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Perio - Exam 2 > Pathogenesis - Lecture II > Flashcards

Pathogenesis - Lecture II Flashcards

1
Q

Tell me the critical pathway model of pathogenesis.

A

Normal flora->Pathogenic flora

If immune response (neutrophil clearance) occurs, then gingivitis and limited disease. If NOT, bacterial penetration.

Bacterial penetration

  • Can lead to systemic exposure
  • Or initial periodontitis

Monocyte/lymphocyte axis

Cytokines and inflammatory mediators

Inflammation and tissue destruction

Pocketing and bone loss

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2
Q

RER produces what?

A

Proteins and antibodies

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3
Q

Antibodies expressed on the surface of bacteria are called what?

A

Phenotype

PMNs recognize the Fc fragment

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4
Q

What is the most common antibody?

A

IgG - 80-85% of total serum immunoglobulin

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5
Q

Tell me about IgG.

A

Monomer

Attach to phagocytes
Complement fixation
-Opsonization
-Agglutination

*Can cross placenta

21 day half life

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6
Q

Tell me about IgM

A

Pentamer (Looks like 5 IgGs)

5-10% of serum immunoglobulin

10 day half life

Complement fixation

Can combat capsules

Agglutination, complement, leads to inflammation

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7
Q

Tell me about IgA.

A

Looks like a dimmer of IgG

10% of total serum

6 day half life

Secreted in saliva, milk, mucus, and other secretions

Protection of mucus membranes by preventing attachment of organisms

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8
Q

Tell me about IgD.

A

Looks like IgG

<1% of total serum

3 day half life

Antigen receptor on B lymphocytes

Facilitates development and maturation of the antibody response

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9
Q

Tell me about IgE.

A

Looks like a taller IgG.

<0.01% of total serum

2 day half life

Attaches to mast cells and basophils
-Antigen reacts with cell-bound IgE to release granules contents

Involved in many allergic reactions

*Helps expel parasites

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10
Q

What holds the long chains together?

A

Disulfide bonds

*Some bacteria release enzymes to break disulfide bonds

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11
Q

T/F - Light chains are highly variable, and the heavy chains are heavily conserved.

A

TRUE

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12
Q

T/F - The Fab region binds the antigen.

A

TRUE

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13
Q

B cells come from where?

A

Bone marrow

Also, nodes and bursae

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14
Q

How does the primary response differ from the secondary response?

A

Primary - High IgG and High-ish IgM

Secondary - 20x’s higher IgG and about the same about of IgM

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15
Q

What is an antibody response that is beneficial for bacteria?

A

Polyclonal response

  • Virulence factor for bacteria turns on a lot of antibodies
  • This creates a needle in the haystack situation
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16
Q

What are 3 beneficial antibody related responses for the host?

A

Local response

Systemic response

Monoclonal response

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17
Q

The macrophage comes from what stem cell, then what cell, then becomes a macrophage?

A

Myeloid stem cell

Monocyte

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18
Q

T/F - Macrophages are mobile and have LONG half-lives.

A

TRUE

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19
Q

T/F - LPS stimulates macrophages.

A

TRUE

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20
Q

Macrophages, dendritic cells, and plasma cells all express MHC class _____.

A

II

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21
Q

IL-1 produced by __________ plays an important role in tissue ___________ associated with periodontal disease.

A

Macrophages

Breakdown

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22
Q

Most people are what type of genotype?

A

Genotype positive - Hypersensitive

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23
Q

What host based risk factors cause monocyte dysregulation?

A

Diabetes

Smoking

*Increase inflammation, MMP expression, and concomitant tissue destruction

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24
Q

CD8 binds what MHC?

A

MHC I

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25
T/F - CD8 CELLS ARE CYTOTOXIC.
SO DANG TRUE SON
26
CD4 binds what class?
MHC II *Helper cells
27
HIV affects which T cell?
CD4 *Decreases its number and causes an early death
28
What removes NK cells?
CD4
29
T/F - Necrotizing ulcerative periodontitis (NUP), Necrotizing ulcerative gingivitis (NUG), and HIV-associated periodontitis (HIV-P) all describe the same thing.
TRUE
30
What are clinical features of NUP, NUG, and HIV-P?
Pain and spontaneous bleeding Necrosis and cratering Edema and intense erythema Extremely rapid bone loss
31
What are cytokines?
Low molecular weight proteins that mediate interactions b/t lymphocytes, inflammatory cells, and other cells
32
T/F - Cytokines are referred to as interleukins.
TRUE
33
T/F - Cytokines may be pleiomorphic (Have different biological activities from different cells), AND different cytokines may elicit similar responses.
TRUE
34
What is a good mnemonic for the interleukins 1-5?
Hot T Bone stEAk IL-1 - HOT —Fever IL-2 - T —T cells produced and activated IL-3 - Bone marrow —Stimulates bone marrow to make more cells IL-4 - E —IgG into IgE production and B cell development IL-5 - A —IgA production and eosinophils
35
Tell me about IL-1 (alpha and beta).
Osteoclast activity CD4 activation B cell maturation *PMN and macrophage chemotaxis* NK cell activity *Secreted by monocytes, macrophages, B cells, fibroblasts, PMNs* Found in GCF *Decreases after perio treatment
36
Tell me about IL-2 (alpha and beta - T-cell growth factor).
General immune responses * Stimulates macrophages* * Secreted by CD4 and NK cells* Increases during periodontitis
37
Tell me about IL-3.
Increases growth/differentiation’s of hematopoietic cells Stims mast cell growth and histamine secretion *Secreted by activated CD4 and NK cells*
38
Tell me about IL-4 (B cell growth factor).
B cell activation, proliferation, and differentiation T cell growth Secreted by CD4 Increases in periodontitis
39
Tell me about IL-5.
Induces B cell proliferation ENHANCES IgA PRODUCTION Secreted by CD4 cells *NOT is periodontal disease
40
Tell me about IL-6.
Stims plasma cell production *Along with IL-1, it activates CD4 cells* Secreted by CD4, macrophages, monocytes, and fibroblasts Increases during gingival inflammation Has a role in bone resorption
41
Tell me about IL-7.
NOT IMPORTANT T cell proliferation Secreted by bone marrow stromal cells
42
Tell me about IL-8.
Stims ICAMS and ECAMS and PMN and MMP activity Increases PMN adherence to endothelial cells *Secreted by macrophages* —*In response to IL-1 and TNF-alpha* High in perio lesions with JE and macrophages HIGH IN DISEASE
43
Tell me about IL-9.
Induces proliferation of CD4 in absence of antigen/antigen presenting cells Promotes growth of mast cells SECRETED BY CD4 cells
44
Tell me about IL-10.
Inhibits the antigen presenting capacity of monocytes SECRETED BY CD4
45
What are IFNs?
Interferons (Alpha, beta, gamma)
46
Tell me about IFNs.
Glycoproteins produced by leukocytes, fibroblasts, and T cells **ANTIVIRAL ACTIVITY** Bone resorption - Increases osteoclastic activity
47
TNF-alpha does what?
STIMS ENDOTHELIAL RESPONSE Produced by macrophages and CD 4 cells Necrosis of some tumors PRODUCED AFTER STIMULATION OF MACROPHAGES BY LPS Can activate osteoclasts ALPHA INCREASES PMN ADHERENCE TO ENDOTHELIAL CELLS Increases PMN phagocytosis and chemotaxis
48
Tell me about TNF-beta.
Cytotoxic to fibroblasts Plaque antigens favor generation of TNF-beta cells and lead to tissue damage in periodontal disease
49
What are 5 characteristics of gingivitis?
More G- enters sulcus Pocketing Venules activated -Expression of IL-8, ICAM-1, E-selectin Infiltration with B and T cells, plasma cells, and macrophages *PMNs prominent*
50
Tell me 5 mediators of the proinflammatory/destructive periodontitis.
IL-1-beta TNF-alpha (Tumor necrosis factor-alpha) Interferon-gamma (IFN-gamma) Prostaglandin E2 (PGE2) Matrix metalloproteinases (MMPs)
51
Tell me 5 mediators of the anti-inflammatory/protective periodontitis (Healthy state).
Transforming growth factor-beta (TGF-beta) IL-1 receptor antagonist IL-10 IL-4 Tissue inhibitors of matrix metalloproteinases (TIMPs)
52
What signaling molecules are high in disease?
IL-1beta TNF-alpha INF-gamma PGE2 MMPs
53
What signaling molecules are high in health?
IL-4 IL-10 TGF-beta IL-1 ra TIMPs
54
IL-4 is special, why?
It is found in health, or at least a less diseased state *Indicator that a site is becoming healthy*
55
What are MMPs?
Primary proteinases involved in periodontal tissue degradation
56
What do MMPs do?
Degrade extracellular matrix molecules (collagen, gelatin, elastin) Tissue destruction and attachment loss
57
What molecules inhibit MMPs?
TIMPs Arrestin - Tetracycline and low dose doxycycline inhibit MMP activity —Changes pH and affects growth
58
What is in the GCF in periodontal disease?
Enzymes IgX’s Cytokines Alkaline phosphatases Beta-glucuronidase IgG4 IL-1-beta Elastase PGE2
59
T/F - Inflamed periodontal tissues possess high levels of PGE2 capable of inducing gingival inflammation and bone resorption.
TRUE
60
What is PGE2?
Breakdown product of arachidonic acid **Very biologically active in low levels - in vitro and in vivo
61
What are 3 activities of arachadonic acid metabolites?
Induces increased vasopermeability Inducer of MMP secretion by monocytes and fibroblasts to trigger CT destruction Osteoclasts activity synergistically auctioned with IL-1 and TNF-alpha to enhance the effects of these molecules
62
What are 3 markers for disease activities that arachondonic acid metabolites?
2-3 fold increase in periodontal disease 5-6 fold increase during periods of active disease progression GCF-PGE2 levels increase prior to attachment level changes can predict future attachment loss
63
What are some txs of periodontitis with drugs that inhibit prostaglandin synthesis block bone loss?
NSAIDs block PGE2 synthase Suppression of PGE2 synthesis w/ these drugs greatly diminishes attach;ment and bone loss *There is an association b/t disease activity and PGE levels in tissues and elimination of PGE2 with NSAID treatment leads to concomitant diminution of disease progression
64
T/F - Data show that the GCF-PGE2 levels are substantially higher in high risk pts.
TRUE - Refractory pts - Early onset periodontitis - Diabetic pts
65
T/F - GCF-PGE2 at healthy sites w/in these special groups are HIGHER than in clinically healthy sites from pts w/ conventional periodontal disease or never diseased sites.
TRUE
66
What are the 2 models that exist for hyperresponsiveness?
Infection and LPS exposure can lead to systemic elevations of TNF-alpha, IL-1beta, and GM-CSF which are all capable of up-regging PGE2 secretion Genetic basis on chromosome 5
67
What are PGE2s?
Prostaglandins -Proinflammatory —Edema —Fever —Pain
68
What are 4 factors for systemic modifications of periodontal disease status?
Host stress Physical stress Social effectors Environmental stress
69
T/F - NONcopers are the ones that get periodontal disease.
TRUE
70
Host stress is mediated by what?
CNS neuropeptides | -Corticotropin releasing factor (CRF)
71
What does CRF do?
Depresses lymphocyte fx leading to inhibition of antibody secretion Impairs PMN killing fx Up-regs release of IL-1 and TNF-alpha by monocytes Increased inflammation
72
IL-2, PGE2, TNF-alpha are what?
Inflammatory mediators
73
If PMNs are handcuffed by host activities, what is more prevalent?
Periodontal disease
74
Once we get past PMN clearance, as in the infection overwhelms it, then what happens?
Disease goes systemic and lymphocyte activity increases

Perio - Exam 2 (8 decks)

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