Pathogenesis Part 2 Flashcards

(51 cards)

1
Q

Initial lesion

A

clinically healthy gingivaE

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2
Q

arly lesion

A

mild gingivitis

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3
Q

Established lesion

A

Chronic/severe gingivitis

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4
Q

Advanced lesion

A

Periodontitis

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5
Q

Eubiosis

A

State of balance and health within a microbiome

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6
Q

Dysbiosis

A

State of imbalance in the microbiome within the body

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7
Q

In clinically healthy gingival tissues, small number of what is in the sulcus?

A

neutrophils

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8
Q

Gingival CT contains a small number of

A

inflammatory cells, mainly neutrophils

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9
Q

Initial lesion develops how long after plaque accumulation?

A

2 to 4 days

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10
Q

Describe what happens in initial lesion

A
  • Bacterial products activate resident leukocytes and stimulate endothelial cells
  • Blood capillaries in CT dilate and elevate vascular permeability
  • Crevicular fluid flows out of sulcus
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11
Q

Chemotactic gradients of _____ and _______ direct the neutrophils from the vasculatrue into the tissues and toward the junctional epithelium

A

IL-8 and ICAM-1

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12
Q

What are the steps of activation and migration of phagocytic cells from BVs

A
  1. Tethering/rolling
  2. Integrin activation
  3. Firm adhesion
  4. Extravasation
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13
Q

What does LFA-1 play a role in?

A

leukocyte adhesion and migration

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14
Q

ICAM-1, E-selectin and VCAM are adhesion molecules that are expressed by endothelial cells and are important for

A

leukocyte migration during an inflammatory response

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15
Q

ICAM-1 is a ligand for

A

LFA-1

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16
Q

When activated, leukocytes bind to endothelial cells via

A

ICAM-1/LFA-1 and then transmigrate into tissues

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17
Q

What happens w/initial lesion if local factors are eliminated?

A

Vascular changes resolve and the tissue reverts to a normal state

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18
Q

What happens w/initial lesion if local factors remain (hyperactive host response)?

A

Initial lesion progresses to early lesion

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19
Q

What are effects of continued plaque accumulation?

A
  • Levels of antigens increase
  • Increased migration of neutrophils and monocytes
  • Vasodilation and increased vascular permeability
  • Edema and erythema
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20
Q

How soon after plaque accumulation does initial lesion start to develop?

A

1 week

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21
Q

Describe what is happening during early lesion

A
  • Increased in prolif of capillaries, vascular permeability, vasodilation and gingival crevicular fluid flow
  • Large numbers of infiltrating leukocytes
24
Q

Early lesion. In gingival CT, it is mainly

25
Describe gingival CT of early lesion
- Degeneration of fibroblasts (mainly by apoptosis) - Collagen destruction that results in collagen depleted areas
26
27
What happens to early lesion is local factors remain?
Early lesion may persist or progress to established lesion
28
How soon after plaque does established lesion occur?
2-3 weeks
29
Describe established lesion
- Dense inflam cell infiltrate - Accumulation of inflam cells in CT (mainly plasma cells and B lymphocytes)
30
In the established lesion, there is increased release of
matrix metalloproteinases and lysosomal enzymes from neutrophils (cause destruction of colalgen fibers and ground substance)
31
In established lesion, what is there significant depletion of?
Colalgen
32
In established lesion, the pocket epi can become ulcerated showing
low resistance to probing and possible bleeding on probing
33
Progression to advanced lesion is influenced by what?
- Composition and quantity of the microbial biofilm - Host immune/inflam factors - Local and systemic risk factors
34
What is the function of neutrophils?
Primary mediators of the innate host defense. Phagocytose and kill bacteria and release lysosomal enzymes, cytokines and ROS
35
Describe the protective role of neutrophils in periodontal health
- Kill bacteria by phagocytosis (Deficiencies in neutrophil migration and function result in increased susceptibility to infections and developemnt of severe periodontitis)
36
Describe the destructive role of neutrophils in perio tissue loss
- Release large quantities of enzymes as they migrate through tissues (Cause breakdown of structural components of periodontium and development of collagen depleted areas)
37
What are characteristics of the advanced lesion (periodontitis)?
- Predominance of neutrophils - Dense inflam cell infiltrate in gingival CT - Continued colalgen breakdown results in areas of collagen depleted CT - Apical migration of JE - Alveolar bone resorption - Plaque bacteria proliferate apically
38
Gingival sulcus
Between tooth and surrounding gingival tissue in healthy sites
39
Periodontal pocket
Pathologically deepened gingival sulcus
40
Psuedopocket
enlarged gingival sulcus formed by coronal advancement of gingival margin due to inflam and gingival enlargement No attachment loss or bone loss
41
Suprabony
Bottom of pocket is coronal to level of adjacent bone
42
Intrabony
Bottom of pocket is apical to level of adjacent bone
43
hat causes the destruction of the collagen fibers in CT?
- Resident and inflam cells secrete MMP - Macrophages and fibroblasts phagocytize fibers - Fibroblasts can degrade collagen fibrils by extending cytoplasmic processes into the PDL cementum
44
JE of a pocket is ________ than JE of a healthy sulcus
shorter
45
What are examples of anti-inflammatory cytokines?
IL-4, IL-10, IL-1Ra, IL-1F5 and TGF-beta
46
IL-4
Key regulator in humoral and adaptive immunity
47
IL-10
produced by Tregs, monocytes and B cells Has immunosuppressive effects
48
IL-1Ra
Binds to the IL-1 receptor and blocks the effect of IL-1
49
IL-1F5
antagonizes the inflammatory effects of IL-1B and LPS
50
TGF-B
Regulates the proliferation, differentiation and function of lymphocytes, macrophages and other cells. Promotes the generation and function of Treg cells, plays a role in repair and tirrus regeneration
51