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Periodontics I > The inflammatory Periodontal Lesion > Flashcards

The inflammatory Periodontal Lesion 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 by saying periodontitis is host-related?

A

Susceptibility of host plays role in progression of gingivitis to periodontitis

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5
Q

What model of disease progression states that “continuous throughout 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 over time 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

progressive 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 burst 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 burst of activity during one period of life; prolonged period of inactivity = remission; cumulative extent 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. functio 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 responsible for in adaptive immunity?

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 are developed in the:

A

thymus

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27
Q

List the functions of T-lymphoctyes:

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 can differentiate into two major forms including:

A
  1. CD4
  2. CD8
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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 cells (cytotoxic T cells)

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31
Q

List the roles of helper T cells:

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

List the roles of cytotoxic T cells:

A
  1. 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-regulated T & B cells

A

Suppressor 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 two main components of humoral immunity?

A
  1. antibodies
  2. complement
43
Q

Antibody that is the first responder & largest in size:

44
Q

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

45
Q

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

46
Q

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

47
Q

Antibody on mast cells & involved in allergic reactions:

48
Q

Part of both the innate & adaptive immune systems; a biochemical cascade that helps clear pathogens by lysis, opsonization, binding 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 & lysis:

A

Complement activation

54
Q

Also called T regulatory cells that function to down-regulate T & B cells and prevent autoimmune disease:

A

T suppressor 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 hour 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 reaction:

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 & acted upon
  4. presence & 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 & 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 or 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 factors (plaque retention factors) that modify the inflammatory response: (5)

A
  1. calculus
  2. caries
  3. restorations (defective)
  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)
  3. HIV/AIDS
  4. Medications
75
Q

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

A
  1. Leukocyte Adhesion Deficiency (LAD)
  2. Hypophosphatasia
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 within the initial lesion?

81
Q

What are considered “cells of chronic inflammation”?

A

Lymphocytes & with increased chronicity we eventually see 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. degredation 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 3mm 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 persist with the initial lesion
  • Increased GCF
  • Pseudopocket formation
  • Cells of chronic inflammation appear & then dominate
A

Early lesion

90
Q

Do cells of chronic inflammation appear with the early lesion?

91
Q

What shift of cells do we see with the initial lesion 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 release of cytokines and ALSO activation 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 & host’s defense system)

99
Q

In what type of lesion do we see proliferation of JE rete pegs & 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)

Periodontics I (17 decks)

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