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Periodontics I > The inflammatory periodontal lesion #2 > Flashcards

The inflammatory periodontal lesion #2 Flashcards

1
Q
  • plaque-induced
  • inflammation (edema + BOP)
  • No destruction of PDL & bone
  • No apical migration of epithelial attachment
A

Gingivitis

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2
Q

Epithelial attachment =

A

junctional epithelium

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3
Q
  • plaque-induced
  • inflammation (edema + BOP)
  • destruction of bone
  • apical migration of epithelial attachment
A

Periodontitis

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4
Q

What do we mean when we say “periodontitis is host-related”?

A

susceptibility of host plays a role in progression of gingivitis to periodontitis

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5
Q

What model of disease progression states that “continuous through out life at same rate of loss” i.e. everyone gets perio disease:

A

continuous model

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6
Q

What model of disease progression states “progressive loss overtime of some sites; no destruction in others; time of onset and extent vary among sites”

A

Progressive model

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7
Q

saying “periodontal disease affects mainly posterior teeth” would align with:

A

progresive model

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8
Q

What model of disease progression states “activity occurs at random at any site; some sites show no activity; some sites have one or more bursts of activity; cumulative extent of destruction varies among sites

A

Random burst model

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9
Q

Saying “periodontitis is different in various sites in the same individual and it is difficult to predict attachment loss” aligns with:

A

random burst model

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10
Q

What model of disease progression states “several sites have one or more bursts of activity during one period of life; prolonged period of inactivity = remission; cumulative extend of destruction varies among sites; some sites don’t develop attachment loss; bursts due to risk factors:

A

Asynchronous multiple burst model

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11
Q

What does asynchronous mean in the asynchronous multiple burst model?

A

not occurring at same time

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12
Q

Signs of inflammation:

A
  1. rubor (redness)
  2. calor (heat)
  3. dolor (pain)
  4. tumor (swelling)
  5. function laesa (loss of function)
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13
Q

Inflammation is a _____ phenomenon

A

vascular

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14
Q

Inflammation includes what two components?

A
  1. Vasculitis
  2. Leukocyte migration
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15
Q

Describe the components of vasculitis (3)

A
  1. dilation
  2. venous stasis (congestion)
  3. increased permeability
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16
Q

First defense = _____ immunity

A

innate

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17
Q

How does innate immunity work?

A

kills by phagocytosis

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18
Q

What cells are involved in innate immunity?

A
  1. PMNs
  2. Monocytes
  3. Macrophages
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19
Q

Describe innate immunity:

A

non-adaptive; genetic

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20
Q

Second defense = _____ immunity

A

adaptive

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21
Q

How does adaptive immunity work?

A

production of immunoglobulins by antibodies

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22
Q

What cells are involved in adaptive immunity?

A
  1. B-cells
  2. T- cells
  3. plasma cells
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23
Q

What are the plasma cells in adaptive immunity responsible for?

A

produce specific antibodies to individual antigens

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24
Q

Activated B-cells become:

A

plasma cells

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25
Q

Plasma cells produce:

A

immunoglobulins

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26
Q

T lymphocytes ar edeveloped in the:

A

thymus

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27
Q

List the functions of T-lymphocytes

A
  1. antigen presentation
  2. help b-cells divide
  3. destroy virally infected cells
  4. can down-regulate immune response
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28
Q

T-cells an differentiate into 2 major forms including:

A

Cd4 and Cd8 cells

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29
Q

MHC class II molecules =

A

CD4 cells (helper t-cells)

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30
Q

MHC class I molecules =

A

CD8 (cytotoxic T-cells)

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31
Q

List the roles of helper T-cells:

A
  1. help B cells
  2. control leukocyte development
  3. activate innate cell lining
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32
Q

List the roles of cytotoxic T cells:

A

destroy virally infected target cells

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33
Q

List cells that function in immunity: (4)

A
  1. PMNs
  2. Macrophages
  3. B- Cells
  4. T-cells
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34
Q

What immune cell is being described below?

  • phagocytosis
  • produce lysosomal enzymes
A

PMNs

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35
Q

What immune cell is being described below?

  • phagocytosis
  • process antigens
  • cytokine secretion
A

macrophages

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36
Q

What immune cell is being described below?

  • produce antibodies
A

B-cells (plasma cells)

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37
Q

What immune cell is being described below?

  • Helps b-cells divide
A

Helper T cells (CD4)

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38
Q

What immune cell is being described below?

  • down-regulates T and B cells
A

Supressor T-cells (Cd8 & Cd25)

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39
Q

What immune cell is being described below?

  • Kills virally-infected cells
A

Natural Killer T cells (CD56)

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40
Q

What immune cell is being described below?

  • Destroys infected cells
A

Cytotoxic T- cells (Cd8)

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41
Q

What immune cell is being described below?

  • Kills infected cells
A

Killer T-cell (Cd28)

42
Q

What are the main two components of humoral immunity?

A
  1. antibodies
  2. complement
43
Q

Antibody that is the 1st responder and largest in size:

44
Q

Antibody that is the 2nd responder, most abundant, and can cross the placenta:

45
Q

Antibody that is found in saliva, and also a dimer:

46
Q

Antibody that is co-expressed with IgM and unsure of role:

47
Q

Antibody on mast cells & involved in allergic reactions:

48
Q

Part of both of the innate and adaptive immune systems; a biochemical cascade that helps clear pathogens by lysis, opsonization, blinding, and clearance of immune complexes:

A

Complement

49
Q

Portion of the immunoglobulin that is specific for antigen binding:

50
Q

Constant portion of the immunoglobulin:

51
Q

Antibody promotes phagocytosis:

A

opsonization

52
Q

Antibody prevents bacterial adherence:

A

neutralization

53
Q

Antibody activates complement enhancing opsonization and lysis

A

complement activation

54
Q

Also called t-regulatory cells that down-regulate T and B cells and prevent autoimmune disease:

A

T-supressor cells

55
Q

Mononuclear cells that kill cells sensitized with antibody (via Fc receptors):

A

Killer cells

56
Q

Kill virally infected and transformed target cells that have not been previously sensitized:

57
Q

Activation in connective tissue; will become macrophages:

58
Q

48 hr lifespan in the blood with migration to sites for phagocytosis:

A

Neutrophils

59
Q

Cause damage by exocytosis (e.g. histamine release)

A

Eosinophils

60
Q

Contain mediators of inflammation (histamine, prostaglandins, leukotrienes, and cytokines); involved in allergic reactions:

A

Mast cells

61
Q

Cells that are in some way functionally similar to mast cells:

62
Q

Soluble, locally active polypeptides; regulate cell growth, differentiation, & function; produced by cells of the immune system:

63
Q

Specific cytokines may have different biologic properties dependent on: (4)

A
  1. their concentration
  2. the cells that produce them
  3. the cells being attracted and acted upon
  4. presence and extent of ECM
64
Q

What cytokine is being described?

  • pro-inflammatory: stimulates osteoclasts, fibroblasts, & macrophages
65
Q

What cytokine is being described?

  • pro-inflammatory: stimulates T and B cells
66
Q

What cytokine is being described?

  • pro-inflammatory: attracts & activates PMNs
67
Q

What cytokine is being described?

  • pro-inflammatory: activates osteoclasts
68
Q

What cytokine is being described?

  • Vasodilation
  • Pyrogenic
  • Releases mediator from mast cells
  • Cell-mediated cytotoxicity
69
Q

What growth factor is being described below?

  • Stimulates epithelial cells & fibroblasts
70
Q

What growth factor is being described below?

  • stimulates fibroblasts
A

PDGF & FGF

71
Q

What growth factor is being described below?

  • stimulates epithelial cells
72
Q

Can we accurately predict which patients with gingivitis will develop periodontitis?

A

NO- but we can assess risk factors such as habits and systemic disorders

73
Q

List some mechanical (plaque retention) factors that modify the inflammatory response: (5)

A
  1. calculus
  2. caries
  3. defective restorations
  4. prosthesis
  5. tooth anatomical factors
74
Q

List some systemic factors that modify the inflammatory response: (4)

A
  1. Diabetes
    2 . Hormonal (puberty & pregnancy)
  2. HIV/AIDS
  3. Medications
75
Q

List some genetic factors that modify the inflammatory response: (2)

A
  1. Leukocyte Adhesion Deficiency (LAD)
  2. Hypophosphotasia
76
Q

The “initial lesion” develops in:

77
Q

With the initial lesion, cells of _____ are present

A

acute inflammation

78
Q

What is increased with the initial lesion?

79
Q

What starts to form with the initial lesion?

A

pseudopocket

80
Q

What are considered “cells of acute inflammation” that are present with the initial lesion?

81
Q

What are considered “cells of chronic inflammation”?

A

lymphocytes & with increased chronicity eventually plasma cells

82
Q

What are the two types of virulence factors that are released into the periodontal tissues following the deposition of plaque?

A
  1. stimulation of host defense systems
  2. degradation of host tissues
83
Q

When bacteria from the plaque utilize virulence factors that function to stimulate the host defense systems, what is occurring?

A
  • cells are stimulated to release cytokines and chemoattractant factors (IL-8)
  • inflammatory cells are signaled in
84
Q

When bacteria from the plaque utilize virulence factors that function to degrade host tissues they use enzymes such as:

A
  1. collagenase
  2. trypsin-like enzymes
  3. keratinase
  4. phospholipase A
85
Q

The following are clinical features of the ____.

  1. increased GCF flow
  2. sulcus increases from 0 to 3 mm by formation of a pseudopocket
  3. alveolar bone is normal on the radiograph
A

Initial lesion

86
Q

PMN diapedesis: _____ “slow” the PMNs and cause them to “roll”. Cytokines activate ______ on the endothelial cells for PMN attachment.

A

Selectins; ICAM receptors

87
Q

Put the following steps in order:

  • adherence
  • chemotaxis
  • phagocytosis
  • diapedesis
  • killing + digestion + aggregation
A
  1. diapedesis
  2. chemotaxis
  3. adherence
  4. phagocytosis
  5. killing + digestion + aggregation
88
Q

The “early lesion” appears within:

89
Q
  • Acute inflammation persists with the initial lesion
  • increased GCF
  • Pseudopocket formation
  • cells of chronic inflammation appear and then dominate
A

Early lesion

90
Q

Do cells of chronic inflammation appear with the early lesion?

91
Q

What shift in cells do we see with the initial to the early lesion?

A

Acute cells of inflammation (PMNs) to chronic cells of inflammation (T-cells)

92
Q

In an early lesion ____ loss continues and ____ activation begins

A

Collagen; MMPs

93
Q

How is collagen lost with the early lesion?

A

Microbial factors (LPS & antigens) stimulate the release of cytokines and ALSO activations and release of MMPs

94
Q

MMPs:

A

matrix metalloproteinases

95
Q

includes 28 metal-dependent endopeptidases (proteases) with activity against most, if not all, extracellular matrix macromolecules (used for normal tissue remodeling)

96
Q

Important sub-class of MMPs:

A

interstitial collagenases

97
Q

With the early lesion, collagen loss is up to:

98
Q

What causes collagen destruction in the early lesion?

A
  1. PMNs products
  2. cytokines
  3. MMPs

(so a combination of bacterial products and host’s defense system cause the destruction)

99
Q

In what type of lesion do we see proliferation of JE rete pegs and the T-cell lesion?

A

Early lesion

100
Q

Is there bone loss with the early lesion?

A

no (but we do have loss of collagen in the CT)

Periodontics I (18 decks)

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