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Endodontics > After Midterm: Lec Dentin Pulp Complex 2 > Flashcards

After Midterm: Lec Dentin Pulp Complex 2 Flashcards

1
Q

Most accepted theory of dentin sensitivity:

A

Hydrodynamic

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2
Q

The other 2, not as accepted theories:

A

transduction, direct innervation

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3
Q

Are nerves present in dentinal tubules?

A

yes

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4
Q

Nerves that are directly activated in the dentinal tubules:

A

free nerve endings

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5
Q

Theory of transduction:

A

sensation is transduced from odontoblasts to nerves through junctions

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6
Q

Are there GAP junctions bw odontoblasts and nerves?

A

no

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7
Q

Hydrodynamic theory:

A

inward and outward movements of dentinal fluid activates sensory fibers by mechanotransduction

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8
Q

Causes of fluid movement:

A

dehydration, osmotic changes (sugary foods), mechanical probing, thermal probing

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9
Q

Stimuli leading to pulpal response:

A

direct exposure, crack, caries, restorative proc, cold, heat, osmotic differential

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10
Q

1’ cause for endo failure:

A

bacteria

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11
Q

TF? Direct exposure of the pulp to the oral environment will always require endo.

A

T

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12
Q

Do caries need to be in pulp to cause pulpal changes?

A

no

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13
Q

These can get to the pulp before caries:

A

Bacteria and their byproducts

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14
Q

Most common cause of pulpal pathosis:

A

caries

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15
Q

When is bacteria able to enter tubules:

A

once it reaches the DEJ

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16
Q

TF? The pulp only get irritated once the bacteria reaches it.

A

F. before

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17
Q

TF? Caries must reach the pulp before necrosis starts.

A

T

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18
Q

Inflammation and necrosis occur via:

A

toxic action, immune response, or frank invasion of bacteria

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19
Q

Ondontolbasts can be damaged due to:

A

deep preparations, drying of tubules, not enough water during drilling

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20
Q

TF? The pulp does not need to be exposed to undergo necrosis.

A

T, microabscess can lead to this

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21
Q

how do dentinal tubules changes as you approach the pulp?

A

inc in diameter and number

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22
Q

How does the dentin change as you approach the pulp?

A

more permeable

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23
Q

Cold stimuli, fast or slow response?

A

fast

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24
Q

Cold stimuli, inward or outward flow?

A

outward

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25
Q

Cold stimuli causes:

A

fluid contraction

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26
Q

Cold stimuli, expansion or constriction?

A

constriction

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27
Q

Is outward flow negative or positive pressure?

A

negative

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28
Q

Heat, inward or outward flow?

A

inward

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29
Q

heat response, slower or faster response?

A

slower

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30
Q

Heat response, negative or positive pressure?

A

positive

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31
Q

Heat stimuli, fluid expansion or contraction?

A

fluid expansion

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32
Q

Heat stimuli, slower or faster expansion?

A

slower

33
Q

Produces stronger nerve response, outward or inward flow?

A

outward

34
Q

Produces stronger nerve response, cold or hot stimuli?

A

cold

35
Q

Most common cause of osmotic differential:

A

sugars (refined carbs)

36
Q

Direction of fluid flow in dentinal tubules:

A

deeper tubules to coronal tooth structure

37
Q

Where in the tooth is there a lower osmotic pressure/ less solute?

A

deeper part of tubule

38
Q

TF? The deeper part of the tubule has a higher osmotic pressure/ more solute.

A

F, coronal portion

39
Q

TF? Pain after eating, expect carious lesion.

A

T

40
Q

What does the unyielding walls of dentin lead to:

A

limited space for pulpal swelling

41
Q

What does the constricted blood source of the pulp lead to:

A

limited blood supply, subject to “strangulation” by swelling.

42
Q

What does the tooth being surring by PDL/bone lead to?

A

PDL/ bone infalmmation

43
Q

Major blood source for tooth:

A

apical foramen

44
Q

3 major factors of pulpal response to irritants:

A

intensity, duration, host response

45
Q

TF? Innate immunity is specific immunity

A

F. non-specific

46
Q

Aspects of innate immunity:

A

histamine, bradykinin, arachidonic acid, neuropeptides

47
Q

What do histamine, bradykinin, arachidonic acid, neuropeptides all result in:

A

vasodilation, vascular permeability

48
Q

Cells that make histamine:

A

mast cells

49
Q

Products (?) of arachidonic acid:

A

prostaglandins, thromboxanes, leukotrienes

50
Q

Neuropeptides:

A

Calcitonin gene-related peptide (CGRP), Substance P (SP), Neurokinin A (NKA)

51
Q

Innate immunity, specific or non-specific?

A

non-specific

52
Q

Complement effect on bac:

A

cell lysis

53
Q

Phagocytes involved in innate immunity:

A

dendritic cells, PMN, mac

54
Q

PMNs, acute or chronic response?

A

acute

55
Q

mac, acute, chronic, or response to both?

A

chronic

56
Q

Goal of phagocytes:

A

engulf and remove bac and their byproducts

57
Q

TF? All cells involved in innate immunity are involved in antigen presentation.

A

F

58
Q

1st arrivers in innate immunity:

A

PMNs

59
Q

What do both B and T cells release?

A

cytokines –> more inflammation

60
Q

TF? T cells are involved in humoral immunity.

A

F. cell mediated

61
Q

What does pulp vitality depend upon?

A

normal cap blood flow and transcapillary fluid exchange

62
Q

Can the pulp become necrotic without being infected?

A

yes

63
Q

What can result in fluid displacement to be incompatible with pulp vitality?

A

marked deviations from normal pressure throughout pulp

64
Q

TF? Pulp can bc necrotic wo being infected.

A

T

65
Q

Pressure cycle:

A

fluid leaves vasculature, inc interstitial pressure, dentin = pressure can’t dissipate, microvasculature shutdown, release of breakdown products, necrosis, inc interstitial osmotic pressure, osmotic attraction draw more fluid from caps, inc interstitial pressure, inc necrosis, inc vessel permeability w fluid outflow and pressure inc, reversal s futile w formation of inflammatory exudate

66
Q

Fluid leaving the vasculature, does this inc interstitial hydrostatic or osmotic pressure?

A

hydrostatic

67
Q

Do solutes inc or dec interstitial osmotic pressure?

A

inc

68
Q

What draws more fluid from capillaries after solutes inc the interstitial osmotic pressure?

A

osmotic attraction

69
Q

As interstitial pressure increases, _this__ inc/dec.

A

necrosis inc

70
Q

TF? Vessel permeability dec w fluid outflow and increase in pressure.

A

F. inc

71
Q

Direction of pulpal necrosis:

A

coronal-apical direction

72
Q

inflammation moves apically as __ moves apically.

A

antigens

73
Q

Does the pulp die via strangulation at the apex?

A

no

74
Q

As pulpal necrosis spread through pulp, is the PDL affected or infected?

A

affected

75
Q

This is req for periapical disease:

A

bacteria

76
Q

When does inflammatory response in bone begin?

A

once antigens are beyond apical foramen

77
Q

What happens as bone is resorbed due to antigens leaving apical foramen?

A

granulation tissue filsl the space –> LEO

78
Q

TF? Pulp must be necrotic and infected to have a LEO.

A

T

79
Q

How to determine whether there is a LEO:

A

pulp test

Endodontics (22 decks)

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