Evolution of Inflamm Perio Lesion (Lecture 4) Flashcards

1
Q

What are the 1st wave of cells to the inflammatory site?

A

Neutrophils (PMNs)

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2
Q

Interesting: Cytoplasmic granules of Basophils contain-Histamine (duh), Platelet Acivating factor, Heparin (anticoagulant-so why have platelet active..nvm), my favorite _____, and SRS-As (Slow-reacting substances of anaphylaxis-leukotrienes)

A

TNF-a

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3
Q

What are the 5 main cytokines/lymphokines released by monocytes/macrophages?

A
  1. IL-1 (osteoclastic activation, B-lymphocyte activation, and activation of CD8 lymphocytes)… 2. IL-6 (osteoclast activation) 3.TNF-a (activator of endothelium and inflammatory mediator) 4.INF (interferon – interferes with virus replication) 5.LIPID mediators of inflammation: prostaglandins, leukotrienes, and platelet activating factor (PAF)
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4
Q

What cell Activates macrophages, Activates CD8 (cytotoxic) T lymphocytes, and Activates B-lymphocytes to secrete immunoglobulin????

A

CD4 Helper T Lymphocyte

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5
Q

Which cell Destroys target cells by synthesis and release of cytotoxin, e.g., perforin and granzyme??

A

CD8 Cytotoxic Lymphocyte

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6
Q

What do CD8’s do their damage with? (4)

A

1.Cytotoxins (lymphokines) 2.INF-g 3.TNF-a 4. TNF-b

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7
Q

MOST DEFINITELY on the test: Cellular Stages of inflame—-Intial: _____……ACUTE: ______…..Chronic: _____

A

PMNs….PMNs, Macrophages, few Lymphocytes….FEW PMNs and Macrophages…MOSTLY Lymphocytes and Plasma Cells

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8
Q

________:defined as a dense localized collection of inflammatory cells, primarily neutrophils, accompanied by tissue necrosis. With time the accumulation of inflammatory cells are surrounded and walled off by immature connective tissue and proliferating capillaries.

A

Abscess

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9
Q

GINGIVITIS VS PERIODONTITIS! Plaque necessary

to initiate the disease?

A

G: YES P: YES

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10
Q

GINGIVITIS VS PERIODONTITIS! Clinical signs of inflammation?

A

G: YES P: MAYBE!!!

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11
Q

GINGIVITIS VS PERIODONTITIS! Bone loss

A

G: hell no P: hell YES

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12
Q

GINGIVITIS VS PERIODONTITIS! PDL destruction

A

G. nope P. yep

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13
Q

GINGIVITIS VS PERIODONTITIS! Apical migration of JE

A

G. nope P. yep

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14
Q

Does everybody with poor plaque control eventually develop gingivitis?

A

YES

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15
Q

Does everybody that has gingivitis because of poor long-term plaque control eventually develop periodontitis?

A

NO

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16
Q

_______ is necessary and sufficient to initiate gingivitis

A

Plaque

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17
Q

Plaque is necessary but not _______ to initiate periodontitis…IN ORDER to DEVELOP periodontitis it requires _________!!!!!

A

sufficient… A susceptible host!!!!!!

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18
Q

A patient’s _______ is extremely important in the pathogenesis of perio disease.

A

immunology

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19
Q

Immune system = provides a defensive process but also may account for most of the ________ observed in gingivitis and periodontitis

A

tissue injury

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20
Q

What did the Shri Lanka study show us?

A

That with uncontrolled plaque only 8% had rapid periodontal disease! 81% had mild progression and 11% had no problems!

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21
Q

The progression of perio disease is probably an ________ multiple burst model

A

asynchronous

22
Q

Since perio disease is typically a ‘random burst model’ see your pt every ___ months.

A

3 months (bacteria take 9-12wks to recolonize)

23
Q

What do we use to slow down MMP (metalo matrix proteinase)

A

deoxycycline

24
Q

________: soluble, locally active polypeptides that regulate cell growth, differentiation and/or function

A

Cytokines

25
Q

IMPORTANT CYTOKINES: Pro-inflammatory: stimulates osteoclasts, fibroblasts, macrophages

A

IL-1

26
Q

IMPORTANT CYTOKINES: Pro-inflammatory: stimulates B and T cells

A

IL-6

27
Q

IMPORTANT CYTOKINES: Pro-inflammatory: attract and activates PMNs

A

IL-8

28
Q

IMPORTANT CYTOKINES: Pro-inflammatory: activate osteoclasts

A

TNF-a

29
Q

IMPORTANT CYTOKINES: Vasodilation Pyrogenic Release mediator from mast cells Cell-mediated cytotoxicity

A

PGE2

30
Q

What are the 4 Growth Factors?

A

TGF, PDGF, EGF, FGF

31
Q

Is there Gingival Crevicular Fluid present in clinically healthy gingiva? Art there PMNs and Macrophages?

A

Yes there sure is!…yep a small amount of PMNs and MO’s

32
Q

When does an INITIAL gingivitis inflammatory lesion develop?

A

2 to 4 days

33
Q

REMEMBER: Acute = PMNs, Chronic = Lymphocytes

Increase in chronicity = _______

A

plasma cells

34
Q

What are the two basic categories that virulence factors cause?

A
  1. Stimulates the host (IL-1, TNF-a,PGE2, LPS induced) 2.Degrades the host (hyaluronidase, collagenase, phospholipase a)
35
Q

WHEN does the EARLY lesion develop? (NOT INITIAL lesion :)

A

4-7days

36
Q

70% loss of collagen in gingival lamina propria.

A

Early Lesion

37
Q

A chronic inflammatory cell infiltrate begins to appear, i.e., lymphocytes and macrophages.

A

Early Lesion

38
Q

eginnings of pseudopocket formation.

A

Early Lesion

39
Q

Loss of gingival stippling, Bleeding on probing

A

Early Lesion

40
Q

The ____ gene family encodes 28 metal-dependent endopeptidases with activity against most, if not all, extracellular matrix macromolecules.

A

Matrix Metalloproteinases MMP

41
Q

______ most active in periodontal disease: • Interstitial Collagenases • Stromelysins • Gelatinases • Metalloelastases

A

MMP’s

42
Q

Host MMPs most active in periodontal disease are:

A

MMP-1 MMP-2 MMP-8 MMP-9 MMP-12 MMP-13

43
Q

After ___-___ weeks the early lesion transitions to the established lesion.

A

2-3 weeks

44
Q

No or slight histologic evidence of bone loss

A

established gingival inflammatory lesion

45
Q

The _______ lesion is the final stage of

gingivitis

A

established

46
Q

RETE PEGS in JE?

A

Early gingivitis

47
Q

RETE PEGS and MicroUlcers in JE?

A

Established Gingivitis

48
Q

The _______ Lesion: Alveolar bone resorption, Activation of osteoclasts, MMPs, Cytokines
• IL-1, IL-6, IL-8, TNF-α, Prostaglandins • PGE2, Leukotrienes

A

ADVANCED

49
Q

What 3 things causes pocket formation in periodontitis?

A

1.Apical migration of JE 2.Loss of CT fiber attachment: Gingival fiber ligament, PDL 3. Loss of bone

50
Q

What % of bone loss occurs BEFORE its detected on a radiograph????

A

30%-50% of volume/density needs to be lost before

detection on radiograph!!!!

51
Q

What is the Normal CEJ-Bone Crest distance? (biological width)

A

1.5-2mm