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Immunology Flashcards

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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

25
part of both innate and adaptive immunity systems. (A biochemical cascade that helps clear pathogens by lysis, opsonization, binding, and clearance of immune complexes).
Complement:
26
– now T-regulatory cells, | down-regulate T and B cells (CD8 ,CD25expression); prevent autoimmune disease
T suppressor cells
27
- mononuclear cells that kill cells | sensitized with antibody (via Fc receptors) (CD28cells which were signaled by CD8 cells)
K (Killer) cells
28
- kill virally infected and transformed target cells that have not been previously sensitized (CD56 cells)
NK (Natural Killer) cells
29
- activation in connective tissue | ►will become macrophages*
Monocytes (5%)
30
(> 70%)* - 48 hours lifespan in | blood with migration to sites for phagocytosis
Neutrophils
31
(2-5%) - cause damage by | exocytosis (eg: histamine release)
Eosinophils
32
- contain mediators of inflammation (histamine, prostaglandins, leukotrienes and cytokines)-involved in allergic reactions
Mast cells
33
(< 0.5%) - are in some ways | functionally similar to mast cells
Basophils
34
• Definition: soluble, locally active polypeptides; regulate cell growth, differentiation, function; produced by cells of the immune system
Cytokines
35
: (cytokine) Pro-inflammatory: stimulates osteoclasts, fibroblasts, macrophages - most important proinflammatory mediator of periodontits
IL-1
36
:(cytokine) Pro-inflammatory: stimulates T and B cells
IL-6
37
: (cytokine) Pro-inflammatory: attracts and activates | PMNs
IL-8
38
: (cytokine) Pro-inflammatory: activates osteoclasts
TNF
39
``` : (cytokine) Vasodilation Pyrogenic Releases mediator from mast cells Cell-mediated cytotoxicity ```
PGE2
40
What 2 growth factors are needed to stimulate fibroblasts?
PDGF | FGF
41
What growth factor stimulates epithelial cells and fibroblasts?
TGF
42
What growth factor stimulates epithelial cells?
EGF
43
Can you accurately predict which gingivitis cases will progress to periodontitis?
No
44
``` 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) ```
Healthy
45
``` • 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 ```
Initial Lesion
46
``` 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 ```
Initial
47
``` • 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** ```
Early Lesion
48
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
Matrix Metalloproteinases | MMPs
49
How much collagen loss is expected in early lesion?
up to 70%
50
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
Early lesion
51
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
Established lesion
52
Which lesion of gingivitis has micro ulcerations of sulcular epithelium?
Established lesions
53
Which lesion of gingivitis is a b cell to plasma cell lesion?
Established lesion
54
Which lesion of gingivitis involves t cells and horizontal migration of JE?
Early lesion
55
``` Clinical Features of _____ lesion 1. Edema 2. Erythema 3. Bleeding on probing (BOP) 4. Gingival changes: • color, contour, consistency 5. No bone loss ```
Established lesion
56
``` _____ 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 ```
Advanced lesion
57
``` 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 ```
Advanced
58
How much volume/density needs to be lost of bone before detection on radiograph?
50%
59
_____ is the primary etiology | for both gingivitis and periodontitis
Plaque

Perio 1 (12 decks)

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