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AU 15- Periodontology > Host Response to Periodontal Bacteria > Flashcards

Host Response to Periodontal Bacteria Flashcards

1
Q

What are the four major microbial virulence factors?

A
  1. Ability to invade periodontal epithelium
  2. Damaging bacterial enzymes
  3. Immunostimulatory molecules
  4. Direct cytotoxic effects of bacterial metabolic waste products.
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2
Q

Which bacterial species are known to be good invaders of the periodontal epithelium?

A

A.a

P.g

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3
Q

_______ are Arg-Specific Proteases that are associated with P.gingivalis.

A

Gingipains

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4
Q

_____ from gram negative bacteria and ______ from gram positive bacteria are immunostimulatory molecules (virulence factors).

A

LPS

Lipoteichoic Acids

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5
Q

Which immunostimulatory molecule is produced by bacteria and stimulates leukocyte chemotaxis?

A

Formylpeptides

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6
Q

What are three mechanisms of periodontal defense against pathogenic bacteria?

A
  1. Prevention of bacterial entry (Passive protection)
  2. Innate Immune Response (non-specific, first line)
  3. Acquired/Adaptive Immune Response (specific, second-line, antibody)
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7
Q

Shedding of _______ into the oral cavity inhibits bacterial colonization of mucosa (passive protection).

A

epithelial cells

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8
Q

How does “positive fluid flow” act as a passive protective mechanism of periodontal defense?

A

GCF starts in the capillaries of the connective tissue and flows through the junctional epithelium in order to clear the pocket/gingival crevice. This countercurrent discourages bacterial adherence

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9
Q

Gingival crevicular fluid originates as ________ fluid.

A

gingival tissue interstitial

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10
Q

Inflammation is associated with increased _______.

A

Permeability (leakage of proteins through gaps)

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11
Q

Epithelial cells are attached by _______ that will lose their integrity in the case of inflammation.

A

tight junctions

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12
Q

Which line of defense includes the complement system, defensins, and cytokines?

A

Innate Immunity (first line of defense)

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13
Q

What are defensins?

A

anti-microbial peptides

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14
Q

_____ and _____ are universal signals of infection that help recruit inflammatory cells.

A

IL-8

TNF-alpha

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15
Q

Which cytokine is responsible for attracting neutrophils in the early stages of infection?

A

IL-8

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16
Q

________ function of neutrophils (PMNs) and macrophages is part of the innate response.

A

Phagocytic

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17
Q

What is the purpose of the complement system?

A

C3a and C5a molecules act to recruit phagocytes, opsonize bacteria, activate mast cells, and eventually lyse bacterial cells more quickly.

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18
Q

Ag recognition, immune memory, and clonal expansion are hallmarks of ________ immunity.

A

adaptive (specific)

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19
Q

True or False: The flow rate of crevicular fluid is greater than that of saliva.

A

False. Saliva is much greater.

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20
Q

How does innate immunity play a major role in defense of the oral cavity?

A

By clearing bacteria before they colonize and by

releasing antimicrobial peptides and histamines

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21
Q

_______ play a major role in induction of the innate immune response.

A

TLRs

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22
Q

True or False: TLRs are expressed by all cells; including epithelial cells, PMNs, monocytes, and macrophages.

A

True

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23
Q

What is the action of TLRs?

A

They signal for cells to produce cytokines, chemokines, antimicrobial peptides, nitric oxide, and eicosanoids. Major role in induction of the innate immune response.

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24
Q

LPS is a gram_____ bacterial virulence factor that activates _______.

A

negative

the complement system, PMNs, macrophages, and B-cell mitogen activity

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25
Q

True or False: LPS (endotoxin) stimulates bone resorption and prostaglandin synthesis.

A

True

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26
Q

______ induces Tumor Necrosis Factor Alpha.

A

LPS

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27
Q

Within the complement system, the classic pathway is activated by _______ and the alternate pathway is activated by _______.

A

bacterial antibody

contact with a bacterial cell wall

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28
Q

What is the end result of complement activation?

A

Enhanced swelling (inflammation)
Opsonization of bacteria/Phagocytosis
Formation of the attack complex/Lysis

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29
Q

Which cells will produce cytokines (3)?

A

Macrophages
Bone cells
Fibroblasts

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30
Q

Which two important cytokines are pro-inflammatory?

A

IL-1 and TNF-alpha

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31
Q

Which cytokine is primarily responsible for chemotactic activity?

A

IL-8

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32
Q

_______ are mediators of innate immunity.

A

Prostaglandins

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33
Q

From what are prostaglandins derived?

A

metabolism of arachidonic acid

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34
Q

Prostaglandins induce _______ and cytokine production.

A

vasodilation

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35
Q

PGE2 is a prostaglandin that induces the production of matrix _________ by fibroblasts and osteoclasts which damages periodontal tissue.

A

metalloproteinases

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36
Q

Which cells produce matrix metalloproteinases?

A

fibroblasts

osteoclasts

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37
Q

True or False: Matrix metalloproteinase concentration is higher in inflammed gingiva than in healthy ginigiva.

A

True

38
Q

Which matrix metalloproteinase is responsible for degrading the major structural protein in gingiva?

A

PMN collagenase

39
Q

Why would the host want to degrade its own collagen matrix via metalloproteinase?

A

to allow neutrophils to gain better and quicker access

40
Q

What is the action of proteinase inhibitors in innate immunity?

A

to antagonize inflammation by inhibiting degradation of matrix proteins; Alpha2 macroglobulin and Alpha1 antitrypsin

41
Q

Name two important antimicrobial peptides that mediate the innate response.

A

Defensins

Calprotectin

42
Q

______ are produced by salivary gland epithelial cells in order to inhibit bacteria and fungi.

A

Defensins

43
Q

_______ is produced by epithelial cells, PMNs, monocytes and macrophages to inhibit bacteria and fungi.

A

calprotectin

44
Q

How does calprotectin inhibit bacteria and fungi?

A

by chelating zinc

45
Q

_____ cells release vasoactive amines in order to change the permeability of capillaries. They are found in connective tissue around mucosal surfaces.

A

Mast

46
Q

PMNs are made in _______ and deployed from the blood to assist with innate immunity.

A

bone marrow

47
Q

Acute inflammation or injury ______ vascular permeability, resulting in redness, edema, and increased ________ flow.

A

increases

gingival crevicular fluid

48
Q

Cleavage products ____ and ____ of the complement system will activate mast cells and release histamine, Nitric Oxide, ____ and _____.

A

C3a
C5a
IL-1
TNF-alpha

49
Q

What will bacterial LPS stimulate? What is LPS?

A

Stimulation of macrophages

Lipopolysaccharide endotoxin present in bacteria

50
Q

What are the four mechanisms for antimicrobial release from PMNs in the early stages of infection?

A
  1. Secretion
  2. Respiratory burst (H2O2 causes dna damage)
  3. Phagocytosis (efficient; granule filled lysosome)
  4. Lysis or apoptosis (worse case scenario)
51
Q

Mechanisms of bacterial killing by PMNs can be either ______ or ______.

A

oxidative

non-oxidative

52
Q

What does elastase degrade?

A

extracellular matrix

53
Q

How is a chemotactic gradient established adjacent to the junctional epithelium?

A

Neutrophils leave post-capillary venules through gaps in the endothelial cells. They then travel through the connective tissue toward the junctional epithelium and crevice. Chemotactic molecules are highest near the JE.

54
Q

Which chemotactic molecules are most important in attracting PMNs?

A

LTB4, IL8, fmet-leu-phe, and C5a

55
Q

A leukocyte contacts, _____, _____, and then extravasates out of a blood vessel prior to reaching the site of inflammation.

A

rolls, sticks

56
Q

PMN extravasation involves ______molecules for adhesion and _______ molecules which bridge the gap between cells and extracellular matrix.

A

e-selectin

integrin

57
Q

PMNs release granules which contain what kind of mediators?

A

Microboidal enzymes, serine proteases, metalloproteases, and acid hydrolases

58
Q

In chronic periodontitis, is the number of plasma cells less than or greater than B lymphocytes?

A

Plasma cells > B lymphocytes

59
Q

In chronic periodontitis, is there a greater proportion of B or T lymphocytes?

A

more B than T

60
Q

In chronic periodontitis, which cell type makes up about 50% of the cells in the periodontal lesion?

A

plasma cells

61
Q

True or False: LPS, bacterial proteins, or other compounds can serve as an antigen.

A

True

62
Q

Macrophages and _______ cells function as Antigen Presenting Cells.

A

Langerhans

63
Q

How many glycoprotein chains does a T-cell receptor have? What are the types?

A

two

alpha and beta

64
Q

The alpha and beta glycoprotein chains have _______ that determine the type of immune response.

A

variable segments

65
Q

True or False: T-cell receptors are different between chronic and aggresive periodontitits.

A

True

66
Q

What are cytokines?

A

messenger proteins that transmit signals to other cells

67
Q

What do Th1 cytokines regulate?

A

cell mediated immunity (IL-2, IFN-gamma, TNF-alpha)

68
Q

What do Th2 cytokines regulate?

A

proliferation of B cells (IL-4,5,6,10,13)

69
Q

The balance between stable and progressive periodontitis rests on which cytokine?

A

IL-10

70
Q

High levels of IL-10 is associated with _____ progressive periodontitis.

A

less

71
Q

What do Tc Cells do when they recognize MHC class 1 bound to antigen?

A

they destroy the infected cell

72
Q

Are Tc Cells commonly found in periodontitis?

A

No, not many Tc Cells are found which suggests that viruses and invasive bacteria are not major players

73
Q

Humoral immunity is triggered in response to _______.

A

soluble antigens

74
Q

Ag-Ab complexes will activate ______ and facilitate ______.

A

complement

opsonization

75
Q

Th2 cytokines (IL4,5,6,10,13) activate B cells to ______.

A

plasma cells

76
Q

What are the two types of B cells?

A

conventional

autoreactive

77
Q

What are conventional B cells?

A

they produce antibodies against bactera; levels decrease in healthy and treated sites

78
Q

What are autoreactive B cells?

A

they produce auto-antibodies; levels do not decrease after treatment

79
Q

After a B cell is activated by an antigen, what are its three fates?

A
  1. becomes memory cells specific to that antigen
  2. secretes antibody to that antigen
  3. becomes plasma cells that will make antibody to that antigen
80
Q

What is avidity?

A

Ag-binding differs among antibody subclasses; not all are capable of effective opsonization or complement activation

81
Q

Which is more common in chronic periodontitis, IgG1 or IgG2?

A

IgG1

82
Q

Which is more common in aggressive periodontitis, IgG1 or IgG2?

A

IgG2

83
Q

Which is less effective, IgG1 or IgG2?

A

IgG2

84
Q

What is different about antigen recognition in IgG2 compared to other subclasses?

A

IgG2 recognizes carbohydrate antigens (LPS)

most others recognize protein antigen

85
Q

Periodontal microbe specific antibodies are produced by plasma cells within the _______ and travel back to the gingiva via blood vessels.

A

Lymph nodes

86
Q

Antibodies are produced locally by _____cells which are controlled by type ____ helper cells; cell-mediated immune activity is regulated by type____ helper cells.

A 
plasma
antibody (type 2)
cell-mediated (type1)
87
Q

_______ of relevant immune cells takes place within the periodontal lesion.

A

Homing

88
Q

______ cells are among the most predominant and active secretory cells in advanced periodontal lesions.

A

Plasma

89
Q

True or False: the ratio IgG subclasses are similar in serum and GCF.

A

True

90
Q

True or False: An individual’s ability to mount a specific Ab response to bacteria in the subgingival biofilm does not indicate a patient’s susceptibility to disease or ability to respond to treatment.

A

False

91
Q

_______ are essential polysaccharides and polynucleotides that differ little from one pathogen to another but are not found in the host.

A

PAMPS

AU 15- Periodontology (11 decks)

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