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Perio 1 > Immunology > Flashcards

Immunology Flashcards

1
Q

– Plaque-induced
– Inflammation (edema/bleeding upon probing)
– No destruction of PDL and bone
– No apical migration of epithelial attachment
Epithelial attachment = Junctional epithelium

A

Gingivitis

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2
Q 
–Plaque-induced
–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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3
Q
  1. Plaque-induced similar to gingivitis.
  2. Host-related (susceptible host).
  3. Each site is individualized or a specific
    environment.
  4. A % of affected population experiences
    severe destruction.
  5. The progression of the disease is
    probably
A

Periodontitis

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4
Q

______ model (1940-1960’s) of periodontitis
– Progressive loss over time of some sites
– No destruction in others
– Time of onset and extent vary among sites
– (i.e. Periodontal disease affects mainly
posterior teeth.)
- gingival col

A

Progressive

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5
Q

________ model (1980-2000’s) of periodontitis
– Activity occurs at random at any site
– Some sites show no activity
– Some sites have one or more bursts of activity
– Cumulative extent of destruction varies
among sites
– (i.e. Periodontitis is different in various
sites in the same individual and it is
difficult to predict attachment loss.)

A

Random burst

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6
Q

________ model of periodontitis
(1980-2000’s)
– Several sites have one or more bursts of
activity during one period of life
– Prolonged period of inactivity; remission
– Cumulative extent of destruction varies
among sites
– Some sites don’t develop attachment loss
– (asynchronous=not occurring at same time)
– Bursts due to Risk Factors

A

Asynchronous multiple burst

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7
Q

What are the least common teeth lost to periodontitis?

A

Mand canine and 1st PM

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8
Q

What is the most commonly lost tooth to perio disease?

A

Max 2nd molars

2nd: 1st max molar

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9
Q

What are the 5 signs of inflammation?

A
  • Rubor (redness)
  • Calor (heat)
  • Dolor (pain)
  • Tumor (swelling)
  • Functio Laesa (loss of function)
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10
Q

Inflammation is a ____ phenomenon

A

vascular

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11
Q

do blood vessels dilate or constrict due to inflammation?

A

Dilate

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12
Q

What are the first cells to defense in inflammation?

A

PMNs
Monocytes/macrophages
(phagocytosis)

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13
Q

What are the mediators of 2ndary defense?

A

B and T cells

Plasma cells produce antibodies

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14
Q

– Activated B-cells become Plasma cells

– Plasma cells produce immunoglobulins

A

B lymphocytes

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15
Q

– developed in the thymus
– several functions (antigen presentation)
– help B-cells divide; can destroy virally infected cells;
can down-regulate immune response

A

T lymphocytes

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16
Q

(TH0/TH1/TH2)
• help B cells to divide
• control leukocyte development
• activate innate cell lining

A 
• CD 4 - MHC class II molecules
– T helper cells
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17
Q
  • MHC class I molecules
    – T cytotoxic
    • destroy virally infected target cells
A

• CD 8

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18
Q

phagocytosis; produce lysosomal enzymes

A

PMNs:

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19
Q

phagocytosis; process antigens;

cytokine secretion

A

Macrophages:

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20
Q

• Plasma cells: produce antibodies

A

B-Lymphocytes

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21
Q

: first responder; largest in size

A

IgM

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22
Q

: second responder; most abundant; crosses

placenta

A

IgG

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23
Q

salivary IgA; a dimer

A

IgA:

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24
Q

: on Mast cells, allergic reactions

A

IgE

25
Q

part of both innate and adaptive
immunity systems. (A biochemical cascade that
helps clear pathogens by lysis, opsonization,
binding, and clearance of immune complexes).

A

Complement:

26
Q

– now T-regulatory cells,

down-regulate T and B cells (CD8 ,CD25expression); prevent autoimmune disease

A

T suppressor cells

27
Q
  • mononuclear cells that kill cells

sensitized with antibody (via Fc receptors) (CD28cells which were signaled by CD8 cells)

A

K (Killer) cells

28
Q
  • kill virally infected
    and transformed target cells that have not been
    previously sensitized (CD56 cells)
A

NK (Natural Killer) cells

29
Q
  • activation in connective tissue

►will become macrophages*

A

Monocytes (5%)

30
Q

(> 70%)* - 48 hours lifespan in

blood with migration to sites for phagocytosis

A

Neutrophils

31
Q

(2-5%) - cause damage by

exocytosis (eg: histamine release)

A

Eosinophils

32
Q
  • contain mediators of inflammation
    (histamine, prostaglandins, leukotrienes and
    cytokines)-involved in allergic reactions
A

Mast cells

33
Q

(< 0.5%) - are in some ways

functionally similar to mast cells

A

Basophils

34
Q

• Definition: soluble, locally active polypeptides;
regulate cell growth, differentiation, function;
produced by cells of the immune system

A

Cytokines

35
Q

: (cytokine) Pro-inflammatory: stimulates osteoclasts,
fibroblasts, macrophages
- most important proinflammatory mediator of periodontits

A

IL-1

36
Q

:(cytokine) Pro-inflammatory: stimulates T and B cells

A

IL-6

37
Q

: (cytokine) Pro-inflammatory: attracts and activates

PMNs

A

IL-8

38
Q

: (cytokine) Pro-inflammatory: activates osteoclasts

A

TNF

39
Q 
\: (cytokine)
 Vasodilation
Pyrogenic
Releases mediator from mast cells
Cell-mediated cytotoxicity
A

PGE2

40
Q

What 2 growth factors are needed to stimulate fibroblasts?

A

PDGF

FGF

41
Q

What growth factor stimulates epithelial cells and fibroblasts?

A

TGF

42
Q

What growth factor stimulates epithelial cells?

A

EGF

43
Q

Can you accurately predict which gingivitis cases will progress to periodontitis?

A

No

44
Q 
Clinically \_\_\_\_\_ Gingiva**
• Some neutrophils and 
macrophages are present in 
connective tissue
• A few neutrophils are migrating 
through the JE
• No collagen destruction
• Intact epithelial barrier
• Gingival crevicular fluid is 
present
• Appears clinically healthy 
(Color, Contour, Consistency)
A

Healthy

45
Q 
• Develops in 2 to 4 days
• Cells of acute inflammation present
• Increased GCF flow
• Start of pseudopocket formation
– Remember: 
Acute = PMNs 
Chronic = Lymphocytes
Increase in chronicity ►►►Plasma cells
A

Initial Lesion

46
Q 
Clinical Features of \_\_\_\_\_
Lesion
• Increased GCF flow
• Sulcus increases from 0→3 mm by 
formation of a pseudopocket
• Alveolar bone is normal on the 
radiograph
A

Initial

47
Q 
• 4-7 days
• Acute inflammation persists (initial 
lesion►►), increased GCF, 
pseudopocket formation
• Cells of chronic inflammation appear and 
then dominate 
• (chronic→shift to T lymph. from PMNs)
Collagen loss continues**
MMPs Activation begins**
A

Early Lesion

48
Q

The family includes 28 metal-dependent endopeptidases (proteases) with activity
against most, if not all, extracellular matrix macromolecules. (used for normal tissue remodeling)
Sub-Classes
- Interstitial Collagenases** - Gelatinases
- Stromelysins - Secreted RXKR (Arg-X-Lys-Arg)
- Membrane type - Metalloelastase

A

Matrix Metalloproteinases

MMPs

49
Q

How much collagen loss is expected in early lesion?

A

up to 70%

50
Q

Clinical Features of ___ Lesion

  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
A

Early lesion

51
Q

The ____ Lesion
1. Acute inflammation persists
-After 2-3 weeks early lesion shifts to
established lesion (a stable lesion)
-Chronic inflammation dominates
• Activated B-lymphocytes → Plasma cells**
2. PMN “wall”: host tries to contain the infection
-Micro-ulcerations of pocket epithelium (causes BOP)
-More proliferation of JE
-More elongation of epithelial rete pegs into
connective tissue
3. Bystander Damage
4. Two-edged “sword” of immune system

A

Established lesion

52
Q

Which lesion of gingivitis has micro ulcerations of sulcular epithelium?

A

Established lesions

53
Q

Which lesion of gingivitis is a b cell to plasma cell lesion?

A

Established lesion

54
Q

Which lesion of gingivitis involves t cells and horizontal migration of JE?

A

Early lesion

55
Q 
Clinical Features of \_\_\_\_\_ lesion
1. Edema
2. Erythema
3. Bleeding on probing (BOP)
4. Gingival changes:
• color, contour, consistency
5. No bone loss
A

Established lesion

56
Q 
\_\_\_\_\_ lesion
• Features of periodontal breakdown
1. Pocket formation
a. PDL destruction
b. Apical migration of JE
c. Bone resorption
2. Asynchronous Multiple Burst Model (?)
a. Short bursts of disease activity
b. Long periods of quiescence
3. Bystander damage
4. Host balance of damage/repair is upset
A

Advanced lesion

57
Q 
Clinical Features of\_\_\_\_\_\_\_
Lesion
1. Periodontal pocket formation 
2. Pocket epithelium ulceration
3. Radiographic bone loss
– 50% of volume/density needs to be lost before 
detection on radiograph
4. Bleeding on probing
5. Changes in gingival color, contour, consistency
6. Attachment Loss
7. Mobility
A

Advanced

58
Q

How much volume/density needs to be lost of bone before detection on radiograph?

A

50%

59
Q

_____ is the primary etiology

for both gingivitis and periodontitis

A

Plaque

Perio 1 (12 decks)

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