Pratique du Shadowing: Endodontics | Pulp Biology and Tooth Pain | INBDE, ADAT - Apprendre l'anglais à l'oral avec YouTube

Hey everyone, this is Ryan here and welcome back for this next series on endodontics,

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Hey everyone, this is Ryan here and welcome back for this next series on endodontics,

one of the main clinical topics that appears on part two of the dental board exams.

It's actually tied with pharmacology with having the least amount of questions of all the sections.

There are only 31 questions out of a total 500.

So with that being said,

like all of my videos,

I'm going to be focusing only on the highest yield things you need to know.

While I'm gearing these videos for exam preparation,

they are also designed to give you a nice overview of these topics for clinical application and general knowledge.

So first, we're going to go over the biology of the dental pulp,

because much of endodontics is focused on pulpal health,

since endodontics literally translates to the knowledge of what's within teeth.

So the pulp is obviously very important.

So the pulp is the innermost part of the tooth and is generally very soft and vascular.

So let's talk about what specifically is contained within this tissue.

So the pulp contains loose fibrous connective tissue with nerves,

blood vessels, and lymphatics.

Again, very vascular.

It contains fibroblasts, which secrete fibrous connective tissue.

It also houses the odontoblasts, which secrete dentin.

Now the type of dentin depends on the stage of root formation.

So it's considered primary dentin before root formation is complete,

and secondary dentin after root formation is complete.

But odontoblasts secrete both types of dentin.

It also contains undifferentiated mesenchymal cells,

which can differentiate into a specific type of cell,

which we'll revisit later, called secondary odontoblasts.

So the confusing thing here is that secondary odontoblasts do not secrete secondary dentin.

They actually form tertiary dentin to protect the pulp from injury.

But these undifferentiated misenchymal cells are basically stem cells that can later on divide and become new cells.

So the pulp is also surrounded by hard dentin.

So that's what those odontoblasts have secreted as the tooth was forming and after it has completed formation.

And so this hard dentin creates a pressure system which limits its ability to expand.

So the pulp, if pressure is building up and some infection has taken place,

it has a lot of trouble expanding against this hard dentin.

Also, it lacks collateral circulation,

which limits its ability to cope with infection.

So basically, there's one way in, one way out.

For a two-rooted tooth, I guess it has two ways in and two ways out.

But there are less avenues for immune cells to reach the pulp.

So the pulp tissue as compared to,

say, the skin of your face is already compromised structurally in terms of being able to fight an infection.

One, for the pressure buildup,

and two, for less avenues for immune cells to reach that component.

So the pulp is already anatomically more driven to infection,

at least more easily.

So let's talk about that.

The dentin and pulp defense.

What can we do for,

or what can the pulp do rather,

to fight off or defend itself from an infection?

So sclerotic dentin is basically very hard dentin.

The calcification has occurred of dentinal tubules in response to slowly advancing caries or just aging,

just the physiological process of this dentin getting harder over time.

So sclerotic dentin would be a pulpal response to slowly advancing caries.

Now we have this thing called reactionary dentin,

which is a reaction to minor damage.

So reactionary reaction to minor damage.

And some sources would call this another word for secondary dentin.

Now, reparative dentin is repair for major damage.

And some textbooks and some sources will refer to this otherwise as the tertiary dentin.

And this makes sense because minor damage wouldn't be enough to destroy the original odontoblasts that are present,

so it allows them to lay down some dentin.

While major damage would destroy the original odontoblasts,

and so then those undifferentiated mesenchymal cells need to step up

and become secondary odontoblasts and lay down tertiary dentin as basically a last resort.

However, many sources just refer to both of these together as tertiary dentin.

But I wouldn't worry too much about these details.

It's not too, too important.

More important is to know that reactionary is for minor damage,

whereas reparative is for major damage.

That's much, much more important to know than all the secondary and tertiary stuff.

So in endodontics and operative dentistry,

there's this technique referred to as pulp capping,

where you place a calcium hydroxide liner,

which irritates odontoblasts, and they'll form either this reactionary or reparative dentin,

depending on how close you are to the pulp.

So this sort of dynamic response of odontoblasts and these secondary odontoblasts to lay down new dentin,

sort of to form this dentinal wall that forms a barrier and defends the pulp.

So the tooth is very alive,

as long as it's not necrotic,

and it can respond dynamically to infection, which is pretty cool.

And now, of course, we have pulpal necrosis,

where the tooth is dead,

the pulp has been compromised,

and that's the response to rapidly advancing caries or other severe damage.

And the tooth has lost the battle and the pulp is now dead.

So in all of these cases,

the main cause of serious pulpal injury is always bacteria.

So bacteria can come from a plethora of sources,

mostly from, let's think, dental caries or cavities,

and the bacteria are small enough where they can penetrate beyond the obvious caries

and cavities through dentinal tubules to reach the pulp.

And that's when problems can start occurring.

The patient can be in pain and the pulp can become infected and can die eventually.

All right, so now let's talk about more specifics of the histology of the dental pulp.

So from outside to inside,

we have, well, first we have dentin,

that's this darkest layer right here,

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and then the pre-dentin is the innermost portion of dentin.

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That's the lighter portion here,

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and it's lighter because it's not mineralized,

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and it's located directly adjacent to what we would consider the actual pulp.

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So the odontoblastic layer is where all of these nuclei are.

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These are the odontoblasts that are laying down dentin right on the outside,

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just adjacent to the pulp tissue.

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So the odontoblasts, again, are actually part of the pulp,

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but they are forming the dentin just outside of it.

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Now right next to, or right inside the odontoblastic layer,

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is the cell-free zone of whale,

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and that's this zone right here where there are almost zero nuclei present,

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and that's because there are no cells there.

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In this region, you'll often see

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nerve bundles and we'll talk more about nerves in the next coming slides

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and then right inside of that is the cell rich zone

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and that's where we have a lot more nuclei

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and then inside of that would be the pulp core the central part of the pulp

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and we will talk more about that as well when we're referring to nerves Okay,

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so we have this thing called dentinal pain.

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And so this is conducted by these A-delta fibers.

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So that's probably the first thing we've talked about so far that's extremely important,

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and I would definitely, definitely know that for the exam.

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This one, the A-delta fiber,

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is large, it's myelinated, and it's an afferent nerve,

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which means, or afferent nerve,

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that means it's carrying nervous information from outside the body.

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It's carrying it peripherally towards the center,

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so it's bringing information into the body.

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And so it's, as you can see in this picture, it's large.

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It's at least larger than this one that we're going to talk about in the next slide.

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It's myelinated.

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That's what these darker red portions are and the nodes of Ranvier between these myelinated sheaths and its afferent.

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So the dentinal pain that's conducted by these A delta fibers is a sharp transient first pain.

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So if you stub your toe,

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that's the initial really sharp pain that you would feel from that.

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These fibers course coronally through the pulp,

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so they're coronally as opposed to,

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say, centrally, which is where the C fibers are going to be.

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And dental pain is more often than not associated with cold temperatures.

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And now the second type of pain is pulpitis pain,

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and that's conducted by these C fibers.

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So when we compare them to the A-delta fibers,

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they're small, they're unmyelinated, and they're also afferent nerves.

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They're carrying this pain information.

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As I said before, they course centrally in the pulp stroma.

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This one is involved with dull, throbbing second pain.

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So after you stub your toe,

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and it hurts a lot initially,

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and then it kind of is sore and achy a little bit later,

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that would be the second pain.

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And this is more often associated with heat.

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So now that we talked about both of these,

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you can see this chart here,

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or this graph, with time on the x-axis,

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and the A delta axons are transmitting this first pain,

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super painful, and then the second pain sort of creeps up later,

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and it's a lot longer,

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maybe not quite as intense,

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but it's managed a lot later.

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So those are the two different types of pain and the two different types of fibers associated with each of those pains.

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Now I'll go back one slide real quick

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because I wanted to mention that the A delta fibers are transmitting dentinal pain because they are associated with the pulpo-dentinal complex.

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And so that means where the pulp and the dentin meets,

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it's a bit more easily provoked because dentinal pain is further on the outside,

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you can say, and because the fibers aren't central to the pulp,

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they're more coronal, they're more on the outside,

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along the outside border, they're more easily provoked than the C fibers,

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which are located more central.

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And so you can think of it,

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the progression of pulpal inflammation can change a pain response from

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this first pain with a delta axons to become second pain transmitted by the C axons.

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Alright, next I want to talk about these two really important terms for pain sensitization.

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And there are some graphs and drawings you can check out for these terms,

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but I actually thought they were very confusing,

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so I'll try to explain these important terms as best as I can.

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First we have hyperalgesia, which is a heightened response to pain.

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And then that's compared to allodynia,

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which is a reduced pain threshold.

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So that's pain due to a stimulus that does not normally provoke pain.

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So hyperalgesia would be where you have inflammatory mediators in the pulp that can increase the intensity of a pain stimulus.

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In other words, something that's usually painful becomes even more painful.

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And for allodynia, I have a great way to remember this.

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And a great example of allodynia is sunburn.

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So usually touching your skin doesn't hurt,

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but when it's badly sunburnt,

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it physiologically hurts when you touch your skin.

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And aloe is something you often use to treat symptoms of sunburn.

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So I think of it like sunburnt skin is an example of allodynia.

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and aloe being, again, the thing that you would often grab when you're experiencing these terrible symptoms of a bad sunburn.

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So hopefully that can help you differentiate and remember between these two important pain sensitization terms.

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And last, I just wanted to review the concept of referred pain,

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which is important in all of dentistry and particularly endodontics.

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So preauricular pain often refers from mandibular molars since both share V3 innervation.

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Okay, so what does this all mean and why is it important for anodontics?

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So preauricular is referring to the region in front of the ear

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and you'd think pain in front of the ears may be referred from say maxillary molars because,

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well, they're anatomically much closer.

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But with how the innervation of the face works,

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as we can see in this diagram,

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although they may be anatomically closer,

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they share, or this area in front of the ear,

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shares V3 innervation with the mandibular molars.

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Since V3 is the mandibular nerve,

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the mandibular nerve, that is what shares innervation with this part of the ear.

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These molars are often innervated by V2 or the maxillary nerve,

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and that's not associated with the preauricular region.

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The reason I bring this up is because this itself can be a test question.

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It's something that you could easily think,

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well, just because the maxillary molars are closer to the ear,

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maybe that could be some referred pain where you feel pain in this region because those molars are acting up,

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but really it's more to do with how the innervation is mapped out onto the face.

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So that's it for this video.

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I hope you found it helpful in our introduction to endodontics and how pain is transmitted from the teeth.

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Please leave a like if you enjoyed this video and subscribe to my channel for more on endodontics and all things dentistry.

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Thanks so much for watching and I'll see you guys in the next video.

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Why practice speaking with this video?

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