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Periodontics I > Week 3 Immunology Lecture > Flashcards

Week 3 Immunology Lecture Flashcards

1
Q

describe gingivitis

A
  • plaque induced
  • inflammation (edema/BOP)
  • no destruction of PDL and bone
  • no apical migration of epithelial attachment
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2
Q

what epithelium is involved with epithelial attachment

A

junctional epithelium

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3
Q

describe periodontitis

A
  • plaque induced
  • inflammation (edema/BOP)
  • destruction of bone
  • apical migration of epithelial attachment
  • not all cases of gingivitis progress to periodontitis
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4
Q

periodontitis is:

A

-plaque induced
- host related - susceptible host
- each site is individualized or a specific environment
- a % of affected population experiences severe destruction

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5
Q

what are the models of disease progression

A
  • continuous model (1900s-1950s)
  • progressive model (1940s-1960s)
  • random burst model (1980s-2000s)
  • asynchronous multiple burst model (1980s-2000s)
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6
Q

describe the continuous model

A

continuous throughout life at same rate of loss
- everyone gets perio disease

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7
Q

describe the progressive model

A
  • progressive loss over time of some sites
  • no destruction in others
  • time of onset and extent vary among sites
  • periodontal disease affects mainly posterior teeth
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8
Q

describe the random burst model (1980s-2000s)

A
  • 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
  • periodontitis is different in various sites in the same individual and it is difficult to predict attachment loss
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9
Q

desribe the asynchronous multiple burst model

A
  • several sites have one or more bursts of activity during one period of life
  • prolonged period of inactivity; remission
  • cumulative extent of destruction varies among sites
  • some sites dont develop attachment loss
  • bursts due to risk factors
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10
Q

what are the signs of inflammation

A
  • rubor (redness)
  • calor (heat)
    -dolor (pain)
  • tumor (swelling)
  • functio laesa (loss of function)
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11
Q

inflammation is a ______ phenomenon

A

vascular

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12
Q

what happens in inflammation:

A

-vasculitis
- leukocyte migration

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13
Q

what happens in vasculitis

A
  • dilation
  • venous stasis (congestion)
  • increased permeability
  • transudate
  • exudate
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14
Q

what is the 1st defense in immunity

A
  • innate
  • non-adaptive, genetic
  • kills by phagocytosis
  • PMNs
  • monocytes/macrophages
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15
Q

what is the 2nd defense in immunity

A
  • adaptive
  • production of immunoglobulins by antibodies
  • highly specific
  • B and T cells involved
  • plasma cells produce specific antibodies to individual antigens
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16
Q

describe B lymphocytes

A
  • activated B cells become plasma cells
  • plasma cells produce immunoglobulins
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17
Q

describe T lymphocytes

A
  • developed in the thymus
  • several functions - antigen presentation
  • help B cells divide; can destroy virally infected cells; can down regulate immune response
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18
Q

what are the 2 major forms of T cells

A

CD4 and CD8

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19
Q

describe the CD4 cell and what is recognizes

A
  • recognizes MHC Class II molecules
  • T helper cells - TH0, TH1, TH2
  • help B cells divide
  • control leukocyte development
  • activate innate cell lining
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20
Q

describe the CD8 cell and what it recognizes

A
  • recognizes MHC Class I molecules
  • T cytotoxic
  • destroy virally infected target cells
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21
Q

what do PMNs do

A
  • phagocytosis
  • produce lysosomal enzymes
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22
Q

what do macrophages do

A
  • phagocytosis
  • process antigens
  • cytokine secretion
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23
Q

what is another name for B lymphocytes and what do they do

A
  • plasma cells
  • produce antibodies
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24
Q

what are the types of T lymphocytes and what do each do

A
  • T-helper (CD4): helps B cells divide
  • T-suppressor (CD8 and CD25): down regulates T and B cells
  • NK cell (natural killer cell and CD56): kills virally infected cells
  • T-cytotoxic cell (CD8): destroys infected cells
  • K (killer T cell and CD28): kills infected cells
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25
Q

what are the components of humoral immunity

A
  • antibodies
  • complement
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26
Q

describe IgM

A
  • first responder
  • largest in size
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27
Q

describe IgG

A
  • second responder
  • most abundant
  • crosses placenta
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28
Q

describe IgA

A

-salivary IgA
- a dimer

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29
Q

describe IgD

A
  • co-expressed with IgM
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30
Q

describe IgE

A
  • on mast cells
  • allergic reactions
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31
Q

what immune system is the complement system a part of

A

innate and adaptive

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32
Q

what is the complement system and what does it do

A

a biochemical cascade that helps clear pathogens by lysis, opsonization, binding, clearance of immune complexes

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33
Q

what does the Fab region of immunoglobulins do

A

specific antigen binding

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34
Q

what is the Fc portion of the immunoglobulin

A

constant portion

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35
Q

what are t-suppressor cells

A
  • now t-regulatory cells
  • down- regulate T and B cells
  • CD8 and CD25
  • prevent autoimmune disease
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36
Q

what are K (killer) cells

A
  • mononuclear cells that kill cells sensitized with antibody via Fc receptors
  • CD28 cells which were signaled by CD8 cells
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37
Q

what are NK (natural killer cells)

A
  • kill virally infected and transformed target cells that have not been previously sensitized
  • CD56 cells
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38
Q

what percentage do monocytes make up and what do they do

A
  • 5%
  • activation in CT
  • will become macrophages
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39
Q

what percentage do neutrophils make up and what do they do

A
  • greater than 70%
  • 48 hours lifespan in blood with migration to sites for phagocytosis
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40
Q

what percentage do eosinophils make up and what do they do

A
  • 2-5%
  • cause damage by exocytosis
  • histamine release
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41
Q

what do mast cells do

A

contain mediators of inflammation such as histamine, prostaglandins, leukotrienes and cytokines
- involved in allergic reactions

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42
Q

what percentage do basophils make up and what do they do

A
  • less than 0.5%
  • functionally similar to mast cells
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43
Q

what are cytokines

A
  • soluble, locally active polypeptides
  • regulate cell growth, differentiation, function
  • produced by cells of the immune system
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44
Q

specific cytokines may have differnet biologic properties dependent on:

A
  • their concentration
  • the cells that produce them
  • the cells being attracted and acted upon
  • presence and extent of ECM
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45
Q

what does IL-1 do

A

-pro-inflammatory
- stimulates osteoclasts, fibroblasts, and macrophages

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46
Q

what does IL-6 do

A

pro-inflammatory
- stimulates T and B cells

47
Q

what does IL-8 do

A

pro-inflammatory
- attracts and activates PMNs

48
Q

what does TNF do

A
  • pro-inflammatory
  • activates osteoclasts
49
Q

what does PGE2 do

A
  • vasodilation
  • pyrogenic
  • releases mediator from mast cells
  • cell-mediated cytotoxicity
50
Q

what does TGF do

A

stimulates epithelial cells and fibroblasts

51
Q

what does PDGF do

A

stimulates fibroblasts

52
Q

what does EGF do

A

stimulates epithelial cells

53
Q

what does FGF do

A

stimulates fibroblasts

54
Q

what are risk factors for perio

A
  • smoking
  • HIV and DM
55
Q

patients with risk factors are more likely to have:

A

attachment loss

56
Q

what are the criteria for clinically healthy gingiva

A
  • some neutrophils and macrophages are present in CT
  • a few neutrophils are migrating through the JE
  • no collagen destruction
  • intact epithelial barrier
  • gingival crevicular fluid is present
  • appears clinically healthy in color, contour and consistency
57
Q

what are the mechanical inflamatory response modifiers that are plaque retention factors

A

-calculus
- caries
- restorations: defective margins, subgignival margins, overcontoured margins
- prosthesis
- tooth anatomical factors such as palatogingival grooves and furcations

58
Q

what are the systemic inflammatory response modifiers

A
  • uncontrolled/controlled diabetes
  • PMN defects
  • hematological
  • hormonal: pubery and pregnancy
  • immune disturbances
  • HIV/AIDS
  • medications
  • nutrition deficiencies
59
Q

what are the genetic inflammatory response modifiers

A
  • Leukocyte adhesion deficiency
  • hypophosphatasia
  • agranulocytosis
  • neutropenia
  • lazy leukocyte
  • downs syndrome
  • paipillon- lefevre
  • chediak-higashi
  • ehlers danlos
60
Q

describe the inital lesion

A
  • develops in 2-4 days
  • cells of acute inflammation present
  • increased GCF flow
  • start of pseudopocket formation
61
Q

what are the cells of acute infalmmation

A

PMNs

62
Q

what are the cells of chronic inflammation

A

lymphocytes

63
Q

what are the cells that appear when chronicity increases

A

plasma cells

64
Q

what are the 2 types of virulence factors

A
  • stimulation of the host defense systems
  • degradation of the host tissues
65
Q

describe the types of virulence factors that stimulate the host defense system

A
  • stimulates cells to release cytokines and chemoattractant factors such as IL-8
  • attracts inflammatory cells
66
Q

what are the enzymes that are virulence factors that degrade the host tissues

A
  • collagenase
  • trypsin like enzymes
  • keratinase
  • phospholipase A
67
Q

what is released in the bacterial to host interaction

A
  • increased release of IL-1
  • increased release of IL-6
  • increased release of IL-8
  • increased release of TNF
  • increased release of PGE
68
Q

what is the mechanism of action in poor plaque control

A
  • bacterial byproducts are released into perio tissues called virulence factors
  • stimulation of epithelial cells and fibroblasts to release IL-8 into the CT which attracts and activates PMNs
  • PMNs are present in the CT
  • PMNs are attracted to and near JE and sulcular epithelium
69
Q

what is the mechanism of action in plaque accumulation

A
  • virulence factors are relased into perio tissues
  • stimulation of inflammatory celsl to release cytokines into the CT
  • PMNs are attracted near and to the JE and sulcular epithelium
70
Q

what are the clinical features of the initial lesion

A
  • increased GCF flow
  • sulcus increases from 0->3 mm by formation of a pseudopocket
  • alveolar bone is normal on the radiograph
71
Q

what slows the PMNs in diapedesis and cause them to roll

A

selectins

72
Q

what do cytokines activate on endothelial cells for PMN attachment in diapedesis

A

ICAM receptors

73
Q

describe the early lesion

A
  • 4-7 days
  • acute inflammation persists -> increased GCF, pseudopocket formation
  • cells of chronic inflammation appear and then dominate
  • chronic -> shift to T lymph from PMNs
  • collagen loss continues
  • MMPs activation begins
74
Q

how is collagen lost

A
  • microbial factors: LPS and antigens
  • stimulate release of cytokines
  • activation and release of MMPs
  • a combination of bacterial products and host’s defense system
75
Q

what are MMPs

A

a family that includes 28 metal dependent endopeptidases (proteases) with activity against most if not all ECM macromolecules used for normal tissue remodeling

76
Q

what are the subclasses of MMPs

A
  • interstitial collagenases
  • stromelysins
  • membrane type
  • gelatinases
  • secreted RXKR
  • metalloelastase
77
Q

in the early lesion collagen lost is up to:

A

70%

78
Q

what is the early lesion histopathology

A
  • collagen loss
  • PMNs accumulation in gingiva and sulcus
  • cells of chronic inflammation accumulate and predominate : t-cell lesion
  • fibroblasts show cell damage
  • rete pegs proliferation of JE into CT
  • no bone loss
79
Q

what are the clinical features of the early lesion

A
  • edema of gingiva
  • increased GCF flow
  • loss of gingival stippling
  • erythema of gingival margin
  • no migration of JE attachment
  • alveolar bone is normal- no bone loss
  • reversible
80
Q

what are the host defenses in the established lesion

A
  • inhibit dramatic plaque growth thus it
  • prevents infection becoming dramatically worse
  • stand off exists, since plaque unable to be eliminated and there is a
  • shift to a B-cell/plasma cell lesion
81
Q

describe the established lesion

A
  • acute inflammation persists
  • PMN wall: host tries to contain the infection
  • bystander damage
  • two- edged sword of immune system
82
Q

how long does acute inflammation persist in the established lesion

A

2-3 weeks early lesion shifts to established lesion - a stable lesion

83
Q

describe the PMN wall in the established lesion

A
  • micro ulcerations of pocket epithelium
  • more proliferation of JE
  • more elongation of epithelial rete pegs into CT
84
Q

describe the established lesion disease activity

A
  • two processes: damage and repair
  • shift to activated B cell-plasma cell lesion
  • highly vascular
  • immature CT
85
Q

what are the types of damage done in the established lesion disease activity

A

bacterial and immunological

86
Q

what are the effects on ground substance in established lesion

A
  • bacterial enzymes produce proteases and hyaluronidase
  • fibroblasts, macrophages, PMNs produce gelatinase, stromelysin
87
Q

what are the mechanisms that cause the loss of collagen in the established lesion

A
  • decreased rate of synthesis
  • increased rate of breakdown
88
Q

describe connective tissue repair in the established lesion

A
  • attempt to minimize tissue damage
  • fibroblasts are cytokine-regulated and synthesize ECM
  • recruitment of new cells- cytokine regulated, chemotactic collagen and elastin fragments
  • tissue inhibitors of metalloproteases- the shut off mechanissm
89
Q

is there bone loss in the established lesion

A

no

90
Q

what is the histopathology of the established lesion

A
  • cellular damage of fibroblasts, epithelium
  • collagen loss increases
  • micro ulcerations of pocket epithelium
  • persistance of acute inflammation
  • marked numbers of PMNs in pocket
  • degradation of ECM
  • dense T-cell, B-cell and plasma cell infiltrate
  • JE proliferation and extension into CT
  • elongation of rete peg ridges
91
Q

what are the clinical features of the established lesion

A
  • edema
  • erythema
  • BOP
  • gingival changes: color, contour, consistency
  • no bone loss
92
Q

the _____ is the final stage of “pure” gingivitis

A

established lesion

93
Q

the established lesion can remain stable for:

A

weeks, months or even years before it progresses to periodontitis

94
Q

what are the features of periodontal breakdown in the advanced lesion

A
  • pocket formation
  • asynchronour multiple burst model
  • bystander damage
  • host balance of damage/repair is upset
95
Q

what is happening in pocket formation in the advanced lesion

A
  • PDL destruction
  • apical migration of JE
  • bone resorption
96
Q

what is the periodontitis definition

A
  • pocket formation results from apical migration of JE
  • loss of fiber attachment - cementum and PDL
  • loss of bone
97
Q

what is happening in alveolar bone resorption in the advanced lesion

A
  • activation of osteoclasts
  • ruffled border produced- active site
  • hydrolytic enzymes released
  • cytokines released
  • prostaglandins produced
  • leukotrienes produced
98
Q

what are leukotrienes

A

inflammatory mediators and involved in allergic reactions

99
Q

what is the mechanism of bone loss in advanced lesion

A
  • microbial factors:LPS
  • activates inflammatory cells to release IL-1 and PGE2
  • activates PMNs to release collagenase (MMP-8)
  • collagen loss
  • activates osteoclasts to release collagenase for bone (MMP-13)
100
Q

what is the histopathology of the advanced lesion

A
  • PMNs
  • B cells, plasma cells dominate
  • inflammatory infiltrate
  • extension of lesion into PDL and bone
  • loss of collagen continues
  • cytopathologically altered plasma cells
  • progressive pocket formation- attachment loss
  • quiescence and exacerbation
101
Q

what are the clinical features of advanced lesion

A
  • periodontal pocket formation
  • pocket epithelium ulceration
  • radiographic bone loss
  • BOP
  • changes in gingival color, contour, and consistency
  • attachment loss
  • mobility
102
Q

what percentage of volume/density of bone needs to be lost before detection on radiograph

A

50%

103
Q

what are the immune cells in the initial lesion

A

PMNs and macrophages

104
Q

what are the immune cells in the early lesion

A
  • PMNs
  • macrophages
  • T-lymphocytes
105
Q

what are the immune cells in the established lesion

A
  • PMNs
  • macrophages
  • T-lymphocytes
  • B-lymphocytes
  • plasma cells
106
Q

what are the immune cells in the advanced lesion

A
  • PMNs
  • macrophages
  • T-lymphocytes
  • B-lymphocytes
  • plasma cells
107
Q

what is the tx for gingivitis

A

reversible
- suppression of microflora for plaque-induced gingivitis through scaling, polishing and patients daily removal of plaque

108
Q

what is the tx for periodontitis

A
  • irreversible
  • suppression of microflora through SRP, surgery and maintenance
  • modulation of host with low dose doxycyline- collagenase inhibitor
109
Q

what is necessary and sufficient to intitiate gingivitis

A

plaque

110
Q

is plaque necessary and sufficient to initiate peridontitis

A

necessary but not sufficient

111
Q

primary etiology of periodontal disease is:

A

bacterial plaque in a susceptible host

112
Q

immune system provides a defensive process but also may account for most of _______ observed in gingivitis and periodontitis

A

tissue injury

113
Q
A

Periodontics I (13 decks)

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