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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
What are the two common microbiota associated with health?
Facultative and Gram (+)
26
What are the two common microbiota associated with Periodontitis?
Anaerobes and Gram (-)
27
T or F. Everbody develops gingivitis but only susceptible patients will develop periodontitis
True
28
What is the positive and negative affect of our Immune System?
Positive- Provides a defensive process Negative- Accounts for tissue injury observed in gingivitis and periodontitis
29
What is was the study conducted in Sri-Lanka?
- No dental treatment - No plaque control - 100% gingivitis - 81 % Moderate Alveolar bone loss rate - 8% rapid rate - 11 % no progression
30
Periodontitis is similar to gingivitis in that ___________
It is Plaque- induced
31
Periodontitis is subject related int that a _______ is required
Susceptible host (immune system)
32
In Periodontitis, only a ______ % of the population experiences ________
- Small | - Advanced destruction
33
In Periodontitis the progression of the disease is probably an ________________ model
Asynchronous multiple burst model
34
What is a continuous model?
ALL sites show a continuous an progressive loss of CAL over time
35
What is the Random burst model?
- ALL sites exhibit progressive loss over time | - Random burst of disease activity with periods of quiescence
36
What is the Asynchronous multiple burst model ?
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
Why are Subantimicrobials prescribed? | Example?
So host does not have destructive reaction Ex: Doxycycline give 20 mg dose (MMP is stunted) for 90 days 2X a day
38
What do MMPs do?
- Chemotaxis: PMNL, Macrophages, CD4/8 cells - Induction of acute phase response - Activation of osteoclasts - Inhibition of fibroblast growth - Inhibition of collagen synthesis
39
Steroids targets what?
Phospholipase to reduce inflammation after surgery
40
Singulair targets what?
5-lipoxygenase
41
Aspirin, NSAIDsm Cox-2, Indomethacin targets what?
Cyclooxygenase
42
What are the effects of Arestin?
Controls bleeding, and bacteria in area without having a systemic effect. Note: Can be placed sub gingival 1mg
43
What are Cytokines?
Soluble, locally active polypeptides that regular cell growth, differentiation and or function
44
Specific cytokines may have different biological properties dependent on what 4 things?
1) Concentration 2) Cell type of origin 3) Target cell 4) Type of extracellular matrix
45
What are the functions of PGE2?
1) Vasodialtion 2) Pyrogenic 3) Release mediator from mast cells 4) Cell mediated cytotoxicity
46
What are the Growth factors and what do they stimulate?
``` TGF= Stimulates epic cells & fibroblasts PDGF= Stimulates fibroblasts EGF= Stimulates epic cells FGF= Stimulates fibroblasts ```
47
Describe healthy gingiva
- Some PMNs and macrophages present - Few PMNs migrating thru JE - No collagen destruciton - Intact epithelial barrier - Gingival crevicular fluid present
48
What is the INITIAL lesion of gingivitis?
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
What are the cells for Acute, Chonic, and increased chronicity?
Acute= PMNs Chronic= Lymphocytes Increase in chronicity= Plasma cells
50
What are the virulence factors that stimulates the host?
- Stimulates the host cells to release cytokine (IL-1, TNF and PGE2) and chemoattractant factors (IL-8) - Attract inflammatory cells (LPS)
51
What are the virulence factors that degrade the host?
Enzymes: 1) Hyalyronidase 2) Collagenase 3) Trypsin-like enzyme 4) Keratinase 5) Phospholipase A
52
What is the EARLY lesion of gingivitis?
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
MMP genes family encodes 28 _________________
metal- dependent endopeptidases
54
What do Matrix Metalloproteinases (MMPs) work against?
MOST all extracellular matrix macromolecules Note: Most are secreted as INACTIVE pro-enzymes
55
Which MMPs are most active in periodontal disease?
1) Interstitial Collagenases 2) Stromelysins 3) Gelatinases 4) Metalloelastases
56
Specific Host MMPs (6) most active in periodontal disease?
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
What are some examples of where MMP may be used to breakdown extracellular matrix?
1) Embryonic development 2) Tissue remodeling 3) disease processes, arthritis, metastasis, and thromboembolism
58
Describe the ESTABLISHED Lesion of Gingivitis or "Transition to Periodontitis"
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
What are the Clinical Features of the Established Lesion ?
1) Edema 2) Erythema 3) Bleeding upon probing 4) Gingival changes: color, contour, consistency 5) NO BONE LOSS
60
The established lesion is the ________ Stage of gingivitis
final
61
The established lesion can remain stable for _______, ______ or even ______ until it develops to periodontitis
weeks months years
62
T or F. The mechanisms of change from gingivitis to periodontitis is well understood
False; is not well understood
63
T or F. In the established lesion is difficult to predict which patents will develop periodontitis, but we can identify risk groups
True
64
In the stages of gingivitis, EARLY occurs in how many days?
4-7 days
65
In the stages of gingivitis, INTIAL occurs in how many days?
2-4 days
66
In the stages of gingivitis, ESTABLISHED occurs in how many days?
14-21 days
67
In the stages of gingivitis, which stage has B-cell or Plasma cells? Which has only T-cells?
- Established | - Early
68
In the ADVANCED Lesion "Periodontitis" which cells are involved in Alveolar bone resorption
1) Activated osteoclasts 2) MMPs 3) Cytokines (IL-1, IL-6, IL-8, TNF-a) 4) Prostaglandins (PGE2) 5) Leukotrienes
69
What does pocket formation result from?
1) Apical migration of JE 2) Loss of CT fiber attachment - Gingival fiber ligament - PDL 3) Loss of bone
70
What is the Histopathology of the Advanced Lesion?
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
In an Established Lesion what are the soft tissue reactions?
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
What are the clinical features of advanced lesion?
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
Lesions in _______ bone can't be seen on radiographs
Cancellous
74
Perforation of _________ bone required before radiographic detection
Cortical bone
75
The normal CEJ-bone crest distance = ___________
1.5-2.0 mm
76
T or F. Significant bone loss present before any radiographic evidence
True
77
Significant attachment loss proceeds bone loss by 6 to 8 months
True
78
T or F. There must be 20%-40% density loss before radiographic detection
False 30-50%
79
Regarding the Pathogenesis Human Periodontitis Model, what are the risk factors for the Host Immuno-Inflammatory response and CT & bone metabolism?
1) Environmental Factors | 2) Genetic Risk Factors
80
Regarding the Pathogenesis Human Periodontitis Model, Clinical Signs of disease initiation and progression lead to what?
Microbial challenge
81
Regarding the Pathogenesis Human Periodontitis Model., What 2 factors leave the "Host Immuno-inflammatory response to the CT & bone metabolism?
1) Cytokines & Prostanoids | 2) MMP (Matrix metalloproteinases
82
The Microbial Challenge will present ______________ and ______________ to the Host ImmunoInflammatory response?
1) Antigens | 2) Lipopolysaccharide & Other virulence factors
83
The Host Immuno Inflammatory Response will present ______________ and ______________ to CT & bone metabolism?
1) Cytokines & prostanoids | 2) Matrix metalloproteinases
84
CT & bone metabolism will lead to what-------> _______
Clinical signs of signs of disease initiation & progression
85
Regarding the Pathogenesis Human Periodontitis Model,, Tissue breakdown products & Ecological factors are due to what 2 things?
1) Microbial Challenge | 2) Clinical Signs of Disease

Periodontics D2 (12 decks)

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