Exam 1; Pathogenesis of Periodontitis Flashcards

(73 cards)

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
Does GCF flow rate increase or decrease with clinical inflammation
increase
26
This stain is for protein indicates GCF volume
ninhydrin
27
There is cytokine-mediated up-regulation of this in the initial lesion
adhesion molecules on endothelial cells
28
These adhere to post-capillary venues and begin to migrate through the JE into the gingival sulcus
PMNs
29
Chemotaxis by PMNs is induced by what two things
``` host factors (IL-8, C5a) molecules released by bacteria ```
30
In the initial lesion, this is subjacent to JE
vasculitis
31
In the initial lesion, there is increased migration of what
leukocytes into the JE and gingival sulcus
32
In the initial lesion, these are present extravascularly
serum proteins
33
In the initial lesion, what is altered in its most coronal portion
the JE
34
What is lost in the initial lesion
perivascular collagen
35
This occurs within 4-7 days of plaque development, inflammation is not clinically evident
early lesion
36
In the early lesion, what is subjacent to the JE
lymphocytes and PMNs
37
In the early lesion, what is undergoing cytopathic alterations
fibroblasts
38
In the early lesion, this undergoes destruction which creates space for infiltrate
collagen
39
In the early lesion, these cells on the JE and SE proliferate
basal cells
40
In the early lesion, these invade the coronal portion of the lesion
epithelial rete pegs
41
The dentogingival plexus is extremely permeable following what
minor trauma or inflammation
42
In the early lesion, there is an accumulation of lymphoid cells
immediately subjacent JE
43
In the early lesion there is cytopathic alteration in what
resident fibroblasts
44
What is also in the established lesion besides macrophages and serum proteins
T, B, and plasma cells
45
In the established lesion the activated T cells produce what
cytokines
46
In the established lesion, the plamsa cells produce this
Ig and cytokines
47
In the established lesion, these produce MMPs and TIMPs
fibroblasts
48
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
permeable pocket epithelium (PE)
49
This is loaded with PMNs and is not attached to the tooth surface
permeable pocket epithelium (PE)
50
The established lesion may have this evident
early pocket formation
51
True or False | There is no apical migration of JE and non bone loss at this stage
True
52
In the advanced lesion stage there is a switch from what cells
T to B cell predominance signals conversion from gingivitis to periodontitis
53
In the advanced stage lesion there is destruction of CT attachment to the root surface and apical migration of what
of epithelial attachment indicates the first clinical sign of periodontitis
54
Bone destruction begins where
around communicating blood vessels along the crest of the septum
55
In the advanced lesion, what is the percentage is plasma cells
50%
56
True or False | In the advanced lesion, there is extension of lesion into alveolar bone and PL with significant bone loss
True
57
What are 5 commons modifyling factors of periodontitis
``` diabetes pregnancy puberty menopause smoking ```
58
The modifying factors can influence these five things
``` susceptibility to gingivitis and periodontitis plaque growth and composition clinical presentation disease progression response to periodontal therapy ```
59
What are the four oral and periodontal effects of diabetes mellitus
xerostomia candida infections periodontits multiple periodontal abscesses
60
Periodontits in diabetes patients increases what
insulin resistance
61
What does diabetes do to the host response system in periodontitis
PMN function, chemotaxis is impaired cytokines, monocytes, and macrophages have a more destructive phenotype connective tissue has a decreased matrix
62
This hormone, common in pregnancy, puberty, and menopause affects salivary perioxidases and increases collagen metabolism and the vascular response
estrogen
63
True or False There is an increase in gingival inflammation and and increase in bleeding during the mental cycle in those women with gingivitis
True
64
gingivitis is seen in about how many pregnancies
35-88% and is highest during the 2nd (best time to treat) and 3rd trimesters
65
What does pregnancy do to the microbiotia
increases certain species
66
What does pregnancy do to host effects
increases vascular permeability but a decrease in PMN chemotaxis
67
What is the main proponent of gingivitis in menopausal women
due to decreased absorption and increased elimination of calcium
68
True or False | Osetoprorsis in post-menopausal women causes periodontitis
False; it may not cause it, but may affect the severity of the disease
69
Tobacco smoking causes what to occur
deep probe and pocket depths but less gingivitis and BOP
70
What does tobacco do to bacteria
smokers have more plaque | increases certain bacteria species
71
What does smoking due to the host
less BOP due to decreased blood vessels, etc. lower amounts of GCF lower PMN function
72
Smoking results in a poor or great response to surgical treatment and nonsurgical treatment
poor
73
What is the main factor of diabetes that causes periodontitis
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