Sweep 1.1 Flashcards

(68 cards)

1
Q

Mediators of innate immunity:

A

Prostaglandins
Matrix metalloproteinases
Proteinase inhibitors
Antimicrobial peptides

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2
Q

Prostaglandins (especially PGE2) induce

A

vasodilation and cytokine production

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3
Q

PGE2 induces

A

production of matrix metalloproteinases by fibroblasts and osteoclasts, which damage periodontal tissues

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4
Q

Mediators of innate immunity: Matrix metalloproteinases

A

Degrade extracellular matrix
Example: PMN collagenase (degrades the major structural protein in gingiva)
Concentrations are higher in inflamed gingiva than in healthy gingiva

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5
Q

Mediators of innate immunity: Proteinase inhibitors

A

Antagonize inflammation
Inhibit degradation of matrix proteins
Alpha-2 macroglobulin: broad spectrum proteinase inhibitor
Alpha-1 antitrypsin: broad spectrum proteinase inhibitor and potent inhibitor of PMN collagenase

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6
Q

Mediators of innate immunity: Antimicrobial peptides

A

Defensins:
Calprotectin:

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7
Q

Defensins: Inhibit

A

bacteria and fungi. Produced by mucosal surfaces and salivary gland epithelium.

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8
Q

Calprotectin:

A

Inhibits bacteria and fungi by chelating zinc. Produced by epithelium, PMNS, monocytes, macrophages.

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9
Q

Acute inflammation or injury increases vascular permeability, resulting in redness, edema, and increased

A

gingival crevicular fluid flow

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10
Q

PMN deliver

A

antimicrobial substances to bacteria in the early stages of infection

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11
Q

T-cell receptor has

A

T-cell receptor has 2 glycoprotein chains ( and ) with variable segments

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12
Q

Variable segments determine the

A

type of immune response

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13
Q

TCR in periodontitis

A

different before and after therapy

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14
Q

TCR different between

A

chronic and aggressive periodontitis

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15
Q

2 types of T-helper cells -

A

differ in cytokine profiles

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16
Q

Cytokines are messenger proteins that

A

transmit signals to other cells
Th1: IL-2, IFN-gamma, TNF-alpha
Th2: IL-4, 5, 6, 10, 13

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17
Q

3Cytotoxic T cells (Tc) activated by

A

cytokines

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18
Q

Tc cells respond to

A

intracellular pathogens

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19
Q

Antigens from these pathogens bind

A

MHC I molecules

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20
Q

Tc cells recognize this antigen presentation and

A

destroy infected cells

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21
Q

Not many Tc cells are found in

A

periodontitis, suggesting that viruses and invasive bacteria are not major players

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22
Q

B cell response

Humoral immunity

A

(antibody mediated) triggered in response to soluble antigens

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23
Q

Ag-Ab complex activates

A

complement

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24
Q

Ag-Ab complex facilitates

A

opsonization

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25
Th-2 cytokines activate
B cells to plasma cells
26
2 types of B cells- | Conventional:
produce antibodies against bacteria, levels decrease in healthy and treated sites
27
Autoreactive:
produce auto-antibodies, levels do not decrease after treatment
28
Efficacy of B cell response | Avidity:
Ag-binding differs among antibody subclasses. Not all are capable of effective opsonization or complement activation.
29
IgG2
chronic periodontitis, but IgG2 predominates in aggressive periodontitis.
30
Antigen recognition:
IgG2 recognizes carbohydrate antigens (LPS), while other subclasses mainly recognize protein Ag
31
Homing of relevant immune cells takes place within the
periodontal lesion.
32
Th2 cells outnumber
Th1 cells in chronic periodontal lesions.
33
Plasma cells are among the most predominant and active
secretory cells in advanced periodontal lesions.
34
The ratio of IgG subclasses are similar in
serum and GCF.
35
An individual’s ability to mount a specific
Ab response to bacteria in the subgingival biofilm may indicate a patient’s susceptibility to the disease and ability to respond to treatment.
36
Stomadeal epithelium releases factors which initiate
epithelial-ectomesenchymal interactions.
37
Dental lamina forms
Bud stage Cap stage Bell stage
38
Ectomesenchyme condenses around
dental organ (DO)
39
Forms dental follicle (DF) | Gives rise to
periodontium | Dental papilla determines shape and form of tooth
40
Embryogenesis
Crown forms first Outer and inner enamel epithelium proliferate apically Hertwig’s epithelial root sheath(RS) Odontoblasts (OB) form dentin Inner cells of RS secrete enamel-related proteins (amelogenins) RS fenestrates Ectomesenchymal cells of follicle contact root surface Amelogenin induces differentiation of these cells into cementoblast (**remember this for later) Cementoid forms Fibers of cementoid intermingle with immature dentinal fibres
41
Limits of free (marginal) gingiva | Macroscopic
Extends from FGM to FGG
42
Limits of free (marginal) gingiva | Microscopic
Extends from FGM to JE
43
No MGJ on
palate
44
Interdental papilla | Shape depends on
the contact relationships between adjacent teeth width of approximal tooth surfaces course of CEJ
45
Col – central zone that curves down. Turns over VERY quickly.
Concavity seen in contact areas of premolar / molar region Non-keratinized epithelium (similar to junctional epithelium), will stay this way as long as two teeth are in contact (protected from friction).
46
Oral epithelium Keratinized, stratified, squamous epithelium (keratinocytes). Layers
1- basal layer (stratum basale or stratum germinativum) 2- prickle cell layer (stratum spinosum) 3- granular cell layer (stratum granulosum) 4- keratinized cell layer (stratum corneum)
47
Orthokeratinized
(no nucleus)
48
Parakeratinized
(nuclear remnants)
49
From the basal layer to the granular layer: Cytoplasmic tonofilaments and number of desmosomes
increase. | The number of organelles decreases.
50
Cells of oral epithelium
``` Keratinocytes (90%) Clear cells (arrows) -melanocytes (synthesize melanin pigment) -Langerhans cells (defense cells)** -Merkel’s cells (sensory ```
51
Basement membrane | 2 layers
Lamina lucida(LL) -adjacent to basal cells (400 A) Lamina densa(LD)- adjacent to connective tissue Hemidesmosomes(HD)- dense plaques that attach epithelium to the basement membrane. Desmosomes: Pairs of hemidesmosomes
52
Lamina densa(LD)-
adjacent to connective tissue | Anchoring fibers project from LD into connective tissue
53
Microscopic anatomy of stippling | Boundary between
``` OE and underlying CT: CT projects into epithelium CT papillae epithelial ridges or rete pegs intervene When rete pegs fuse it is seen as stippling Rete pegs are missing at JE site. ```
54
JE does not correspond to Free Gingival groove until
tooth reaches final position, and as person ages, this relationship stops (recession). NOTE: the above is an unerupted tooth.
55
Differences between JE and OE
Size of the cells-JE>OE – means metabolically active. Size of intercellular space- JE>OE – allows fluid and neutrophils to flow. GCF = gingival cravicular fluid Number of desmosomes- JE
56
Collagen
Characteristic cross-banding Produced by fibroblasts, cementoblasts and osteoblasts Most abundant
57
Reticulin
Numerous adjacent to basement membrane | Around blood vessels
58
Oxytalan
mostly in pdl Run parallel to long axis of tooth Keep things from collapsing
59
Elastic
around blood vessels
60
Fibroblasts-
aligned along principal fibres
61
Osteoblasts-
line bone surface
62
Cementoblasts-
line cemental surface
63
Osteoclasts-
multinucleated, crete ruffled surface of bone epithelial cells nerve fibers
64
epithelial cell rests of Mallassez:
remnants of the Hertwig’s epithelial root sheath.
65
Cementum thickness increases by gradual apposition throughout life. Cementum thickness in cervical portion of the root:
20-50 m
66
Cementum thickness in apical portion of the root:
150-250 m
67
Alveolar bone Consists of bone formed both by | cells from the
dental follicle | cells independent of tooth development.
68
Alveolar bone
``` Cancellous bone Cortical bone –hard flat bone Bone marrow adipocytes vascular structures undifferentiated mesenchymal cells Remodels in response to forces and tooth movement ```