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
Q

what do TLRs do for immuntiy

A

recognize MAMPs and signal cells to make cytokines, chemokines, antimicrobial peptides, NO and eicosanoids
responds to ox LDL

26
Q

in chronic periodontitis, describe the relative amount of plasma cells to Blymphocytes to T lymphocytes

A

plasma cells > B lymphocytes > T lymphocytes

27
Q

Th1 cytokines involved in chronic periodontitis

A

IL-2, IFN gamma, TNF alpha

28
Q

Th2 cytokines involved in chronic periodontits

A

IL-4, 5, 6, 10, 13

29
Q

t/f. in chronic periodontitis, IgG2

A

true. IgG2 is predominant in aggressive periodontitis annd recognizes LPS

30
Q

t/f. Th2>Th1 in chronic periodontitis

A

true. plasma cells are the most predominant and active secretory cells in advanced periodontitis

31
Q

an advanced periodontitis lesion is characteristic of what stage in periodontitis

A

4

32
Q

what happens in advanced periodontits

A

plasma cells dominat the ct, PMNs dominate the JE, apical migration of the JE = attachment loss