The Inflammatory Periodontal Lesion Flashcards

(82 cards)

1
Q
  • plaque induced
  • inflammation (edema/bleeding upon probing)
  • no destruction of PDL and bone
  • no apical migration of epithelial attachment
A

Gingivitis

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2
Q

Describe the destruction of PDL and bone and apical migration of epithelial attachment with gingivitis:

A

No destruction of PDL & bone
No apical migration of epithelial attachment

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3
Q

Epithelial attachment =

A

junctional epithelium

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4
Q
  • plaque-induced
  • inflammation (edema/bleeding upon probing)
  • destruction of bone
  • apical migration of epithelial attachment
A

Periodontitis

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5
Q

If you stop brushing & flossing will you develop gingivitis?

A

yes

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6
Q

Keystone pathogens of gingivitis:

A

p. gingivalis & Agregatibacter actinomycetecomitans

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7
Q

If you stop brushing and flossing and develop gingivitis, start brushing again and have optimal oral hygeine, is the gingivitis reversible?

A

yes

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8
Q

What are some factors that make someone a susceptible host for periodontitis?

A

diabetics, smokers, immune conditions

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9
Q

T/F: Not all cases of gingivitis progress to periodontitis

A

True

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10
Q

In other words, periodontitis is:

  1. ______ similar to gingivitis
  2. _____ ( susceptible host)
  3. Each site is ___ or ____ environment
  4. A % of affects population experiences _____
  5. The progression of the disease is probably…
A
  1. plaque-induced
  2. host-related
  3. individualized or specific
  4. severe destruction
  5. ….
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11
Q

Models of disease progression:

A
  1. continuous model (1900 -1950s)
  2. progressive model (1940-1960s)
  3. Random burst model (1980s-2000s)
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12
Q

Why does periodontal disease start in the posterior teeth?

A

Due to the gingival col- it creates a perfect valley where bacteria can thrive and the tissue is NON-keratinized

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13
Q

Red complex: (3)

A

P. gingivalis
T. Forsynthia
T. Denticola

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14
Q

The red complex species are associated with:

A
  1. bleeding upon probing
  2. progressive bone loss
  3. progressive attachment loss
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15
Q

What model of disease progression states “continuous through life at same rate of loss”

A

Continuous Model

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16
Q

What model disease progression coincides with the following example:

“everyone gets perio disease”

A

Continuous model

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17
Q

What model of disease progression states:
- progressive loss over time of some sites
- no destruction in others
- time of onset and extends vary among sites

A

Progressive model

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18
Q

What model disease progression coincides with the following example:

” periodontal disease affects mainly posterior teeth”

A

Progressive model

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19
Q

What model of disease progression tends to fit best when there are random areas of disease progression while some areas seem to be unaffected?

A

Asynchronous multiple burst model (1980s-2000s)

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20
Q

T/F: Maxillary teeth are less susceptible to perio disease than mandibular teeth

A

false- maxillary teeth more susceptible due to the trifurcated roots

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21
Q

What would be the reason for seeing bone loss progression more severely on the maxillary 2nd molars compared to the mandibular second molar?

A

The maxillary teeth have trifurcation vs. the bifurcation on the mandibular molars- this trifurcation can make it harder to keep clean

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22
Q

What teeth are least likely to be lost to perio disease?

A

mandibular canine & mandibular 1st premolar

(because the maxillary canine is right next to the first premolar which has a mesial concavity)

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23
Q

Signs of inflammation: (5)

A
  1. rubor (redness)
  2. calor (heat)
  3. dolor (pain)
  4. tumor (swelling)
  5. functio laesa (loss of function)
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24
Q

When there is an insult to the body - the first Lin e of defense is ____ and the body sends these players to the area by _____.

A

WBCs (neutrophils)

Dilation of blood vessels

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25
Inflammation is a ____ phenomenon
vascular
26
When you see purplish change in the gingiva this is a sign of:
stagnant blood flow (chronic inflammation)
27
What type of cells are the "migrators" in inflammation?
leukocytes
28
Signs of vasculitis in an inflammatory response include:
1. dilation 2. venous stasis (congestion) 3. increased permeability (transudate & exudate)
29
List some examples of innate immunity:
- skin - saliva - gingival crevicular fluid
30
Anytime the immune system goes out of control, this can result in:
autoimmunity
31
T cells can differentiate into 2 major forms:
CD4 & CD8
32
T/F: The innate and adaptive immune system work completely separate
False- the adaptive immune system goes back and helps out the innate immune system and they kinda work together
33
Two individuals with - Same plaque - Same amounts of bacteria - Same species of bacteria One person develops periodontitis and the other does not. Why might this be?
Due to the host immune response differing
34
Molecules that are secreted to send signals to other cells. A component of humoral immunity:
Complement
35
Bacteria cause disease when _____.
attach to the epithelium
36
One of the biggest mediators of destruction in periodontal disease:
Cytokines
37
Pro-Inflammatory cytokine: stimulates osteoclasts, fibroblasts macrophages
IL-1
38
What destroys bone, osteoclasts or osteoblasts?
osteoclasts
39
Pro-inflammatory cytokine: stimulates T and B cells:
IL-6
40
Pro-inflammatory cytokine: attracts and activates PMNs:
IL-8
41
Pro-inflammatory cytokine: activates osteoclasts
TNF
42
Cytokine that is responsible for vasodilation, is pyrogenic, releases mediator from mast cells and is involved in cell-mediated cytotoxicity:
PGE2
43
In women, what cytokine is regulated by estrogen levels, causing more issues in menopausal women?
IL-6
44
Whenever there is tissue breakdown, ____ is released
prostaglandin
45
Growth factor that stimulates epithelial cells AND fibroblasts:
TGF
46
Growth factors that stimulates fibroblasts: (2)
PDGF & FGF
47
Growth factor that stimulates/ heals epithelial cells:
EGF
48
FGF:
Fibroblast growth factors
49
EGF:
Epithelial growth factor
50
What causes bleeding upon probing?
ulceration of the junctional epithelium
51
In health when we probe, the probe stops short of the:
junctional epithelium
52
When probing, if the sulcular epithelium is in tact:
there will be no bleeding upon probing
53
When probing, if the sulcular epithelium is NOT in tact, this would result in:
bleeding upon probing
54
What situation might there be abscence of bleeding upon probing if someone has gingivitis/periodontitis?
smokers
55
Can we accurately predict which patients with gingivitis are going to progress to periodontitis?
Exactly, NO but we can identify risk factors
56
Risk factors for gingivitis progressing into periodontitis?
1. habits (smoking) 2. systemic disorders (HIV and diabetes)
57
Patients with risk factors are more likely to have:
attachment loss
58
In clinically healthy gingiva 1. Some ____ and ____ are present in connective tissue 2. A few ____ are migrating through the ___ 3. No ____ destruction 4. Intact ____ barrier 5. ____ is present 6. Appears _____ healthy (color, contours, consistency)
1. neutrophils & macrophages 2. neutrophils; JE 3. collagen 4. epithelial 5. gingival crevicular fluid 6. clinically
59
A condition that may cause young kids to have susceptibility to periodontal disease:
Hypophosphotasia
60
List some examples of GENETIC inflammatory response modifiers: (9)
1. Agranulocytosis 2. Neutropenias 3. Lazy leukocyte 4. Leukocyte adhesion deficiency (LAD) 5. Down syndrome 6. Papillon-Lefevre 7. Chediak-Higashi 8. Hypophosphatasia 9. Ehlers-Danlos syndrome
61
Initial lesion of gingivitis develops in:
2-4 days
62
- Develops in 2-4 days - Cells of acute inflammation present - Increased GCF flow - Start of pseudo-pocket formation
Initial lesion
63
Cells of acute inflammation:
PMNs
64
Cells of chronic inflammation:
lymphocytes
65
As inflammation increases in chronicity what cells may be present?
Plasma cells
66
What are two types of virulence factors?
1. stimulation of the host defense systems 2. Degradation of host tissues
67
Virulence factors that stimulate the host defense systems stimulate cells to release ____ (examples: ____) & _____ (example: ___)
cytokines (ie. IL-1, TNF and PGE) & chemoattractant factors (ie. IL-8)
68
Virulence factors that degrade host tissues are enzymes which include: (4)
1. collagenase 2. trypsin-like enzymes 3. keratinase 4. phospholipase A
69
Early lesion of gingivitis occurs in:
4-7 days
70
- Develops in 4-7 days - Acute inflammation persists (from initial lesion) - Increase GCF - Pseudopocket formation - Cells of chronic inflammation appear and then DOMINATE
Early Lesion
71
Describe the shift of cells present we see form initial lesions to early lesions:
PMNs---> T Lymphocytes
72
Early lesion may also be known as:
T-Cell lesion
73
What is the dominate cell of early lesion?
T-cells
74
In early lesions, ______ continues and _______ begins
collagen loss; MMPs Activation
75
Clinical features of early lesion: (7)
1. Edema of gingiva 2. Increased GCF flow 3. Loss of gingival stippling 4. Erythema of gingival margin 5. No migration of JE attachment 6. Alveolar bone is normal- no bone loss 7. Reversible
76
If you see a patient that has bleeding upon probing, what stage of lesion presents?
Established
77
Established lesion is characterized by breakage in the:
sulcular epithelium
78
The established lesion is characterized by loss of:
collagen
79
The loss of collagen in an established lesion results in: (2)
1. decreased rate of synthesis 2. increased rate of breakdown
80
Histopathology of the established lesion: 1. Cellular damage of _____ & ____ 2. ____ loss increases 3. ____ of pocket epithelium 4. Persistence of ____ 5. Marked numbers of _____ in pocket 6. Degradation of _____ 7. Dense ___, ___, & ___ infiltrate 8. ____ proliferation & extension into ___ 9. Elongation of ___
1. fibroblasts & epithelium 2. collagen 3. micro-ulcerations 4. acute inflammation 5. PMN's 6. extracellular matrix 7. T-cell, B- cell, & plasma cell 8. JE; CT 9. rete peg ridges
81
Attachment loss ____ bone loss by about _____
PRECEDES; 6 months
82