host responses to periodontal bacteria Flashcards

1
Q

where does bacteria attach and colonize to induce damge to perio tissues

A

in the gingival crevice and some invade perio soft tissue

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2
Q

how can a bacteria cause perio damage

A
  • Release substance to directly damage host cells

- Activate host’s own inflammatory and immune systems leading to host tissue damage (most damage)

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3
Q

what are the major microbial virulence factors

A

Ability to invade epithelium
Direct cytoxic effects of bacterial metabolic waste
Damaging bacterial enzyes
Immunostimulatory molecules

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4
Q

what are the bacterial metabolic wastes that can damge periodontal tissue

A

Ammonia
Indole compounds
Fatty acids (propionic and butyric acids)
HS

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5
Q

what bacterial enzymes can damage periodontal tissue

A

Leukotoxin

Gingipains

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6
Q

what are the immunostimulatory molecules

A
LPS from gram negative
Lipoteichoic acids from gram positive
Gingivapins
Formylpeptides
Other surface antigens
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7
Q

what is the action of leukotoxin

A

Kills neutrophils and macrophages (phagocytic cells)

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8
Q

what doe Gingipains do

A

Degrade many proteins

- interleukins

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9
Q

what is the action of formylpeptides

A

Interact with phagocytic cells to induce chemotoxis

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10
Q

what is the passive protection of the periodontium

A

PRevention of bacterial entry via periodontal eptihlium

- shedding of outer layer

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11
Q

what is the first line of active defense of the periodontum

A

Innate/nonspecific immune system

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12
Q

what is the second line of active defense

A

Acquired (adaptive) immune response - specific

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13
Q

what stops bacteria from entering in the first place

A

Shedding of epithelial cells into the oral cavity
intact epithelial barrier
Possitive fluid flow into the gingival crevis

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14
Q

what epithlium is crutial for stopping bacterial entry

A

Junctional epithelium

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15
Q

what is the roll of connective tissue in preventing bacterial entry

A

Lots of vessels to flow and flush out bacterium

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16
Q

what does gignival crevicular fluid originate as

A

Gingival tissue interstitial fluid

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17
Q

what happens to the vessels of the periodontum connective tissue with inflammation

A

dilation leads to opening a vessels and leaking

  • plasma and compliments leave
    • adema and redness
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18
Q

what is included in the innate immune repsonse

A

Complement system
Oral mucosa production of anti-microbial peptides
Oral epithelium produced pro-inflammatory cytokines
Antimicrobial effects of antibodies, lactoferrin, lysozyme
Phagocytic function of neutrophils and macrophages

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19
Q

what does the complement system lead to

A

Induces bacterial lysis
promote phagocyte recruitment (chemotaxis)
promote phagocytic by opsonization of bacterial
Activates mast cells, increasing

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20
Q

what are universal signs of infection

A

Il-1Beta and TNF-alpha

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21
Q

what do IL-1 beta and TNF-alpha do

A

Recruit inflammatory cells

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22
Q

what does Il-8 do

A

attract neutrophils in early stage of infections

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23
Q

what does adaptive immunity respond to

A

BActerial Ag

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24
Q

what are the halmarks of adaptive immunity

A

Ag recognition
Immune memory
Clonal expansion

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25
Q

do antimicrobial compounds only kill bacteria

A

No, kill fungi too

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26
Q

what is the host defense hierarchy

A

Serum complement
Neutrophils (acute inglammation)
Monocyte/macrophages (chronic inflammation)
Lymphocytes (systemic)

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27
Q

where in the mouth can bacteria colonize

A

Supra and subgingival environments

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28
Q

what are the supragingival environments that bacteria can colonize

A
Tongue
Oral mucosa
Tonsils
Saliva
Supragingival plaque
Others
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29
Q

what are the subgingival environments that bacteria can colonize

A

Periodontal soft tisse
Dentinal tubules
Furcations
Subgingival calculus

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30
Q

how long does it take for neutrophils to begin fighting bacteria

A

1/2 hours

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31
Q

what are monocytesand macrophages life length and location

A

Long life cels that are preposisioned in tissue

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32
Q

what are the actions of monocytes and macrophages

A

phagocytize and make biochem mediators

present antigens to the acquired immune response on MHC for the lymphocyte

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33
Q

what kind of bacteria tend to be subgingival

A

anaerobic

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34
Q

what kind of bacteria tend to supragingival

A

anaerobic

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35
Q

what is the roll of SecA in saliva

A

Prevents bacteria attachment

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36
Q

what is the roll of histatins

A

antimicrobial peptide

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37
Q

what covers the oral mucosa

A

mucous coat

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38
Q

what is the action of mucins and agglutinin

A

cause bacteria to clump together and fall out of solution

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39
Q

what response do toll-like receptors work in

A

Induce the innate immune response

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40
Q

what do toll-like receptors recognize

A

Conserved microbial-associated molecular patterns (LPS, lipoteichoic acid and flagellae)

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41
Q

what cells express Toll-like receptors

A

all cells including:

  • epithelial cells
  • PMNs
  • monocytes
  • macrophages
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42
Q

what do TLR’s signal for cells to do

A

Produce cytokines, chemokines, antimicrobial peptides, NO and eicosanoids

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43
Q

what happens what your immne system senses LPS

A
Complement activation
Macrophages secrete cytokines
lymphocytes devide
B cell mitogen activity
Bone resorbs
secretion of proteoglycans and TNF-alpha
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44
Q

what is the Classical pathway for the complement system

A

uses antibodies to sense

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45
Q

what is the alternative pathway for the complement system

A

uses bacterial celll wals

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46
Q

what does complement system eventually lead to

A

Cleavage of PR to give progenerators with specific activites

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47
Q

what do the proteins of the complement system do

A

direct lysis of bacteria
inflammation
Phagocytosis

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48
Q

what does opsonition of C3b do

A

leads to phagocytosis by macrophages

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49
Q

what are the rolls of C3a and C5a in the complement system

A

Chemotactic: attract neutrophils

  • mast cell degranulation
  • vascular permiability
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50
Q

what do cytokines do

A

Coordiation of Inflammatory and immune response

- coordinate reaction to bacteria

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51
Q

what cytokines are pro-inflammatory

A

Il-1beta

TNF-alpha

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52
Q

what cytokine is has chemotactic activity

A

IL-8

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53
Q

what do prostaglandins do

A

Induce vasodilation and cytokine production

54
Q

what prostaglandin is a proinflamitory cytokin

A

PGE2

55
Q

what is the roll of PGE2

A

induces production of matrix metaloproteinases by fibroblasts and osteoclas

56
Q

what do metalloproteinases do

A

Degrade the ECM (may damage tissue)

57
Q

what matrix metalloproteinase degrades the major structural protein in gingiva

A

PMN colagenase

58
Q

how does the concentratio of matrix metalloproteinase change over time

A

High in inflamed gingiva than helahty gingiva

59
Q

what do Proteinase inhibitors do

A

Antagonize inflammation

inhibit degradation of matrix proteins

60
Q

what is alpha-2 macroglobulin

A

Broad spectrum proteinase inhibitor

61
Q

what is alpha-1 antitrypsin

A

Broad spectrum proteinase inhibitor

inhibitor of PMN collagenase

62
Q

what are definis

A

inhibit bacteria and fungi

63
Q

what produces densins

A

Salivary gland epithelium

64
Q

what des calprotein do

A

Inhibit bacteria dn fungi by chelating zinc

65
Q

what produces calprotectin

A

Produced by epithelium, PMNs, monocytes, and macrophages

66
Q

where do neutrophils come from

A

Depoyed from the blood

67
Q

where are macrophages found

A

found in organs and tissues

68
Q

where are mast cells found

A

Throughout the body

- esp connective tissue subjacent to mucosal surfaces

69
Q

what do neutrophiles look like

A

Mutli-lobed

70
Q

how long do neutrophils circulate

A

1 day

71
Q

what does acute inflammation or injury does

A

increases vascular permeability
redness
edema
increased gingival crevicular fluid flow

72
Q

what are the cleavage products of compliment proteins

A

C5a, C3a

IL-1, TNF

73
Q

what does C5a and C3a do

A

acitvates mast cells to release Histomine, NO, interleukin and TNF

74
Q

what are the action of IL-1, TNF

A

activates endo cells for adhesion reception to immobilize cells

75
Q

what is the most numerous innate immune response

A

PMN’s

76
Q

what do PMN’s contain to fight infection

A

Contain granules b/f going to the periphery

77
Q

what are oxidative mechanisms by PMNs used to kill bacteria

A

USes ROS to form an oxidative complex

78
Q

would PMNs create HOCl or H2O2

A

Prefer HOCl because it is better at killing microbes and damages host less

79
Q

how does PMNs kill stuff

A

Surrounds bacteria and creates a phagosome

- pours granules, glycolysis to decrease pH

80
Q

what is the innate immunity

A

The inherent biological responses

81
Q

what is adaptive/acquired immunity related to

A

Based on recognition of antigens, immune memory and clonal expansion

82
Q

how does cell populations change in chronic periodontitis

A

Plasma cells(50%)> B lymphocytes > T lymphocytes

83
Q

what kind of immunity are plasma cells a part of

A

Acquired immunity

84
Q

what kind of immunity are neutrophils and macrophages part of

A

Innate

85
Q

what do antigen presenting cells do

A

digest and present antigens to T helper cells

86
Q

what do antigen presenting cells present antigens with

A

with MHC class II

87
Q

what part of immunity are T helper cells part of

A

acquired immunity

88
Q

what do Th1 Cells help to fight

A
cancer
intercellular infections( Virus and bacteria)
89
Q

what do Th1 cells activate

A

Cytotoxic C cells

also can kinda activate B lymphocytes

90
Q

what immunity are Th2 cells assocaited with

A

humeral immunity

91
Q

what do Th2 cells do to fiht periodontal bacteria

A

release antibodies

activate B lymphocytes to make antibodies

92
Q

what is the action of IL-10 released by Th2 cells

A

force B lymphocytes to mature to plasma cells

93
Q

what can serve as an antigen

A

LPS
bacterial proteins
other bacterial compounds

94
Q

what can act as a antigen presenting cell

A

Macrophages

Langerhan cells

95
Q

what do plasma cells do

A

create lots of antibodies

96
Q

what is the action of B1 lymphocytes

A

Autoimmune dissorders to attack self

97
Q

what is the action of B2 lymphocytes

A

Fight pathogens

98
Q

what does the veriability of T cells give

A

Different types of immune resposnes

99
Q

what is the important of Il-10 in immune responses

A

Balance between th1 and th2

100
Q

what is the T-cell receptor made of

A

2 glycoprotein chains (Alpha and beta) with variable segnments

101
Q

what do the variable segments of the T cell receptor do

A

Types of immune reponse

102
Q

what happens to the TCR before and after therapy

A

changes before and after therapy

103
Q

is TCR the same betwen chronic and aggressive perio

A

No, different

104
Q

how are the twupes of T helper cells different

A

HAVE differnet cytokine progiles

105
Q

what does Th1 secrete as a cytokine

A

Il-1
IFN-gama
TNF-alpha

106
Q

what does Th2 secerete asa cytokine

A

Il-2, 5, 6, 10, 13

107
Q

what all does IL-10 do to balance Th1 and Th2

A

slows down responses
inhibit macrophages
tells macrophages to make antibodies

108
Q

is lots of IL-10 a stable, or unstable system

A

Stable

109
Q

what activates Cytotoxic T cells

A

cytokines

110
Q

what do Cytotoxic T cell respond to

A

Intracellular pathogens

111
Q

what do antigens from intracellular pathogens bind to on cytotoxic t Cells

A

MHC 1 molecules

112
Q

what happens when Cytotoxic T cells recognize an antigen presented via MHC1

A

destroy the infected

113
Q

are there a lot of Cytotoxic T cells in periodontitis

A

No, because viruses and invasive bacteria are not really there

114
Q

what triggerst humoral immunity

A

In response to soluble antigens

115
Q

what activates complementation

A

Ag-Ab complex

116
Q

what facilitates opsonization

A

Ag-Ab complex

117
Q

what causes B cells to change to plasma cells

A

Th-2 cytokines

118
Q

how do Convenstional B cels chang in helathy’treated sites

A

Decrease in helathy and treated sites

119
Q

how do Autoreactive B cells change in healthy and treated sites

A

do not decrease after treatment

120
Q

what does the complement system eventually form

A

Membrane attack complexes

121
Q

what can antigbodies alone do

A
Block entery of toxins and viruses (IgM, IgG, IgA)
Immobilized bacteria (IgM>IgG)
Agglutinates bacteria (IgM> IgG)
122
Q

what can antibodies plus complements do

A

Lyse bacteria

123
Q

what can antibodies plus cells do

A

Opsonize bacteria, fungi for phagocytosis (IgG)

Activates extracellular killing (IgG)

124
Q

what is avidity

A

Ag-bidning differs among antibody subclasses

125
Q

are all antibodies capable of effective opsonization or complement activation

A

No

126
Q

is there more IgG2 or IgG1 in chronic periodontis

A

More IgG1

127
Q

is there more IgG2 os IgG1 in agggressive periodontitis

A

more IgG2

128
Q

what type of antigen does IgG2 recognize

A

carbohydrate antigens (LPS)

129
Q

what do most subclassesof antibodies recognize

A

Protein antigen

130
Q

what is the systemic humoral response to plaque antigens

A
  1. antigens diffuse through junctional eptiehlium
  2. langerhan cells process antigen
  3. Antigen presenting cells (macrophages and langerhan cells) go to lymphocyes
  4. antigen presenting cells reach lymph nodes to stimulte lymphocytes
  5. perio microbe specific antibodies produced by plasma cells in lymph nodes and travel to gingiva via the blood
  6. antibodies leave circulation to go to the crevice
  7. antibody acts on microbes
131
Q

how does the local cellular immune response to plaque antigens in the gingival crevice act

A
  1. peridontically specific B cells and T cell proliferate within the lymph and blood streem
  2. perio specific lymphocytes home back to the periodontium to begin cell mediated immune function
  3. antibodies produced locally by plasma are controlled by Th2 cells. Cell mediated immunity mediated by TH1