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Transcribed by Amit Amin 09/26/2014

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[Diagnosis & Treatment of Oral Diseases] [39-40] [Pathogenesis of Periapical
and Pulpal Pathosis] by [Dr. Sigurdsson ]

*TRANSCRIBERS NOTE*
1. He mumbles a bit and has an accent so I tried my best but there were
some parts I just didnt understand.
2. He used a bunch of sides not on the ppt. I tried my best to follow what
the video showed. He threw in a bunch of picture slides and stuff.

[1] [Intro]
[Dr. Sigurdsson] Good morning. Welcome. It's 8 o'clock. It's early for this. What I'm
going to be talking to you today. Just one question. Two hours right? Two sessions
b/c I'm obviously not Dr. Rosenberg. You should know this by now. He was
supposed to give you the lecture but he didn't realize the date. He asked me to take
over. You have my version on the internet already. The last few slides may be in
slightly different order. Sorry about that. I didn't realize when I turned it in that it
might be in slight reverse order from the pdf I sent in yesterday. Don't think it
makes a different. IT should be the same slides except one more slide that I threw in
last minute when it comes up so don't worry about it. The task today is to really
start to tie in root canals and endodontic and really figure out about pulp biology,
pathogenesis of pulpal and periapical pathosis. It's a white topic and will certainly
approach what Dr. Bush should have spoken to you about earlier this week. Some of
the stuff I'm showing you will be reiterated not repeated b/c there's going to be a
different slant to it in the next few weeks. I want to give you a good overview, a good
basis of those three main issues and then we can move on to understand a little bit
better our patients and what we are trying to do. Let me see now if it works.

[2] [Endodontics]
[Dr. Sigurdsson] Here we go. So the issue is what is endodontic? I mentioned this
before to this group. I think it was last spring when we last spoke. Endodontic is
really a nut-shell the prevent or treatment of peri-apical periodontitis. Prevention
means even a restoration in a tooth w/ a healthy pulp is a prevention of that disease
occurring b/c your preventing the offending material from getting into the pulp/
root canal/ periapical tissues. That is really in a nutshell what we are. We are either
preventing or if the bacteria got into the canal, got all the way down to the apical
area, then we have a periapical disease but if the same thing goes we're trying to get
rid of it. We're going to come back to this in details later on.

[3] [The prevention of]
[Dr. Sigurdsson] The first part of the course that we do in endo and you are doing
really already in certain ways is treatment of vital, non-infected pulps. That is really
the key understanding that everything you do to a tooth, there is a pulp or was a
pulp at one time involved and it is effected by everything. So pulpal therapy when
we have a reversible pulpitis that means there is an irritation to the pulp and
remember and you should remember that from basic cariology that even when
caries is in the enamel there is reaction in the pulp. Removing caries from even not
Transcribed by Amit Amin 09/26/2014

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reaching the dentin is by this definition a pulp therapy. You have some pulpitis,
inflammation in the tissue and you're reversing it. Sometimes you have to do what
we call pulpectomy. Now remember that pulpectomy means that the pulp is
irreversibly inflamed. It's not going to heal itself. It's gone beyond it's ability to heal
if you remove the source of irritation and then you do pulpectomy or removing the
whole pulpal tissue. Please don't write you did a pulpectomy on a necrotic tooth b/c
there is no ectomy to be done there b/c the tissue is already gone. You're doing
debridement, your treating a necrotic tooth so we're here only talking about vital
pulp.

[4] [The prevention of]
[Dr. Sigurdsson] And we all know that, you have deep decay, you have deep caries.
Deep something. You might actually here if you think it's reversible pulpitis error on
the site or taking your chances. You will start to see that very soon. You have a deep
decay in the tooth but you didn't see the pulp, therefore the treatment dictates you
restore the tooth but you have to do something else also. You have to remind the
patient there might be a situation might be like this where even though there's not a
breach into the pulp, the bacteria may have gotten close, the bacterial byproducts
have started to effect the pulpal tissue inside and it might be irreversible. You
should always treat it conservatively no question about that if you don't have an
exposure but you need to start building into patient's mind, weeks down the road
they might have pulpitis and then pain which of course means we have to remove
the tissue. W/o telling patients anything at this stage, they will get terribly upset w/
you. You place a new nice filling there and now you have to drill on it again. You're
not a good dentist are you? If you build the expectation on the patient this may
happen b/c we know it happens in several of the cases. Not always not 50%. It's
probably irreversible pulpitis in deep caries is somewhere b/w 20-30% though I'm
taking that number out of a hat b/c we don't really don't know but that's my
expectation. 70-80% of them are going to be fine and thus it's worth the risk.

[5] [The prevention of]
[Dr. Sigurdsson] Of course, if you see the pulp then we know there is no turning
back. There are a lot of articles/ lot of discussion going on in the literature right now
where they do pulp capping with all kinds of fancy materials, bioceramtics, MTA, all
of kinds of materials. The problem is w/ many of those, with one exception when
you have a very young tooth with immature roots meaning root open teeth, it is
usually not worth it b/c you already have massive necrosis, massive inflammation
going on in the tooth. That will mean, whatever you do right here, if you leave all
that affected tissue in there or infected tissue in there, it is not going to heal. The
impression, even some of the research we read is that it works b/c the patient is
called a week later/ 10 weeks later and they say I'm fine I have no pain. The
problem is that many of these cases the pulp becomes necrotic w/o any further
symptoms. The patient has a massive problem w/ the tooth but he/she is unaware
of it b/c there was no further pain associated w/ the necrosis of the tissue. Don't be
fooled to think you can get away w/ it when you have a pulpal exposure. We need to
do the root canal therapy. There is no it/ buts.
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[6] [The treatment of]
[Dr. Sigurdsson] Really, this is the slide that should be basically lecture. The lecture
is pulpal and periapical pathosis. It is a very simple one answer. 90+ percent 99% of
the problems w/ the pulp and periapical area is bacteria flat out. How they get there,
what allows them to get there, all of those things we will discuss to some detail later
on this morning. This is the list you dont' have to remember any list of anything.

[7] [Role of Bacteria]
[Dr. Sigurdsson] However, at least if you're ever thinking about going into
endodontic you should know this article. This is the pivotal article that was
published now almost 50 years ago that proved for the first time, though it was not
the cleanest study the best study maybe w/ the modern knowledge/ technology that
when you have an open tooth, open cavity, oral bacteria, you will develop periapical
lesion. This study was done in germ free rats, laboratory rats that had very
minimum oral flora. If you exposed the pulp in those animals the pulp survived.
There were no periapical lesions formed. If there were normal rats, of course
laboratory rats not rats from the street, had a normal oral flora, same kind of cavity
preparation into the pulp w/in 2-3 weeks there was a massive periapical lesion. It
was known before this 65 study that this would most likely happen but that's the
first time it was really documented in a cross over study so that to us is very pivotal
discussion. You might even hear now some dentist say it can be the lysosomes or
other things, or even materials used that cause periapical lesions. Fungi, viruses
maybe. Spirochetes, but they are never found alone. They are only found along w/
bacteria.

[8] [The treatment of]
[Dr. Sigurdsson] What happens? I think I've shown you this before you have a large
lesion, you find the offending tooth, and it will heal. 90% of the time, if not higher
now w/ modern technology you can heal the periapical lesion if it's properly done
and kept in mind the reason for this lesion is bacteria. Canal disinfection and I warn
you that once you graduate in a couple years you will be bombarded w/ materials
and technology in endo that tells you can do one appointment quick and easy and
don't have to worry about b/c the instrument is so nice, looks so good, and fills so
quickly. The problem is that is those technologies have lost the sight of this right
here. That there is bacteria in there. Yes you can get rid of the bacteria 50-60% of
the time but that's not a very good offering where you do a 2 appointment endo
where you get rid of the bacteria 90% of the time. 30% difference and therefore a
higher failure rate. The beauty of dentistry is that patients are so mobile and not
loyal to you that you don't see if the root canal fails, the patient is likely to move
away or is pissed at you and is going to go somewhere else. Many perception is that
this is fine to do in one appointment. Thats the reason behind it. We'll talk about
this in some detail later. Remember I showed you this also I think last year, last
spring was even the obturation on the last lesion like this is not that important. It is
the disinfection. This was a patient of mine who actually I started the root canal
therapy on that premolar, he vanished for 9 months with the calcium hydroxide in
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there, no obturation, but perfect healing. That's the key. Get rid of the bacteria and
you have a good outcome irrespective of what you put into the canal. More extreme
case. This kid was sent to me some years ago w/ this massive lesion that you can
hopefully see on it. The oral surgeon was going to extract those two teeth and
enucleate (that's what it sounds like) the lesion but mom was really upset about it
and asked for a second opinion and ended up in my lap for whatever reason. Test
the teeth and we will go through the testing and everything else both clinically and
in lectures. This tooth was non-responsive. 14 year old kid. History of sports, history
of lot of activity. Pathophysiology probably some trauma on the tooth some years
before. Became necrotic w/ the trauma. Bacteria eventually found its way in there.
This is just treatment of CaOH. Placed it in after 6 weeks. Good healing after 3
months. Great healing. He's now ready for obturation and he kept both his teeth.
Again, the oral surgeon lost the site of yes, lesions esp. in young individuals can form
very rapidly, the root can look aggressive but there is only reason for it. It's bacteria.
Of course it can be cancer. It can be all kinds of bad things. We can go in there and do
biopsies put when you find a necrotic tooth in an area like this the most obvious first
treatment is to just do endo and see what happens. That's the reason why I called
him in actually. I called him in after 3 weeks and then 6 weeks and no question he
doesn't need surgery.

[9] [Vital Pulp Therapy]
[Dr. Sigurdsson] So what are the requirements for success in endodontic? Pulpal
status. If you are actually doing vital pulp therapy and you're capping a pulp, if it's
healthy if there is no bacteria/ minimal bacterial byproducts are into the pulp, you
can argue that the capping will be over 90% successful. I will talk about that a little
bit later one. When do we do that in a healthy pulp or in trauma. You break the tooth
or the kid breaks the tooth, the pulp is just sitting there. Few hour exposure, few
days exposure. That's a healthy pulp. You can expect very good success rate. If you
cap inflamed pulp where you did not remove all of the inflammation or irritants of
you pulp and you're below 30% . The reason of course being even though you might
not have a breach into the pulp, there is massive inflammation going on. You see left
and right here it differs b/w healthy pulp and affected/ infected pulp. Once you get
the exposure the massive, necrosis here, massive amount of inflammation going on.
Really to hope for this to survive, if you placed just a filling right up here, this would
not survive. This thing would continue and erode the whole tissue in the hope that
the canals are still healthy. The only time you would do that again would be in young
kids w/ immature teeth you want to try to buy time or allow the roots to continue to
form, apices to close and then do the endo. You're buying 2-3 years at the most.

[10] [Pulp capping]
[Dr. Sigurdsson] Telling the truth well, there's a study out of Germany some years
ago now that looked at minimal exposure. The issue here is that many think you just
scooping out the decay and you have a pinpoint exposure (<1mm exposure of the
pulp). Why not, the patient is fine asymptomatic, put the dycal on top of it or the
glass ionomer and build w/ that rather than go through (some word I don't
understand). Good argument. Dr. Barthel, at Columbia decided to follow this. He had
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54 teeth that had no symptoms before. The patients were fine, minimum exposure,
chip a layer of sealant meaning Dycal, IRM, and other composite or amalgam on top
of it. So 3 layers of protection. Follow up success only 37%. Failure 45%.
Questionable 18. What does questionable mean? The tooth was not responding to
EPT or cold so there was no really conformation that the pulp was vital but there
was no periapical problems. The failure had definitely. Many of the patients thought
they were fine since they were asymptomatic. No pain. Yet, they had a periapical
lesion.

[11] [Pulp capping]
[Dr. Sigurdsson] Now seeing them back 10 years down the road, success 13%.
Failure 80%. Questionable now 7%. Again, I know you're taught partial or I don't
know what you call it, pulp capping in some other areas especially in stages where
you leave a bit of infected dentin leave it there for a while, let it calcify, and then go
back and scoop it out or leave it there and whatever. I'm not saying it doesn't work,
and I agree w/ that sometimes it is indicated especially for financial reasons for
many individuals but you have to be mindful this was done in grown ups that the
outcome long-term is very poor. At least according this study and many studies.
Short term it might be fine. It might want to buy time. You want to buy patients the
opportunity to gather some money before they can afford the root canal. That's
acceptable in my mind but you have to warn the patient that the outcome is not
guaranteed. Far from it. thats the whole purpose of it. So when you are being taught
now to do pulp capping in other areas throw in this article and let's see what they
say.

[12] [Endodontic Diagnosis]
[Dr. Sigurdsson] Keeping w/ the line of this discussion of why we do root canal
therapies, we do it when the pulp is necrotic. No question about that. That's obvious.
We have to do it then. WE do it when the pulp is irreversibly inflamed. That
sometimes can be challenged into decide but I can tell you categorically, if you have
caries exposure, the pulp is irreversibly inflamed. It will always necrose. Eventually
it will take it maybe 10 years but it will go there. And of course, sometimes we do
endo b/c the treatment plan dictates that. You might have a tooth that is broken
down. Still the pulp is healthy but you need a post. You need some restorations,
retention, or you're going to do an over denture on the reduced couple teeth left.
then you do endo. That's fine. Thats a good diagnostic term b/c the treatment plan
requires it.

[13] [Scope of Endodontics]
[Dr. Sigurdsson] But we are about basically. We are trying to retain natural teeth.
This is always a competition. You will be faced w/ this over and over again w/ the
implants should you do endo w/ a crown and everything else or should you just
drop in an implant w/ a crown. Cost right now is slightly cheaper to do endo than
placing an implant but that's being washed out more and more. But remember,
implant is a foreign body. Tooth natural tooth being saved is the patient's own and
there is now a trend in certainly the implantology to realize that the success rate
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that they are claiming is not quite correct but more importantly we've been
comparing apples and oranges when we say success of endo and success of
implants. The reason being is that a successful implant is an implant that stays. It
may have implantitis (I think that's how you spell it), it may have very poor bone
integration but it's there. It's functional and the patient is able to function on it.
Failure in endo is that we see on the radiograph something periapically. Patient
might be asymptomatic. The patient is doing fine but b/c we put in a white line into
the root canal system, gutta percha, and the lesion didn't go away, we call that a
failure, but the patient is fine. He is functioning with the tooth. We are now adjusting
the endodontic to talk about the retention like implant people and almost now the
success rate is now even or slightly higher. When you hear about endo being 80%,
70% successful please read into it, what is the definition of that success and I argue
w/ you and I'm absolute that no one can say I'm correct but I know it's the issue that
we were very hard on ourselves w/ the definitions and fortunately we are learning
from implant people that it is not quite. So of course what is endodontic is about? It
is about pulp biology, microbiology. it's a discipline. We are also, us and endodontic,
and as dentist as you part of endodontic, very much diagnosis part of it. Especially
differential diagnosis. I will talk to you a lecture or two later this year bout that.
Really this here, is the most clinical what you do for your patient. Is the pain in the
jaw on the lower left side in the fat of a smoker actually a tooth ache or is it his
heart? Is he having a heart attack? Big decision and you have to known that. Of
course we then need to know if it is the odontogenic which tooth is involved.
Another part of endodontic is relievable of pain/ swelling, emergency procedures,
regenerative procedures, and treatment of dental trauma. I know Dr. Busch
probably approached this a bit but I want to put this in context to the what the rest
of my lecture is.

[14] [Contraindications to endodontic]
[Dr. Sigurdsson] So any contradictions to endo? Overall very few. The main issue
that you are faced w/ probably w/ the next 2 years at this school is the restorability
of this tooth. is it worth it? Do you have do quite extensive restoration. Do you have
to do periodontal surgery. All these things to save the tooth. Again if you can't, if the
patient is willing why not, but sometimes it's just beyond reason so there lies the
main contraindications. The second issue though I put two question marks is b/c it's
listed in many textbooks is the access to the tooth. It's so hard, the patient can only
open a few mms. You just can't get your drill to even cut the access level, let alone do
the root canal therapy. Well to me, that is very rare that I cannot get to the tooth and
I don't do the endo. I've done it on patients w/ an opening of 3-4mms. There are
techniques. Endodontics can certainly do it. Don't condemn a tooth before you talk
to an endodontist. See if she/ he is willing to do it, if you can't do it yourself. Of
course the main goal of this training here, is that you can do more than half if not
2/3rd of the endo if you so decided. Thats the whole goal of what we're trying to do
here. Of course the third reason is medical reasons. Is the patient stable enough? Is
the patient healthy enough.

[15] [Medical Contraindications]
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[Dr. Sigurdsson] And you know the issue uncontrolled diabetes for example. That is
a patient that should not be in an endo chair except for maybe an emergency but not
a routine treatment. Of course, recent myocardial infarction is something that again,
patient is usually very unstable and you don't want to any elected, you want to get
him out of pain obviously but not a routine endo. Hypertension, I know you have all
kinds of numbers floating around. Some say over 300, some say diastolic over 100. It
depends on whom you read, where you are, but I agree w/ both and actually in our
endo clinic right now, our rule of thumb if we're going to do endodontic surgery, if
the combined numbers if over 250/260 and the diastolic is approaching we're not
going to do it. Routine endo on a patient that is known to be hypertensive but is
trying to control it w/ diet or more likely medication is approaching combined
number of 270/300 it's ok but I certainly would not rather do it for obvious reasons.
Thats about it. The extreme, undiagnosed symptoms might indicate something else.
We'll talk about that later in the year about differential diagnosis. What can else be
there.

[16] [Prognosis of]
[Dr. Sigurdsson] So what is the prognosis of endo. You need to know that. You need
to be able to tell patient what you think what is going to come out of this. Why
should you rather have root canal then implants for instance. And this is a fairly 10
year old study but it was the largest one we ever found. They looked at 1.5 millions
treatments across the U.S. and using the definition, the same definition as the
implant people used, meaning the tooth is still there some years down the road, 8 as
we recall. We're in 97%. Are they all healthy? I don't know. B/c the study was not
(mumbles again). It's just using the same as the implant rate, is the tooth treatment
and did it stay? To be honest w/ you, if you look at the endo literature, you will find
a different number. The pulp is necrotic in periapical lesion we say 80-85% success
rate. Remember that means we can heal the apical lesion. It doesn't mean that the
tooth might have to be extracted. Of course if it's vital, it's approaching this. If you
did the proper endo and remembered to use your rubber dam, and that's the
hardest part of the whole thing right now, students who graduate in the U.S. to use
rubber dam for endo then you have this no question about it. And remember of
those 1.5 million teeth, moth of them were done by GPs in that study. This was just a
comprehension multi-centered study. They were done by general practioners not
endodontist. So you guys can do it once you gradate here. There's no question about
it.

[17] [Consider relationship of the pulp]
[Dr. Sigurdsson] Let's now go into the biology and the pathophysiology we just
have to remember this even though this is very old schematic drawing not a real
histology but it's nice to tip your hat to the old guys and we have a very unique
relationship. Remember the periodontal ligament and the periapical space that is
always there. This is exaggerated and that's the reason why I liked the picture b/c
you know that it is much thinner proportionally and then we have the hard tissue.
We have the pulp tissue. Therefore we have a very unique situation.

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[18] [Endodontics Relieves Pain]
[Dr. Sigurdsson] Very much part of the endo is the pain and pain issues. We need
to really work on that as well as well as a part of the outcome. I'll come back to that
in just a minute.

[19] [Normal Pulp]
[Dr. Sigurdsson] I want to just stay w/ the normal pulp a little first. Remember
richly vascularized. Very well defined odontoblast layer that you find right
underneath and the rest is undifferentiated mesenchymal and stromal cells in the
body. This is normal healthy pulp.

[20] [Normal Pulp]
[Dr. Sigurdsson] We have all these denticles. All kinds of things that seem to
happen w/ increased age in the pulp tissue. You have less cells, more of these guys
right now. Does it make a difference? No. Actually, it does not make a difference
what so ever. Some decades ago, there were thought that these denticles or pulp
stones/ pearls were indicative of irritation in the tissue. Therefore if it was seen on
the radiograph some dentist thought if they saw it they needed to do endo. This is
just a natural aging process that does not have to do anything w/ the healthy pulp.

[21] [Pulp Anatomy]
[Dr. Sigurdsson] We have to remember though that the pulp is sitting in a very
unique situation compared to any other tissue except the brain b/c it is encaged w/
bone. No other tissue in our body is encaged like that except the brain b/c any tissue
can expand if it is inflamed if it has things like that but of course obviously the pulp
cannot.

[22] [Pulp Vitality]
[Dr. Sigurdsson] That's where we come in w/ the pulp biology/ pathophysiology
and then we have the first question is what is vitality? Anyone define that for me?
What is vitality by definition. Now I'm not talking about pulp necessarily. You're
being alive but is that life. Do you feel something or is it something else? Let's go
first and answer your question in a minute. You see it on a slide of course. How do
we measure the vitality of a pulp? We use cold, we use heat, we use electric pulp
test. Thats the test we will teach you and train you to use to diagnose the health/
vitality of the pulp. However, the problem is sometimes we have mentioned this but
we don't have it, it's expensive and not around. Vitality of a tissue is this. It's blood
circulation actually. It's not new in the variation if you will. Vitality means that we
have a tissue that has blood circulation through it. There lies the problem that go
back here, heat, cold, EPT does not measure that. There we have a major problem
b/c when we are looking into the pulp. This is actually a resin cast of a pulp horn in
a dog sacrificed for the culture of science I guess, you see how intricate it is. This is
the vitality and what I thought we know as a very young endodontist 20 some years
ago that by 2014 we would have a tester that would tell us yes there is a blood
circulation going on which has increased b/c there is inflammation or decreased b/c
it is partially necrotic. We don't have it yet. WE still rely on the same old same old.
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[23] [Pulpal Circulation]
[Dr. Sigurdsson] This is what we're looking at. The pulpal circulation and there's a
large, esp. this is an open apex as you can see, you can see a lot of vascularity there.
We have as well connected, collateralized the blood vessels are unique also. They
are very thin vessels and they have a lot of A-V shunts. If you don't remember what
those are, that's basically a bypass shunt if this is the pulp, on the incisal edge, it will
be on the other end in the apical area. If the pressure inside the pulp encasement
(tooth), increases, these AV shunt will open up and try to reduce the pressure so
there is less blood flow into the crown portion of the tooth. Of course over the years,
the increased age and irritance meaning orthodontics, restorations, abrasions, and
all sort of things that happen. Of course these blood vessels become less numerous
and they change over the years. The issue is that, it has perceived to have an effect
on the healing rate or the healing capacity of the bone. But no study has shown it
does actually. Pulp even in an old person seems to be able to heal if you allow it
properly w/o any problems as easily as anything else. Just also want before I go into
the inflamed pulp,

[24] [Innervation]
[Dr. Sigurdsson] is to talk a little bit about innervation. Again, this is a repeat of
what you should have somewhere else but it's always good to remind you the right
cells. The pulp has really 3 of the basic fibers. A-Beta, A-delta, and C fibers. Again, it
changes w/ age and exposures or irritants meaning that the ratio b/w the two seem
to shift. We don't know why. We don't understand it very well.

[25] [No title]
[Dr. Sigurdsson] Of course the remember we have the neurofibers going into the
tubuli at least in the coronal segment about 1/3-->1/2 the distance of the dental
tubuli. We don't know what's beyond there. It's argued some tell you they know and
others say they don't know. I don't know. This is not my research so I don't know.

[26] [Basic Mechanism]
[Dr. Sigurdsson] But we have to remember mechanisms for pain is. In the incisal
area of the pulp, the nerve fibers are every tubuli. In the cervical area you have only
7% of the tubuli that are innervated. Isn't that interesting? Every patient that you
get w/ cold sensitivity is not complaining b/c the dentin is exposed on the lingual
side of the canine or somewhere like that, but rather b/c of the exposure under the
cervical area. Yet I'm just telling you the innervation that is a lot less. Can I explain
it? No. But it's an interesting fact if you will. So normal healthy pulp has small and
large A-deltas. What are the A-deltas? They are pain fibers. They are pretty much
on/off fibers. meaning there is something that they perceive as being painful. They
kick and you get that sharp shooting pain. They have very little encoding of pain.
They just kick. The more they kick, the number of them kick, the more the pain will
be. The C-fibers are very different. They are also exclusively pain fibers or almost
exclusively but they have heat sensitivity as well. In the pulp, the C fibers are almost
always what we call silent. They are not reactive. Then we have some Beta. Some
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people dont' really understand why we have Beta b/c they are not pain fibers. They
are propriosensitive fibers, they are pressure sensitive fibers. That's probably just to
control the pressure inside the pulp.

[27] [Sensory Fibers]
[Dr. Sigurdsson] and you have this/ you should have this. I want you to highlight
the difference b/w the two here. The A-delta and the C fibers in what the patients
feel. What you will feel. The sharp picking cold sensitivity is the A-delta fibers. That's
the normal activity of the normal pulp. The long burning, lasting, strange fibers, pain
sorry, is associated w/ the C fibers. That if you have the report meaning the patient
tells you the achy, throbbing, burning sensation in the tooth tells me one thing and
one thing only. The pulp is really inflamed and really in trouble. B/c what we have,
we have A-fibers w/ sharp pain very short duration, that is the normal function of a
healthy pulp. If you put cold on a tooth, the patient feels it immediately.

[28] [Pulpal Fibers]
[Dr. Sigurdsson] That's A-Delta. But w/ the C fibers there are unmyelinated, they
are very slow b/c of the light myelination. They have low threshold. They create
very dull, achy, radiating pain. There lies the key b/c the issue is that once you have
the inflammation going on you have a problem w/ the pulp. A-Delta fibers are
always active, always expected to kick when you test the tooth in a normal but when
you have the really severe inflammation, the C fibers will give. That's the key in
diagnosis.

[29] [Neurofibers]
[Dr. Sigurdsson] Skip

[30 number] [Dentinal Hypersensitivity]
[Dr. Sigurdsson] So, hydrodynamic theory. Has anyone discussed that w/ you yet?
Yes. Ok. So you know all the don't give it to Branstrom give it to Gysi.

[31] [Hydrodynamic Theory]
[Dr. Sigurdsson] Remember it's just the theory is that you have flow of fluids
backwards forwards. He explains almost everything in the literature except now
we're realizing that the odontoblast can talk to each other. This might change. You
might be outdated in a few years w/ that. I just wanted to highlight that.

[32] [Aging of the Pulp]
[Dr. Sigurdsson] Let's go back to the aging and the pathology or the
pathophysiology of what's going on. So, young pulp has a lot of vascularity, a lot of
fibers, and of course a lot of nerve fibers as well. When you get old, the vascularity,
neural fibers go down. You test the tooth. it doesn't respond. Does it mean it's
necrotic? Not really. It means you have fewer nerve fibers that means the patient is
not responding and you have a lot of calcifications going on there. And of course you
have a lot of these guys. (slide not on the file showing tooth decay). Sorry about the
quality of the film. I didn't realize it was so low resolution. That you know these
Transcribed by Amit Amin 09/26/2014

11
teeth are very aged. The patient might not be very old, but these teeth are certainly
worn down and aged.

[33] [Aging of the Pulp]
[Dr. Sigurdsson] As I said before, I got a little ahead of myself the issue is that aging
pulp contra to popular opinion, older patients seems to heal as well at least from the
pulpal standpoint so you know there is no issue, no contraindications of doing either
endodontic therapy or doing vital tooth therapy on these guys.

[34] [Aging of the Pulp]
[Dr. Sigurdsson] We have to remember that even though it's no difference in
healing the chamber, you might be thinking oh, the upper central is easy to do, you
need to take a good radiography you need to investigate the tooth. Of course
previous treatment history might effect the ease of the treatment. Finding this canal
here where you see that canal doesn't start until you're about bone level if you not
further down, you're drilling down and the small tooth where you may have maybe
a quarter of a (mm) going to each side by perforation and then ruining the tooth.
You're not saying you shouldn't do it, you have to be very careful and mindful of
that.

[35] [Aging of the Pulp]
[Dr. Sigurdsson] The other thing is that the issue when we talk about age changes
in the pulp, they can occur for two reasons. One is just a natural, my pulp chamber is
smaller than yours obviously since I'm much older. However, trauma including
drilling, restoration, blunt force trauma can also show aging changes in pulp.

[36] [Aging of the Pulp]
[Dr. Sigurdsson] And of course in cases of trauma, any trauma, the chronological
age of the patient has nothing to do w/ the situation of the pulp both histologically
as well as morphology. this is a 14 year old kid. You can see very open canal on one
side. You can see no canal on the other side. That again is from extreme aging of the
pulp b/c the kid had a trauma from years earlier, the tissue reacted by
overcalcification. It had probably very few nerve fibers, very few blood vessels left,
it's still vial . We think so b/c the periapical area is normal and the patient is
responding to electric pulp testing. Does it a root canal? No. Does it need to be
monitored? Absolutely. It needs to be monitored almost like an ER, you need to
check this every year at least b/c the centers might turn into a periapical lesion.

[37] [Aging of the Pulp]
[Dr. Sigurdsson] What are the ages just to recap what I've been saying is the
morphological and histological. To some degree physiological as well.

[38] [Aging of the Pulp]
[Dr. Sigurdsson] We just remembered also, that it's just not even over time,
especially molars. You will see this trend meaning that there might be almost two
(some work he mumbles) that these, the secondary/ tertiary dentin joins right here
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12
and you have almost two systems going on. Very commonly you see this. There
should be a chamber as you know up here but the kind of the roof and the floor of
the chamber seems to kind of grow faster. That means when you cut the direct
access in the center of tooth, you might be drilling and drilling and all of a sudden
you're through. So take a good radiograph. Take a new radiograph. Especially in an
older patient and try to figure it out. More extreme, this had been referred to me as
the dentist had drilled all the way down to here. The furcation is right here and not
found anything. Again, same thing. These can be treated and you can even treat
them yourself if you're careful. Now once you start in the clinic next year, remember
if you have a tooth like this and you want to try you can do the evening sessions up
in 7W where we do have the microscopes available to actually play w/ b/c this
actually requires microscope to be able to find the canal w/o destroying what is left
of the tooth.

[39] [Induced Aging]
[Dr. Sigurdsson] So induced aging. What do I mean by that? well I think you all are
not already guilting pulps you will.

[40] [Operative Trauma]
[Dr. Sigurdsson] What we're talking about is (goes to a different slide called
odontoblastic process). Remember we have shown you the schematics of these guys
before. Now this is real thing. You have the odontoblastic layer, you have the
odontoblastic process going into the dentin. What happens if you're not careful
when you're cutting for a restoration, cutting for a crown is that b/c of the
hydrodynamics going on there, you will start to suck in the cells. These are actually
cell bodies of our odontoblastic layer on the dentin that was actually cut w/o cooling
so you do two things. You desiccate or dehydrate the dentin or you create a suction
effect of the hydrodynamics and you suck them in. Once you suck them in like this
they're dead. They're not going to crawl back out and survive. They will have a
problem.

[41] [Repair following cavity prep]
[Dr. Sigurdsson] this you will see here inflammation one week after the
preparation. There is a problem here. It's not going to cure the pulp but this area
right now here is compromised b/c there's partial necrosis going on there. If
bacteria find its way through the dental tubulin right here it has diminished defense
of the tooth and pulp products they say, the bacteria can stop itself if it's quicker
what does the pulp do? It tries if it happens in a localized area if it's not, it just a
small area. It builds a reparative or secondary dentin/ tertiary. Hopefully we see
another odontoplastic layer going on. And in extreme you will see this after a crown
preparation. You will see the pulp horns are absolutely gone and this is just tertiary
dentin that was formed. This is the good scenario. The bad scenario is that you've
created so much necrosis in the pulp that it's kicked into irreversible pulpitis. Again,
it might be asymptomatic, it might not be infected yet, but there is no host defense
left in there b/c there is no blood supply, vitality left. Therefore, you will not get this,
but you rather as soon as the bacteria gets in there, it's a primal opportunity for the
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13
bacteria to create problem. So you have to remember, the frictional heat if you're
using any kind of burr sharp, dull, I don't care. Of course the duller the burr is the
more frictional heat you create especially w/ the high speed turbine but you need to
cool it. This is the reason why you cool your burrs. It's not b/c it smells awful when
you cut the dentin. It is b/c you're trying to reduce the dehydration and the sucking
effect of the dental tubuli and therefore killing of the odontoblastic layer. I just read
a study looking at survival of pulp in cases where they are cutting crowns. Dental
students. Fairly large, study it's going to be published w/in the next few weeks and
actually, 13% of all teeth that were in the paper, meaning they were confirmed to be
vital and the dental student did the crown preparation, about 7% did not survive the
preparation. The rest were still alive after that. 36% did not survive the
temporization and impression. Does it mean that as a dental student you will do
this? I think every time we do a crown preparation there is a risk. Of course you
guys might take a longer time and thus there is a slight increased risk. I would like to
see this study done w/ more experienced dentist and I argue it's probably the same.
They're too quick. The point I'm trying to make is, anytime you cut for a crown,
before even starting given that this is a 10-15% chance that the patient will need a
root canal therapy you should do two things. A) warn the patient. Yes the pulp might
be healthy right now or at least alive, it might be compromised b/c there is a reason
you're doing a crown. Remember there is broken down tissue, there is old
restorations. There might be a lot of leakage. I'm not saying the dental student killed
the pulp b/c they might have been compromised before of the reasons why you're
placing a crown. There's no way to access that. You need to warn the patient. 10% of
these will die due to this procedure and the patient will then be very happy if it
doesn't happen but then be warned if it does happen. The second thing you need to
remember is just to remember these numbers. Try to reduce it. Be careful w/ it. use
water, use coolant, use appropriate ways to control and use fresh new burrs b/c
again dull burrs will burn. So I think it's clear that I need coffee right now. We will
meet again in about 10 minutes or so. Any question by the way? You need coffee too
I guess. That's alright. We'll do that together.

[42] [Pulpal Circulation]
[Dr. Sigurdsson] Ok guys. Let's get moving. I have been asked to actually share w/
you the version I'm talking from and unfortunately I cannot till after we're done
today b/c the issue I realized when I was in a rush when I knew I was giving this
lecture yesterday, I grabbed an old version of this lecture and shared that and when
I started to look at it, to share it w/ you I have to share it w/ you I have to send it to
my department who sends it to someone else to download it. We have no privileges
in endo. As of today, to get this directly to you, I'm going to ask for that this
afternoon so we can actually do this real time. Right now, unfortunately, I know the
slides are there but they might be in slightly different order. I'm terribly sorry about
that. My brain is scattered everywhere. What I was talking about before the break is
the aging changes of the dentin as such and the pulp and all that. I want to talk about
the blood vessels a little bit.

[43] [Vascular Changes]
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14
[Dr. Sigurdsson] And the uniqueness of the blood vessels in the pulp is of course
what we're talking about that we have easily when we have inflammation going on.
You having different pressure. There's a vasodilation and you start to have a leaky
blood vessel. You all know that. It's just a part of the natural inflammatory process.
[44] [Inflammation]
[Dr. Sigurdsson] We have remember these two. Margination that occurs in the
blood vessels and then they start to leak if you will w/ the immune cells are
chemotaxically attracted to the area. The leak out. That of course starts to increase
the pressure. Not a problem in the tissue that just expands when it's inflamed but of
course, we have dentin on the other side. Now you have a problem. You have a tooth
competing w/ things going on. There's a need for leakage blood vessels b/c you
want to get rid of the offending material that is coming in or what you're doing when
you're cutting the tooth. At the same time of course, the pressure increases b/c of
that. The interstitial pressure increases b/c of the leaky blood vessel and the pulp
starts to shut it down through the AV shunting and all of a sudden we have a very
compromised situation b/c less blood through, more heat on the cut angle that's
also part of the cooling system internally you're in trouble. You're going to kill the
pulp if you're not careful.

[45] [Tissue Damage]
[Dr. Sigurdsson] Of course then you have the mast cells all that. I'm not going into
that detail.

[46] [Host Response]
[Dr. Sigurdsson] This is actually a slide from Dr. Rosenberg whom he is very proud
of. I'm going to share w/ you what he always says when he lectures on this, he has a
print out in a larger form than you have in your computer now. If you want that,
entertain him by going to 7W, find Dr. Rosenberg and ask him for a print out of this
inflammatory host response to tissue damage. Remember we have bacterial physical
or chemical entry. All of them can cause this but of course in dentistry we're mainly
talking about bacterial or the physical heat damage that you cause or dehydration
w/ the cutting. You have tissue damage and you start to have this classical
inflammatory mediated reaction which I'm not going to go into details. You should
have learned it and memorized it. You start to get inflammation but that starts to
feed the frenzy. That's normal for every other tissue and healthy for every other
tissue in your body except the pulp. W/ there we start to have now a vicious cycle
that's very hard to break. Of course it causes other things, the adaptive and innate
system and all kinds of other things and you have all this things that you all like I
said should have learned somewhere else. But two things that I want to highlight.
Let me do it differently.

[47] [Neurogenic Inflammation]
[Dr. Sigurdsson] This is my simplified version of the (says some word that I can't
understand). And again, the key is that you have some kind of trauma to a blood
vessel, you have this thing that you have here, and now we have this evil little thing
right there. I spoke to you to about the C fibers before that once you have quite a bit
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15
of inflammation going on all the serotonins, braikinins, prostaglandins, leukotrienes,
everything else that is inflammatory mediated affects the C fibers. Affects it in two
ways. Increases it's firing which is the second slide in a minute. It also of course
wakes it up and causes it to relay pain to the brain but it's a different kind of pain.
When I'm trying to diagnose if is reversible, irreversible pulpitis I always ask the key
questions. Please describe the pain to me. if the patient is confused just say is sharp
shooting, or dull aching. Give them those two choices. Sharp shooting might be leaky
restoration or cervical area exposed. That's normal. That's very likely to be
reversible. Dull aching, radiating, yes. This is most likely pulpitis. How bad is it? We
have to figure it out. That is b/c of the activation of C fibers. I said they do other
things. The problem w/ the C fiber is that their neuropeptides CGRP and Substance
P primarily and those on their own are inflammatory mediators. They will cause
further inflammation and that's the loops that starts the neurogenic inflammation
which occurs everywhere in the body. The problem is in the pulp, the system has no
flexibility. That is sometimes what we believe causes necrosis on it's own. it just
goes into overdrive. It doesn't stop. The AV shunts kill the blood circulation and it's
a vicious cycle and you lose it. Is it that simple? Probably not but certainly it explains
a lot of things.

[48] [Pathogenesis of the pulp]
[Dr. Sigurdsson] So, going back to the theme. True pulpal pathosis. Now we have to
do a split here. I've spoken about trauma, I've spoken about when we crack the
tooth, we cause pulpal necrosis or pulpal inflammation but that really doesn't do
anything but that. We need an active stimulator to maintain the problem and there
is only one reason why we really go into trouble w/ the pulp and that's the bacteria.
Yes we can compromise the pulp such that it is more susceptible to the bacteria but
the bacteria is the thing.

[49] [Pathogenesis of the pulp]
[Dr. Sigurdsson] So prior to bacterial invasion of the pulp it is compromised like I
said by all the things that I mentioned. Or I mentioned so far but that's the key.
Remember that if you do something to the pulp, it is compromised, and then the
opportunistic issue which is the bacteria gets there and causes the problem.

[50] [Pathway of microbial entry]
[Dr. Sigurdsson] So this is just an overview of all possibilities. Caries, trauma,
cracks, cavity preparations. Even root absorptions b/c remember especially in the
cervical area you have cementum layer which is impermeable to bacteria. You do a
perio therapy. You're scrapping, you're scaling, you're cleaning the calculus that is
building up here. Do you know when to stop and you're into the dentin? No you
can't. There is no way to do it. We can't do it. Now by root planning you are opening
up the tubuli and if the pulp is healthy underneath it will defend itself. It will create
a new layer of reactive dentin but if the pulp is compromised already b/c you just
cut a crown on it or something like that Boom! you have a problem. Bacteria will get
there and cause a problem.

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16
[51] [Dentin Bonding]
[Dr. Sigurdsson] But, does it happen all the time? No. This is a trauma pulp exposed
on both teeth and you can easily actually and predictably treat that w/o having to
worry about a pulp.

[52] [Uncomplicated Crown Fracture]
[Dr. Sigurdsson] Because, the only except to everything I've been saying so far is
fresh dental trauma. When we have what we call uncomplicated crown fractures
that means that you broke the tooth but it didn't expose the pulp. The biological
consequences/ pulp consequences are very minimal if any unless we mess it up. We
can further damage the pulp but if we do the natural thing which....

[53] [Uncomplicated Crown Fracture]
[Dr. Sigurdsson] ...is basically do the esthetic repair and if it's less than 1/2 a mm
which means that you see pink through the dentin fracture you don't have to do
anything. You just etch, bond, and either bond the piece back on as I did in that case
or you build up w/ composite. If it is less than .5mm-1mm in you put a Dycal on top
of the deepest portion of it and then you restore it.

[54] [No title]
[Dr. Sigurdsson] Picture of incisor. Even when you have the pulp exposed like this
in a trauma, up to 48-72 hours you find...

[55] [Complicated Crown Fractures]
[Dr. Sigurdsson] ...there is minimal inflammation. Maybe 1 or 2 mm down into the
pulp. Why? Well two things. Usually this is for young individuals. The pulp is more
robust. Quicker to respond to it. If you don't do anything of course there will be
necrosis.

[56] [Complicated Crown Fracture]
[Dr. Sigurdsson] For some reason it's not showing all of my slides. I have no idea
why. What that slide was going to show you is, that after 48 hours there is actually
pulp polyp forming in these cases. Rather than you get the bacteria in. More than 48
hours you start packing bacteria and then you start to see the classical reaction as
you saw w/ decay.

[57] [Inflammatory Reactions]
[Dr. Sigurdsson] So, just as you remember the tissue damage has to be there and
then we have to have some mediators going on.

[58] [The bacterial invasion]
[Dr. Sigurdsson] The bacterial invasion of the pulp will always going to be if we
don't treat whether it's trauma or caries or whatever it is. First localized, massive
inflammation, zones of necrosis, complete necrosis of the pulp. So you start very
localized, you get more massive, you get zones of necrosis as I showed you before,
you get into this like this. Even though rot not into the pulp yet, you see the area of
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17
necrosis already. The endotoxins and the bacteria cross through these tubuli and get
there no question about it.

[59] [The end result]
[Dr. Sigurdsson] End result we have something like this where you have two
cardinal signs of trouble. You follow the PDL space and you to start to lose right
here, pick it up here, and I hope you can all appreciate the lesion right there. This is
a tooth w/o caries. What happened? Most likely trauma. Possibly that the enamel
and cementum didnt' meet here and now the patient is getting older and the
bacteria is find it's way there. There are many ways but remember (something
something Fitzgerald I think). If you see this you know there is bacteria and if you
look at the histology this is a younger tooth though admittedly you have massive
periapical lesions.

[60] [Apical Dynamics]
[Dr. Sigurdsson] Classically we talk about it in the zones. You have infected tissue
in the canal. You have the exudative zone. You have pus formation in that area. Then
you have granulation tissue and fibrotic tissue around in these chronic situations.
This is just the classical model of the body trying to kind of encapsulate the problem.
This can go on for weeks and weeks if not years and decades and the patient is most
often asymptomatic.

[61] [Host defense mechanism]
[Dr. Sigurdsson] Of course what is going on is that you have a lot of cytokines going
on in there or you have the endotoxins that actually are chemotactic to the
inflammatory. You have a lot of things going on. We will discuss this to some degree
in other areas but most certainly should have gotten the basics already.

[62] [Diagnostic Information]
[Dr. Sigurdsson] I just want to go back to this issue that even when you have a
periapical lesion this was a fairly large study looking at about 1/1,000 charts in
Michigan dental school some years ago. They looked at the charts, every radiograph
they could find, and they identified over a thousand patients w/ periapical lesions
either as connection w/ root canal therapy but more likely no therapy had been
done but there was a lesion on it but they did not find any report in the charts and
40% of the time the patient was ever complaining about pain in the tooth. It doesn't
mean that all those 40% or 400/1000 never had any pain but they did not have
enough to have significant pain that they would seek care b/c of it. This indicates it's
a low grade if any pain. So even when you have a periapical lesion which you know
now started out w/ local inflammation, spread into necrosis in the canal, and then
periapical pathosis, no pain. So the fact a patient is asymptomatic does not mean
there is anything.

[63] [Pain Issues]
[Dr. Sigurdsson] The question of course then begs are all patients have they the
same pain reaction? Do some patients actually report more pain than others if you
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have the same stimulus and actually we're of 80 people in a room here. I can argue
that if I place the same stimulus on all of us we would see 80 different reactions.
That's not b/c we're macho/ we're strong. There are a lot of other things going on.

[64] [Pain Issues]
[Dr. Sigurdsson] There are a lot of variables going on. It's terribly important to put
that into context w/ endodontic diagnosis and the pathophysiology b/c that also
plays a role when you're trying to figure out if it's reversible/ irreversible pulpitis or
something else. Age for instance, it seems that of course w/ the neurological changes
that occur in the pulp, the older patients have less chief complaint of pulpitis b/c
there is just fewer nerves to convey it. Also age at least in some cultures makes the
patients more stoic. They are less likely to complain even though they have aches
and pains they don't complain about it or they're taking medication b/c of other
pain and that masks pulpal pain. Sex. Does it make a difference. Men or women.
Depends in context. For younger woman, premenopausal there is a difference in
pain reports compared to males. Less of a difference post menopause but there is a
difference. It can vary also w/ the psychological aspects of it so it's a very
complicated relationship but it is an issue. Ethnicity. It plays a quite a bit of role in
pain measurements. In one direction or another direction no we can't say all b/c this
is an issue. Person in this is Caucasian person there is going to be different but there
is a cultural difference certainly if not ethnicity difference. Also, playing on that is a
little bit the issue of maybe background of the patient. Just before I came to the U.S.
many years ago I had been reported to the authorities for prescription writing. What
was I writing? Ibuprofen. B/c in Iceland, my native country ibuprofen is only for
doctors not dentist. Now you're growing up and you're buying it over the counter. I
knew it was a good pain medication for pulpal pain but I was not allowed even as a
dentist to sign it. In Iceland of course what you do if you have pain, you deal w/ it
differently. Over here, you deal w/ it w/ pills b/c that's the environment that you're
in. There's nothing to say or worse or better than the others but in Iceland you
couldn't get the pain medications that you can get here. You dealt w/ it differently.
You coped w/ it. You did whatever you needed. Most of course, just drink but that's
a different story. Educational level, that plays a huge role when you're trying to
diagnose a patient. The more educated patients give you more information but they
also might throw in something that is important to you but it isn't so you always
have to take that into consideration. Social status, income. Higher income usually
more demanding patients. Expect you to quick fix and things like that also less
tolerant to pain. Family background, anxiety, depression, coping skills, very
important issue. And just vulnerability. Some patient feel that they're really under
the gun therefore their pain increases. You need to talk to the patient about this.
We're going to talk about this in my lecture about differential diagnosis in more
detail. Don't worry about it. Of course experience/ expectations play a very high
role. Studies just published, just coming out again large comprehensive, multi-
centered study looking at the expectation of patients in endodontic. Most patients
were very happy b/c you had a tooth ache and you went to the dentist/ endodontist
and the pain went away. About 10% of the patients the pain didn't go away. They
were very upset. Very upset. Actually probably reported much higher pain rating
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then what they were actually experiencing just b/c they were expecting the pain to
go away and it didn't for various reasons so we have to keep that in mind.

[65] [Genetics and gender]
[Dr. Sigurdsson] Genetics and gender also are really something that is very
fashionable to research right now. There is no question this plays a huge role. We're
not going into that right now. We'll talk about that maybe later.

[66] [Cartoon]
[Dr. Sigurdsson] Skip

[67] [Stoma]
[Dr. Sigurdsson] Just going to wrap things up. Just go through a little bit here. We
should be done in about 10 minutes or so. What else can this cause? If we leave the
periapical lesion untreated, for a while the pus would break out to the surface
somewhere most likely. If it is actively pus forming lesion it could be on the face.
This was actually from a canine. This is from a premolar. Strange location.
Absolutely, but that's what happens. You need to not only look intra-oral in these
patients, you need to look extra=orally. The premolar was treated. Things went
away very quickly.

[68] [Bacteria in the periapical area]
[Dr. Sigurdsson] Even though we see these stomas, we see these fistulas, I cause it
sinus tracts, it is basically pus from the pressure going out. It's not active bacteria.
We as a rule have found that in periapical lesions, you rarely find bacteria alive. You
find bacteria byproducts from the gram negatives of course you find the LPS or
things like that but you dont' find alive bacteria. There are a few exceptions. Of
course we also know that by some of the sampling techniques we have done in the
past. We might not have been capturing some of the sensitive bacteria so maybe this
is changing.

[69] [Unusual case]
[Dr. Sigurdsson] But we know that there are a few bacteria that can survive
outside. The actinomyces is most notorious. Why is actinomyces difficult? Does
anyone remember that from bacteriology? What does it do? It creates sulfur
granules which creates a calcification around the colony. This makes the
immunological system of the body much more harder to attack b/c the bacteria is
almost sheltered inside these capsule of our body. Therefore, many times if you
suspect actinomyces you need to apicalectomy to get rid of the lesion.

[70] [Bacteria in the periapical area]
[Dr. Sigurdsson] Another study some years ago found that actually there can be in a
very long standing periapical lesion a plaque like structure on the outside of the
root. That means there is bacteria b/c plaque doesn't form w/o bacteria. We know
that there are some things going on but this is usually then when you try to do the
endo it doesn't want to heal.
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[71] [The periapical area]
[Dr. Sigurdsson] Of course yeast have been now identified in several of these
lesions but and again, you mainly associated it when you do routine root canal
therapy and it doesn't want to heal. There are theories out there right now that
yeast might be playing a role there.

[72] [The periapical area]
[Dr. Sigurdsson] The periapical area. This is a slide that's not on your handout right
now. It'll be on the handout this afternoon is regarding the viruses. So anaerobic
bacteria are really the reason 99% of the time; however, more recent time in the last
few years we're seeing Herpes viruses are being able to measure out of these
periapical lesions. Herpes or Epstein-Barr viruses that seems to be associated w/
large lesions, symptomatic lesions. Of course the problem is, we don't know where
these viruses are coming. They could be coming actually, they have infected the
immunological cells that are actually fighting the infection so they have nothing to
do w/ the pathophysiology or they might be doing something and increasing, like I
said there is a correlation b/w the size of a periapical lesion and these viruses being
found. These studies are very few and they're not conclusive. They don't show a
cause-and-effect relationship. They only show yes, we find them in more likely in
the larger lesions but that might be b/c the lesion is so large there's more
immunological reaction to the lesion therefore more likely that the cells that were
infected by the viruses were brought to the scene of the crime rather than they were
causing it or the perpetrators of the crime. This is something we need to follow. You
as a dentist need to follow b/c they might change completely sometimes the
antibiotic regiment or treatment regiment if this proves to be true. To be continued
when we know this is a study that took purpose last year.

[73] [Periapical pathosis]
[Dr. Sigurdsson] But of course, just to keep in line, let's go through the definitions
of this and then we are basically over what we have going on. We can have
periapical abscess, periapical granuloma, radicular cyst, and it then can go over into
osteomyelitis. The beauty of endodontic or the endodontic lesions that it is
exceedingly rare if not unreported in a healthy person that this continues all the way
to osteomyelitis. There seems to be something in our bodies that the peripical
abscess, yes will certainly go into granuloma or for a cystic structure that can
expand and be quite destructive. There is no question about that but having
osteomyelitis in this context is exceedingly rare compared to when you extract a
tooth or you place an implant. Why? I can't explain that but that's just so we can
draw really a good line right there. That's the beauty of it.

[74] [Periapical Pathosis]
[Dr. Sigurdsson] What are the classifications. This is something that you need to
learn. You need to have b/c you're not expected especially once you go into the
electronic health records you need to pick the right category for every patient that
you're looking at. Classifications are normal periapical tissue. The patient is
Transcribed by Amit Amin 09/26/2014

21
asymptomatic. They might have a necrotic tooth, might be vital, the pulp might be
vital, but you don't see anything on the radiograph and the patient is asymptomatic.
You tap on the tooth you palpate the tooth and it's normal. Next step is symptomatic
apical periodontitis. That means you still might not have anything on the radiograph
but you tap on the tooth, you press on the tooth, you palpate the area and the
patient reports pain. That is symptomatic apical periodontitis. Might not be anything
on the radiograph, might be something on the radiograph. That's neither here, not
there. This can even be when you have still vital tissue. There's so much
inflammation in the pulp it's starting now exiting the apex and causing now
inflammation around the tooth in the PDL. Can be spontaneous discomfort of pain
and of course palpation, percussion is most likely the identification of this. You
might but that's really over emphasized in my view, that you might have a vital PDL.
People look at the radiographs. That's a quarter of a mm larger. Doesn't mean
anything. You can take a slightly different angulation and heal it. The thing is you're
looking for the symptoms by definition you have symptomatic apical periodontitis.
That's what we're talking about.

[75] [Periapical Pathosis]
[Dr. Sigurdsson] Now the next one is asymptomatic apical periodontitis. That
almost sounds contradiction. But that's these chronic large lesions that you see.
There's a lot of inflammation but for whatever reason the patient is not feeling it. No
pain whatsoever. It usually comes as a second. You start w/ symptomatic and then it
burns over/ turns over to chronic apical, asymptomatic, sorry that's the new
definition. Patient is always pain free. Pulp necrotic, lamina dura lost, you can see
changes on the radiograph, you know there is a problem w/ the pulp and the tooth,
the tissue but there is no symptoms. Of course if you do a histology, you have a
periapical granuloma or cyst. Now doe it make a difference whether you have a
granuloma or cyst? Treatment wise, outcome wise, does anyone know? I don't
know. That's the reason I'm asking it. IN the old days, we thought if you had a cyst if
would heal less. That was the dogma based on two studies that were flawed. Once
people realized how flawed these studies were, they were biased in one direction
we don't know. The general sense within the endo community, it doesn't make a
difference. It makes a difference to get rid of the offending material, whether it's a
cyst or granuloma, both of them will most likely will heal.

[76] [Periapical Pathosis]
[Dr. Sigurdsson] The third sort of side view of this is then b/c we have
asymptomatic periapical and then we can have acute apical abscess. It can be
localize or diffused. It is always liquefaction from the pulpal origin. That's the
driving force. Remember now this is basically what you see swelling. Local swelling
or (something I can't understand). There might be radiographic lesion, it might not
be. Again in material. Of course you get the severe inflammatory response almost
always if not bacteria or bacteria byproducts. Rapid onset, usually moderate to
severe discomfort/ swelling. Treatment is get rid of the tooth or get rid of the
offending tissue by doing endo or initiating endo therapy.

Transcribed by Amit Amin 09/26/2014

22
[77] [Periapical Abscess]
[Dr. Sigurdsson] Of course we see it all the time. Im sure you've seen it already.
You have a tooth and actually endo was started and then it lost. Here is another area
that is not.
[78] [Cellulitis]
[Dr. Sigurdsson] you have a localized or diffuse cellulitis like this. Again if it's
localized you might want to stop and drain just to relieve the pressure, get the
patient more comfortable. It doesn't affect the healing one way or another. Draining
it doesn't speed up the healing. Doing the proper endo will speed up healing but the
draining and the IND we do on these guys are for palatal reasons except when it is
going down into the throat, retropharyngeal space. That of course can be life
threating situations then you have to drain, get the pus out rather than letting it go
in but it's not going to speed up the healing. Cellulitis like this is most likely doing
endo, the only scary thing is when you start to go around the eye. Remember the
cavernous sinus that can allow bacteria to go bacteria to go back into the brain
through the venal portal there so you need to be careful w/ these patients that they
are under control and they might need antibiotic therapy.

[79] [Periapical Pathosis]
[Dr. Sigurdsson] Chronic apical abscess by definition relatively or completely
asymptomatic. Very long-standing. Usually clear radiolucency. No question about it.
I know it's a little bit confusing b/c they changed the nomenclature so this is
somewhat overlapping. I know when you have a have a (something) down in the
clinic later on, is it a chronic apical abscess or asymptomatic periapical abscess
what's the difference there? The difference is mainly when we start to say it's
chronic, it's long standing you know it's been there for a long time. It didn't happen
last week, last month. There lies the definition. You have something like this. This is
asymptomatic. Patient is normal. This is just a chronic apical abscess. This one
would maybe more on the border line going back to this asymptomatic. This is more
recent. Patient is not symptomatic you don't see a clear cut difference from the
bone. There is something there but not quite. So that's the issue. Now it's the test
and I want you to be very honest w/ me w/ the next radiograph. This is very
important.

[80] [Pictures of radiographs]
[Dr. Sigurdsson] Radiographs. What's the main problem here. What's the problem
here? Nope. Nope. Of course we always focus on either the pin that's out there or the
pin that's inside the pulp chamber and this is actually a case that I happened to be
walking by the clinic a few years ago. I saw a periodontist just starting the surgery
on this and why did I say hang on a minute here, you're not treating the main
problem. This one has a chronic periapical lesion w/ a very sclerotic canal which has
possibly pain into the chamber. The patient is asymptomatic or has some perio
problems and the periodontist of course diagnosed it as a periodontal problem
which is correct in a certain way. But you can do the best perio surgery in patching
and healing of this but you're not going to save the tooth b/c if I can't go in and find
the canal and treat the periapical lesion, the tooth is going to be lost. Remember this
Transcribed by Amit Amin 09/26/2014

23
is the test like I said. Every time you take a radiograph esp. in endo. You need to see
the whole root, you need to see the surrounding tissue around the root area and
make a proper diagnosis. That periodontist was working mainly from bitewings.
Just happened to have this one. What did I do. I drilled through. Yes I did find the
canal. Yes I was able to treat it and then the periodontal surgery was done. That
would be a completely waste of time and money of the patient. Be careful w/ it and
of course you never know where the lesion is. We're talking about pathogens. The
only thing I didn't mention very well that I think it will be covered in another lecture
by a different Dr. in a different lecture later on is vertical fractures. Vertical fractures
in teeth are, roots will always cause pulpal symptoms if not pulpal necrosis b/c the
fracture was we usually talk about J shaped lesion. You have a lesion on the side of
the root and it goes around to the apex of the tooth. The problem w/ it is that
sometimes it's very hard to see on the radiograph if not impossible. The diagnosis is
based on maybe symptoms maybe not, the radiograph appearance, the J shaped
lesion and you can put a cone into the very narrow but deep pocket. This will cause
pulpal necrosis and most likely lose the tooth but don't be fooled always. This s a
case of mine that I did 3-4 years ago and the patient just had the crown placed one.
Not the greatest crown in the world, but she paid a few thousand dollars for the
procedure but I told her it's hopeless. She asked me can you help me. I decided to
put some CaOH and it was not a vertical fracture but rather a lateral canal that
allowed the bacteria to populate not only at the apex but this zone in 3 months time.
So even when we have a diagnosis of vertical fracture get a second opinion. You
might have something. W/ that I'm going to stop. Any questions/ any discussion?
Like I said I promise w/in the hour I'll have downloaded the new version. I'm
terribly sorry about the confusion but it is what it is. All best. See you around guys.