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Perio I Supplemental Cards > Pathogenesis > Flashcards

Pathogenesis Flashcards

1
Q

what are the 5 cardinal signs of inflammation?

A
  • redness (rubor)
  • swelling (tumor)
  • heat (calor)
  • pain (dolor)
  • loss of function (functio laesa)
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2
Q

describe the immune system

A
  • innate response
    • non-specific
  • acquired response
    • adaptive
    • specific
  • fundamentally different
  • both required for host immune competency
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3
Q

what are 5 components involved in plaque accumulation and initiation of gingivitis?

A
  • mast cells
  • acute phase proteins
  • complement
  • PMNs
  • antibodies
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4
Q

describe the inflammatory effects of tissue injury

A

release of chemical mediators that increase permeability of adjacent small blood vessels

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5
Q

describe the inflammatory effects of blood vessel dilation and increased permeability to plasma, which may clot

A
  • tissues swell due to plasma leakage
  • elevated temp from increased blood flow in dialated vessels
  • redness
  • pain from increased fluid in tissues and direct effect of chemicals on sensory nerve endings
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6
Q

describe the inflammatory effects when circulating WBC adhere to walls of altered blood vessels

A

WBC chemotaxis through vessel walls and to area of injury induce phagocytosis of foreign material and tissue debris and initiate Ab production

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7
Q

what cells release histamine? what is the inflammatory effect?

A
  • mast cells
  • dilation and increase of permeability of small blood vessels: constriction of bronchi
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8
Q

what cells release chemotactic factors? what is the inflammatory effect?

A
  • mast cells
  • eosinophil and PMN chemotaxis
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9
Q

what cells release interleukins 3, 4, 5, and 6? what is the inflammatory effect?

A
  • mast cells
  • many interactions
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10
Q

what cells release TNF alpha? what is the inflammatory effect?

A
  • mast cells
  • recruitement of granulocytes to area of inflammation; inducement of fever
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11
Q

what cells release leukotrienes? what is the inflammatory effect?

A
  • mast cells
  • dilation of small blood vessels; constriction of bronchi; chemotaxis of leukocytes
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12
Q

what cells release prostaglandins? what is the inflammatory effect?

A
  • mast cells
  • increase in vascular permeability; regulation of immune response
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13
Q

acute phase proteins (ACP) are a class of proteins whose plasma concentrations do what in response to inflammation?

A
  • positive ACPs will increase plasma concentraiton
  • negative ACPs will decrease plasma concentration
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14
Q

which ACP plasma proteins increase due to microbial infection? and which ones are associated with increased risk of heart disease?

A
  • CRP
  • fibrinogen
  • complement
  • mannose-binding protein
  • metal-binding proteins
  • alpha1-antitrypsin, alpha1-antichymotrypsin
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15
Q

what are 2 well established risk factors for cardiovascular disease?

A

tobacco smoking and high LDL

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16
Q

recent evidence has identified CRP as an important risk factor for MI. how much does CRP increase the risk?

A

2-5 fold increased risk

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17
Q

describe complement

A
  • activated by Ag - Ab interaction (IgG and IgM)
  • consists of at least 11 proteins and glycoproteins
  • 10% of proteins in normal sera
  • not affected by immunization
  • synthesized in liver, small intestine, F (?), and other mononuclear cells
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18
Q

name the 5 main leukocyte cell types and their relative percentages in the blood

A
  • granulocytes
    • PMNs - 55-65%
    • eosinophils - 2-4%
    • basophils - 0-1%
  • mononuclear phagocytes
    • monocytes - 3-8%
  • lymphocytes
    • several types - 25-35%
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19
Q

what is the typical life span of a PMN?

A
  • short half-life of 5-90 days
  • it is a terminal cell
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20
Q

what are some functions of PMNs?

A
  • phagocytosis
  • release of enzymes
  • release of chemical mediators
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21
Q

describe the movement of PMNs

A
  • leaves circulation to get to site of action by squeezing through walls of the blood vessel
  • steps:
    • sticks to endothelium (selectins, adhesins)
    • squeezes through endothelium (diapedesis)
    • chemotaxis (inflammatory mediators, bacteria)
    • kills bacteria by phagocytosis
    • dies
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22
Q

name 8 neutrophil chemoattractants and their sources

A
  1. leukotriene B4 - macrophage/monocytes
  2. IL-8 - macrophage/monocytes
  3. platelet activating factor - many cells
  4. C5a, C5 adesArg - serum/plasma
  5. f-Met peptides - bacteria
  6. neutrophil chemotactic factor - mast cells
  7. endothelial IL-8 - endothelium
  8. IL-1 - B cells, macrophages
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23
Q

describe PMN phagocytosis

A
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24
Q

describe PMN binding

A
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25
Q

describe the 3 types of PMN granules

A
  • azurophilic granules (primary granules)
    • myeloperoxidase, bactericidal/permeability-increasing protein (BPI), defensins, elastase, and cathepsin G
  • specific granules (secondary granules)
    • alkaline phosphatase, lysozyme, NADPH oxidase, collagenase, lactoferrin, and cathelicidin
  • tertiary granules
    • cathepsin and gelatinase
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26
Q

describe PMN respiratory burst

A
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27
Q

host risk factors can act as modifiers of disease expression of genetic/induced neutrophil defects like decreased killing and dysregulation. what are 4 of these risk factors?

A
  • leukocyte adhesion deficiency (LAD)
  • papillon lefevre syndrome
  • diabetes
  • smoking
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28
Q

what are epitopes?

A

antigenic determinants that sit on bacterial cells and allow antibodies to bind

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29
Q

what are 4 responses of antibodies?

A
  • local response
  • systemic response
  • monoclonal response
  • polyclonal response
30
Q

macrophages are ___ cells with a ___ half life

A
  • mobile
  • long
31
Q

describe macrophage phagocytosis

A
32
Q

describe LPS stimulation of macrophages

A
33
Q

describe macrophages as antigen presenting cells

A
34
Q

what it IL-1’s role in periodontal disease

A

it is associated with tissue breakdown

35
Q

___ and ___ are the 2 host based risk factors involved in monocyte dysregulation.

A

diabetes and smoking

36
Q

what are results of monocyte dysregulation?

A
  • increase inflammation
  • MMP expression
  • concomitant tissue destruction
37
Q

what are the ultimate fates of CD4 T cells and CD8 T cells?

A
  • CD4 T cells
    • memory cells
    • Th1 (causes macrophage activation)
    • Th2 (active in the antibody response)
  • CD8 T cells
    • memory cells
    • Tc cells (kill target cells directly)
38
Q

necrotizing ulcerative periodontitis (NUP), necrotizing ulcerative gingivitis (NUG), and HIV-associated periodontitis (HIV-P) all share what 4 clinical features?

A
  • pain and spontaneous bleeding
  • necrosis and cratering
  • edema and intense erythema
  • extremely rapid bone loss
39
Q

what are cytokines and inflammatory mediators?

A

low molecular weight proteins that mediate interactions among lymphocytes, inflammatory cells and other cellular elements in connective tissues

40
Q

today, most cytokines are referred to as ___

A

interleukins, but some still retain biologic activity name (ex. TNF, TGF, interferon, etc.)

41
Q

cytokines may be pleiomorphic. what does that mean?

A
  • they can elicit different biologic activities from different cells
  • different cytokines may elicit similar responses
42
Q

describe IL-1 alpha and beta

A
  • pleiomorphic
  • includes osteoclast (OAF) and lymphocyte (LAF) activities
  • CD4 activation
  • B-cell maturation
  • PMN and macrophage chemotaxis
  • increases NK cell activity, fibroblast procollagen, PGE2 and bone resporption
  • secreted by monocytes, macrophages, B-cells, fibroblasts, PMNs, epithelial cells, and other stimulated cells
  • found in gingival tissue, GCF
  • decreased after periodontal treatment
43
Q

describe IL-2 alpha and beta

A
  • general role in immune responses
  • stimulates macrophages
  • modulates and induces NK function and proliferation
  • secreted by CD4 and NK cells
  • increases in periodontal tissues in periodontitis
44
Q

describe IL-3

A
  • supports growth/differentiation of hematopoietic cells
  • stimulates mast cell growth and histamine secretion
  • secreted by activated CD4 and NK cells
45
Q

describe IL-4

A
  • B-cell activation, proliferation and differentiation
  • T-cell growth
  • macrophage function
  • growth of mast cells
  • secreted by CD4 cells
  • B-cell IgE synthesis
  • increases in periodontal tissues in periodontitis
46
Q

describe IL-5

A
  • induces B-cell proliferation
  • enhances IgA production
  • secreted by CD4 cells
47
Q

describe IL-6

A
  • stimulates plasma cell production
  • with IL-1 activates CD4 cells
  • secreted by CD4, macrophages, monocytes, fibroblasts and endothelial cells
  • increases in sites of gingival inflammation
  • role in bone resorption
48
Q

describe IL-7

A
  • induces T-cell proliferation by expressing IL-2 and IL-2 receptors
  • secreted by bone marrow stromal cells
49
Q

describe IL-8

A
  • chemotactic for PMNs
  • increases PMN adherence to endothelial cells
  • secreted by macrophages in response to IL-1, TNFalpha
  • present high levels in perio lesions associated with JE and macrophages
  • high in disease vs health
  • stimulates PMN MMP activity
50
Q

describe IL-9

A
  • induces proliferation if CD4 cells in absense of antigen/antigen presenting cell
  • promotes growth of mast cells
  • secreted by CD4 cells
51
Q

describe IL-10

A
  • inhibits the antigen presenting capacity of monocytes
  • secreted by CD4 cells
52
Q

describe IFNs (alpha, beta, and gamma)

A
  • glycoproteins produced by leukocytes, fibroblasts, t-lymphocytes respectively
  • antiviral activity
  • enhance macrophage activity (gamma), t-cell activity, NK-cell activity
  • plays a role in bone resorption, by inhibiting proliferation and differentiation of progenitors of osteoblasts
53
Q

describe TNF (alpha and beta)

A
  • produced by macrophages and CD4 cells, respectively
  • cause necrosis of some tumors
  • TNF alpha produced after stimulation of macrophages by LPS
  • TNF beta (lymphotoxin)
  • TNF alpha and beta can activate osteoclasts leading to bone resorption
  • alpha increases PMN adherence to endothelial cells
54
Q

describe TNFa (alpha and beta)

A
  • alpha increases PMN phagocytosis and chemotaxis
  • effect on PMN and macrophages play a role in vascular changes seen in period dx
  • TNF beta cytotoxic for fibroblasts
  • plaque antigens favor generation of TNF beta cells and/or direct lymphotoxicity leading to tissue damage seen in periodontal disease
55
Q

what are characteristics of established gingivitis?

A
  • microbial plaque that is better organized and more gram negative enters sulcus
  • small gingival pocket with pocket epithelium forms
  • more venules become activated; enhanced expression of IL-8, ICAM-1, E-selectin; enhanced PMN migration
  • enlarging infiltrate with B and T cells, plasma cells, macrophages
  • PMNs are prominent
56
Q

what are 5 proinflammatory/destructive mediators of events that occur in periodontitis?

A

these are high in disease, low in health

  • IL-1beta
  • TNFalpha
  • IFN-gamma
  • PGE2
  • MMPs
57
Q

what are 5 anti-inflammatory/protective mediators of events that occur in periodontitis?

A

these are high in health and low in disease

  • TGF-beta
  • IL-1 receptor antagonist
  • IL-10
  • IL-4
  • TIMPs
58
Q

what are MMPs?

A
  • matrix metaloproteinases
  • primary proteinases involved in periodontal tissue degradation
    • family of 17 metalloproteinases
    • degrade extracellular matrix molecules (collagen, gelatin, elastin)
    • good evidence participate in tissue destruction and AL
59
Q

what are inhibitors of MMPs?

A
  • chemically modified tetracycline and low-dose doxycycline
  • appear to be good candidates for inhibiting the destruction of periodontal structures
60
Q

what are components of crevicular fluid that contribute to the diagnosis of periodontal disease?

A
  • enzymes, immunoglobulins, inflammatory mediators, cytokines, cell/tissue degradation products
  • alkaline phosphatase, glucuronidase, IgG4, IL-1 beta, elastase, AAT, and PGE2
61
Q

what are arachidonic acid metabolites?

A
  • inflamed periodontal tissues posess high levels of PGE2 capable of inducing gingival inflammation and bone resorption
  • pathology seen in periodontal diseases can be theoretically attributable to PGE2, especially in the presence of IL-1 and TNFalpha
  • levels in the periodontal tissues are in the micromolar range
62
Q

in what 3 ways do arachidonic acid metabolites exhibit evidence for their role in periodontal disease?

A
  • activities
  • marker for disease activity
  • treatment of experimental periodontitis
63
Q

what are activities of arachidonic acid metabolites that provide evidence of its role in periodontal disease?

A
  • induces increased vasopermeability and vasodilation leading to redness and edema
  • potent inducer of MMP secretion by monocytes and fibroblasts to trigger connective tissue destruction
  • osteoclast bone resorption is triggered by a synergistic action with IL-1 and TNF alpha to enhance the effects of these molecules
64
Q

describe how arachidonic acid metabolites function as markers for periodontal disease activity

A
  • 2-3 fold increase in gingivitis and periodontal disease compared to health
  • 5-6 fold increase during periods of active disease progression based on longitudinal attachment loss
  • GCF-PGE2 levels increase prior to attachment level changes and can be used as a screening test to predict future attachment loss
65
Q

describe how treatment of experimental periodontitis provides evidence of the role of arachidonic acid metabolites in periodontal disease

A
  • treatment of experimental periodontitis with drugs that inhibit prostaglandin synthesis block bone loss (best evidence for AAM role)
  • non-steroidal anti-inflammatory drugs (NSAIDS) block PGE2 synthase (cyclooxygenase, COX, PGH synthase)
  • suppression of PGE2 synthesis with these drugs greatly diminishes attachment and bone loss limiting peridontal disease progression
  • compared to other host mediators, prostaglandin data indicate an association between disease activity and PGE levels in tissues and elimination of PGE2 with NSAID treatment leads to a concomitant diminution of disease progression
66
Q

arachidonic acid metabolites

recent data suggest that GCF-PGE2 levels are substantially higher in high risk patients, which include…?

A
  • refractory
  • early onset (EOP, IAP)
  • diabetic (IDDM)
67
Q

arachidonic acid metabolites

in patients who have refractory disease, early onset periodontitis, or diabetes, GCF-PGE2 levels are ___ in clinically healthy sites compared to patients with conventional periodontal disease or never diseased sites

A

higher

68
Q

arachidonic acid metabolites

data shows that elevated GCF-PGE2 levels in patients with refractory disease, early onset periodontits, or diabetes, is also associated with what?

A
  • a hyperresponsibe monocyte PGE2 trait systematically
  • this hypersecretory state leads to the concept of individual susceptibility to periodontal disease
69
Q

arachidonic acid metabolites

what are the 2 models for hyperresponsiveness?

A
  • chronic infection and LPS exposure might lead to systemic elevations of TNF alpha, IL-1beta, and GM-CSF, which are all capable of up-regulating monocyte PGE2 secretion
  • alternatively, there is extensive data which establish a genetic basis in the region of the HLA-DR region of chromosome 5 in the area of TNFbeta genes
70
Q

what are 4 systemic modifications of periodontal disease status?

A
  • host stress
  • physical stress
  • social effectors
  • environmental stress
71
Q

the effects of host stress are mediated by what?

A

central nervous system neuropeptides, like corticotropin releasing factor (CRF)

72
Q

how does CRF mediate host stress?

A
  • CRF depresses lymphocyte function leading to inhibition of antibody secretion
  • CRF impairs neutrophil phagocytic and killing function
  • CRF up-regulates the release of IL-1 and TNF alpha by monocytes
  • adrenohypophyseal axis (psychoneuroimmunology) ie increased inflammation

Perio I Supplemental Cards (7 decks)

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