Immunology Flashcards

1
Q

What are THREE roles commensal bacteria play in periodontal defence?

A
  • Competitive barrier (nutrients, ecological niche)
  • Physical barrier
  • Immunological barrier (constant sampling “state of perpetual excitement” and tolerance to commensals)
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2
Q

What’s so bad about High Endothelial-like Venules (HEVs)?

A

They are lumpy vessels that produce turbulent flow to allow WBCs to transmigrate through endothelium into site. The angiogenesis of HEVs may explain greater inflammation at sites of periodontitis.

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3
Q

What are THREE bacterial virulence factors that may trigger an immune response in gingivitis/periodontitis?

A
  • LPS
  • Lipotechoic acid
  • Proteases (e.g. MMP, gingipains)
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4
Q

What do adhesion molecules have to do with perio pathogenesis?

A

They allow for greater transmigration of WBCs -> increased inflammation

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5
Q

What are FOUR cells of the periodontium and their roles in perio pathogenesis?

A
  • Gingival epithelial cells (sampling, tolerance, cytokine prodn, physical barrier)
  • Fibroblasts (cytokine prodn)
  • Monocytes (IL-6/8 prodn, precursor for macrophage, osteoclast, dendritic cells)
  • Neutrophils (degranulation -> collateral damage)
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6
Q

What are TWO mechanisms through which tolerance to commensal bacteria may be achieved?

A
  • PAMP (pathogen associated molecular pattern) on commensal undergoes biochemical modification to render them ‘stealth’
  • Commensals produce tolerance signals
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7
Q

What are TWO things that detect MAMPs/PAMPs?

A

TLR (toll-like receptor) and PRR (pattern recognition receptor)

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8
Q

What is the difference in PMNs in aggressive perio vs. chronic perio?

A
  • High PMN count in aggressive perio

- Low or faulty PMN in chronic perio

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9
Q

What are TWO cytokines involved in osteoclast differentiation and activation?

A
  • M-CSF (Macrophage colony stimulating factor)

- RANKL (from osteoblasts and T-cells)

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10
Q

Describe the THREE components in the immune response process in periodontitis.

A
  1. Activation and cytokine release from gingival cells, mast cells, endothelial cells, fibroblasts, monocytes
  2. Vascular changes (PMN migration) and RANKL (osteoclast activation)
  3. Adaptive immune system activated
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11
Q

What is ONE mechanism to explain the link between periodontitis and Rheumatoid Arthritis?

A
  1. P.gingivalis citrullination of host or bacterial proteins
  2. Anti-citrullinated protein antibodies formed
  3. Auto-immune attack of citrullinated host proteins in joints
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12
Q

What are FOUR steps through which cigarette smoke promotes chronic inflammation at the periodontium?

A
  1. Cigarette smoke triggers epithelial cells to release pro-inflammatory cytokines
  2. Cytokines recruit and promote survival of innate immune system cells (neutrophils, macrophages) that release more pro-inflammatory cytokines
  3. Result is chronic inflammation, impaired innate and altered adaptive
  4. Adaptive immune system more likely to be autoreactive
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13
Q

What are FIVE requirements for successful eradication of a virus?

A
  • Available effective attenuated vaccine
  • Antigen stable virus
  • No assymptomatic carriers
  • Absence of animal reservoir
  • Public cooperation
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14
Q

What are the general herd immunity thresholds?

A

80-95%, depending on specific disease.

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15
Q

Vaccine-preventable diseases (measles and pertussis) are becoming more common. What are THREE reasons why?

A
  • Anti-vax movement
  • Waning efficacy of vaccines and pathogen adaptation
  • Travel to endemic areas
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