The Inflammatory Periodontal Lesion Flashcards

1
Q
A
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2
Q
  • Plaque-induced
  • Inflammation (edema/bleeding upon probing)
  • No destruction of PDL & bone
  • No apical migration of epithelial attachment
A

Gingivitis

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3
Q

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

A

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

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4
Q

Epithelial attachment =

A

Junctional epithelium

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5
Q
  • Plaque-indued
  • Inflammation (edema/bleeding upon probing)
  • Destruction of bone
  • Apical migration of epithelial attachment
  • Not all cases of gingivitis progress to periodontitis
A

Periodontitis

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6
Q

If you stop brushing & flossing will you develop gingivitis?

A

yes

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7
Q

Keystone pathogen of gingivitis:

A

p. Gingivalis & Aggregatibacter actinomycetemcomitans

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8
Q

If you stop brushing and flossing and develop gingivitis, and then you resume brushing and flossing with optimal oral hygiene, is the gingivitis reversible?

A

Yes

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9
Q

What determines if a case of gingivitis will progress to peridontitis?

A

the susceptibility of the host

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10
Q

What are some factors that result in a susceptible host in terms of gingivitis progressing to periodontitis?

A
  1. smoker
  2. diabetes
  3. immune conditions
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11
Q

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

A

True

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12
Q

In other words periodontitis is:

  1. _____ similar to gingivitis
  2. _____ (susceptible host)
  3. Each site is ____ or ____ environment
  4. A % of the affected 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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13
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

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14
Q

What bacteria are in the red complex?

A
  1. P. Gingivalis
  2. Tanerella Forsyth..
  3. T. Denticola
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15
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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16
Q

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

A

Continuous model (1900-1950s)

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17
Q

What model of disease progression coincides with the following example:

“everyone gets perio disease”

A

continuous model

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18
Q

What model of disease progression states:

  • progressive loss over time of some sites
  • no destruction in others
  • time of onset and extent may vary among sites
A

progressive model (1940-1960s)

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19
Q

What model of disease progression coincides with the following example:

“Periodontal disease affects mainly posterior teeth”

A

progressive model

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20
Q

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

A

Asynchronous multiple burst model (1980-2000s)

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21
Q

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

A

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

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22
Q

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

A

False- maxillary teeth are more susceptible due to trifurcated roots

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23
Q

Which teeth are the least likely to be lost to periodontal disease?

A

Mandibular canine & mandibular 1st premolar

This is because the bone is more dense in the mamdinular in addition to the maxillary canine being next to the maxillary first premolar which has a mesial concavity leading to collateral damage)

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24
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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25
Q

When there is an insult to the body- the first line of defense is ______ and the body sends these players to the area by ____

A

WBCs (neutrophils)

Dilation of blood vessels

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26
Q

Inflammation is a ____ phenomenon

A

vascular

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27
Q

When you see purplish change of color in inflammation this is a sign of ______ and is due to _____

A

chronic inflammation; blood flow is stagnant

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28
Q

What type of cells are the “migrators” in inflammation?

A

Leukocytes

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29
Q

Signs of vasculitis in an inflammatory response include:

A
  1. dilation
  2. venous stasis (congestion)
  3. increased permeability (transudate & exudate)
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30
Q

List some examples of innate immunity:

A
  • skin
  • saliva
  • gingival crevicular fluid
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31
Q

Any time the immune system goes out of control this can result in:

A

autoimmunity

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32
Q

T cells can differentiate into two forms:

A

CD4
CD8

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33
Q

T/F: The innate & adaptive immune system work completely separately

A

False- they work together

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34
Q

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?

A

Due to the host immune response differing

(one may have a heightened response compared to the other)

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35
Q

Molecules that are selected to send signals to other cells; a component of humoral immunity:

A

complement

36
Q

Bacteria cause disease when _____

A

attach to the epithelium

37
Q

One of the biggest mediators of destruction in periodontal disease:

A

Cytokines

38
Q

Pro-inflammatory cytokine; critical because it can stimulate osteoclasts (destructive), fibroblasts & macrophages:

A

IL-1

39
Q

What destroys bone- Osteoclasts or osteoblasts?

A

Osteoclasts

40
Q

Periodontal susceptibility test looks for:

A

IL-1 genotype

41
Q

Pro-inflammatory cytokine, stimulates T & B cells:

A

IL-6

42
Q

Pro-inflammatory cytokine, attracts & activates PMNs:

A

IL-8

43
Q

In women, this cytokine is regulated by estrogen levels:

A

IL-6

44
Q

Pro-inflammatory cytokine that activates osteoclasts:

A

TNF

45
Q

Cytokine that is responsible for vasodilation, is pyrogenic, releases mediator from mast cells and is involved in cell-mediated immunity:

A

PGE2

46
Q

Whenever there is tissue breakdown ____ is released

A

Prostaglandin

47
Q

Growth factor that stimulates/heals epithelial cells and fibroblasts:

A

TGF

48
Q

Growth factor that stimulates/heals fibroblasts:

A

PDGF & FGF

49
Q

Growth factor that stimulates/heals epithelial cells:

A

EGF

50
Q

FGF:

A

Fibroblasts growth factor

51
Q

EGF:

A

Epithelial growth factor

52
Q

What causes bleeding upon probing when pressure is too hard:

A

ulceration of junctional epithelium

53
Q

In health when we probe, the probe stops short of the:

A

junctional epithelium

54
Q

When probing, if the sulcular epithelium is intact:

A

there will be no bleeding upon probing

55
Q

When probing, if the sulcular epithelium is NOT intact, this would result in:

A

bleeding upon probing

56
Q

What situation might there be an absence of bleeding upon probing if someone has gingivitis/periodontitis?

A

smokers

57
Q

Can we accurately predict which patients with gingivitis are going to develop periodontitis?

A

Exactly- no, but we can identify risk factors

so one appointment no, but if we are seeing the patient over time and are seeing the etiology and knowing the risk factors it is easier to predict

58
Q

Risk factors for gingivitis progressing into periodontitis?

A
  1. habits (smoking)
  2. systemic disorders (HIV & DM)
59
Q

Patients with risk factors are more likely to have:

A

attachment loss

60
Q

In clinically health 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)

A
  1. neutrophils & macrophages
  2. neutrophils; JE
  3. collagen
  4. epithelial
  5. gingival crevicular fluid
  6. clinically
61
Q

List some examples of GENETIC inflammatory modifiers: (9)

A
  1. agranulocytosis
  2. neutropenias
  3. lazy leukocyte
  4. leukocyte adhesion deficiency (LAD)
  5. Down’s syndrome
  6. Papillon-Lefevre
  7. Hypophosphatasia
  8. Chediak-Higashi
  9. Ehlers-Danlos syndrome
62
Q

A condition that may cause young kids to have susceptibility to periodontal disease:

A

Hypophosphatasia

63
Q

Initial lesion of gingivitis develop in:

A

2-4 days

64
Q
  • developed in 2-4 days
  • cells of acute inflammation present
  • increased GCF flow
  • start of pseudopocket formation
A

Initial lesion

65
Q

Cells of acute inflammation:

A

PNMs

66
Q

Cells of chronic inflammation:

A

Lymphocytes

67
Q

As inflammation increases in chronicity what cells may be present?

A

Plasma cells

68
Q

What are the two types of virulence factors?

A
  1. stimulation of the host defense systems
  2. degradation of host tissues
69
Q

Virulence factors that stimulate the host defense systems stimulate cells to release ____ (example: ____) & ____

A

cytokines (i.e. IL-1, TNF & PGE) & chemoattractant factors (IL-8)

70
Q

Virulence factors that degrade host tissues are enzymes which include: (4)

A
  1. collagenase
  2. trypsin-like enxymes
  3. keratinase
  4. phospholipase A
71
Q

Early lesions of gingivitis develop in:

A

4-7 days

72
Q
A
73
Q
  • Develop in 4-7 days
  • acute inflammation persists, increased GCF, pseudopocket formation
  • cells of chronic inflammation appear and then dominate
A

Early lesion

74
Q

Describe the shift of cells present we see from initial lesions to early lesions:

A

PNMs —-> T lymphocytes

75
Q

Early lesions may also be known as:

A

T cell lesion

76
Q

What is the dominate cells of early lesions?

A

T cells

77
Q

In early lesions _____ loss continues and ____ begins

A

collagen loss; MMPs activation

78
Q

Clinical features of early lesion: (7)

A
  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
79
Q

If you see a patient that has bleeding upon probing, what stage of lesion presents?

A

Established

80
Q

Established lesion is characterized by breakage in the:

A

sulcular epithelium

81
Q

The established lesion is characterized by loss of:

A

collagen

82
Q

What causes the loss of collagen in an established lesion? (2)

A
  1. decreased rate of synthesis
  2. increased rate breakdown
83
Q

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 ____
A
  1. fibroblasts & epithelium
  2. collagen
  3. micro-ulcerations
  4. acute inflammation
  5. PNMs
  6. extracellular matrix
  7. T-cell, B-cell & plasma cell
  8. JE; CT
  9. rete peg ridges
84
Q

Attachment loss precedes bone loss by about:

A

6 months

85
Q
A