3. Pathogenesis of Pulpal Disease Flashcards

1
Q

Dentin pulp complex

• We are still talking about pulp biology and things that are connected to inflammation and
disease in the pulp
• Dr. Kim talked about the aspect from the pulp side
• Dr. Wolff talked about cariology
• Setzer is going to go into more detail and sum up those two topics
• Particularly on innervation of pulp
• Recap - This slide is just a quick review:
• Number 1: we always talk about a dentin + pulp complex
• We are not just talking about the pulp, because we always know that it is
part of an encasing in dentin and in enamel and in cementum

• It is important to note that we have the dentin, the shell that encases the pulp
tissue, and at the border we have the ____ (responsible for building the
tooth and secreting the dentin

A

odontoblasts

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2
Q

DENTIN PULP COMPLEX

Characteristically, these odontoblasts are lined like a wall in the periphery of the pulp
• That is why we call it the ____ cell layer, towards the end of the ____,
towards the center part of the dentin, on the outer layer of pulp tissue

A

odontoblast

dentin

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3
Q

DENTIN PULP COMPLEX

• This is the enlarged view of the blue box in the previous slide
• We also have a characteristic zone between the mineralized dentin and the odontoblast
itself, that’s the ____, that is the un-____ portion of the dentin, before
mineralization sets in, since this was just produced by the odontoblasts
• This is something to keep in mind for later, as it will play a role in resorption. Because resorption can only eat up ____ tissue, thus it will always stop at the ____ layer, the pre-dentin

• Or if the resorption is happening externally, it will stop at the ____
layer, if it comes form outside the root

• Then we have the dentinal tubules, which is where the ____ processes were, and still are housed inside the dentin, form the secretion/formation of the dentin itself

A

pre-dentin
mineralized
mineralized
un-mineralized

precementum

odontoblastic

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4
Q

Types of dentin

Primary: circumpulpal ____, mantle dentin, bulk of tooth
Secondary: continuing deposition by ____
Tertiary (reparative dentin): reaction to ____ (attrition, caries, restoration)

• We have primary dentin,
• Secondary dentin, which are the initial deposition of the dentin while the dentin is made and the tooth is filled
• And in the secondary dentin, you have the continuing deposition by the
odontoblasts

  • Tertiary dentin, which is formed when we have an ____ to the pulp (attrition, carious restoration, bacterial onslaught, etc.)
  • The other word for this type of dentin is ____ dentin (or reactionary dentin)
A

dentin
odontoblasts
stimuli

attack
reparative

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5
Q

Structure of Dentin

Dentinal tubules number
42360 - ____
39010 - middle
8190 - apical

Apical root dentin
fewer and more ____
dentinal tubules

• This is different density of dentinal tubules
• If you look at the root dentin:
• Usually you have less dentinal tubules in the apical portion of the root canal
• Coronal dentin has more
• Middle has a little less than coronal
• It is significant to note that the apical has far fewer dentinal tubules
• Because: if you have invasion of dentinal tubules with bacteria, you will have
much more of an infection in the ____ aspect than the apical
• More tubules that can be filled in coronal

A

coronal
sclerotic
coronal

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6
Q

Structure of dentin

• Pics of dentinal tubules
• Important thing to know:
• “is that we have different types of dentin, also how this is called (points to the stuff
in between the little tube openings), the ____ dentin, for example, and the
intratubular dentin in between the dentinal tubules”
• I think peri and intra are synonyms. He didn’t clarify.

A

peritubular

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7
Q

Odontoblast

• Inside those dentinal tubules, we will have ____, nerve fibers and
some other things (we will see later)

A

odontoblastic processes

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8
Q

Microscopic Zones of the Dental Pulp

OB layer
Lines the outer ____ wall and consists of the ____ of odontoblast. ____ dentin may form in this area from the apposition of odontoblast.

Cell-free zone
____ cells than odontoblastic layer. ____ and capillary plexus located here

Cell-rich zone
Increased ____ of cells as compared to cell- free zone and also a more extensive ____ system

Pulpal-core
Located in the ____ of the pulp chamber, which has many cells and an extensice vascular supply, similar to ____ zone

• We also have characteristic zones of the pulp:
1) Odontoblastic layer – outr later – reads box
2) Cell-free zone – reads box then adds: ____-fibers that are going to make the
innervation of the dentin, they will have a lot of nerve fiber concentration in this
layer
3) Cell-rich zone – reads box then adds: it is interesting because you are going to
have the ____-fibers, the other fibers that innervate the pulp, are going to be mostly
located here, around the central portion near the blood vessels that will be in that
area
4) Pulpal core – even more extensive vascular supply

A

pulpal
cell bodies
secondary

fewer
nerve

density
vascular

center
cell-rich

Adelta
C

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9
Q
  • [NOTES TO HERE]
    • ____ > OB goes into tubules > ____ with cell bodies > ____ zone with nerve fibers into the tubules > ____ zone and ____ core
A
pre-dentin
OB
CF
CR
pulpal
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10
Q

Functions of the Dental Pulp
____: blood supply for pulp and dentin.
____: changes in temp., vibration and chemical that affect the dentin and pulp.
____: the pulp involve in the support, maintenance and continued formation of dentin.
____: triggering of inflammatory and immune response.
____: Development and formation of secondary and tertiary dentin which increase the coverage of the pulp.

A
nutrition
sensory
formative
defensive
protective
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11
Q

Constituents of the Dental Pulp

Cells: Odontoblast, Fibroblast, white-blood cells,
Macrophages and Lymphocytes. No fat cell. ____ stem cells
Blood Vessels
Nerves
Extracellular Matrix: Mostly ____ fibres and collagen fibres (Type ____ and Type ____, Elastin, Glycosaminoglycans, Fibronectin, Basement Membrane).
Ground substance: Act as a medium to transport ____ to cells and metabolites of the cell to the blood vessels.

• The pulp is described as a loose conn tissue > lots of fibros
• Adult stem cells > dental pulp SC 
	○ New formation and resvasc of pulp following trauma, or necrotic pulp
		§ SC from PA area can regrow tissue
A
adult
reticular
I
III
nutrients
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12
Q

Healthy pulp
• Where pulp is open > and pulp is healthy: will see network of BV inside the pulp
○ If pulp is not inflamed > would not see a lot of ____
§ Description for appearance of pulp > if pulp has undergone inflam changes > profuse ____

Pathogenesis of Pulpal disease
• See changes in the dentinal structure > the decay area corresponds to the same section in the pulpal tissue
○ Dentinal tubules from OB connect them, and then extend OB processes from the dentin

A

bleeding

bleeding

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13
Q

Pathogenesis
• If the pulp is affected by decay and endotoxins (LPS) > causes pulp to react with an ____ defense reaction
○ First: OB, then ____ cells that will start to trigger the first immune response from the pulp
○ ____ tries to wall pulp if assault is not too quick/aggressive, at the same time the pulp tries to hold off bacteria by building a wall > ____ dentin > pulp is trying to get away from toxins of any bacteria

* Reaction to a cavity prep
* No decay > \_\_\_\_ irritation from preparing a cavity > would see corresponding again > \_\_\_\_ dentin formation
A
immune
dendritic
OB
tertiary/reactionary
mechanical
tertiary
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14
Q

Possible causes of pulpal inflammation
____
trauma
____ disease iatrogenic (perio, prosth)

BUT No. 1 Cause of Pulpal Inflammation: ____!!

• Different types of irritation that cause pulpal inflammation
	○ Caries is the foremost cause of inflam from bacteria
• Doesn't mean you have a fracture where pulp is open > can be a \_\_\_\_ > irritation to the pulp
	○ Where trauma is exerted on teeth a long time ago > no explanation why it happens \_\_\_\_ later you may see reactions to the pulp (5-15 years ago)
		§ Internal resorptions > cells start to eat up dentin structure from inside (OC's), can also see external (PDL might've been damaged) > go through calc/sclerofication of the root canal chamber
		§ Long term changes assoc with low grade inflam that's constantly going on in the pulp
• P disease may affect pulp > connections of inner portion of root canal to root structure [???]
	○ General perio disease with 4-5mm pocket > internal inflam inside the pulpal tissues
• Iatrogenic
	○ SRP > transient inflam inside pulpal tissues
	○ Cavity > transient inflam inside the pulp Chemical and maybe mechanical inflam
A

fracture
periodontal
caries
concussion

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15
Q

Pulpa response to carious lesion

• \_\_\_\_ theory > causes pain coming from the tooth from fluid movement coming from inside the dentin tubules
	○ Showed when early enamel caries (small decay) could be remineralized; in these situations > see \_\_\_\_ changes if only enamel is affected inside the dental pulp
	○ When does endo start?
		§ The very moment when you have initial \_\_\_\_ decay > changes to the inside of the tooth (\_\_\_\_ tissues) > dental decay > carious exposure of the pulp tissues
A

hydrodynamic
inflam
enamel
pulpal

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16
Q

Progression of Caries-induced pulp diseases

• Microbial insult > responsible in the beginning for a pulpitis (inflam that happens inside the pulpal tissues)
	○ This may happen w/ or w/o pain
		§ Pain threshold is too high, or not enough inflam going on at this point
		§ Pulp necrosis > no pain sometimes!
• [???]
• May have inflam that may \_\_\_\_ itself it it's not strong enough
	○ Repaired decay > filling > arrested and inflam regresses
	○ If bacteria are strong enough > may go from reversible pulpitis to \_\_\_\_ and then leads to pulp necrosis and to a AP w/ inflam around the root tip
A

reverse

irreversible pulpitis

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17
Q

Pulpitis

Inflammatory disease
requiring endodontic therapy (root canal treatment) The

• Bacteria starting to cause havoc > when bacteria hit enamel and dentin > can be \_\_\_\_ (took bacteria out) > can be \_\_\_\_ pulpitis
• If the inflame has progressed too much > inflam cannot be reversed > \_\_\_\_ > endodontic therapy
	○ Most commonly used endo therapy > RCT
		§ For an adult person w/ a \_\_\_\_ mature root developmen
• Inflam on right isn't just superficial, and not reversible > massive inflammation taking over
	○ Will not have a situation where one snapshot in time your entire pulp from a horn down ot the end of RC is just inflamed in the same way across the board
		§ Always diff \_\_\_\_ of this inflam inside the pulpal tissues > related to the location of bacteria and their toxins in relation to their pulpal tissues
		§ Inflammation in this example centers around where the decay is trying to break through the pulpal tissues
		§ Also in this example > only one pulp horn is inflamed; the other pulp is healthy
		§ Could be calcification or RC that's split
• Vital pulp therapy > only remove the \_\_\_\_ part
	○ Now we have materials that can be placed directly into the pulp and it tolerates it > now becoming more popular
	○ Only problem > no one can say how deep the level of inflam inside the pulp > can only go by clinical signs of inflam > bleeding
		§ Pulpotomy > removed part of the pulp > drill until the \_\_\_\_ stops and place the filling material and hope for the best
		§ More difficult for irreversible pulpitis > don't know how deep to take parts of the pulp out
• Filling materials that we had caused inflam by themselves
• Looking into deeper portion of the RC > healthy pulp
A
arrested
reversible
irreversible
completed
stages
inflamed
bleeding
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18
Q

Case 1

• First thing when patient arrives > \_\_\_\_ history form
• And then ask for the \_\_\_\_
	○ Correct treatment is to address the CC
	○ Then tests on a patient to figure out dx
• The inflammation here is very severe
	○ Cold test > spray on cotton and place on tooth (on a number of them!)
		§ Inform the patient of the normal response
			□ \_\_\_\_ ourselves and the patient
		§ Pain on the tooth in question > take cotton pellet and place it slightly
			□ If severe inflam > will feel it \_\_\_\_ > cold causes fluid movement in the tubules, and the nerve fibers will react with a painful response
A

medical
CC
calibrate
right away

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19
Q

Case 1

• Test teeth adj to the one with a problem
• \_\_\_\_ > artifact that something appears very dark next to an opaque filler material
	○ Clinical test, or may appear different on a BW
• On #2
	○ The pulp is adjusted > when cold > no \_\_\_\_
	○ Even if there is pulp, in the roots, the cold will not reach this area
		§ The pulp that reacts to the cold is normally in the \_\_\_\_ portion
• On #3
	○ Feels it a lot (+++) > strong reaction to the cold from the patient
	○ Also \_\_\_\_ > 10-30 seconds
• On #4
	○ Still has a strong reaction
	○ Patient says its lingering > place the cold
		§ Temp change to the tooth is pain; the receptors in \_\_\_\_ is only the receptors that respond to temperature! Both teeth give a lingering response > unlikely > patient gives a lingering response when cold on tooth > two fillings are \_\_\_\_ > extremely good conductor for temp > clinically: separate the fillings so they don't transmit the cold
A
burnout
reaction
crown
lingering
pulp
metal
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20
Q

Case 1

• Percussion
	○ Tap on tooth from two directions:
		§ Occlusal in the \_\_\_\_ axis of the tooth
			□ Testing the apical part of the tooth; any inflam at the tip of the root > would hurt
				® Apical changes if disease progresses > bacteria reaching the end of the RC > may cause inflam at the apical PDL
		§ Hit the crown from the \_\_\_\_
			□ Testing lateral inflam, but most of the the time it's at the end of the \_\_\_\_ tip
		§ Place finger on soft tissues next to the root tip > swelling bc of an abscess from  a root tip
• Palpation
	○ Pressure in area of the root tip to see if it hurts the patient
• Question response from cold test > electricity
	○ Patient holds onto something > electric current through the patient > may feel a tingling in the tooth
	○ The electricity would get to the roots if part of the pulp was \_\_\_\_ (like the previous example)
• If goes to the end > nerve probably isn't alive anymore
• From CC, dental history and test > severe pulpitis in #3 it is an irreversible pulpitis
	○ Some pulpitis may be w/o pain
	○ This patient had symptoms > \_\_\_\_
• Any diagnosis is two fold > the \_\_\_\_, and the status of the \_\_\_\_ (apical) structures
	○ So far we described the pulpal dx, and since the patient had pain when tapping on the tooth > know that there's something in the \_\_\_\_ area as well > \_\_\_\_ in addition!

• Pulp is bleeding a lot > severe inflam
A

long axis
side
root

removed
sympamatoic irrev pulp
pulp
periapical
periapical
sympto apical perio
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21
Q

Possible origins of endodontic pain

Hyperalgesia (increase in perceived ____ of painful stimulus)

AND/OR

Allodynia (reduction in ____ threshold, triggering of a pain response from stimuli which do not normally provoke ____)

• DENTAL PAIN > \_\_\_\_ pulp (beginning of disease before necrosis) > that may become degen pulp (way to die) > pain may come from: \_\_\_\_ fluid, pressure, and from inflam mediators (CGRP, substance P) that causes sensi of nerves and nerve sprouting; now when bac is not only superficial, and manage to get into pulp > will start to breakdown > bacteria can cause a \_\_\_\_ inflammation (by themselves), or their byproducts can cause inflam as well
	○ Other things may happen that is conencted to brain and pain modulation
		§ Hyperalgesia
			□ Situation where something would normally cause very little pain but with inflammation > inc pain sensation when inflam is already kicking in at the same time
				® I.e. Cold on tooth > everyone will feel it but should be brief and removed; if you have inflam in addition that already painful response, it will hurt BADLY
		§ Allodynia
			□ Something hurts you that wouldn't normally hurt you
A

magnitude
threshold
pain

inflamed
edema
PA

22
Q

Nociceptive Mechanism
Pulp is notorious as a source of pain
Pain = most cases it is the pathology they present with - instead of the expert treatment.

(a) ____ pain system where the nerve fibers carry only information related to pain.
(b) There are several types of ____
(c) Basic neuronal pathway for pain input in the trigeminal system contains ____ neurons.
(d) The basic ____ pathway for modulating pain begins in several brain sites, of which the periaqueductal gray (PAG), nucleus raphe magnus (NRM), and dorsal raphe (DR) are the most prominent.
(e) Balancing of input from dedicated pain system with ____ modulation is the basis of the current understanding of pain.
(f) In inflammation, neuropeptides and cytokines, among other effects, initiate activity in nociceptors and awaken silent nociceptors in a process known as ____ sensitization.
(g) When noxious input continues for a long time, changes in sensitivity occur in the central nervous system that may become permanent. This is ____ sensitization.

A
dedicated
nociceptors
three
neuronal
descending
peripheral
central
23
Q

Healthy Pulp: ____, cold, or ____ stimuli will elicit a mildly painful response when applied to exposed dentin.

Inflamed Pulp: hot, cold, or osmotic stimuli, will evoke pain from the tooth when applied to exposed dentin even at levels ____ elsewhere. Stronger pain is thought to indicate a greater degree of ____.

____ (non- physiological) stimuli directly activate the nerve fibers.

* Stimuli to pulp and it's healthy > pain is transient
* Stronger pain > greater degree of \_\_\_\_
A
hot
osmotic
innocuous
inflammation
electrical
inflam
24
Q

Innervation of dentin

• Back to the tubules > OB process inside, there are other things as well:
	○ \_\_\_\_
	○ \_\_\_\_ filled space (dentinal)
	○ Extension of \_\_\_\_ cell
		§ Cells found interwoven into the OB layer > thought to be the first cells involved in immune response of the pulp in repsonse to bac insult
	○ Nerve fiber
A

collagen
fluid
dendritic

25
Q

Nociceptive Mechanism

Nociceptive endings pass between the ____ and into the dentinal tubules in some areas but primarily in the ____ beneath the cusps.
In animal models, beneath the cusps up to 80% of the tubules are ____.
The most widely accepted explanation of pulpal nerve fiber activation is the “____ hypothesis (theory)” which suggests that movement of the contents of the dentinal tubules either in or out stimulates nociceptors in or near the dentin by deforming the cell membrane.

Caries that did not cause cavitation may have ____ below the lesion.

Any damage to the pulp is thought to be due to the penetration of ____ and their toxins, leading to inflammation of the pulp.
Clinically, any tooth with strong hot and/or cold response has an inflamed pulp.

A
odontoblasts
pulp horns
innervated
hydrodynamic
inflammation
bacteria
26
Q

Nociceptive mechanism

	• Painful response when these nerve fiber endings are provoked
• High innervation in dentin in the area of pulp horns underneath the cusps > 80%
• Not every tubule will stay have an OB \_\_\_\_ > at one point will have had it bc the OB was responsible to make the dentin around the process > this OB may have retired
	○ Many of them will have a process
		§ But just bc you have a process doesn't mean that automatically that it is together with a nerve fiber inside the dentinal tubule
		It would have had it because an odontoblast with an odontoblastic process was responsible to make the dentin around that odontoblastic process. But that odontoblast may have gone so there is no odontoblastic process. But many of these dentinal tubules will have an odontoblastic process.
• Fluid in dentinal tubule > create movement after temp changes hit the tooth > nerve fiber inside the dentinal tubule that's moving back and forth > 
is giving you a \_\_\_\_ response. The pain is coming from the \_\_\_\_ fibers
(nociceptors) getting provoked inside the dentinal tubules.
A

process
painful
nerve

27
Q

Nociceptive mechanism

Pulpal nociceptors are non- mylelinated could be the terminals of both Aδ and C fibers.

Adelta fiber
Diameter: \_\_\_\_
Velocity: \_\_\_\_
Location: \_\_\_\_
Pain: \_\_\_\_
Threshold: \_\_\_\_
Stimulation: \_\_\_\_
Inflammation: \_\_\_\_
Hypoxia: \_\_\_\_
C-fiber
Diameter: \_\_\_\_
Velocity: \_\_\_\_
Location: \_\_\_\_
Pain: \_\_\_\_
Threshold: \_\_\_\_
Stimulation: \_\_\_\_
Inflammation: \_\_\_\_
Hypoxia: \_\_\_\_
A
2-5um
4-23 m/s
peripheral
sharp, pricking
low
thermal, osmotic
intial phase
sensitive

0.4-1.2 um
0.4-2.0 m/s
perivascular
burning, aching
high
noxious heat
later phase
resistant

28
Q

Nociceptive Mechanism

• A delta fibers
	○ Two subtypes: slow and fast
• A beta fibers (ignored)
• C fibers
	○ Nociceptive fibers
• For innervation and pain perception: a delta and c fibers
• MUST KNOW THE TABLE
• Great difference in speed of nerve fibers > myelination (A delta)
• Location
	○ Nerve plexus in the \_\_\_\_ zone > peripheral location of the a delta fibers
	○ Perivascular C fibers > in the \_\_\_\_ of the pulp around the BV towards the pulpal core
• A delta fibers > give a sharp pain sensation; while C fibers give a burning/duller pain sensation
	○ More diff to elicit a pain response form the C fiber (threshold is much higher)
• Typical stimulation > evaluation of the quality of pain that the patient gets > looking for thermal osmotic changes in the a delta synthesis
	○ [???]
• Hypoxia
	○ Lack of O2
• Diagnose a patient with pulp necrosis > no rxn to cold test, and no response from the EPT > do a RCT > get to lower portion of RC > should be necrotic, but the patient feels it > C fibers where some may \_\_\_\_ on in the extremely hypoxic enviro > the cell body (not the extension) is not located inside the pulp, it is located outside of the root structure

• If there is pain coming from C fibers (and only them) > patient may not be able to \_\_\_\_ where the pain is coming from
	○ In progressed stages of inflam > majority of A delta are dead > patient may not be able to say which tooth it is (otherwise, they can directly target if A delta were alive)
• Can use the different qualities of the nerve fibers to diagnose the patient
A

cell free
center
linger
localizable

29
Q

A-delta :
____ Pain
Primarily ____
Can be ____

C:
____ pain
____ receptors
Poorly ____

A

sharp
mechanoreceptors
localized

dull
mechano and chemo
localized

30
Q

Brannström’s Hydrodynamic Theory

Rapid and outward movement of dentinal tubule fluid causes ____ distortion of ____ fibers resulting in brief and sharp pain

• Fluid movement in the tubules > brief, sharp pain response > hydrodynamic theory
A

mechanical

Adelta

31
Q

C-fibers - ____ pain, indication of possible patho-physiology
- ____ pain (C fibers)

• C fibers progressive state of inflam > already has a heat response > delayed pain
	○ Takes a while for the temp change to get to the deeper portions of the pulp
	○ Not as \_\_\_\_ as putting something cold on the tooth
	○ Throbbing pain is coming from the \_\_\_\_ (C fibers are wrapped) in advanced stages of inflam
A

dull
dull
instantaneous
pulse

32
Q

Pain response - normal pulp

• Have dentin, with the tubules, with the OB layer and pulp and now nerve fibers
	○ A delta (#1, 2, and 3)
	○ Some tubules will have innervation (up to \_\_\_\_% around the pulp horn, but not all!)
	○ Not once single fiber per dentinal tubule > will split in the end and will go into different tubules > end up with a set of tubules that are close to each other > innervated by nerve 1, and another area that is innervated 2 and 3 and so on
	○ These sections of dentin > form a receptive field > cold on tooth > certain areas of dentin, depending on how large the area is > may get a response from one \_\_\_\_ (one nerve fiber), or may get it from 2+ nerve fibers
		§ The more nerve fibers are firing > the \_\_\_\_ the pain response you will get
• Normally: may have some tubules that are close and some are innervated by different fibers, but very little \_\_\_\_ of these fields
A

80
RF
stronger
overlap

33
Q

Normal pulp response

• Pain reaction diagram
	○ Patient will have a painful response with cold and remove the cold > pain goes away (the blue) > this is a \_\_\_\_ reaction
	○ Normally do not get a \_\_\_\_ fiber response (no inflam, only healthy tooth!)
A

normal

c

34
Q

Clinical correlation in humans

• Inflam mediators that are happening inside the solutions on the tooth
	○ Different responses in terms of pain
	○ Sharp response to \_\_\_\_, may get a \_\_\_\_ response (C fiber)
A

NaCl

dull

35
Q

A-fibers v. C-fibers

* Where responses are coming from
* Inflam mediated responses from \_\_\_\_ fiber
* Heat is from the \_\_\_\_ fibers
* Probing/air blast/drilling > \_\_\_\_ fibers
A

c
c
adelta

36
Q

A-fibers v C-fibers

A-fibers

  • ____ sensitivity
  • ____, thermal and mechanical sensitivity

C-fibers

  • NO ____ sensitivity
  • ____ and thermal sensitivity

ALL sensitive to ____

• A delta > responsible for the sensitivity that is coming from the dentin
	○ Sensitive teeth > patients wwho \_\_\_\_ and exposed cervical aras on teeth > sensitive to air, touch and will know that is mediated by a delta
	○ One of the differences
• If there is a real inflam process in the pulp > all of these can react with inc pain to htermal mech snesitivitiy
	○ Osmotic changes will cause an increase in pain sensi
A

dentin
osmotic

dentin
mechanical
grind

37
Q

Heat
•Heating a tooth slowly, even to122-144 degrees F will not cause ____ to respond.
•Mean C-fiber stimulation threshold ____ degrees F.
•Normal physiologic temperature (98 deg.) can cause spontaneous firing of ____ during inflammation.

• Not easy to apply and test on tooth
• Not done on regular basis
• A delta fibers will not repsond to heat very well
• Very slowly raising the temp and put something on tooth and it goes up an dup > a delta do not respond
	○ C fibers will respond but they have a threshold of 110F
	○ In a non-\_\_\_\_ enviro
• In a nutshell > non-inflamed situation > apply heat and it goes slwoly up > noramlly do not get a painful response
	○ But if you have inflam changes in the pulp > normal \_\_\_\_ temp can cause a spontanoues firing of the nociicpeotrs of the \_\_\_\_ fibers when you have the heat increase inside the pulp
• Inflam is a typical diagnosis when a patient tells you they have a painful response to heat
A

adelta
110
nociceptors

inflamed
physio
C

38
Q

Heat

A-delta response is ____ and ____ dependent.

•Heated Gutta-percha: ____F when applied to the teeth.
+70.2 0F (+21.50C)

•Endo Ice: -15.160F.
-113.7 0F (-45.40C)

• A delta may respond to heat only when have \_\_\_\_ increase in temp
	○ Dynamic and gradient response
A

dynamic
gradient
168.8
rapid

39
Q

Nerve Changes in Inflammation
Conductance

• Nerve changes with inflam
• A is not ifnlamed, and B is inflamed
	○ Increased firing in presence of \_\_\_\_
A

inflam

40
Q

Nerve Changes in Inflammation
Receptive Fields

• Inc in \_\_\_\_ fiels
A

receptive

41
Q

Pain Response - Inflamed Pulp

• When inflam starts inside the pulp > modulation and peripheral sensi taking place within the pulp
• Concept > \_\_\_\_ (CGRP, sub P, bradykinin) > released based on commands from CNS in brain > cause additional \_\_\_\_ and neuromodulation (inflam) in the nerves that are in periphery of pulpal tissues of a delta fibers
• In healthy pulp, \_\_\_\_ looked differenryl
	○ Pain response changes with an inlfamed pulp
	○ Neuropeptides are causing the nerve fibers (1, 2 and 3) > create more \_\_\_\_ at the end of the nerve > nerve sprouting
	○ Based on neuroinflam mediators > nerve will have more \_\_\_\_ endings then it used to have and into dentinal tubules
	○ May not only have tubules with a nerve fiber ending that had in healthy situation, but also may expand reach > RF is getting larger and now some RF that mightve had little interaction before, now they're starting to \_\_\_\_ much more
	○ Bc of the inflam > many more nociceptive fiber endings in the tubules, with more RF overlapping > stimulate this now > much more painful respnse bc more nerve fiber endings are reacting to the original stimulus
A
inflam mediators
nerve sprouting
RF
nerve endings
nociceptive
overlap
42
Q

Pulpal pathology - reversible pulpitis

• \_\_\_\_ > can get back to normal

• Same pain reaction diagram > something cold to the tooth > inflam has ahappened > more \_\_\_\_ involved
• Cold on the patient's tooth > \_\_\_\_ painful response bc of the inflam changes
• Do not have \_\_\_\_ fiber response as of yet
	○ Bc they're early and reversible changes inside the dental pulp
A

reversible

RF
larger
C

43
Q

Pulpal pathology - irreversible pulpitis

• Pulp wants to react with the same \_\_\_\_ response (PMN, odonto) but the bacteria are more \_\_\_\_, or the immune system is down > trying to recruit as much response as can but bac is overcoming > tubules > pulp > immune defense has to go further away > may kill pulp tissue \_\_\_\_ > infalm in deeper portions of pulp > pulp is breaking down > \_\_\_\_ after compartment of pulp is breaking down
A

immune
aggressive
locally
compartment

44
Q

Irreversible Pulpitis

A-delta : ____ and longer lasting pain
Can be ____

C: ____ throbbing pain
Poorly ____
____ Response

* Seeing responses not only from a delta, but also from the C fibers (BP changes, throbbing, dull pain)
* Takes a while for a painful response to be elicited from the c fibers bc it takes time for it to travel into the deeper portions of the pulp
* Biphasic response (initial response) from the \_\_\_\_ fibers, and a delayed \_\_\_\_ (deeper portions of the pulp)
A
sharper
localized
dull
localized
biphasic
adelta
c fibers
45
Q

Irreversible pulpitis

• Much deeper and more severe inflammation
	○ Irreversible pulpitis
	○ Cold on tooth > \_\_\_\_ fire much more than when pulp is healthy (just like reversible pulpitis, but not only inc pain, but it may be a little longer and it will \_\_\_\_)
		§ All a delta here
	○ Takes a little bit > after a delay > \_\_\_\_ fibers kick in > another painful response that's coming from the C fibers > \_\_\_\_, aching, and burning pain
		§ Biphasic response
• Phases in waves > c fibers are really activated > BP > \_\_\_\_ pain
• Typical pain diagram seen from a patient
A
adelta
linger
c
dull
pulsing
46
Q

Increased Local Release of Neuropeptides May Contribute to Pain During Irreversible Pulpitis

Role of Neuropeptides = Regulate ____ and Repair

Results: 8 fold inc in ____ in irreversibly inflamed pulp!

Implication: ____ sensation may not correspond directly to the level of inflammation due to NP modulation

* NP involved in the inflam that's happening in pulpal tissues
* CGRP and SP > involved in modulation of the dental pain
* Irreversible inflam pulp > SP goes up in 8 fold increase > directly related to inc in \_\_\_\_ in the pulp
A

inflammation
SP
pain
NP

47
Q

sensory nerves show increased branching (sprouting) in inflamed pulps

* Stained for inflam situation
* Nerves that have in periphery of pulp > undergo \_\_\_\_
A

nerve sprouting

48
Q

Nerve sprouting

• Nerve sprouting
	○ Dentin and tubules and nerve fibers ending with nociceptors going into the tubules
	○ Increases in \_\_\_\_ (the RF) and you may have more \_\_\_\_
	○ Activation of one set of nerve fibers in portion of dentin after insult (cold, osm changes, heat, etc.) > nerve sprouting > more nerve endings grow into dentinal tubules
• Regular nerve fibers > divisions at the end of the nerve fiber > may be a \_\_\_\_ > nodal sprouting as well > ultratermianl sprouting,etc
	○ Get more more of \_\_\_\_ with nociceptors, inc \_\_\_\_ with nociceptors and \_\_\_\_ fields that are overlapping
• More \_\_\_\_ are innervated bc more endings have been created after the inflam process
A
size
overlapping
branch
nerve endings
tubules
larger
nerve fibers
49
Q

Irreversible Pulpitis

Mechanical Allodynia - Lowered ____

Normal ____ Blood Pressure
____ pain
Positive to ____

Thermal Allodynia - Lowered ____
Normal ____ Temperature(37 C)
____ relieves pain

• Positive to percussion > non-inflamed won't hurt, but tap when nerve fiber is \_\_\_\_, or apical tissue is inflamed > it will hurt
	○ Pain coming from the regular pulse in an inflamed situation (from C fibers around the BV in the center of the pulp)
	○ Based on the BP around the area where the nerve fibers are located
• Thermal allodynia
	○ Normal physio temp may cause pain firing 
	○ Ice > pain is down
		§ Can alleviate some of the pain in some situations
		§ \_\_\_\_ fibers may not be alive anymore
A

pain threshold
systolic
pulsing
percussion

pain threshold
physiologic
ice water

inflamed
adelta

50
Q

Peripheral and Central Sensitization

Peripheral Sensitization
•Tissues injured or exposed to a toxin, an ____ response occurs that includes the release of a cocktail of molecules which will interact with nociceptors including ____ (lowering pH), ____ and its metabolites (prostaglandins), bradykinin, ____, serotonin, nucleotides, and ____ (NGF).
•These come from multiple sources and have multiple effects, only some of which are on the nociceptors that they activate and sensitize by a number of mechanisms.

Central Sensitization
•Continuous high-level activity in nociceptors results in serious changes in the ____, the most significant of which is the lowering of the ____ of previously silent nociceptive afferents such that terminals of ____ fibers will activate them.

A
inflammatory
protons
arachidonic acid
histamine
nerve growth factor

nucleus caudalis
threshold
non-nociceptive

51
Q

Where is the Cut-Off Point between Reversible and Irreversible Pulpitis?

The inflammatory process leading to necrosis occurs by compartments and it
gradually migrates in the apical direction.

• Confusion ab normal/necrotic pulp, reversible/irreversible pulpitis
• Clinical situatiosn > nothing is ever 100% clear or textbook
• Conseq #1
	○ Scenarios between normal pulp and necrotic pulp
	○ Doesn't happen immediately > there's a \_\_\_\_ phase in between
		§ Patients may not have \_\_\_\_ that are perfect for one situation or the other
		§ Irreversible pulp can be confused with \_\_\_\_ teeth
			□ May have TMJ issues, muscle pain, etc.
A

transitional
symptoms
grinding