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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
Q

T/F - CD8 CELLS ARE CYTOTOXIC.

A

SO DANG TRUE SON

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26
Q

CD4 binds what class?

A

MHC II

*Helper cells

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27
Q

HIV affects which T cell?

A

CD4

*Decreases its number and causes an early death

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28
Q

What removes NK cells?

A

CD4

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29
Q

T/F - Necrotizing ulcerative periodontitis (NUP), Necrotizing ulcerative gingivitis (NUG), and HIV-associated periodontitis (HIV-P) all describe the same thing.

A

TRUE

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30
Q

What are clinical features of NUP, NUG, and HIV-P?

A

Pain and spontaneous bleeding

Necrosis and cratering

Edema and intense erythema

Extremely rapid bone loss

31
Q

What are cytokines?

A

Low molecular weight proteins that mediate interactions b/t lymphocytes, inflammatory cells, and other cells

32
Q

T/F - Cytokines are referred to as interleukins.

33
Q

T/F - Cytokines may be pleiomorphic (Have different biological activities from different cells), AND different cytokines may elicit similar responses.

34
Q

What is a good mnemonic for the interleukins 1-5?

A

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
Q

Tell me about IL-1 (alpha and beta).

A

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
Q

Tell me about IL-2 (alpha and beta - T-cell growth factor).

A

General immune responses

  • Stimulates macrophages*
  • Secreted by CD4 and NK cells*

Increases during periodontitis

37
Q

Tell me about IL-3.

A

Increases growth/differentiation’s of hematopoietic cells

Stims mast cell growth and histamine secretion

Secreted by activated CD4 and NK cells

38
Q

Tell me about IL-4 (B cell growth factor).

A

B cell activation, proliferation, and differentiation

T cell growth

Secreted by CD4

Increases in periodontitis

39
Q

Tell me about IL-5.

A

Induces B cell proliferation

ENHANCES IgA PRODUCTION

Secreted by CD4 cells

*NOT is periodontal disease

40
Q

Tell me about IL-6.

A

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
Q

Tell me about IL-7.

A

NOT IMPORTANT

T cell proliferation

Secreted by bone marrow stromal cells

42
Q

Tell me about IL-8.

A

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
Q

Tell me about IL-9.

A

Induces proliferation of CD4 in absence of antigen/antigen presenting cells

Promotes growth of mast cells

SECRETED BY CD4 cells

44
Q

Tell me about IL-10.

A

Inhibits the antigen presenting capacity of monocytes

SECRETED BY CD4

45
Q

What are IFNs?

A

Interferons (Alpha, beta, gamma)

46
Q

Tell me about IFNs.

A

Glycoproteins produced by leukocytes, fibroblasts, and T cells

ANTIVIRAL ACTIVITY

Bone resorption - Increases osteoclastic activity

47
Q

TNF-alpha does what?

A

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
Q

Tell me about TNF-beta.

A

Cytotoxic to fibroblasts

Plaque antigens favor generation of TNF-beta cells and lead to tissue damage in periodontal disease

49
Q

What are 5 characteristics of gingivitis?

A

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
Q

Tell me 5 mediators of the proinflammatory/destructive periodontitis.

A

IL-1-beta

TNF-alpha (Tumor necrosis factor-alpha)

Interferon-gamma (IFN-gamma)

Prostaglandin E2 (PGE2)

Matrix metalloproteinases (MMPs)

51
Q

Tell me 5 mediators of the anti-inflammatory/protective periodontitis (Healthy state).

A

Transforming growth factor-beta (TGF-beta)

IL-1 receptor antagonist

IL-10

IL-4

Tissue inhibitors of matrix metalloproteinases (TIMPs)

52
Q

What signaling molecules are high in disease?

A

IL-1beta

TNF-alpha

INF-gamma

PGE2

MMPs

53
Q

What signaling molecules are high in health?

A

IL-4

IL-10

TGF-beta

IL-1 ra

TIMPs

54
Q

IL-4 is special, why?

A

It is found in health, or at least a less diseased state

Indicator that a site is becoming healthy

55
Q

What are MMPs?

A

Primary proteinases involved in periodontal tissue degradation

56
Q

What do MMPs do?

A

Degrade extracellular matrix molecules (collagen, gelatin, elastin)

Tissue destruction and attachment loss

57
Q

What molecules inhibit MMPs?

A

TIMPs

Arrestin - Tetracycline and low dose doxycycline inhibit MMP activity
—Changes pH and affects growth

58
Q

What is in the GCF in periodontal disease?

A

Enzymes

IgX’s

Cytokines

Alkaline phosphatases

Beta-glucuronidase

IgG4

IL-1-beta

Elastase

PGE2

59
Q

T/F - Inflamed periodontal tissues possess high levels of PGE2 capable of inducing gingival inflammation and bone resorption.

60
Q

What is PGE2?

A

Breakdown product of arachidonic acid

**Very biologically active in low levels - in vitro and in vivo

61
Q

What are 3 activities of arachadonic acid metabolites?

A

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
Q

What are 3 markers for disease activities that arachondonic acid metabolites?

A

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
Q

What are some txs of periodontitis with drugs that inhibit prostaglandin synthesis block bone loss?

A

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
Q

T/F - Data show that the GCF-PGE2 levels are substantially higher in high risk pts.

A

TRUE

  • Refractory pts
  • Early onset periodontitis
  • Diabetic pts
65
Q

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.

66
Q

What are the 2 models that exist for hyperresponsiveness?

A

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
Q

What are PGE2s?

A

Prostaglandins

-Proinflammatory
—Edema
—Fever
—Pain

68
Q

What are 4 factors for systemic modifications of periodontal disease status?

A

Host stress

Physical stress

Social effectors

Environmental stress

69
Q

T/F - NONcopers are the ones that get periodontal disease.

70
Q

Host stress is mediated by what?

A

CNS neuropeptides

-Corticotropin releasing factor (CRF)

71
Q

What does CRF do?

A

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
Q

IL-2, PGE2, TNF-alpha are what?

A

Inflammatory mediators

73
Q

If PMNs are handcuffed by host activities, what is more prevalent?

A

Periodontal disease

74
Q

Once we get past PMN clearance, as in the infection overwhelms it, then what happens?

A

Disease goes systemic and lymphocyte activity increases

Perio - Exam 2 (8 decks)

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