immunology and pathogenesis Flashcards

1
Q

what causes periodontal disease

A

bacterial pathogens and the host immune response

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2
Q

t/f. acute inflammation causes vascular permeability

A

true. it then results in redness, edema, and increased GCF flow

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3
Q

bacterial species that invade periodontal soft tissue

A

P gingivalis and Aa

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4
Q

effects of bacterial metabolic waste products

A

ammonia, indole compounds, FA, hydrogen sulfide

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5
Q

damaging bacterial enzymes

A

leukotoxins (Aa) and gingipains (proteases from Pg)

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6
Q

immunostimulatory molecules

A

LPS (G-), lipoteichoic acid (G+), gingipains, formylpeptides (stim. leukocyte chemotaxis)

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7
Q

what does LPS do

A

complement activation, pmn activation, macrophage activation, B-cell mitogen activity, pyrogenicity, stim bone resorption, stim prostaglandin synthesis, induction of TNF-alpha

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8
Q

host defense of gingivitis

A

acute inflammation (also seen in an abscess)

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9
Q

host defense of periodontitis

A

chronic inflammation (also seen in Tb)

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10
Q

after Tx, there is typically an increase or decrease in protease levels?

A

decrease

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11
Q

what do proteinase inhibitors do and what are 2 examples

A

inhibit degradation of matrix proteins

alpha-2 macroglobulin, alpha-1 antitrypsin

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12
Q

what do MMPs do

A

degrade ECM (ex. PMN collagenase)

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13
Q

are there higher or lower concentrations of MMPs in inflamed gingiva

A

higher

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14
Q

what do IL-1beta and TNF-alpha do

A

proinflammatory cytokines that stimulate bone resorption and inhibit bone formation

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15
Q

what does IL-8 do

A

chemotactic activity

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16
Q

PGE2

A

prostaglandin that induces vasodilaiton and cytokine and MMP production

17
Q

t/f. pmns are only in GCF in disease states

A

false. health and disease

18
Q

primary and secondary granules found in periodontitis lesions

A

elastase - primary, lactoferrin - secondary

19
Q

osteoclast activating cytokines

A

IL-1beta, 6, 11, 17, PGE2, TNF-alpha

20
Q

RANKL:OPG ratio

A

RANKL (osteroclast activationg) higher and OPG (ostoblast activating) lower in periodontitis

21
Q

innate immunity defense in periodontitis

A

biofilm, gingival crevice, mechanical barrier

22
Q

acquired immunity

A

acute and chronic inflammatory process

23
Q

how does GCF provide innate immunity

A

carries antibodies, lactoferrin, lysozyme

24
Q

4 steps the innate immune sys takes to provide a defense mechanism

A

oral mucosa makes antimicrobial peptides
oral epithelium produce pro inflammatory cytokines (IL-1B and TNF-alpha, IL-8)
GCF flows to the site of injury
phagocytic function of PMNs and macrophages

25
what do TLRs do for immuntiy
recognize MAMPs and signal cells to make cytokines, chemokines, antimicrobial peptides, NO and eicosanoids responds to ox LDL
26
in chronic periodontitis, describe the relative amount of plasma cells to Blymphocytes to T lymphocytes
plasma cells > B lymphocytes > T lymphocytes
27
Th1 cytokines involved in chronic periodontitis
IL-2, IFN gamma, TNF alpha
28
Th2 cytokines involved in chronic periodontits
IL-4, 5, 6, 10, 13
29
t/f. in chronic periodontitis, IgG2
true. IgG2 is predominant in aggressive periodontitis annd recognizes LPS
30
t/f. Th2>Th1 in chronic periodontitis
true. plasma cells are the most predominant and active secretory cells in advanced periodontitis
31
an advanced periodontitis lesion is characteristic of what stage in periodontitis
4
32
what happens in advanced periodontits
plasma cells dominat the ct, PMNs dominate the JE, apical migration of the JE = attachment loss