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Periodontics D2 > Evolution of the Inflammatory Periodontal Lesion > Flashcards

Evolution of the Inflammatory Periodontal Lesion Flashcards

1
Q

Neutrophils make up __________ of cells that cross the blood vessel to enter ____________

A
  • 1st wave

- inflammtory site

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2
Q

What are the 7 types of responses by Neutrophils?

A

1) Rolling
2) Margination
3) Adhesion/Binding
4) Emigration/Diapedesis
5) Migration/Chemotaxis
6) Phagocytosis
7) Killing/Neutralization of Antigen

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3
Q

What do the Basophil/Mast cell cytoplasmic granules contain?

A

1) Histamine (causes vasodilation & increased vascular permeability(
2) Platelet activating factor
3) Heparin (anticoag)
4) TNF-alpha
5) Slow secreting substance of anaphylaxis (SRS-As)
- Leukotriene C4, D4, and E4

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4
Q

What are the major functions of Macrophages?

A

1) Phagocytosis
2) Antigen recognition
3) Synthesis & release of cytokines & lymphokines

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5
Q

What is IL-1?

A

Stimulates osteoclasts, fibroblasts, macrophages, and activation of CD 8 lymphocytes

Pro-inflammatory

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6
Q

What is IL-6?

A

Stimulates B & T cells

Pro-inflammatory

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7
Q

What is TNF-alpha?

A

activator of endothelium/osteoclasts & inflammatory mediator

Pro-inflammatory

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8
Q

What is INF?

A

Interferon- interferes w/ virus replication

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9
Q

What are lipid mediators of inflammation?

A

Prostaglandins, leukotrienes, and platelet activating factor (PAF)

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10
Q

What is a CD4 Lymphocyte?

A
  • Helper cell that is KEY to immune response
  • Actives macrophages
  • Activates CD8 (cytotoxic) T lymphocytes
  • Activates B-Lymphocytes to secrete immunoglobulin
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11
Q

What is CD 8 Lymphocytes?

A

-(Cytotoxic) T lymphocytes that destroys target cells by synthesis and release of cytotoxin, e.g., perforin & granzymes

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12
Q

Cytotoxins= _________

A

Lymphokines

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13
Q

CD8 synthesize and release what?

A
  • Interfeon gamma (INF- gamma)
  • Tumor necrosis Factor alpha (TNF-a)
  • Tumor necrosis Facor-beta (TNF-b)
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14
Q

B-lymphocytes is a precursor of ________

A

Plasma cells

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15
Q

Plasma cells and B-lymophocytes are capable of synthesis and release of what?

A

Immunoglobulin

Ig G, M, E, D and A

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16
Q

What are the Cellular Population at different stages of inflammation?

A

Initial–> PMNs
Acute–> PMNs, Macrophages, and some lymphocytes
Chronic–> A few PMNs & macrophages, and MOSTLY lymphocytes and Plasma cells

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17
Q

What is a abscess defined as?

A
  • A dense localized collection of inflammatory cells, primarily PMNs and tea necrosis.
  • With time the accumulation of inflammatory cells are surrounded & walled off by immature connective tissue & proliferating capillaries
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18
Q

What are the vascular components of gingiva; inhalation?

A

1) Color
2) Edema/Swelling
3) Bleeding

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19
Q

What is the difference between Perio and Gingivitis?

A

GINGIVITIS- requires plaque to initiate disease and clinical signs of inflammation. (NO bone loss, PDL destruction of apical migration of JE)

PERIODONTITIS- requires plaque, bone loss, PDL destruction, apical migration of JE, BUT may NOT require signs of INFLAMMATION

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20
Q

Everyone with poor plaque control develops _______

A

gingivitis

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21
Q

T or F. Everyone that has gingivitis because of poor long-term plaque control eventually develops periodontitis.

A

FALSE

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22
Q

T or F. Plaque is necessary and sufficient to initiate periodontitis.

A

False (not sufficient)

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23
Q

T or F. Plaque is necessary and sufficient to initiate gingivitis.

A

True

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24
Q

T or F. Development of periodontitis requires a susceptible host

A

True

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25
Q

What are the two common microbiota associated with health?

A

Facultative and Gram (+)

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26
Q

What are the two common microbiota associated with Periodontitis?

A

Anaerobes and Gram (-)

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27
Q

T or F. Everbody develops gingivitis but only susceptible patients will develop periodontitis

A

True

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28
Q

What is the positive and negative affect of our Immune System?

A

Positive- Provides a defensive process

Negative- Accounts for tissue injury observed in gingivitis and periodontitis

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29
Q

What is was the study conducted in Sri-Lanka?

A
  • No dental treatment
  • No plaque control
  • 100% gingivitis
  • 81 % Moderate Alveolar bone loss rate
  • 8% rapid rate
  • 11 % no progression
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30
Q

Periodontitis is similar to gingivitis in that ___________

A

It is Plaque- induced

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31
Q

Periodontitis is subject related int that a _______ is required

A

Susceptible host (immune system)

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32
Q

In Periodontitis, only a ______ % of the population experiences ________

A
  • Small

- Advanced destruction

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33
Q

In Periodontitis the progression of the disease is probably an ________________ model

A

Asynchronous multiple burst model

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34
Q

What is a continuous model?

A

ALL sites show a continuous an progressive loss of CAL over time

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35
Q

What is the Random burst model?

A
  • ALL sites exhibit progressive loss over time

- Random burst of disease activity with periods of quiescence

36
Q

What is the Asynchronous multiple burst model ?

A

1) Several sites have 1 or more burst of activity
2) Prolonged period of inactivity
3) Cumulative extent of destruction varies among sires
4) Some sites DONT develop attachment loss

37
Q

Why are Subantimicrobials prescribed?

Example?

A

So host does not have destructive reaction

Ex: Doxycycline give 20 mg dose (MMP is stunted) for 90 days 2X a day

38
Q

What do MMPs do?

A
  • Chemotaxis: PMNL, Macrophages, CD4/8 cells
  • Induction of acute phase response
  • Activation of osteoclasts
  • Inhibition of fibroblast growth
  • Inhibition of collagen synthesis
39
Q

Steroids targets what?

A

Phospholipase to reduce inflammation after surgery

40
Q

Singulair targets what?

A

5-lipoxygenase

41
Q

Aspirin, NSAIDsm Cox-2, Indomethacin targets what?

A

Cyclooxygenase

42
Q

What are the effects of Arestin?

A

Controls bleeding, and bacteria in area without having a systemic effect.

Note: Can be placed sub gingival 1mg

43
Q

What are Cytokines?

A

Soluble, locally active polypeptides that regular cell growth, differentiation and or function

44
Q

Specific cytokines may have different biological properties dependent on what 4 things?

A

1) Concentration
2) Cell type of origin
3) Target cell
4) Type of extracellular matrix

45
Q

What are the functions of PGE2?

A

1) Vasodialtion
2) Pyrogenic
3) Release mediator from mast cells
4) Cell mediated cytotoxicity

46
Q

What are the Growth factors and what do they stimulate?

A 
TGF= Stimulates epic cells & fibroblasts
PDGF= Stimulates fibroblasts 
EGF= Stimulates epic cells 
FGF= Stimulates fibroblasts
47
Q

Describe healthy gingiva

A
  • Some PMNs and macrophages present
  • Few PMNs migrating thru JE
  • No collagen destruciton
  • Intact epithelial barrier
  • Gingival crevicular fluid present
48
Q

What is the INITIAL lesion of gingivitis?

A

1) Develops in 2 to 4 days
2) Inflammatory cell infiltrate primary PMNs
3) Vasculitis
4) Loss of perivascular CT (collagen)
5) INCREASE in GCF
6) No bone loss or CAL

49
Q

What are the cells for Acute, Chonic, and increased chronicity?

A

Acute= PMNs
Chronic= Lymphocytes
Increase in chronicity= Plasma cells

50
Q

What are the virulence factors that stimulates the host?

A
  • Stimulates the host cells to release cytokine (IL-1, TNF and PGE2) and chemoattractant factors (IL-8)
  • Attract inflammatory cells (LPS)
51
Q

What are the virulence factors that degrade the host?

A

Enzymes:

1) Hyalyronidase
2) Collagenase
3) Trypsin-like enzyme
4) Keratinase
5) Phospholipase A

52
Q

What is the EARLY lesion of gingivitis?

A

1) Evolves @ 4-7 days
2) Acute inflammation persists (PMNs)
3) Chronic inflammatory cells infiltrate begins to appear (lymphocytes & macrophages)
4) 70% loss of collage in gingival lamina propr.
5) Fibroblasts exhibit evidence of damage
6) Beginning psuedopocket formation
7) Edema and erythema of marginal gingiva
8) Increased GCF flow
9) Loss of gingival stilling
10) Bleeding on probing

53
Q

MMP genes family encodes 28 _________________

A

metal- dependent endopeptidases

54
Q

What do Matrix Metalloproteinases (MMPs) work against?

A

MOST all extracellular matrix macromolecules

Note: Most are secreted as INACTIVE pro-enzymes

55
Q

Which MMPs are most active in periodontal disease?

A

1) Interstitial Collagenases
2) Stromelysins
3) Gelatinases
4) Metalloelastases

56
Q

Specific Host MMPs (6) most active in periodontal disease?

A

MMP1 - Interstitial collagenase & fibroblast collagenase

MMP2 Fibroblast Gelatinase; Type 4 collagenase

MMP 8- PMN collagenase

MMP- 9 PMN Gelatinase; Type 4 collagenase

MMP 12- Macrophage Elastase

MMP 13- Fibroblast Collagenase

57
Q

What are some examples of where MMP may be used to breakdown extracellular matrix?

A

1) Embryonic development
2) Tissue remodeling
3) disease processes, arthritis, metastasis, and thromboembolism

58
Q

Describe the ESTABLISHED Lesion of Gingivitis or “Transition to Periodontitis”

A

1) AFTER ( 14-21 DAYS) 2-3 WEEKS the early lesion transition to established
2) PMNs persisted but chronic inflammatory cells infiltrate dominates (i.ed lymphocytes, macrophages, and plasma cells)
3) Micro ulceration of pocket epithelium
4) Elongation of epithelial rete pegs
5) No or slight histologic evidence of bone loss
6) Continued loss of collagen & severe fibroblast degradation

59
Q

What are the Clinical Features of the Established Lesion ?

A

1) Edema
2) Erythema
3) Bleeding upon probing
4) Gingival changes: color, contour, consistency
5) NO BONE LOSS

60
Q

The established lesion is the ________ Stage of gingivitis

A

final

61
Q

The established lesion can remain stable for _______, ______ or even ______ until it develops to periodontitis

A

weeks
months
years

62
Q

T or F. The mechanisms of change from gingivitis to periodontitis is well understood

A

False; is not well understood

63
Q

T or F. In the established lesion is difficult to predict which patents will develop periodontitis, but we can identify risk groups

A

True

64
Q

In the stages of gingivitis, EARLY occurs in how many days?

A

4-7 days

65
Q

In the stages of gingivitis, INTIAL occurs in how many days?

A

2-4 days

66
Q

In the stages of gingivitis, ESTABLISHED occurs in how many days?

A

14-21 days

67
Q

In the stages of gingivitis, which stage has B-cell or Plasma cells?

Which has only T-cells?

A
  • Established

- Early

68
Q

In the ADVANCED Lesion “Periodontitis” which cells are involved in Alveolar bone resorption

A

1) Activated osteoclasts
2) MMPs
3) Cytokines (IL-1, IL-6, IL-8, TNF-a)
4) Prostaglandins (PGE2)
5) Leukotrienes

69
Q

What does pocket formation result from?

A

1) Apical migration of JE

2) Loss of CT fiber attachment
- Gingival fiber ligament
- PDL

3) Loss of bone

70
Q

What is the Histopathology of the Advanced Lesion?

A

1) PMNs
2) Plasma cells, Lymphocytes, Macrophages
3) Extension of lesion into PDL & bone
4) Loss of collagen continues
5) Cytopathology altered plasma cells
6) Progressive pocket formation with cell-mediated bone resorption (osteoclastic)
* Attachment loss

71
Q

In an Established Lesion what are the soft tissue reactions?

A

1) Bacterial invasion
2) Increased epithelial spacing
3) Increased epithelial turnover
4) Epithelial loss of intermediate, tight, and gap junctions
5) Host cells membranes damaged & rupture
6) Epithelial basal lamina damage

72
Q

What are the clinical features of advanced lesion?

A

1) Perio pocket formation (attachment loss)
2) Pocket epi ulceration
3) Radiographic bone loss
- 30-50% NEEDS to be LOST to show up on X-ray
4) BOP
5) Changes in gingival color, contour, consistency
6) mobility

73
Q

Lesions in _______ bone can’t be seen on radiographs

A

Cancellous

74
Q

Perforation of _________ bone required before radiographic detection

A

Cortical bone

75
Q

The normal CEJ-bone crest distance = ___________

A

1.5-2.0 mm

76
Q

T or F. Significant bone loss present before any radiographic evidence

A

True

77
Q

Significant attachment loss proceeds bone loss by 6 to 8 months

A

True

78
Q

T or F. There must be 20%-40% density loss before radiographic detection

A

False 30-50%

79
Q

Regarding the Pathogenesis Human Periodontitis Model, what are the risk factors for the Host Immuno-Inflammatory response and CT & bone metabolism?

A

1) Environmental Factors

2) Genetic Risk Factors

80
Q

Regarding the Pathogenesis Human Periodontitis Model, Clinical Signs of disease initiation and progression lead to what?

A

Microbial challenge

81
Q

Regarding the Pathogenesis Human Periodontitis Model., What 2 factors leave the “Host Immuno-inflammatory response to the CT & bone metabolism?

A

1) Cytokines & Prostanoids

2) MMP (Matrix metalloproteinases

82
Q

The Microbial Challenge will present ______________ and ______________ to the Host ImmunoInflammatory response?

A

1) Antigens

2) Lipopolysaccharide
& Other virulence factors

83
Q

The Host Immuno Inflammatory Response will present ______________ and ______________ to CT & bone metabolism?

A

1) Cytokines & prostanoids

2) Matrix metalloproteinases

84
Q

CT & bone metabolism will lead to what——-> _______

A

Clinical signs of signs of disease initiation & progression

85
Q

Regarding the Pathogenesis Human Periodontitis Model,, Tissue breakdown products & Ecological factors are due to what 2 things?

A

1) Microbial Challenge

2) Clinical Signs of Disease

Periodontics D2 (12 decks)

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