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23 Endodontics > 3 - Etiology of Pulpal Disease > Flashcards

3 - Etiology of Pulpal Disease Flashcards

1
Q

what are pulpal irritants

A

living and non-living

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2
Q

examples of living pulapl irritatngs

A

bacteria, fungii, viruses

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3
Q

examples of non-living pulpal irritants

A

mechanical, thermal, and chemical

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4
Q

what are bacterial toxins

A
  1. endotoxin
  2. LPS
  3. exotoxin
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5
Q

what is an endotoxint

A

bacterial toxin part of bacteria

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6
Q

what is an exotoxin

A

bacterial toxin excreted by microorganism

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7
Q

are bacterial toxins very potent and cause cell damage

A

YES

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8
Q

what are microbial irritants

A
  1. bacterial proper
  2. microbial toxins (endo and exotoxins)
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9
Q

is direct pulp exposure a prerequisite for pulapl resonse and inflammation

A

NO

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10
Q

what are factors affecting pulapl response

A
  1. Virulence of bacteria
  2. Ability to release inflammatory fluids
  3. Host resistance
  4. Amount of circulation
  5. Lymph drainage
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11
Q

If bacterial invasion of pulp is severe sooner or later what happens

A

damage will become extensive and
spread throughout the pulp

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12
Q

___ can lead to an interruption of blood flow to the pulp

A

Inflammation

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13
Q

Inflammation can lead to an interruption of blood flow to the pulp, THE PULP THEN WILL BECOME
___

A

NECROTIC

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14
Q

one the pulp becomes necrotic, what is it colonized by ___

A

bacteria

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15
Q

Eventually bacterial byproducts and other irritants from necrotic tissue will diffuse from the ___ into the ___causing destruction of these tissues

A

canal; periapical tissues

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16
Q

what is the Kakehashi Study

A
  • pulp exposure in conventional and germ free rats
  • conventional rats developed pulpal and periradicular lesions
  • germ free rats did not develop lesions
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17
Q

what is considered the most important study in endodontics

A

Kakehashi

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18
Q

what are mechanical irritants to the pulp

A
  1. operative procedures
  2. trauma
  3. ortho
  4. periodontal scaling
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19
Q

what removes cementum therefore exposing dentinal tubules resulting mechanical irritation to the pulp

A

periodontal scaling

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20
Q

what are chemical irritants to the pulp

A
  1. antibacterial agents
  2. acids
  3. acidic liners and bases
  4. temporary and permanent filling materials
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21
Q

what are steps lesion progression

A
  1. release of inflammatory mediators
  2. increased vascular permeability
  3. exudate formation
  4. increase in intrapulpal pressure
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22
Q

where does pressure increase occur? does it progress fast or slowly?

A

occurs in small compartmentalized regions

progresses slowly

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23
Q

does pain associated w/ inflammatory mediators lower the sensory nerve threshold

A

YES

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24
Q

T/F: pain associated w/ inflammation mediators effects vascular permeability resulting in DECREASED tissue pressure

A

FALSE! ELEVATED tissue pressure

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25
Q

does pressure associated w/ inflammatory mediators act directly on sensory nerve receptors

A

YES

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26
Q

describe the special environment of the pulp

A
  1. poor collateral circualtion
  2. pulp surrounded by hard unyielding walls
  3. area of terminal circulation
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27
Q

Among the various forms of dental treatment, ___ are the most common cause
of pulpal injury

A

restorative procedures

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28
Q

what are sources of bacteria in leaky restorations

A
  1. ingrowth from surface (open margins)
  2. bacteria in smear layer
  3. bacteria in deep dentin
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29
Q

Diameter and density of dentinal tubules [increases, decreases] in direct proportion to the depth of the cavity preparation

A

INCREASES

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30
Q

Usually ___mm of dentin thickness is needed to protect the pulp from most irritants

A

2

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31
Q

what is frictional heat

A

drastic increase in temp severely damages pulp

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32
Q

can frictional heat initiate inflammatory response

A

yes

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33
Q

can frictional heat desiccate dentinal tubules

A

yes

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34
Q

preps without coolant can reduce what

A

pulpal blood flow

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35
Q

how to prevent heat

A
  1. use high speed with EFFICIENT water coolant
  2. light pressure (use new burs so less pressure needed)
  3. intermittent cutting
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36
Q

what speed to use high speed at

A

100,000 - 250,000 RPM

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37
Q

preps without coolant can markedly reduce pulapl blood flow. why wouldn’t we want that

A

reduction of blood flow makes tooth necrotic

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38
Q

Use of rubber points at high-speed can increase pulp temperature by ___ degrees Celsius enough to cause pulpal damage

A

16

39
Q

what is an outward movement of dentinal fluid if back pressure can dispace odontoblasts?

A

dentin dessication

40
Q

prolonged air drying should be avoided to avoid what

A

dentin desiccation

41
Q

Impressions or cementation of restorations can produce an outward movement of dentinal fluid. This is what type of force?

A

hydraulic forces

42
Q

Research indicates ___ of
materials to be more important than their
___

A

physical properties; chemical composition

43
Q

Evidence is that pulpal injury after restorations is
mainly caused by ___

A

bacterial microleakage

44
Q

Bacteria will grow underneath a restoration only a in the presence of ___

A

microleakage

45
Q

what are factors that affect microleakage

A
  1. Marginal adaptation of the material
  2. Shrinkage
  3. Contraction gaps
  4. Elastic deformation of tooth structure
46
Q

T/F: In and of itself acid etchants DO appear to produce injury to the pulp

A

FALSE! it does NOT

47
Q

how do acid etchants cause pulpal injury

A
  1. Buffering effect of dentin neutralizes acid
  2. Greatly increases dentin permeability
48
Q

in tooth sensitivity after restoration placement, is discomfort usually a short or long duration?

A

SHORT

49
Q

what to do to avoid sensitivity after restoration placement

A

check occlusion

50
Q

persistent and increasing discomfort after restoration placement might be indicative of what? especially when?

A

indicative of irreversible pulp damage especially if there is spontaneous pain

51
Q

spread of canal inflammation and/or infection occurs thru what

A
  1. apical foramen
  2. lateral canals
  3. dentinal tubules
52
Q

periradicular pathosis can range from ___ to ___

A

slight inflammation to extensive tissue destruction

53
Q

cellular damage occurs thru what

A
  1. release of non-specific inflammatory mediators
  2. specific immunologic mediators
54
Q

in periradicular lesions, products released from ___ contribute to inflammatory process and cause swelling, pain, and tissue destruction

A

activated systems

55
Q

what are inflammatory mediators found in PA lesions

A
  1. vasoactive amines
  2. bradykinin
  3. lysosomal enzymes
  4. complement fragments
  5. leukotrienes
  6. PROSTAGLANDINS
  7. CYTOKINES
56
Q

what are vasoactive amines

A

hismatine, serotonin, etc.

57
Q

what inflammatory mediators are shown to play important role on bone resorption

A

cytokines and prostaglandins

58
Q

what are arachidonic acid metabolites

A

phospholipase A2

59
Q

phosphalipase A2 results from what

A
  1. cycooxigenase
  2. lipooxygenase
60
Q

cyclooxigenase results from what

A
  1. prostablandins
  2. prostacyclin
  3. thromboxane A2
61
Q

lipooxygenase results from what

A

leukotrienes

62
Q

arachidonic acid ->/<- phospholipase A2 pathway is inhibited by what

A

corticosteroids inhibit both pathways

63
Q

what medication affects cyclooxigenase and inhibits prostaglandin, prostacyclin, and thromboxane A2?

A

Aspirin and NSAIDS

64
Q

what medication inhibits prostaglandins

A

COX-2 inhibitors: clebrex

65
Q

what medication inhibits leukotrienes

A
  • some asthma meds
  • some asthritis meds
66
Q

what is an intense pain and/or swelling after a root canal procedure

A

flare up

67
Q

pushing canal contents into periradicular lesions can create a type ___ reaction that could result in severe flare up

A

TYPE I

68
Q

what are mechanical and chemical irritants

A
  1. over-instrumentation
  2. overfills gutta-percha and/or sealer
  3. irrigants
  4. medications
69
Q

what results in endo damage

A
  1. severance of BV
  2. activation of coagulation pathways contribute to inflammation
  3. activation of kinin system and complement cascade
  4. vasoactive amines
  5. foreign body reactions
70
Q

what causes endo damange

A
  1. endo irrigating solutions NaOCl (chlorox)
  2. intracanal medications
71
Q

what are specific mediators

A

antigen/antibody

72
Q

T/F: root canals are a pathway for sensitization

A

TRUE

73
Q

what are immunologic responses

A
  1. antigen (bacteria and their products)
  2. B and lympohcytes and plasma cells
  3. antibodies and T lymphocytes
74
Q

are are antigens of immunologic responses

A
  1. microorganisms
  2. microbial toxins
  3. altered pulp tissue
75
Q

what are specific antibodies of immunologic responses

A
  1. immunoglobulins
  2. immunocompetent cells
  3. IgE and Mast cells
76
Q

IgE and Mast Cells in PA lesions suggest what

A

type I immunologic response may occur

77
Q

what are the elements needed for reactions to be present in human periradicular lesions

A
  1. antigens
  2. immuno-competent cells
  3. specific antibodies (immuno-globulins)
78
Q

T/F: vaious types of immunologic reactions can start, amplify and perpetuate lesions

A

TRUE

79
Q

how to prevent periradicular inflammation

A
  1. avoid pushing debris thru apex
  2. do not over-instrument
  3. do not overmedicate
  4. avoid pushing NaOCl thru apex
80
Q

do periradicular lesions persist until causing agent is removed (bacteria in canals)

A

YES

81
Q

how should canals be sealed to avoid recurrence of pariradicular lesions

A

hermetically sealed

82
Q

if defense mechanisms are compromised, infection can spread where

A

spread into adjacent tissues

83
Q

if defense mechanisms are compromised, is it potentiall grave and result in fatal consequences

A

yes

84
Q

you should worry about the host response for what type of patients

A

immunocompromised patients

85
Q

it is important to distinguish infection from what

A

inflammatory conditions

86
Q

T/F: medications you give to the patient is more important that the local treatment done to patient

A

FALSE! what you do for the patient (local treatment) is more important than any medications you give the patient

87
Q

is it possible for periraduclar tissues that have been destroyed to regenerate with original tissue after endo therapy? why?

A

YES! because irritating stimulus has been removed

88
Q

what periradicular tissues that have been destroyed can be regenerated

A
  1. alveolar bone
  2. cementum
  3. periodontal ligament
89
Q

can dentin regenerate? why?

A

NO! because odontoblasts originate in pulp

90
Q

etiology of endodontic lesions is from what

A

microbes, microbial toxins and/or inflammatory mediators within root canal system

91
Q

what is the first tissue to be destroyed by endo disease

A

PDL of periapical tissues

92
Q

what is the last tissue to fully regenerate

A

PDL of periapical tissues

93
Q

T/F: after successful RCT, all tissue CANNOT be restored to their original state except dentin

A

FALSE!

after sucessful RCT, all tissues CAN be restored to their original state except dentin

23 Endodontics (12 decks)

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