The Inflammatory Periodontal Lesion Flashcards

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
Q

Inflammation is a ____ phenomenon

A

vascular

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26
Q

When you see purplish change in the gingiva this is a sign of:

A

stagnant blood flow (chronic inflammation)

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27
Q

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

A

leukocytes

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28
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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29
Q

List some examples of innate immunity:

A
  • skin
  • saliva
  • gingival crevicular fluid
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30
Q

Anytime the immune system goes out of control, this can result in:

A

autoimmunity

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31
Q

T cells can differentiate into 2 major forms:

A

CD4 & CD8

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32
Q

T/F: The innate and adaptive immune system work completely separate

A

False- the adaptive immune system goes back and helps out the innate immune system and they kinda work together

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33
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

34
Q

Molecules that are secreted to send signals to other cells. A component of humoral immunity:

A

Complement

35
Q

Bacteria cause disease when _____.

A

attach to the epithelium

36
Q

One of the biggest mediators of destruction in periodontal disease:

A

Cytokines

37
Q

Pro-Inflammatory cytokine: stimulates osteoclasts, fibroblasts macrophages

A

IL-1

38
Q

What destroys bone, osteoclasts or osteoblasts?

A

osteoclasts

39
Q

Pro-inflammatory cytokine: stimulates T and B cells:

A

IL-6

40
Q

Pro-inflammatory cytokine: attracts and activates PMNs:

A

IL-8

41
Q

Pro-inflammatory cytokine: activates osteoclasts

A

TNF

42
Q

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

A

PGE2

43
Q

In women, what cytokine is regulated by estrogen levels, causing more issues in menopausal women?

A

IL-6

44
Q

Whenever there is tissue breakdown, ____ is released

A

prostaglandin

45
Q

Growth factor that stimulates epithelial cells AND fibroblasts:

A

TGF

46
Q

Growth factors that stimulates fibroblasts: (2)

A

PDGF & FGF

47
Q

Growth factor that stimulates/ heals epithelial cells:

A

EGF

48
Q

FGF:

A

Fibroblast growth factors

49
Q

EGF:

A

Epithelial growth factor

50
Q

What causes bleeding upon probing?

A

ulceration of the junctional epithelium

51
Q

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

A

junctional epithelium

52
Q

When probing, if the sulcular epithelium is in tact:

A

there will be no bleeding upon probing

53
Q

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

A

bleeding upon probing

54
Q

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

A

smokers

55
Q

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

A

Exactly, NO but we can identify risk factors

56
Q

Risk factors for gingivitis progressing into periodontitis?

A
  1. habits (smoking)
  2. systemic disorders (HIV and diabetes)
57
Q

Patients with risk factors are more likely to have:

A

attachment loss

58
Q

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)

A
  1. neutrophils & macrophages
  2. neutrophils; JE
  3. collagen
  4. epithelial
  5. gingival crevicular fluid
  6. clinically
59
Q

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

A

Hypophosphotasia

60
Q

List some examples of GENETIC inflammatory response modifiers: (9)

A
  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
Q

Initial lesion of gingivitis develops in:

A

2-4 days

62
Q
  • Develops in 2-4 days
  • Cells of acute inflammation present
  • Increased GCF flow
  • Start of pseudo-pocket formation
A

Initial lesion

63
Q

Cells of acute inflammation:

A

PMNs

64
Q

Cells of chronic inflammation:

A

lymphocytes

65
Q

As inflammation increases in chronicity what cells may be present?

A

Plasma cells

66
Q

What are two types of virulence factors?

A
  1. stimulation of the host defense systems
  2. Degradation of host tissues
67
Q

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

A

cytokines (ie. IL-1, TNF and PGE) & chemoattractant factors (ie. IL-8)

68
Q

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

A
  1. collagenase
  2. trypsin-like enzymes
  3. keratinase
  4. phospholipase A
69
Q

Early lesion of gingivitis occurs in:

A

4-7 days

70
Q
  • Develops in 4-7 days
  • Acute inflammation persists (from initial lesion)
  • Increase GCF
  • Pseudopocket formation
  • Cells of chronic inflammation appear and then DOMINATE
A

Early Lesion

71
Q

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

A

PMNs—> T Lymphocytes

72
Q

Early lesion may also be known as:

A

T-Cell lesion

73
Q

What is the dominate cell of early lesion?

A

T-cells

74
Q

In early lesions, ______ continues and _______ begins

A

collagen loss; MMPs Activation

75
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
76
Q

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

A

Established

77
Q

Established lesion is characterized by breakage in the:

A

sulcular epithelium

78
Q

The established lesion is characterized by loss of:

A

collagen

79
Q

The loss of collagen in an established lesion results in: (2)

A
  1. decreased rate of synthesis
  2. increased rate of breakdown
80
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. PMN’s
  6. extracellular matrix
  7. T-cell, B- cell, & plasma cell
  8. JE; CT
  9. rete peg ridges
81
Q

Attachment loss ____ bone loss by about _____

A

PRECEDES; 6 months

82
Q
A