Lecture 7 questions Flashcards

1
Q

what are 4 major microbial virulence factors

A

ability to invade periodontal epithelium (with A. a. and P.g.), direct cytotoxic effects of bacterial metabolic waste products, damaging bacterial enzymes, and immunostimulatoy molecules

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2
Q

what are examples of bacterial metabolic waste products?

A

ammonia, indole compounds, fatty acids, and hydrogen sulfide

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3
Q

what can damage bacterial enzymes?

A

leukotoxin from A. a. and ginigpains from P.g.

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4
Q

what are some immunostimulatory molecules?

A

LPS (endotoxin) from gram - bacteria, lipteichoic acids from gram + bacteria, gingipains, formypeptides, and other surface antigens

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5
Q

what are formylpeptides?

A

small tripeptides that have the ability to interact with receptors of phagocytic cells and induce chemotaxis

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6
Q

what are the 3 mechanism of periodontal disease>

A
  • prevention of bacterial entry (passive protection by periodontal epithelium), innate immune responses (nonspecific, first line of active defense), acquired (adaptive) immune responses (specific, second line of active defense…if the previous 2 don’t hold up against bacteria)
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7
Q

how do we prevent bacterial entry

A

shedding of epithelium cells into the oral cavity inhibits bacterial colonization of mucosa, keeping an intact epithelium barrier, and having positive fluid flow into the gingival crevice to clear the outer epithelium

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8
Q

what does gingival crevicular fluid originate as

A

gingival tissue interstitial fluid from capillaries in gingival CT

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9
Q

what is associated with increases capillary permeability

A

inflammation (clinically we can see edema increase in temp and redness)

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10
Q

what are the 5 innate immune response?

A

complement system, anti-microbial peptides from oral mucosa, pro-inflammatory cytokines in oral epithelium, antimicrobial effect of antibodies, and phagocytic function of neutrophils (PMNs) and macrophages

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11
Q

what is the complement system of innate immunity?

A

induces bacterial lysis in a nonspecific way, promotes chemotaxis (recruits neutrophils and macrophages), promotes opsonization of bacteria, and HELPS ACTIVATE MAST CELLS WHICH INCREASES VASCULAR PERMEABILITY, coats bacteria and makes it more apparent to macrophages and neutrophils (“makes it more tasty”)

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12
Q

which cytokines are universal signal of infection that help recruit inflammatory cells

A

IL-1b and TNF-a

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13
Q

which cytokine attracts neutrophils in the early stages of infection (chemotactic activity)

A

IL-8

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14
Q

what do prostaglandins do?

A
  • induce vasodilation and cytokine production

- PGE2 induces production of matrix metalloproteinases by fibroblasts and osteoclasts which damage perio tissues

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15
Q

what do matrix metalloproteinases do?

A

degrade ECM (eg. PMN collagenase degrades major structural protein in gingiva). CONCENTRATIONS ARE HIGHER IN INFLAMED GINGIVA THAN IN HEALTHY GINGIVA

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16
Q

what do proteinase inhibitors do?

A

antagonize inflammation, and inhibit degradation of matrix proteins (eg. Alpha-2 macro globulin: broad spectrum proteinase inhibitor, Alpha -1 antitrypsin: broad spectrum proteinase inhibitor and potent inhibitor of PMN collagenase)

17
Q

what are antimicrobial peptides

A
  • defensins are produced by salivary gland epithelium and inhibit bacterial and fungi
  • calprotectin are produced by epithelium, PMNs, monocytes, and macrophages, chelates zine and inhibits bacteria and fungi
18
Q

what is adaptive or acquired immunity

A

the seance line of defense, with specific responses to bacterial antigens. involves antigen recognition, immune memory, and clonal expansion

19
Q

which last longer, neutrophils, or monocytes and macrophages?

A

monocytes and macrophages

20
Q

if monocytes and macrophages don’t fix the problem, what’s next

A

lymphocytes come in and if the chronic inflammation is not resolved, then theres a standoff or systemic infection

21
Q

bacteria colonizes supra gingival and sub gingival environments, but only this environment is aerobic

A

supra gingival

22
Q

what do TLRs do?

A

can turn on cytokines and antimicrobial peptides, nitro oxide, and eicosanoids

23
Q

what do secretory IGAs do

A

protect bacteria from attaching to surface of mucosa

24
Q

what do Von Ebner’s proteins function as

A

antimicrobial peptides

25
Q

what does LPS (endotoxin) do

A

complement, PMN, and macrophage activation …b-cell mitogen activity, stimulation of bone resorption, and prostaglandin synthesis, and induction of TNF-a

26
Q

where do we find neutrophils (PMNs)?

A

deployed from the blood and into infection and inflammatory sites

27
Q

where are macrophages found

A

in organs and tissues

28
Q

where are mast cells found

A

throughout the body, especially in CT subjacent to mucosal surfaces