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AU14 Periodontology > Exam 1; Pathogenesis of Periodontitis > Flashcards

Exam 1; Pathogenesis of Periodontitis Flashcards

1
Q

This is attached to enamel

A

the junctional epithelium

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2
Q

This appears to be continuous with the junctional epithelium

A

oral epithelium

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3
Q

What are the tissue ratios in healthy gingiva

A

10% JE
30% OE
60% CT

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4
Q

True or False

There is a large number of PMNs present in the outer portion of the JE

A

False; there are only a few

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5
Q

What is the thickness of the JE

A

thin; 10-20 cell layers thick

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6
Q

What is absent in the gingiva

A

epithelial ridges; rete pegs

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7
Q

This is dense with prominent collagen fiber bundles

A

connective tissue

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8
Q

This is with capillary loops (rete pegs) and the number of loops is constant

A

subepithelial plexus

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9
Q

The anastomoses of supraperiosteal blood vessels (sv) is with what

A

vessels from the bone and PL

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10
Q

These have no loops in healthy gingiva

A

dentogingival plexus (dp)

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11
Q

What are 6 reasons for stability in healthy gingiva

A 
shedding of epithelial cells
intact epithelial barrier
positive flow of the GCF
complement system
PMNs and macrophages
protective effects of antibodies
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12
Q

Histopathological stages in the development of gingivitis and periodontitis were described by who

A

Page and Schroeder

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13
Q

This lesion stage is in the sub gingival stage of gingivitis

A

initial lesion

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14
Q

This lesion stage is in the clinical stage of gingivitis

A

early lesion

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15
Q

This lesion stage is chronic gingivitis

A

established lesion

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16
Q

This lesion stage is in the progression of periodontitis

A

advanced lesion

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17
Q

This type of lesion occurs within 1-4 days of plaque development and has the early stage of inflammation

A

initial lesion

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18
Q

The initial lesion has increased permeability and infiltration to which molecules

A

permeable to; carbon particles and serum proteins that leak out of vessels
PMNs and monocytes in the JE and lymphocytes in the CT

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19
Q

This type of lesion has increased vascular density, decreased perivascular collagen, and increased gingival crevicular fluid

A

initial lesion

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20
Q

Is the initial lesion detectable clinically

A

No

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21
Q

Where do the vessels dilate in the initial lesion, resulting in increased permeability and an increase in GCF flow

A

dentogingival plexus

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22
Q

What is vasodilation induced by in the initial lesion

A

vasoactive mediators like histamine, IL-1, TNF

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23
Q

This is a plasma transduate (health) and inflammatory exudate (disease)

A

GCF

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24
Q

GCF constituents indicate what

A

inflammatory changes and bacterial colonization

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25
Q

Does GCF flow rate increase or decrease with clinical inflammation

A

increase

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26
Q

This stain is for protein indicates GCF volume

A

ninhydrin

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27
Q

There is cytokine-mediated up-regulation of this in the initial lesion

A

adhesion molecules on endothelial cells

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28
Q

These adhere to post-capillary venues and begin to migrate through the JE into the gingival sulcus

A

PMNs

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29
Q

Chemotaxis by PMNs is induced by what two things

A 
host factors (IL-8, C5a)
molecules released by bacteria
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30
Q

In the initial lesion, this is subjacent to JE

A

vasculitis

31
Q

In the initial lesion, there is increased migration of what

A

leukocytes into the JE and gingival sulcus

32
Q

In the initial lesion, these are present extravascularly

A

serum proteins

33
Q

In the initial lesion, what is altered in its most coronal portion

A

the JE

34
Q

What is lost in the initial lesion

A

perivascular collagen

35
Q

This occurs within 4-7 days of plaque development, inflammation is not clinically evident

A

early lesion

36
Q

In the early lesion, what is subjacent to the JE

A

lymphocytes and PMNs

37
Q

In the early lesion, what is undergoing cytopathic alterations

A

fibroblasts

38
Q

In the early lesion, this undergoes destruction which creates space for infiltrate

A

collagen

39
Q

In the early lesion, these cells on the JE and SE proliferate

A

basal cells

40
Q

In the early lesion, these invade the coronal portion of the lesion

A

epithelial rete pegs

41
Q

The dentogingival plexus is extremely permeable following what

A

minor trauma or inflammation

42
Q

In the early lesion, there is an accumulation of lymphoid cells

A

immediately subjacent JE

43
Q

In the early lesion there is cytopathic alteration in what

A

resident fibroblasts

44
Q

What is also in the established lesion besides macrophages and serum proteins

A

T, B, and plasma cells

45
Q

In the established lesion the activated T cells produce what

A

cytokines

46
Q

In the established lesion, the plamsa cells produce this

A

Ig and cytokines

47
Q

In the established lesion, these produce MMPs and TIMPs

A

fibroblasts

48
Q

In the established lesion, the JE and SE proliferate and migrate deep into the CT, the sulcus deepens and the JE is converted to what

A

permeable pocket epithelium (PE)

49
Q

This is loaded with PMNs and is not attached to the tooth surface

A

permeable pocket epithelium (PE)

50
Q

The established lesion may have this evident

A

early pocket formation

51
Q

True or False

There is no apical migration of JE and non bone loss at this stage

A

True

52
Q

In the advanced lesion stage there is a switch from what cells

A

T to B cell predominance signals conversion from gingivitis to periodontitis

53
Q

In the advanced stage lesion there is destruction of CT attachment to the root surface and apical migration of what

A

of epithelial attachment indicates the first clinical sign of periodontitis

54
Q

Bone destruction begins where

A

around communicating blood vessels along the crest of the septum

55
Q

In the advanced lesion, what is the percentage is plasma cells

A

50%

56
Q

True or False

In the advanced lesion, there is extension of lesion into alveolar bone and PL with significant bone loss

A

True

57
Q

What are 5 commons modifyling factors of periodontitis

A 
diabetes
pregnancy
puberty
menopause
smoking
58
Q

The modifying factors can influence these five things

A 
susceptibility to gingivitis and periodontitis
plaque growth and composition
clinical presentation
disease progression
response to periodontal therapy
59
Q

What are the four oral and periodontal effects of diabetes mellitus

A

xerostomia
candida infections
periodontits
multiple periodontal abscesses

60
Q

Periodontits in diabetes patients increases what

A

insulin resistance

61
Q

What does diabetes do to the host response system in periodontitis

A

PMN function, chemotaxis is impaired
cytokines, monocytes, and macrophages have a more destructive phenotype
connective tissue has a decreased matrix

62
Q

This hormone, common in pregnancy, puberty, and menopause affects salivary perioxidases and increases collagen metabolism and the vascular response

A

estrogen

63
Q

True or False
There is an increase in gingival inflammation and and increase in bleeding during the mental cycle in those women with gingivitis

A

True

64
Q

gingivitis is seen in about how many pregnancies

A

35-88% and is highest during the 2nd (best time to treat) and 3rd trimesters

65
Q

What does pregnancy do to the microbiotia

A

increases certain species

66
Q

What does pregnancy do to host effects

A

increases vascular permeability but a decrease in PMN chemotaxis

67
Q

What is the main proponent of gingivitis in menopausal women

A

due to decreased absorption and increased elimination of calcium

68
Q

True or False

Osetoprorsis in post-menopausal women causes periodontitis

A

False; it may not cause it, but may affect the severity of the disease

69
Q

Tobacco smoking causes what to occur

A

deep probe and pocket depths but less gingivitis and BOP

70
Q

What does tobacco do to bacteria

A

smokers have more plaque

increases certain bacteria species

71
Q

What does smoking due to the host

A

less BOP due to decreased blood vessels, etc.
lower amounts of GCF
lower PMN function

72
Q

Smoking results in a poor or great response to surgical treatment and nonsurgical treatment

A

poor

73
Q

What is the main factor of diabetes that causes periodontitis

A

Advanced glycation end products (AGE); harms the immune system (reducing migration, impairing host defenses) and capillary thickening leading to altered connective tissue fibroblast/osteoblast and epithelium

AU14 Periodontology (29 decks)

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