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perio > pathogenesis of periodontitis > Flashcards

pathogenesis of periodontitis Flashcards

1
Q

why would someone have gingival health

A

Superb hygiene

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2
Q

hows the Junctional epithelium in gingival healtyh

A

attached to enamel

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3
Q

how does the oral epithelium and the Junction epithlium relate in gingival health

A

Looks continues

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4
Q

Inflammation in gingival health

A

Virtually absent

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5
Q

tissue volume ratio in health

A

10% JE
30% OE
60% CT

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6
Q

what immune cells are present in gingival health

A

Few PMNs present in the outer portion of the JE

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7
Q

thickness of junctional epithelium in health

A

Thin (10-20 cell layers

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8
Q

are epithelial ridges present in JE during healtyh

A

Absent

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9
Q

how does the CT look in gingival healthy

A

Dense with prominent collagen fiber bundles

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10
Q

what do the vapillaries look in the subepithelial plexus in gingival health

A

has loops that are constant

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11
Q

what do the capillaries look like in the dentogingival plexus in health

A

No loop

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12
Q

why does clinically healthy gingiva remain stable

A 
Shedding of epithelial cells
Intact epithelial barrier
Positive flow of GCF
complement system
PMNs and macrophages
Protective effects of antibodies
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13
Q

why does the subepithelial plexues capillary loops go through the retee pegs

A

Get nutrients and O2 to the epithlium

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14
Q

what is the subclinical stage of gingivitis

A

Initial lesion

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15
Q

what is the clinical early stage of gingivits

A

Early lesion

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16
Q

what is chronic gingivitis(no bone loss yet)

A

Established lesion

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17
Q

what is the stage that is the progression to periodontitis (bone loss)

A

Advanced lesion

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18
Q

when does the inital lesion occur

A

within 1-4 days of plaque development

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19
Q

what does the increased permeability of an inital lesion lead to

A

Carbon particles and serum proteins leak out of vessels

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20
Q

what does infiltration show in the inital lesion

A

PMNs and monocytes in the JE

lymphocytes in the CT (5%)

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21
Q

what happens to the vessels in the inital lesion

A

Vascular density

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22
Q

what happens to collagen in the inital lesion

A

Decreased perivascular colagen

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23
Q

what happens in the gingival crevicular fluid volume in the initial lesion

A

Increases

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24
Q

can you clinically see the inital lesion

A

No

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25
Q

what normally can pass through a vessel

A

Water
salts
small molecules

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26
Q

how do intercelular junction look in an intial lesion

A

Normally closed

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27
Q

what causes dilation of vessels of the dentogingival plexues

A

Vasoactive mediators

histamine, IL-1, TNF

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28
Q

what does gaps forming from dialtion of vessels lead to

A

Increased permeability
fluid and prtein flow out
GCF flow increases
White blood cells can leave

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29
Q

what is Gingival crevicular fluid made of

A 
Plasma transudate (health)
inflammatory exudate (disease)
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30
Q

what does gingival crevicular fluid pass through to get to crevis

A

Through the periodontal tissues

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31
Q

what does the GCF constituents indicate

A

Inflammatory changes

bacterial colonization

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32
Q

what causes GCF flow rate to increase

A

Clinical inflammation

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33
Q

what is used to measure GCF volume

A

Ninhydrin stain for protein

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34
Q

what mediates the up-regulation of adhesion molecules on endothelial cells in an initial lesion

A

Cytokine mediated

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35
Q

what does the adhesion moelcules of endothelial cells in an intiial lesion do

A

Allows PMN’s to adhere to post-capillary venules

- migration

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36
Q

where do PMNs migrate in an inital lesion

A

Through JE into gingival sulcus

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37
Q

what induces chemotaxis by PMNs

A 
Host factors (Il-8, C5a)
Molecules released by bacteria (fMetLeuPhe)
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38
Q

what happens to the JE in the inital lesion

A

Alteration of the most coronal portion of the JE

39
Q

when does an early lesion tend to occur

A

within 4-7 days of plaque development

40
Q

what immunologic cells appear in the Early lesion

A

Lymphocytes and PMNs subjacent to JE

Few Plasma cells

41
Q

how much of the infiltrated connective tissue is there

A

15%

42
Q

what happens to the fibroblasts in an early lesion

A

Undergoing cytopathic alterations

43
Q

can you see inflammation in early lesions

A

yes, clinically evident

44
Q

what happens to the Collagen in early lesions

A

Destroyed

- creates space for infiltrate

45
Q

what happens to basal cells in an early lesions

A

Cells of JE and SE proliferate

rete pegs invade the coronal portion of the lesion

46
Q

what happens to the Dentogingival plexues

A
  • Dilated w/ venules

- extremely permeable following minor trauma or inflammation

47
Q

what happens as JE invades the CT

A

preivously inactive capillary bed opens up and proliferates into the CT papillae

48
Q

why does junctional epithelium proliferate in early lesiosn

A

to compensative and fight plaque

49
Q

what cells are present in an early lesion

A

Macrophages
T cells
B cells
Firboblasts

50
Q

what is clinically seen in an established lesions

A

increased swelling

51
Q

what hapens to crevicular fluid in established lesion

A

increased fluid exudation

52
Q

what cells tend to migrate in an established lesion

A

leukocyte migration

plasma cell increased around blood vessel in coronal CT

53
Q

what happens to the collagen in established lesion

A

loss continues as infiltrate expands

54
Q

what cells become present in an established lesion

A

Macrophages and serum proteins
T and B cells
Plasma Cells

55
Q

What do activated T cells Produce in an established lesion

A 
Cytokines (IL-2, 3, 4, 5, 6, 10 , and 13, TNF-alpha)
Chemotactic substances (MCP, MIP, and Rantes)
56
Q

what do plasma cells produce in an established lesion

A

Produce Ig and Cytokines (IL-6 and TNF-alpha_

57
Q

what do fibroblasts produce in an established lesion

A

MMPs and TIMPs

58
Q

what happens to the JE and Sulcular epithelium in an established lesion

A

Proliferate and migrate deep into CT

59
Q

what happens to the sulcus in an established lesion

A

deepens

60
Q

what happens to just JE during an established lesion

A

JE converted into permeable pocket epithelium

61
Q

what are characteristics of PE

A

not attached to tooth surface

Loaded with PMNs

62
Q

what is an established lesion look like pathologically

A

Chronic gingivitis

63
Q

how does the margin look like in an established lession

A

Rolled gingival margin
lots of redness
bleed on probing

64
Q

is there attachment lost in an established lession

A

No

- probe depth increased but no attachment loss

65
Q

how can one fix an established lession

A

clearing plaque

66
Q

when does an advanced lesion occur

A

Not well known

67
Q

how do cells change in an advanced lesion

A

switch from T to b cell prodminance

-converstion from gingivitis to periodontitis

68
Q

what happens to the CT attachment in an advanced lesion

A

Destruction of CT attachment to root surface

69
Q

what is the first clinical sign of periodontitis

A

migration of epithelail attachment indicates

70
Q

where does bone loss begin in an advanced lesion

A

begins around communicating blood vessels

along crest of septum

71
Q

what does the PE proliferate into an advnaced lession

A

Deep into CT

72
Q

is the PE attached to the tooth in an advanced lession

A

Not attached

73
Q

what is the most common cell in advnaced lesion

A

50% plasma

74
Q

are there lots of cytokines in in advanced lession

A

Small spectrum of pro-inflammatory cytokines

75
Q

what happens if you clear plaque from an advanced lession

A

basal and epithelium have signal die away

- may not get all your attachment back

76
Q

Common modify factors of advanced lession

A

Diabetes
Pregnancy, pubery, and menopause
Smoking

77
Q

modifying factors can influnce what

A 
Susceptibility to gingivitis and periodontitis
Plaque growth and composition
Clinical presentation
Disease progression
Response to periodontal therapy
78
Q

how can diabetes mellitus be a risk factor for oral and periodontal problems

A

Xerostomia
Candida infections
Periodontitis
Multiple periodontal abscesses

79
Q

how much control should you have over diabetes

A

good control will lead to less periodontitis

- poor control=problems

80
Q

what does periodontitis do for diabetes

A

increasees insuline resistance

have a higher incidence of proteinuria and cardiovascular problems

81
Q

what happens in diabetteics after periodontal therapy

A

Glycemic control improved

82
Q

how can diabetes affect periodontis

A

change the bacteria
change host response
efect on periodontal treatement

83
Q

what effect on the host response can diabetes have

A

PMN fuction. chemotaxis impaired
cytokines, monocytes, and macrophages
Connective tissue

84
Q

what can diabetes affect in treatment

A

poorly controled leads to poor results

85
Q

what effect does estrogen have on periodontitis

A

Affects salivary peroxidases

increases collagen metabolism and angiogenesis

86
Q

how does pregnancy affact periodontium

A

increase estrogen
increase vascular response and inflammatory mediates
gingival inflammation increase
increase in gingival bleeding during menstrual cycle

87
Q

how common is gingivitis in pregnancy

A

35-88%

88
Q

when is pregnancy related gingivitus most common

A

2nd and 3rd trimesters

89
Q

what is the second risk factor for periodontitis

A

Smoking

90
Q

what does tobaccco smoking cause in perio

A

Deeper pockets
more attachmnet loss
more tooth loss
less bleeding on probing

91
Q

what can smoking affect

A

Bacteria

Host

92
Q

how does smoking affect reattachment for treatment

A

Poorer reduction in probing depth

poorer attachment gain in nonsurgical treatment

93
Q

what happens to treatment if you quite smoking

A

BEtter treatment outcome

perio (8 decks)

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