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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
describe the 3 types of PMN granules
* 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
26
describe PMN respiratory burst
27
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?
* leukocyte adhesion deficiency (LAD) * papillon lefevre syndrome * diabetes * smoking
28
what are epitopes?
antigenic determinants that sit on bacterial cells and allow antibodies to bind
29
what are 4 responses of antibodies?
* local response * systemic response * monoclonal response * polyclonal response
30
macrophages are ___ cells with a ___ half life
* mobile * long
31
describe macrophage phagocytosis
32
describe LPS stimulation of macrophages
33
describe macrophages as antigen presenting cells
34
what it IL-1's role in periodontal disease
it is associated with tissue breakdown
35
\_\_\_ and ___ are the 2 host based risk factors involved in monocyte dysregulation.
diabetes and smoking
36
what are results of monocyte dysregulation?
* increase inflammation * MMP expression * concomitant tissue destruction
37
what are the ultimate fates of CD4 T cells and CD8 T cells?
* 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
necrotizing ulcerative periodontitis (NUP), necrotizing ulcerative gingivitis (NUG), and HIV-associated periodontitis (HIV-P) all share what 4 clinical features?
* pain and spontaneous bleeding * necrosis and cratering * edema and intense erythema * extremely rapid bone loss
39
what are cytokines and inflammatory mediators?
low molecular weight proteins that mediate interactions among lymphocytes, inflammatory cells and other cellular elements in connective tissues
40
today, most cytokines are referred to as \_\_\_
interleukins, but some still retain biologic activity name (ex. TNF, TGF, interferon, etc.)
41
cytokines may be pleiomorphic. what does that mean?
* they can elicit different biologic activities from different cells * different cytokines may elicit similar responses
42
describe IL-1 alpha and beta
* 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
describe IL-2 alpha and beta
* 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
describe IL-3
* supports growth/differentiation of hematopoietic cells * stimulates mast cell growth and histamine secretion * secreted by activated CD4 and NK cells
45
describe IL-4
* 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
describe IL-5
* induces B-cell proliferation * enhances IgA production * secreted by CD4 cells
47
describe IL-6
* 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
describe IL-7
* induces T-cell proliferation by expressing IL-2 and IL-2 receptors * secreted by bone marrow stromal cells
49
describe IL-8
* 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
describe IL-9
* induces proliferation if CD4 cells in absense of antigen/antigen presenting cell * promotes growth of mast cells * secreted by CD4 cells
51
describe IL-10
* inhibits the antigen presenting capacity of monocytes * secreted by CD4 cells
52
describe IFNs (alpha, beta, and gamma)
* 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
describe TNF (alpha and beta)
* 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
describe TNFa (alpha and beta)
* 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
what are characteristics of established gingivitis?
* 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
what are 5 proinflammatory/destructive mediators of events that occur in periodontitis?
these are high in disease, low in health * IL-1beta * TNFalpha * IFN-gamma * PGE2 * MMPs
57
what are 5 anti-inflammatory/protective mediators of events that occur in periodontitis?
these are high in health and low in disease * TGF-beta * IL-1 receptor antagonist * IL-10 * IL-4 * TIMPs
58
what are MMPs?
* 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
what are inhibitors of MMPs?
* chemically modified tetracycline and low-dose doxycycline * appear to be good candidates for inhibiting the destruction of periodontal structures
60
what are components of crevicular fluid that contribute to the diagnosis of periodontal disease?
* enzymes, immunoglobulins, inflammatory mediators, cytokines, cell/tissue degradation products * alkaline phosphatase, glucuronidase, IgG4, IL-1 beta, elastase, AAT, and PGE2
61
what are arachidonic acid metabolites?
* 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
in what 3 ways do arachidonic acid metabolites exhibit evidence for their role in periodontal disease?
* activities * marker for disease activity * treatment of experimental periodontitis
63
what are activities of arachidonic acid metabolites that provide evidence of its role in periodontal disease?
* 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
describe how arachidonic acid metabolites function as markers for periodontal disease activity
* 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
describe how treatment of experimental periodontitis provides evidence of the role of arachidonic acid metabolites in periodontal disease
* 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
arachidonic acid metabolites recent data suggest that GCF-PGE2 levels are substantially higher in high risk patients, which include...?
* refractory * early onset (EOP, IAP) * diabetic (IDDM)
67
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
higher
68
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 hyperresponsibe monocyte PGE2 trait systematically * this hypersecretory state leads to the concept of individual susceptibility to periodontal disease
69
arachidonic acid metabolites what are the 2 models for hyperresponsiveness?
* 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
what are 4 systemic modifications of periodontal disease status?
* host stress * physical stress * social effectors * environmental stress
71
the effects of host stress are mediated by what?
central nervous system neuropeptides, like corticotropin releasing factor (CRF)
72
how does CRF mediate host stress?
* 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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