilic end of the amphipathic LPS molecule located?

A

exposed to env on the exterior surface of the outer membrane

187
Q

Location of the core region of LPS:

A

in outer leaflet

188
Q

Core region connects:

A

O-antigen to the hydrophobic end of the molecule, lipid A

189
Q

Hydrophobic end of LPS molecule:

A

Lipid A

190
Q

LPS, large or small?

A

large 10kDa +

191
Q

What makes up the hydrophilic end of LPS?

A

polysaccharide or O-specific (somatic)antigen

192
Q

O-specific antigen is aka:

A

somatic antigen

193
Q

Lipid A is embedded here:

A

lipid portion of outer membrane leaflet

194
Q

Fxn of LPS:

A

induce several host derived cyto- and chemokines, cytotoxin

195
Q

TF? The LPS of P.g. is the same as the enteric LPS.

A

F

196
Q

Does P.g. have higher or lower biological activity than enteric LPS?

A

lower, very low endotoxicity

197
Q

Why might P.g. be able to colonize and grow in sterile tissue undetected by the host?

A

low biological activity, very low endotoxicity

198
Q

Outer membrane contains:

A

LPS, phospholipids, lipoproteins and outer membrane proteins

199
Q

P.g. is capable of:

A

adhering to a variety of host tissues and cells, and to invade these cells and multiply

200
Q

Define coaggregation:

A

interaction of pairs of oral bacteria via cognate binding, many species of oral bacteria demonstrate this

201
Q

This may be related to the development of complex biofilms of the OC:

A

coaggregation

202
Q

This contributes to the characteristics of the complex microbial ecology of biofilms:

A

intergeneric coaggregation

203
Q

P.g. is capable of coaggregation w:

A

A.n. two (A.v.), S.gordonii, S. mitis, and fimbriated S.salivarius (n,g,m,s,f)

204
Q

Interaction of P.g w A.n. two (A.v.), S.gordonii, S. mitis, and fimbriated S.salivarius can be altered via:

A

heat, sugars, AA’s, cation chelation, protease tx, (suggesting ligand-receptor interaction)

205
Q

Initial event in pathogenicity of P.g.:

A

adherence in OC

206
Q

P.g. use these for bacterial adherence:

A

fimbriae, proteases, hemagglutinins, and LPSD

207
Q

Fimbriae or pili are what type of appendages?

A

proteinaceous, filamentous

208
Q

How do fimbriae and pili play a role in virulence?

A

by stimulating bacterial attachment to host cells

209
Q

First fimbriae:

A

major, long, or FimA fimbriae

210
Q

Second fimbriae:

A

minor, short, or Mfa1 fimbraie

211
Q

Subunit protein of major fimbriae:

A

fimbrillin (FimA)

212
Q

How does fimbrilin (FimA) act on bacterial interactions w host tissue?

A

by mediating bacterial adhesion and colonization in targeted sites

213
Q

Fxn of major fimbriae:

A

bind and activate various host cells: epi, endo, spleen, peripheral blood monocytes

214
Q

What does the binding and activation of various host cells by major fimbriae result in?

A

release of cytokines (IL-1, 6, 8, TNF, ICAM-1, VCAM-1, P- and E-selectins

215
Q

Adhesion molecules released by interaction of fimbriae and body cells:

A

ICAM-1, VCAM-1, P- and E-selectins

216
Q

Which fimbriae are necessary for bacterial invasion to host cells:

A

major fimbriae

217
Q

appendages in an major fimbriae deficient mutant strain resemble:

A

minor appendages

218
Q

How do major and minor fimbriae vary?

A

size, antigenicity

219
Q

fimA mutant, inc or red of adhesive potential to saliva-coated HA, gingival epi cells, and fibroblasts, as well as bone absorption capability

A

red

220
Q

P.g. can induces:

A

IL-1a, IL-1B, IL-6, and TNF-a cytokine expression in macs

221
Q

P.g., high or low proteolytic activity?

A

high

222
Q

1’ fxn of proteases and peptidases secreted by assacharoltyic bacteria:

A

provide nutrients for growth

223
Q

How many secreted proteinases have been described for P.g. and their concerted activity?

A

at least 8

224
Q

Fxns of secreted proteinases:

A

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
Q

exs of tissue degradation and attenuation of host defense mechs:

A

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
Q

How are the adhesive and enzymatic functions of P.g. proteinases connected?

A

intrinsically

227
Q

P.g. cells bind to and degrade:

A

fibronectin, laminin, fibrinogen, collagen

228
Q

Adhesion and degradation process involve:

A

fimbriae and Arg-X-specific and Lys-X-specific cysteine proteinases

229
Q

The hydrolytic products of these enhance the binding of fimbriae to their substrates:

A

fibronectin or other matrix poteins such as collagen

230
Q

This hydrolyzes fibronectin or other matrix proteins such as collagen:

A

P.g. Arg-X proteinases RgpA and RgpB

231
Q

Proteinases can expose sequences that carry:

A

C-terminal residues

232
Q

What does the exposure of C-terminal residues lead to:o:

A

adhesion promotion (via fimbrial-arginine interaction)

233
Q

How might initial gingivitis progress to more severe?

A

exposure of C-terminal residues –> adhesion promotion thru fimbrial-arginine interaction

234
Q

What might expose hidden receptors that would enhance colonization by P.g.?

A

proteolytic activity assoc w infection of gingival sulcus

235
Q

cysteine proteinases are aka:

A

gingipains

236
Q

Gingipains cleave:

A

after

237
Q

Gingipains comprise a group of:

A

cysteine endopeptidases

238
Q

What % of the general proteolytic activity of P.g. do gingipains account for?

A

85%

239
Q

% of the expressed “trypsin-like activity” of gingipains of P.g.:

A

100%

240
Q

Gingipains, soluble or insoluble?

A

soluble and cell-assoc

241
Q

Gingipains are the products of:

A

3 genes: rgpA, rgpB, kgp (all encode cysteine proteinases)

242
Q

The product of the kgp gene cleaves:

A

after lysine

243
Q

Products of rgp! and rgpB genes cleave:

A

arginine residues

244
Q

How do gingipains contribute to the virulence potential of P.g.?

A

By influencing bacterium-tissues binding, binding to a cognate receptor, or by exposing cryptitope receptors

245
Q

P.g. strains w high levels of this adhere better to epi cells:

A

typrsin-like protease activity

246
Q

Mature forms of Arg-gingipain A and Lys-gingipain posses:

A

a catalytic domain and 3 or 4 hemagglutinin/adhesion (HA) domains linked by noncovalent bonds

247
Q

HA domain sf:

A

hemagglutinin/adhesion domains

248
Q

Degree of homology shared bw HA domains of gingipain A and Lys-gingipain:

A

97%

249
Q

HA domains of gingipain A and Lys-gingipain are implicated in:

A

adherence of P.g. to gingival epi cells

250
Q

Physiological roles of gingipains:

A

expression of virulence factors, stability and/or processing of extracellular and cell-surface proteins

251
Q

Proteases of P.g. may play a role in:

A

host destructive events,

252
Q

How does P.g. adhere to and invade epi cells?

A

targeting specific host receptors, modulating host signalling events and deregulating the host cytokine network

253
Q

P.g and epi interactions lead to:

A

activation of several cascades that regulate transcription of genes that encode effectors and regulators of the immune response

254
Q

These are upregulated by P.g.-epi interactions:

A

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
Q

Members of the red complex:

A

p.g. T.f., T.d.

256
Q

T.f.:

A

Gram-, anearobic, fusiform, unique growth req’s

257
Q

Growth req’s of T.f.:

A

hemin, menadione, L-cysteine, and N-acetylneuraminic acid

258
Q

T.f., fastidious or not?

A

fastidious

259
Q

T.f. often isolated form acute or chronic perio pts?

A

chronic, active

260
Q

PDD that progresses posttherapy:

A

refractory, aggressive form

261
Q

Refractory PDD is assoc ith this organism:

A

T.f.

262
Q

T.f. was freq assoc with ___ colonization and elevated in older pts:

A

P.g.

263
Q

Detection of T.f. is assoc w:

A

early periodontiits

264
Q

TF? T.f. is a risk factor for periodontitis.

A

T

265
Q

Presence of T.f. is assoc with:

A

smokers, positive for aspartate aminotransferase activity, or interleukin-1 genotype (PST test)

266
Q

Test to determine if pt is interleukin-1 genotype:

A

PST test

267
Q

TF? PDD is assoc w lowered resistance to infection.

A

T

268
Q

T.f. is assoc w:

A

viral diseases, HIV, diabetes, Papillon-Lefevre syndrome

269
Q

The robust enzymatic repertoire of T.f. is related to its:

A

asaccharolytic physiology

270
Q

T.f. produces an enzymatic peptidase activity that degrades:

A

benzoyl-DL arginine-naphthylamide (BANA)

271
Q

BANA sf:

A

benzoyl-DL arginine-naphthylamide

272
Q

BANA activity is related to:

A

sites of perio destruction

273
Q

This, produced by T.f. activates gingival fibroblasts to produce elevated levels of IL-6 and TNF-a

A

lipoproteins (BfLP)

274
Q

Fxn of IL-6:

A

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
Q

This is made by T.f. and is thought to be involved in host-cel virulence:

A

sialidase and a trypsin like enzyme

276
Q

TF? T.f. can induce apoptosis.

A

T, could be part of progression of periodontitis

277
Q

What may prevent T.f. and P.g from being destroyed by PMNs?

A

apototic-inducing activity –> elimination of host immune or preimmune cells –> bacterial colonization –> rapid progression of disease

Oral Sciences (16 decks)

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