43/44: Luxation & Micro

Transcribed by Charles Buchanan Date of the Lecture: 10/06/14
[Diagnosis and Treatment of Oral Diseases] [Lecture 45] [Luxation Injuries:

Diagnosis and Treatment] by Dr. Busch
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[Slide 1] [Luxation Injuries: Diagnosis and Treatment]
[Dr. Busch] Luxation injuriesLuxation injuries Let see. Alright.
[Slide 2] [Categories of Luxation Injuries]
[Dr. Busch] So we are talking aboutthis is associated with trauma. Um, There are
categories. What I have done here is I have listed the type of luxation injury in increasing
order of severity. Number 1 in the least severe going up to number 6 is the most severe of
the different types of luxation injuries. So now well go through each one of them
separately.
[Slide 3] [Luxation Injuries]
[Dr. Busch]
Okay. Alright, by definition the luxation histories, there is a history of trauma and as I
talk about the degree of severity, um, the amount of displacement is usually or mounted
types of displacement categorize the different types of luxation injuries.What can happen
from the luxation - luxation means movement. The luxation of the movement of them, if
its too severe the blood vessels of the foramen can be severed. That would cause a
problem. The pulps can undergo necrosis. What you have to do is take X-rays to
determine the degree of displacement. One of the other things we check for on the X-rays
is to see any root fractures. Okay, what you want to do is check the symptoms when the
patient comes in.
[Slide 4] [Concussion]
[Dr. Busch] In sports lately, its a big thing, if any of you follow sports - concussion
injuries. Concussion injury is, I have a feeling, that this guy has a concussion of the brain.
Concussion of the brain, because the brain is in the enclosed skull and it has no room to
move around really, that is why you get the injury to the brain - a brain concussion.
[Slide 5] [Concussion]
[Dr. Busch] So basically the same this that is happening with the tooth because the pulp
is in the enclosed tooth structure that the traumatic injury to the pulp can be called a
concussion because there's no where for it to expand. So the way that you determine a
concussion, as I said, there is a history of trauma. You got hit in the mouth, very common
with any sports injuries. One of the most common is people falling off bicycles. You get
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trauma to the teeth. Now with a concussion, concussion, there is no displacement or no
mobility. There was trauma tooth to tooth. Patient comes in and there are certain things
you are looking for when you are examining the patient. You want to be looking for is
mobile; if theres been displacement; is it still in alignment where it was and is there any
mobility. Is the tooth tendered to percussion? With a concussion, remember this is the
least severe of all the traumatic to all of the luxation injuries. Theres no displacement or
mobility. The only symptom you will have is that the tooth is tendered to percussion as I
said of course there is history of trauma. and the tooth may be discolored. The important
thing when you have a patient who has a history of trauma, you take, you go through
these various symptoms and you record your findings because your findings you're
getting on this initial visit are the base line findings that you will have because typically a
lot of these injuries you're going to see patients in subsequent visits and follow up to see
what is happening. So you must have your baseline findings from the initial time you saw
the patient so that when he or she comes back in you can see if the symptoms have
changed. You can see if things have gotten better, worse or staying the same. You must
record the baseline symptoms.
[Slide 6] [Concussion Treatment]
[Dr. Busch] Okay. So with a concussion, the baseline percussion sensitivity and there
may be some thermal sensitivity. but mostly there is the percussion sensitivity. As I said
you take the radiographs to check if theres a fracture. Now, you'll always take
radiographs of both the maxillary and the mandibular arch. Because, when there is
trauma to the anterior part of the face, you dont know if even though, sometimes, its
only the one arch which feels the brunt of it, which takes pain. You dont know if theres
trauma to the other arch also. So you take radiographs of the maxillary and the
mandibular areas and your looking for root fractures. Alright. Um, because the only
symptom really is the sensitivity to percussion, no root canal treatment is really
indicated at this point. Its just follow up treatments. So say you follow up three weeks -
thats an approximation. But you follow up, you want to see the patient in approximately
three weeks and check periodically at three months. Uh, the reason I say that is because,
uh, every time I talk about about procedure to a tooth - crown prep, filling, whatever, that
is trauma to the pulp. Okay. Anytime you do a deep restoration you warn the patient that
down the road, the patient may end up needing root canal therapy from a procedure
which has been done now. So you want to see the patient at subsequent appointments.
You want to keep checking, checking.
[Slide 7] [Interventional RCT]
[Dr. Busch] Now the reason I saw that and I am disappointed that theres too much light
here. I dont know if you can actually see what is going on in this radiograph. But, what I
was trying to show here, is if you notice a normal canal in the tooth here. You notice a
normal canal in the tooth here. There is no canal in this tooth. The tooth, the nerve, the
chamber of the canal, is completely calcified. Now that happens over time as a result of a
traumatic injury. Whenever you see a patient who comes in with a tooth like this where
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there is no canal. The canal is completely calcified. The first question you ask is there a
history of trauma. Sometimes the patient will remember, sometimes the patient will not.
Sometimes they feel it is rather an innocuous problem and may not remember the trauma.
But whenever you see something like this - when adjacent teeth have normal canals, its
obvious that there was some type of trauma to this tooth so now the reason that I say you
check it periodically is because this calcification did not happen overnight. When you
have adjacent teeth and you see the way now, remember, you know that, that in a young
tooth, that the canal gets smaller normally. Okay. The younger the tooth, the larger the
canal will be. They get, they get. The canals get uh, smaller, normally. If patient comes in,
and you see one canal. The canal of one tooth becoming much more calcified than the
other adjacent teeth, and there is a history of trauma, its actually correct to go in and do
an elective or prophylactic root canal. Because at this point I cant do endodontic here
therapy because theres no canal. So if I see that because of the trauma, the canal is
calcifying, its getting smaller, it is correct to explain to the patient whats going on and
why you are doing it and to initiate the root canal therapy while you can. So thats why I
say there is the importance of continuing the observation.
[Student] So what is the recommended treatment?
[Dr. Busch] For this tooth at this point you have to hope that there wont be any kinds
of symptoms or problems. If this patient should develop a uh, now remember now the
problem that manifested itself, an endodontic problem, would be at the apex. If this tooth
should develop a periopathology at the apex, what do you think that the treatment would
be?.No, you want to keep the toothDid I talk about apicoectomies? I did talk about
apicoectomy. Remember the cause of the infection up here would be, although theres not
macroscopic canal, of course its microscopic and theres still bacteria in here and it can
get out through the various portals of exit. The main portal of exit of course is the
foramen. There are other portals of entrance and exit. There are lateral canals, furcation
canals. So it if became symptomatic we would do surgical procedure, lay back the flap,
go into the area. Cause I know I talked about fenestrations . You would remove the
pathology form here, you shave off part of the tip of the root, by definition apicoectomy ,
and then put a retrograde filling there. Okay, so thats alright. The problem you have,
thats an easy way to solve the problem. The other problem you have is if the tooth
becomes brittle and the patient, now, years down the road, the patient, bites down and
fractures the crown off, typically if you had a canal here, you could restore the tooth with
a posted core and a crown. Now that you have no canal, you cant do that. So thats why
it is correct to initiate root canal therapy when you see the canal calcifying to prevent
those problems.
[Slide 8] [Subluxation]
[Dr. Busch] Okay. Subluxation. Sublation was number two on the list. The subluxation
is very similar to a concussion. Theres no displacement and there no - well maybe there
is a slight- excuse me - there is slight mobility. That is the differentiation between
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subluxation and concussion. With a concussion there is no mobility, with subluxation
there is slight mobility. Thats the definition really of the lunation. There is slight
mobility. You also may get some slight sulcular bleeding. Ill show you what that means
in some other slides. There may be some discoloration and you want to remember that
about 25% of these teeth will become necrotic. 75% wont. Again, this is why you want
to continue to check. Uh, subluxation, there is no endodontic treatment indicator initiated.
But again, you follow up with the patient. You take your baseline symptoms. You take the
uh, percussion, mobility, thermal sensitivity and see at subsequent visits if its got better,
worse or stayed the same. So thats the different between the luxation and subluxation.
There is a slight, slight mobility.
[Slide 9] [Subluxation Treatment]
[Dr. Busch] Okay, so, I was one slide ahead of myself.
So this is what I just told you to do. Observe. No root canal present. Again - make sure
the patient is aware of the need as I showed you in that other case. Now typically, in an
immature tooth, tooth which has an open apex, the trauma will not cause as much
problem to the tooth as if it were a mature tooth where everything is closed because an
immature tooth, the canal is wide open, the apex is wide open. They observe the blow
better.
[Slide 10] [Six year old fell off a bike hit face no fracture of teeth, slight mobility]
[Dr. Busch] So, this patient came in to me. Six year old; fell off a bike; hit his face -
slight mobility. Okay. Classic subluxation. Wide open apex. Prognosis for this tooth -
these teeth are very good. The only one that seems to be traumatized was this immature
central incisor. So we did no treatment. We told the parent to watch and observe.
[Slide 11] [6 Months later child complained of pain in his tooth]
[Dr. Busch] Patient came back 6 months later, 6 months later complaining of pain. Can
you see how much bone loss there is here? Okay. Take a look there.
[Slide 10] [Six year old fell off a bike hit face no fracture of teeth, slight mobility]
[Dr. Busch] Initially, the bone is fine around here.
[Slide 11] [6 Months later child complained of pain in his tooth]
[Dr. Busch] 6 months later, significant amount of bone loss gone.
What do we do with this patient? Any idea? So now what has happened here? Again, he
complained of pain there is a radiolucent area there, there was swelling. What do you
think the tooth is? Vital or non-vital? Cause there still seems some confusion with you
guys about that. The tooth is obviously non-vital now. Unusual for an immature tooth
with an open apex like this to become devitalized from the trauma. Unusual but it
happens. Okay. So the tooth is non-vital and thats what is causing the bone loss. So what
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do we do? Non-vital tooth - we initiate root canal therapy. Okay. Whats the problem
here? Whats the last step of the root canal therapy? Last step of the root canal therapy is
the obturation. Alright. You need a closed apex to obturate the tooth. You cant obturate
this tooth, its not closed at all. Alright. So now Ive said to you that theres been an
evolution, not a revolution in dentistry regarding modes of treatment. I saw this patient
probably 30 years ago. Probably even more. The procedure at the time - there were two
types of procedures - when you were treating a tooth where the tooth had an open apex.
An open apex meaning the apex is not formed and you can not obturate the canal because
there is no closure of the apical area. You have to get closure of the apical area. In a non-
vital tooth, the treatment that we used all the time was called apexification. In a vital
tooth the procedure we used was called a apexogenesis. Now the difference between the
two is if now the scenario in a vital tooth, if the tooth had been fractured, if the crown
had been fractured off and was exposing the pulp, and was painful, we would want to
initiate root canal therapy but because the apex was open we couldnt complete the root
canal therapy. So what we would have done, we would have done a pulpotomy. Taking
the pulp tissue out of the chamber and then put a medicament in the canal, temporary
filling, leaving the vital tissue in the canal to allow the root to continue to form. Thats
apexogenesis. You continue to watch radiographically when the apex is completely
formed, and it would form normally because you left the vital pulp tissue in there and you
could then complete your normal root canal therapy. Okay, pretty simply procedure. All
you had to do was a pulpotomy until the apex was completely formed. With the non-vital
tooth, again theres no vital pulp tissue in here, your not going to get dentin formation.
But what we did with the non-vital tooth, we cleaned out the canal completely, debride
the canal. Placed CaOH in the canal to get a bridge closure across here. Once you got a
closure here then you had something to obturate against and you could then fill the canal.
[Slide 12] [2 Years After Treatment Started]
[Dr. Busch] So this is 2 and it, again, um, the amount of time it would take to get the
closure with the apexification it was not really, it was questionable. You would check
periodically. Ok? So here, I have CaOH in there and what you have here is a bridge
formed across here. If you noticed the bone has filled in. The bone has filled in because I
removed the cause of the problem by cleaning out the canal and then we would fill this
canal with gutta percha. You did not get the continued formation of the root in this
procedure- apexification. Apexogenesis, you did. As I said, it took two years. Ok? Now
what has happened, is theres a material called MTA which, what we would do then with
the MTA is to just clean out the uh, tissue in the canal, make sure that its starting to heal,
and then you could put a barrier of MTA across here. MTA is Portland Cement. MTA
stands for mineral trioxide aggregate. When it started to come out on the market, about 20
some odd years ago, and you would ask the people what is MTA? And theyd say
mineral trioxide aggregate. Oh, its Portland cement. Its a cement. So you would
seal the, you would clean out the canals and when the symptoms subsided you would put
a plug across here with the MTA and then you could fill it. Now, the procedures have
evolved even more. Theres a procedure called regeneration. Regenerative endodontics,
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which I dont have it. But in the regenerative endodontics, even in the non-vital tooth, the
procedures can be done where you can actually continue to get formation of the root. Ok.
So these are some of the changes that have come along over the many years.
[Slide 13] [Lateral Luxation]
[Dr. Busch] Alright. Lateral Luxation. By definition. The tooth is displaced laterally.
Now the lateral- the way its removed laterally is the crown of the tooth is pushed in
labially. Excuse me- palatally. The crown- you have the trauma and the crown is pushed
in towards the palate and what happens when it moves, if you have the crown come in
towards the palate, the apex (the tip of the root) is going to go labially. Thats what- thats
lateral luxation. Ok. Sometimes, the apex of the tooth can go so far that it can go through
the cortical plate.And here, youll have sulcular bleeding and the tooth is very tender to
percussion. So, how would you get a lateral luxation? Come on.
[Slide 14] [title]
[Dr. Busch] Ok. You see a trauma like this? Getting hit like that. If hes not wearing a
mouth guard, it would not be surprising for a tooth to be laterally luxated like that.
Shoulder going to the mouth, the crown of the tooth will go towards the palate. So that
would be a lateral luxation. Um, ok.
[Slide 15] [Lateral Luxation: Soccer Injury- Note Sulcular Bleeding] starting at 30:00
[Dr. Busch] Very common ones I see in soccer also. In soccer, I see all types of
luxation. When two people go to head the ball, what happens? The guy who gets up
higher is the one who gets hit. You have both persons go to head the ball. One guy gets up
high, the other guy jumps in, his head hits the tooth and you have different kinds of
luxation. This is very common in soccer.
[Slide 16] [X-Ray of Lateral Luxation]
[Dr. Busch] Ok. So. Again. The lighting here. Theres too much light.When you take
the- again, like I said, when the patient comes in, you must take your radiographs to
check for displacement and rot fractures. The radiolucent area here. I don't know if you
can see that with this light but there's a radiolucent area there. Now typically, we talk
about radiolucent areas or pathology areas- I discussed the other day- you have pathology
because bone has been destroyed. Thats when you explain to your patient when he has
the asymptomatic necrotic infection- by the way I sent something out in the email to the
entire class yesterday with diagnostic endodontic terms. I said you must know these
terms. You will see these- you must know these terms- it will be on the exam so make
sure you dont ignore that email which was sent out. So you tell the patient that theres a
radiolucency there because the bone is thinner. Well, here, theres a radiolucency. Its not
because of pathology but because the tooth has been displaced. The tooth has moved -
there is a space there now. So thats why it shows up as a radiolucent area there.
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[Slide 17] [Lateral Luxation - Sulcular Bleeding]
[Dr. Busch] So you should be able to see what I was talking about here with the lateral
luxation. You can see- although this is only a two dimensional picture- you can see where
the crown is pushed palatally. Its not in line with the other teeth here and this is why I
talk about the sulcular bleeding. You see the bleeding around the sulcus there? So thats
the sulcular bleeding. I believe this is the same person. I took the picture at a different
angle so you can see how the tooth is displaced laterally, that the crown of the tooth has
gone towards the palate.
[Slide 18] [Lateral Luxation Treatment]
[Dr. Busch] Ok. So whats the treatment with a lateral luxation? Now we start to get
more involved. Concussion - basically you dont do anything. Subluxation- you have
some mobility, not much treatment. But lateral luxation, you must realign the- get the
tooth back into proper alignment. Ok. You have to get the tooth back into proper
alignment. How are you going to do that? Remember, the crown has been pushed to the
palate. The apex of the tooth has gone out labially.The way you have to do that is push on
the apical area, push down, and then move the crown from the palate back into position
into the normal labial position. If youve heard about, uh, subluxations of the jaw where
the mandible is displaced. The condyle goes out of place, sometimes, I had heard about it
in school some time, I had never had a patient who had it. One patient. And it was lucky
my partner was treating her. And it was opened wide a long time, the treatment was done-
she couldnt close her mouth again because of the dislocation of the mandible. The
treatment there, I dont know if youve heard, what you have to do in order to get the
mandible back in place- you must put your thumbs on the side of the teeth. You dont put
your thumbs on the teeth. You put your thumbs down, you push the mandible down and
back. So thats basically what youre doing with this tooth which has a lateral luxation.
Youre pushing apically- from the apex down and then the crown, youre pushing from
the palate to the labial to get it back into position. Alright. So I forgot that I even had this
here.
Ok. Splint the tooth. This is where I differ with some people. What I worry about with
some of these traumatic injuries is resorption of the roots and significant problems.
Resorption of the roots and loss of the tooth. I believe that with a lateral luxation, because
of the amount of trauma and damage to the PDL and all the fibers, that it is wise to
initiate root canal therapy on a tooth that has had lateral lunation which you have to
replace. Even though you dont have any kind symptoms, it will be very painful to
percussion but I believe the judicious thing is to start RCT on that tooth. I know other
people will argue with me and say that it may not be necessary. I understand that.
Personally, I would rather err on the side of safety to try to prevent any kind of root
resorption. And later on, Ill show you what Im talking about. Ok.
[Slide 19] [Five Year Span] - SKIP
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[Slide 20] [Extrusive Luxation]
[Dr. Busch] Extrusive Luxation. By definition- lateral- if its pushed laterally:
extrusive. The tooth is knocked out. So here, the tooth is knocked out of the socket and
its going to extend longer. You must replace the tooth. You have to push it back in place
and splint it.
[Slide 21] [Extrusive Luxation IMAGE]
[Dr. Busch] Heres an evidence of extrusive luxation. You can see where this tooth has
been , is extruded. You can also see discoloration of the tooth.
[Slide 22] [Extrusive Luxation IMAGE]
[Dr. Busch] The same person, just different lighting on the picture. And you see the
tooth is extruded. You can also see that, as I said before, when you get the trauma, more
than one tooth may be traumatized. Here you have fractures here and here. Sometimes,
they say, if the the tooth is fractured- if they fracture the crown like that, that actually
may even save the tooth because the forces can be dissipated from the fracture. A tooth-
these teeth probably, you notice theyre not discolored, this one is discolored, this is
extruded. But the fracture here, although a slight fracture here - these teeth can probably
just be restored with bonding. Of course, you would want to follow these teeth up. See if
there are any detrimental changes in time. As I showed you, that other tooth which-where
its calcified- you want to continue to watch all of these teeth to see if there are any
detrimental changes and if treatment-other treatment has to be initiated.
[Slide 23] [Radiograph of Extrusive Luxation]
[Dr. Busch] Ok. Now here, again, this is even more obvious. You can see, this is the X-
ray of the extruded tooth. You can see here is the tooth in normal position where the apex
is-normal position. And here, the tooth was extruded. You can see it coming out. The
radiolucent area there, again, is just the socket where the tooth was removed from. You
want to get the tooth back up into that area. And then splint the tooth and initiate RCT.
And you dont have to initiate RCT that day, but it should be done within a short period
of time. Sometimes, with the amount of trauma to the patient, the lips can be swollen, it
can be bleeding, so maybe youre not going to do it that day. But you do want the tooth
back in place as quickly as possible- whether it be the lateral or extrusive luxation. And
then splint it in place.
[Slide 24] [Extrusive Luxation Images]
[Dr. Busch] Ok.
[Slide 25] [Intrusive Luxation]
[Dr. Busch] Intrusive luxation. Obviously, just the opposite of extrusive luxation. Here,
the tooth is pushed in. Its not predictable, really when theres a traumatic blow as
opposed to which of these types of lunation will happen. It depends upon how the tooth
or teeth were hit - at what angle? So the intrusive luxation, the tooth is pushed up into the
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socket to varying degrees. Sometimes the tooth can be pushed up so far that you may not
even see the tooth, you might think that the tooth was lost-completely evulsed. The tooth
is pushed up, its firm in the socket. You must check the radiographs if you want-
especially if you dont see the tooth. You would have to take a radiograph to see if the
tooth was there. So we talked about repositioning the tooth. Lateral lunation, I told you
how to reposition. Extrusive luxation, you push up. Intrusive luxation, you have to get the
tooth back into place also. How are you going to do that? Ok?
[Slide 26] [Intrusive Luxation Treatment]
[Dr. Busch] So there, with the intrusive luxation, theres a lot of damage. And again, it
says will probably cause replacement resorption. Pulpal necrosis is very common. So we
know that, so were going to initiate RCT before these problems happen. So if youre
lucky enough, if it was an immature tooth, it may spontaneously re-erupt. You dont
have- so the immature tooth is what I showed you before, what I talked about where the
root is not completely formed. Thats an immature tooth that will probably re-erupt and
come down by itself. In a mature tooth, it has to be repositioned. If you dont re-position
it in a judicious amount of time, the teeth can ankylose and become very difficult to
move, if possible at all once theyre ankylosed. So, how do you reposition it? You can-
either with an orthodontic appliance or surgery. Once the teeth- tooth or teeth- are put
back into place and theyve splinted, then root canal should be initiated. So. Theres a
difference in treatment- again we went down: concussion, subluxation, lateral luxation,
extrusive luxation, and intrusive luxation. The only one where Id say I differ in opinion
from other people is the lateral luxation. Based upon that, I would not hold you to give
me a definitive answer on an exam for lateral luxation, the others I might.
[Slide 27] [CONCLUSION] - SKIP
[Slide 28] [Avulsion]
[Dr. Busch] Ok. Avulsion is the ultimate luxation. Its luxated so much its out of the
mouth. Its removed from the socket, its gone.
[Slide 29] [Avulsion Treatment]
[Dr. Busch] Whats the treatment for avulsion? Replace the tooth in the socket as soon
as possible - ASAP. Do not handle the root. Why? Why dont we handle the root? What
are we worried about? Were worried about trauma to the PDL around the root. You hold
the tooth by the crown. You get it back in as quickly as possible. You wash the tooth off.
You gently wash it off. It was knocked out. Its on the ground. Its on the ground, its
dirty. You dont have to sterilize the tooth. Wash it off. Get rid of any dirt, schmutz,
whatever and put it back into the socket. Stabilize it. Initialize RCT. I dont know if
youve gotten this in pedo or whatever. What is the most- what do we worried about with
the avulsed tooth. We worry about root resorption- replacement resorption. What is the
prognosis of the tooth depend upon whether or not if you get it back in place and stabilize
it. What is the one thing supposedly that affects the prognosis? Its the time out of the
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socket. After 30 minutes, 30 minutes, the prognosis is much worse. Now, Ive said here,
warn of poor prognosis. Umm. Ive treated a number of patients who have had the teeth
avulsed. It used to be, and here I go again about what has evolved. It used to be, and
people tend to, typically, a person who has a tooth avulsed, knocked out, is not going to
think to go to an oral surgeon- excuse me, endodontist. The patient or the patients parent,
whatever, typically theyre going to think to go to the family dentist. Ok? So these are
treatments that all of you guys can do. So they go to the family dentist. And the family
dentist will either decide to treat the tooth him or herself or frequently, what they used to
do was send them to an oral surgeon. An oral surgeon would replace the teeth, wire the
teeth, splint them together, leave the splint on for 6 weeks, then take the splints off, and
then youve got resorption start already. Once the resorption starts, the prognosis is
extremely poor. Once the resorption starts, its very difficult if not impossible to get it to
stop it. Alright. So. Im a real pessimist about avulsed teeth because Ive seen a number
of them where the oral surgeon sent the patient to me after the 6 weeks and the resorption
has started already. I had one patient. He was at Boy Scout Camp. They say Be
Prepared. They were prepared. I dont remember exactly how it happened but something
happened and his upper central was knocked out. They knew exactly what to do. They
washed the tooth off, they didn't handle the root, because you dont want to disturb the
PDL. They gently washed it off, they re-placed it, got to the dentist very quickly and it
was replaced in minutes. The patient came to me, no resorption had started. I started the
RCT, initiated the RCT, took the pulp out, put CaOH in there, let it sit for 6 weeks. It was
a mature tooth, apex was formed. After 6 weeks, I obturated the tooth with gutta percha.
It looked great. Everything was done perfectly - just by the text book, exactly where it
was supposed to be. I followed this young man for years. For about 6-7 years, everything
was perfect and then all of a sudden, the roots started to resorb. And once they started to
resorb, it just went and the tooth had to be lost. And I said, if this one didnt work where
everything was done perfectly, I will never guarantee to anyone that even when its done
perfectly that it will be fine. It does increase the chances that sometimes it will be
successful. I wasnt lucky enough to have that. OK. So.
[Slide 19] [Five Year Span]
[Dr. Busch] Now, the case I get. Young girl comes to me. Two teeth. The two centrals
had been avulsed, replaced by an oral surgeon and he had wire splinted them for 6 weeks.
Now she comes to me. These two centrals. You can see resorption has started on this one.
Alright. This is an immature tooth, no resorption has started yet. I say ok, great. We have
a good prognosis for this tooth. This one, not so good because the resorption started
already. Now if you remembered, I said at the beginning- the procedure that we used to
use when there was an open apex was called apexogenesis. So I said this tooth is still
vital, the apex is still open, Im going to treat this tooth differently than this one. So this
tooth, I decided to just do a pulpotomy and do apexogenesis. This one, since the
resorption had already started, I said this tooth has a real poor prognosis and Im just
going to try do whatever we can to retain this tooth as long as possible. Now I believe
10
she was about 8 y/o, well ok so that leaves- if the upper centrals come in at about 6 y/o
and about 3 years until closure, so the apex should be closed at about 9 years old. This
one should be almost closed. She was 8 y/o so that was my rationale. This one, Im not
happy with. Well do whatever we can. This one is going to be fine. So, long story short,
five years later, after I had treated this tooth the way I thought it was a good idea, you
could see that the root is completely gone. Completely resorbed away. Replaced with
resorption with bone. It is unbelievable how stable a tooth can be with so little root
because its ankylosed and you have the replacement resorption until the point where it
virtually does fall out. Whereas this one, where I thought it had such a poor prognosis, I
put CaOH for I dont remember how long, ultimately filled it with gutta percha and this
one remained in the mouth longer than the one that I thought that I was treating properly.
I made a mistake. I learned from my mistake. Any time the tooth is avulsed, I initiate
RCT right away. So learn from my mistakes. However now, again, she was 8 y/o,
prognosis was poor, I made a mistake. But, this was 5 years later, shes 13 y/o now. You
have more restorative options. A lot of times when you have a traumatic injury, even if
you cant retain the tooth forever, if you can retain the tooth long enough - especially if
its a kid- so that now you have better restorative options and the kid had the teeth all
these years as opposed to having to have some kind of removable appliance, youve done
a service.
[Slide 27] [Conclusion]
[Dr. Busch] So, the conclusion is what I was talking about. Boy, Im good - two
minutes. Concussion/ Subluxation. Observe, record the baseline. Thats very important
the baseline. No indication, no root canal indicated but observe. I said observe
radiographically approximately at 5 years because if you start to see the canal calcifying,
jump in and do the root canal while you still can so it doesn't become completely
calcified.
The other luxation, theyre pretty much the same. Reposition, stabilize, initiate RCT.
CaOH in the canals. OK. Thats it for this lecture. Now Dr. Adamo is going to come up
and teach you everything you have to know about microbiology, endodontic
microbiology.
[Slide 30] [The End]
[Dr. Busch] Any questions about that? As I said, Im not sure why because I know that
I posted all of these PowerPoints and I have them here but it may be that have to do
something so that you can view it. But again, the diagnostic terms which I sent out to you
yesterday, make sure you know them.
[Diagnosis and Treatment of Oral Diseases] [Lecture 46] [Endodontic Microbiology]
by Dr. Adamo
[Slide 1] [Endodontic Microbiology Title Slide]
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[Dr. Adamo] Thats good. This is good. Alright. Alright, if you want to start now,
because its a very long involved thing. Do you want to take a break? Further break
anybody? Thats it then. From the boss. Alright. Umm. Endodontic microbiology is a
really intense field so youre expected of course to know your chapter. I think youre
doing Walton and Torabinejads book and, uh, theres also Pathways of the Pulp which
the PGs mainly use. So theres plenty of text references for these things aside from the
literature itself which is constantly being updated. Um, but lets get- before we get into the
specifics of it, uh different states and how the bacteria function as polymicrobial
communities really. We want to just go into the history, a little bit of it, just so you
understand how this thing came to be.
[Slide 2] [Teeth Image]
[Dr. Adamo] Cause back in the 19th century and early 20th century, they were pretty
clueless about bacteria- the role of bacteria in endodontic infections. And its big one
because when all the people come in like this, thats what youre dealing with. If it
periodontal, its localized, its usually draining, gingival. You see it in the mouth but dont
generally have a face thats blown up because theres drainage by definition. But with
endodontic infections, you know, acute apical abscess, the oral surgeons and the
endodontists are dealing with this but of course general dentists have to see this first and
may be dealing with this in entirety. So its important to have an overview of the process
so that you can, a little bit, micromanage. You know, theres way too much antibiotic
prescription for situations which are not helped at all by antibiotics. Uh, and, there has to
be a clear view of the progression. So anyways, the first person, really the father of oral
microbiology was Willeby Daton Miller and in the late 19th century, he indicated that he
was sure that bacteria had a role in endodontic and root canal infections.
[Slide 3] [Role of Bacteria]
[Dr. Adamo] And in 1919, Henrissi and Hartzel (?) found that- they analyzed normal
pulp and found that it was sterile. So they reasoned that a healthy pulp must be
protected from bacterial invasion. And conversely, if you had bacteria in the canal, youd
better clean it out. So he also made the observation, which was very out of his time, that
to prevent acute infection, those with a chronic apical periodontitis- you know, those that
we would notice today as being an X-ray with a big shadow but the tooth doesn't
bother the pt, they don't feel anything, in fact they dont feel hot or cold either,
thats how you know pretty much that its necrotic. But, uh, he figured that you better
take them out, or do RCT in order to prevent an exacerbation of an acute apical abscess.
And you know consequently, subsequent deep space infections which frequently
followed if you dont interfere with the process. Now we have antibiotics which help to
contain THAT sort of thing. Thats when you employ antibiotics- when youre trying
to contain the spread of infection. Its not going to get in the root canal. Root canals
are already necrotic by the time the patient has an abscess. So, its the deep space
infection you want to contain. So you do local measures, either extraction which
solves the problem quickly, or incision and drainage, start RCT, get drainage
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through the tooth and or through the soft tissues intraorally and then antibiotic will
also contain it. These are the strategies used when youre keeping a tooth. Removing a
tooth is another story. I just mentioned that because Dr. Busch was just telling me theres
exceedingly too much prescription of antibiotics for pulpal conditions like irreversible
pulpitis and all that. And its not indicated there. The risk of taking those antibiotics far
outweigh any benefit youre going to get for it and thats not the appropriate treatment.
Pulpectomy. Pulpotomy, pulpectomy, or an extraction are really all you can do and you
dont have to get into the realm of deep space infection containment when youre dealing
with an irreversible pulpitis or any kind of pulpitis that isnt necrotic. There couldnt be
a pulpitis if were necrotic.
[Dr. Adamo] So the question is, then they didn't know how to culture it. They said lets
say we get bacteria from the teeth but they would either contaminate it in when they were
getting it or they would put a disinfectant inside of the root canal so the culture that they
would obtain would be useless or, you know, you dont know which bacteria already
would have been killed off by the, or reduced in great number by the medicaments they
would use. They used to use phenolic compounds, creosote, all kinds of stuff. and um,
then of course, they didnt realize that- they were all doing aerobic cultures. Theyd take
a culture, plate it and watch it grow and they couldn't really find out what the pathogen
was because most of the bacteria werent even aerobic- they were anaerobic involved in
these infections.
[Dr. Adamo] So, finally, in the 1960s, and thats how late it was. 1965 was the first time
any group had done a definitive study to establish that you needed, you definitely
needed bacteria to initiate this process of, you know, irreversible pulpitis, necrosis
and abscess. And what they did, Kakehashi and Fitzgerald, published their paper in
1965. And what they had done was expose pulp using sterile techniques in two
categories of rats. One were normal laboratory rats and the others were sterile or
gnotobiotic germ free rats.
[Dr. Adamo] So of course, the germ free rats failed to develop pulpal necrosis. Not
so for the normal rats. And this proved that bacteria are necessary to get pulpal
pathology pathosis. And the question now became- if you want to look it up, I have these
references in the back too on the slides if you have the PDFs. I don't know if you can
access them, I gave them to him. I suppose hell put them in a place that you can get at
them. Ill make sure he does- the question became which bacteria.
[Slide 7] [Anaerobic Bacteria]
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[Dr. Adamo] So, anaerobes were only first isolated in root canals in 1957. Thats
amazing. And they had done that before Stanley, Kakehashi and Fitzgerald had done their
famous study that we just talked about. So it didn't go in sequence necessarily but the
discovery was, they did find them back in that day.
[Dr. Adamo] And then during the following decade - you don't have to know all these
names, its just giving you an idea if youre curious, you know who you can look up
some of the names and see what research or if you run into them in your textbooks, youll
know where they were in the progression of understanding this disease process. Um.
Thanks largely to Moller in Sweden, 1966. His doctoral thesis made people aware within
the dental research community and within dental schools in general that anaerobic
bacteria were the target. We have to culture for them or else we aren't going to learn
anything about this or the disease process and how to contain it. So, by 1976, his student
Sundqvist, this was up in Umea, Sweden way up north - theyre still there. I think
Sundqvist still has a lab there. They, in 76, his doctoral work dealt with trying to
elucidate the nature of the flora inside a root canal infection. And he found they were
polymicrobial facultative and strict as well. And he further elaborated how they might
initiate infection. Well get to lipopolysaccharide endotoxins in a minute. Thats more or
less where he was headed. So he started the ball rolling. Moller made it evident that you
needed to do anaerobic culturing and then Sundqvist went ahead and - what did I do here,
oh - went ahead to sort of clarify what was actually growing in there.
[Dr. Adamo] And um, these other people Griffee, Schein and Schilder. Yes, Schilder
from Boston University, Yamasaki, these are some of the big names.
[Dr. Adamo] So, um, these, for instance, this is what porphyromonas, prevotella- the
black pigmented bacteroides which is what they were called at that time as a group.
These are the strict anaerobes- they look like this and this looks like strep. And strep is
facultative. It can tolerate oxygen as well as we know but it also can live in very low
oxygen content and its always found in these infections, some kind of strep.
[Slide 11] [Predominant Isolates from Infected Root Canals]
[Dr. Adamo] Here are Sundqvists findings in composite form. Major ones, here you
see Peptostreptococcus which we were just talking about and porphyromonas and
prevotella. These two were the bacteroides that were first identified as a major player in
acute endodontic infections - they were always there.
[Slide 12] [Predominant Isolates from Infected Root Canals]
[Dr. Adamo] And then theres also actinomyces. Um. alright, so these actinomyces and
prevotella, and - I mean actinomyces and propionibacteria used to be called arachnea
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because it looked like a spider. And um, Nayers original identification of these things -
thats how he described them. But it produces propionic acid so theyre associated with
propionic acid and therefore- but these two were singled out for being major players in
failed root canals or persistent root canal infections. Notice gram positive rods,
theyre more associated with persistent infections. Gram negative, more with the
initial root canal infection. Well get more into that in a minute.
[Dr. Adamo] Then there was Fabricius, another svenska who figured out, in 1982 that -
what he did was inoculate root canals with 8 commonly found strains in equal proportion
and then observe them over long periods of time. The six month findings were the most
significant but he actually went out longer with 1 or 2 monkeys. And, um, found out that
anaerobic bacteroides strains did not survive without other facultative strains
providing things such as beta hemolytic strep providing nutrients like hemin and
succinate which some of them required to sustain themselves. So theres a little
symbiosis, a little microecology starting to, uh, crop up inside these root canals.
[Dr. Adamo] And he found, uh, by with the passage of time that the strict anaerobes
increased in the apical portions and the facultative strains diminished. So as you get-
logically, it selects for a more anaerobic strain because theres no oxygen higher up in the
canal. As you go further up towards the apex, you would expect to find more aerobic-
anaerobic strains, you know, flourishing. And thats exactly what it was. More strict
anaerobes found in the apical region and a change in the types of flora.
[Slide 15] [Prevalence of Black-pigmented Bacteroides]
[Dr. Adamo] And, um, Sundqvist in 1989, with Johansson and Sjogren investigated the
prevalence of black pigmented bacteroides- and again these names come up as
porphyromonas prevotella as the genus of those bacteroides. And he found those in
the root canals of 72 teeth with apical periodontitis.
[Slide 16] [16 of the 22 root canals]
[Dr. Adamo] He found that nearly 73% in 16 of 22 root canals, where they found these
bacteroides - again prevotella porphyromonas- were associated with acute apical abscess
and purulent discharge. There had been many kinds of studies trying to correlate exact
bacteria with symptoms that doesn't really work that way. So, not to worry about that, but
generally these are found. Any time you have an acute infection, youre going to find
these among other bacteria. And this was the beginning of an awareness of, you know, the
changes that take place sort of a 3-D picture in time. You see how it sweeps through the
canals and these chronic infections are set up. They werent even thinking about biofilms
at that time. That came later. And later molecular studies, of course, have found
prevotella nigrescens as a species often isolated from infections of endodontic origin.
15
And they also- enterococcus fecalis and enteric rods in root filled teeth with symptomless
periapical lesions.
[Slide 17] [The Red Complex]
[Dr. Adamo] But thanks to the advent of PCR and other molecular techniques, a world
opened up. And this was spear-headed by Siqueira and Rocas in Brazil. This became the
next focus of endodontic discovery. And these guys were incredible but- well get- You
know, actually the chapter in Pathways of the Pulp is- the chapter on micro is authored, is
penned by Siqueira and he gets into good detail if youre interested in going further. I
think your textbook is sufficient for the level youre expected to know now. But its
interesting as a reference. You can go back and you get a little more information from the
other one. Anyway, they discovered the Red Complex among many other bacterial
genera. But these three species were found in almost all endodontic infections and root
canals. Tannerella forsythia, Porphyromonas gingivalis who is one of the bacteroides, and
Treponema denticola- well, its a spirochete. Nobody talked about spirochetes before
because they were culturing in anaerobic cultures and, of course, you need to look under
dark field illumination to see spirochetes, or you need to do PCR analysis to find out that,
you know, the genes identify which treponeme is there. So they didnt- that really was
very obscure until the advent of PCR. And this is pretty recent. This is the 21st century
now, the first decade. And the significance of the Red Complex is that these are the
bacteria that are normally identified with periodontal infections. So if you find them in
endodontic infections, thats telling us that some of the pool of bacteria that enter into a
root canal in the anaerobic conditions there with the dead protein for the bacteria to live
on because anaerobes are on the Atkins diet- you know, theyre not interested in
sacrolytes (?) but they will live on dead proteins and set up house in there for a long time.
The immune system can contain them and you get the development of this quiet
asymptomatic apical periodontitis which is typically viewed as a shadow- a periapical
radiolucent lesion- and no symptoms. Patient says I feel fine, nothing bothers me. Then
you test it- cold testing- and electrical pulp tester- no response. So its necrotic and its
not bothering them yet. It's being held held in check. Something changes and it can
exacerbate and become a nasty infection. Um, in any event, we know that some of the
source is periodontal. The periodontal sulcus is a good reservoir for these bacteria. You
have a crack, a filling or lateral canal- it could enter- or gingival recession could get an
entry there.
[Slide 18] [Molecular Techniques]
[Dr. Adamo] Now the most frequent detected endodontic bacteria in endodontically
infected teeth are these 9 phyla. Theyre found pretty much in all the studies now. There
are many other taxa found that they havent identified yet. In fact, about half of them
have yet to be cultivated. Thats what they, uh, currently project. Its amazing. Its so
different from the culture, the older techniques of culture, you know, where they were
looking for 5-8 strains, they were trying to use reductionist mentality. You know, lets find
the one chemical that causes all this, the lipopolysaccharide. Yeah it does all that, but
16
there are many- its much more complicated than that. And biofilms, of course, which
well get into in a minute are key in maintenance and persistence of infection.
[Slide 19] [Bacterial Genera Represented in Endodontic Infections Table]
[Dr. Adamo] Any event, great variation from individual to individual. OK? Current
view is that apical periodontitis is a heterogeneous etiology. Its many different strains
and multiple bacterial combinations that play a role in the progression of these infections.
So, shown here the bacterial genera most commonly found in endodontic infections.
Gram negative bacteria appear to be the most common, as I said before, common
inhabitants in primary endodontic infections and uh several gram positive strains are
there as well but in smaller proportions than the gram negatives. And, um, but whether
theyre gram positive or gram negative - theyre usually a mix- theyre all anaerobes,
facultative and, you know, some, like, strains of strep again. But theyre, this is the
general pattern thats found over and over. The frequency, you know, with PCR, youre
not knowing, you cant really tell its a viable bacteria unless youre doing RNA studies
because if its reproducing then obviously its viable. But, you know, it could be dead, it
could be contaminants, you dont know what. But when you see a high frequency of
certain genera, you know these are probably major players or at least theyre comfortable
inhabiting the micro eco-niche. So there have to be selection pressures that allow them to
survive and they may, therefore, have a role in perpetuating it. Um, ok. So.
[Slide 20] [Table]
[Dr. Adamo] Symptomatic failed cases also associated with gram positive bacteria
when they fail. Either they're recontaminated or there is a consistence of something that
was there and you never eliminated it properly because itd be hiding out in a sluiceway
(=an artificial water channel for carrying off overflow or surplus water) and a little fin,
or a lateral canal which you cant clean with the instruments that we use and the
chemistry that were using. Uh, this is being improved. Photodynamic theory may be
something were using 5 years from now so it can have a longer reaching effect than
sonication and that kind of thing. But these are all therapeutic things that are being
experimented, mainly in vitro right now. And it hasn't gotten so much to the in vivo side.
So anyways, symptomatic failed cases often associated with, let me see here, let me- oh,
before we get off this slide- chronic apical periodontitis is the quiescent phase. We call it
asymptomatic apical periodontitis now but for the Siqueria chose to illustrate it this way.
Um. This is in Walton and Torabinejads text. And, uh, as it progresses to acute apical
abscess, this is the pattern frequency of different genera and acute apical abscess is
characterized by predominance of these species. And note that Treponema denticola over
here, Tannerella forsythia, Porphyromonas gingivalis- the red complex- they all increase
as we become more acute. See? So thats an interesting observation but theyre there.
Those perio bugs are in there and they thrive in that environment as well. And there are
many others, you know, as you see. Youre not expected to memorize all these things or
anything like that. But just have an idea of the general- like the 9 most common phyla-
that slide before. Its good to know, to recognize them. Its not rote recall or anything but
17
you should be familiar with the kinds of bacteria that are found. And mainly, its about
the types and the groups. Not specific ones. Im using, Im mentioning specific ones
because it helps tell the story. Like the Red Complex, you know, you know Oh, ok, so
perio. How else would it get in? Its not in a healthy pulp. Its gotta get in somewhere
and obviously periodontal pocket is an ideal reservoir for these things. Anywhere in the
oral cavity could be. So lets-
[Slide 21] [Microorganisms Detected in Root Canal-Treated.]
[Dr. Adamo] This is the ones that are mostly detected in failed root canal. Gram
positive bacteria. E. faecalis. Enterococcus faecalis is always found in failed cases. And
in different proportions, but its a major player. Were not sure, and we dont really think
its a pathogen as such. It doesnt have great virulence but it has the ability to survive.
Uh, arachnea. Propianobacteria is the arachnea that we talked aboutthis one. Theyre
found, as well. And again. Tannerella forsythia, Treponema denticola, Porphyromonas
gingivalis up here somewhere - or if it isnt it should be. Here it is. And so, those are the
Red Complex again. And then actinomyces. As well as propianobacterium which have
characteristically have been identified with failed cases. Theyre in the molecular studies
as well but its much more, you know, big eye opener, looking at the frequency of these
things as a result of various molecular techniques. There are two basic categories of
molecular techniques. One is broad-base, broad range, fish, DGG. And then there are the
specific ones where they target like DNA, DNA hybridization, etc. Thats where you have
to know what youre looking for before hand. And same thing, kind of, with regular
culturing because you have to know - youre providing a medium and seeing if they grow
in it. If its not appropriate, you might be killing off something thats there and viable. So
thats another issue. But anyway.
[Slide 22] [Virulence Factors]
[Dr. Adamo] Virulence factors. Ok, this sort of refers, as you already know, refers to
attributes or properties of bacteria that promote invasion of the host and/or persistence of
the infection. Just what it sounds like. More virulent, why? They use the genes expressed,
molecules released, that sort of thing. Um. Major ones are endotoxins. LPS-
lipopolysaccharides- while associated with bacteroides bacteria or prevotella
porphyromonas. They releasee LPS from the cell wall and its found on the surface of
gram negative- a lot of gram negative anaerobic bacteria. And it initiates an inflammatory
process. Um, endotoxins, theyre referred to, in some articles or texts, same thing. Thats
what they usually mean when theyre talking about it. There are virulence factors
associated with bacteria that could alter the course and severity of the infection. Uhh, its
noteworthy to the- lipoteichoic acid (LTA) which is associated with gram positive
bacteria. Thats not as virulent. It is, but its in a, its in a much lower weight for weight
basis in these infections so its a player in persistent infections mainly but nearly as much
of a problem as LPS from the gram negatives. Fimbriae, important in attaching to the
surface of the root canal wall or whatever. And it can alter the relationship by attaching to
other bacteria. Capsules act to protect certain bacteria like the bacteroides. They are
18
protected from phagocytosis by forming a capsule. Histolytic enzymes are also, play a
role in inhibiting the bodies defense mechanisms and allow migration of bacteria and
their toxins to spread. Proteases like collagenase, fibrinolysin react with
immunoglobulins and complement, other serum and connective tissue proteins but they
all- uh, hyaluronidase is mentioned a lot, chondroitin sulfatase glucuronidase, they also
further break down the tissues and host defenses. A good example of this is
porphyromonas gingivalis produces collagenase. Its not coincidence that its called
porphyromonas gingivalis because its associated more with perio disease even though
its found in endo disease. And what this perio- what would be a survival factor, a
virulence factor, would be the ability to dissolve collagen and spread through the tissues,
destroying gingival attachment. So P. gingivalis is a collegenase producer. It has a gene
that is usually associated with it. Sometimes the gene is turned off. If its found in a root
canal, some of the studies show it doesnt have that active gene that produces collagenase
but it doesnt need it to survive in that environment. Alright, um. Also damage occurs as a
result of hydrolytic enzymes produced by surrounding neutrophils and PMNs in purulent
infections. Alright?
[Slide 23] [Virulence Factors]
[Dr. Adamo] Extracellular vesicles and short-chain fatty acids. These, um. Extracellular
vesicles are sort of like decoys. They have a tri-laminar structure similar to the bacterias
own outer membrane. And it can bind up specific antigens because its a decoy that thinks
the antigens bind up to that and let the host, the original cell survive. So um, also those
vesicles can contain various enzymes that produces, that allow them to be a player in a
range of activities that are aimed at host cells such as proteolysis and hemolysis.
Adhesion and heme agglutination as well. And anaerobes also produce those short
chained fatty acids. Umm, like propionic acid, butyric acid, isobutyric acid, and they
affect chemotaxis, degranulation, um, phagocytosis of course. Butyric acid inhibits T-cell
blastogenesis and can stimulate IL-1 which is associated with bone resorption. Actually,
gram positive strep are also associated with TNF-alpha and interleukins, so its not only
gram negatives but these are some of the things that are more associated with gram
negatives. Um, low molecular weight products such as, well, Ok, well talk about that
first. Hydrogen sulfide and ammonia are also produced and cause tissue damage but the
polyamines, gram-negatives include the largest amount of polyamines such as putricine,
cadaverine, these kind of chemicals. They regulate cell growth, regeneration of tissues, as
well as their inflammatory modulators. Putricine in total polyamine levels are higher in
necrotic pulps than pulps associated with percussion and spontaneous pain. And teeth
with sinus tracts like chronic apical abscesses have higher levels of cadaverine. These are
observations- help them to identify when they were using classical culturing. But, uh, you
know, its interesting but it doesn't really tell us anything in particular about how that
bacteria will affect the disease process on a macroscopic level.
[Slide 24] [Biofilms]
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[Dr. Adamo] But biofilms. This is important. Taken as an entity now. Now, theyre
beginning to look at biofilms as a significant, one of the most significant virulence factors
involved in development and persistence in endodontic and other chronic infections.
They are microbial communities formed by many different species of bacteria and theyre
associated with a surface- theyre encased, these communities, these colonies are
enclosed in extracellular matrix of their own origin. This ECM is known as EPS which
stands for extracellular polymeric substance. Among inhabitants are gram positive, gram
negative, facultative, strict anaerobes and there is variation from individual to individual
from infection to infection. Not only that, from population to population globally. Thats
hard to get your head around but it does, it starts to clarify that there are patterns that
youre looking for. Once formed- instead of this reductionist thing that the
microbiologists were using 15 years ago, you know its this molecule thats doing it-
now its no, its a complicated ecosystem thats doing it. And its allowing various
chemicals like this to be produced or preventing them from being eradicated by the
immune system. They, once formed, these biofilms, serve to resist elimination, promote
resistance of the pathogens that live there. And one way to describe a biofilm would be as
a metabolically active community of microbes where some species help others to adhere
to solid surfaces while others might form bridges that connect different species, like
water channels, and um, they develop a self-sustaining micro ecosystem. And they can
also detach from the biofilm and again be freed as planktonic bacteria which can go
somewhere else and start the same process.
[Slide 25] [Biofilm Development]
[Dr. Adamo] So this schematic shows the development basically, the development
stages of the biofilm. Um, interaction of planktonic suspended microbial cells. Microbes
already attached to the stratum. This is adhesion, known as adhesion. And then secondary
colonizers attach to that mass- its known as co-adhesion and then the bridging or
clumping of bacteria is referred to as co-aggregation. And of course, in that stage, thats
when planktonic- when bacteria can be freed again and they are in planktonic state.
[Slide 26] [Quorum Sensing]
[Dr. Adamo] So another thing you have to know about, about biofilms is of course
quorum sensing. This is a term thats used, it doesn't have an exact definition but its used
by various researchers to describe cell-cell bacterial communication within these biofilms
and it has some specific attributes such as production, release and detection of these
signaling molecules: autoinducers- lactones made by gram negative bacteria and peptides
made by gram positive bacteria. In sufficient concentration, they can serve to turn on
genes like, you know, antibiotic resistance, producing beta lactamase. And that, of course,
will have an effect on protecting the entire community. It may be produced by one
bacterium but its going to protect all of them if its binding up penicillin, for instance.
Also, harder to eradicate because theyre embedded bacteria. Phagocytes can't get to them
as well. And, um, what else. Theyre, oh. Gene, horizontal gene transfer occurs in these
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biofilms as well. So, you know, they can transfer an antibiotic gene to another bacterium
as well inside this community.
[Slide 27] [Progression to AP]
[Dr. Adamo] Uh, ok. So before we get into, um, host response, I want to touch briefly
on the progression from pulpal infection to pulpal necrosis. Because that has to precede
the development of apical periodontitis. Its a varied, dynamic process and involves
complex immunological and neurological interactions that are covered in many of your
other lectures. But a brief overview is important so you can connect the microbiology to
the etiology of apical periodontitis. After the initial infection of the vital pulp from oral
flora, whether from periodontal tissue or where ever, saliva. They go through various
portals which well also cover in a few minutes. But the pulp became inflamed, see in this
case, these are going down. This was dens invaginatus and bacteria obviously got in
through here. You see an apical periodontitis. After treatment, 6 months or so later, bone
was pretty much filled in. Here, its more obvious. In this tooth, you know, the carious
lesion- either this is a mechanical exposure or caused by the caries which the dentist
excavated. And it, uh, the pulp became necrotic and formed this lesion which you see out
the side which is caused by a lateral canal. And after 6 months or so after doing the endo,
the lesion, it filled it. And you see a little puff of cement, uh, or sealer which had extruded
there so this confirms that it must have been- when you see this kind of lateral, if its not
a lateral periodontal cyst, if its real endodontic pathology, its usually coming through a
lateral canal. You dont have to fill the lateral canal, supposedly. If you just do the main
canal and seal- disinfect it properly and seal it, itll be enough to allow the body to heal
and bone to fill in, but not always. And, uh, you know, not always, sometimes we have to
do additional surgical treatment. But anyway, um, getting back to the progress, they enter
through those portals and then pulps of course, it becomes inflamed. The pulp becomes
inflamed, it causes a pulpitis which is characterized by cold sensitivity. Doc, every time
I breathe in or have something cold, it hurts. Does it go away right away? Yeah. If it
goes away right away, its irreversi reversible, reversible pulpitis, excuse me. It just
means a lower threshold but it doesn't persist. It doesnt have any peculiar symptoms like
spontaneous pain, referred pain. Still might not need endo when its just acute reversible
pulpitis but a localized Cold War ensues with these microbes and the immune system and
during that time, if the pulp is unable to contain and destroy the invaders and wall of
necrotic pulp tissue from the rest of the pulp, then the bacteria and their toxins spread
throughout the whole pulp and overwhelm it. Its in a contained environment, like the
CNS, it cant expand so you can get stasis- necrosis. And then the bacteria thats already
there, they have a food supply. That Atkins diet. An indefinite supply of stuff so they can
really can, uh, expand during this, this, uh, period of time. And when its in that shady
area between necrosis and reversible pulpitis, it becomes irreversible pulpitis. Now how
do we know that? Well the symptoms are different. Patient gets spontaneous pain, or they
have something cold, or you put something cold like an ice cube or an endo device on it.
Well, that doesnt bother me doctorwhoa, whoa, whoa. Wait a minute. You take it
away, its still aching. Itll still hurt. I feel it in my ear now. I feel it in my temple or I
21
feel it down here. They get referred pain, delayed pain. These are our, indicative of C-
fibers. C-fibers in the pulp are the last holdouts. When youre getting C-fiber response,
that means its irreversible pulpitis by definition. You know, it may be accompanied by
symptomatic apical periodontitis where theres inflammation and the tooth is also
sensitive to percussion and even palpation. But that cold response tells you a lot. It tells
you you gotta do endo or else the tooth will have to come out at some point. Its not going
to heal anymore whereas reversible pulpitis - just a little cold sensitive- you put in a new
filling, its cold sensitive, avoid cold, avoid extremes of temperature. Use a straw. Take
NSAIDs for a few days and usually in 2 weeks, that has stabilized. And you got a healthy
pulp again. But when its gone to these kinds of symptoms, thats irreversible pulpitis.
And its only going to go to necrosis. If the patient toughs it out, the next thing is it
doesnt hurt anymore doc. Then you put the ice cube on it and they dont feel it. You put
the EPT on it and they don't feel it. See, it doesn't bother me at all. Sure, because its
now dead. The next thing youre going to do is get a shadow here, or get an acute apical
abscess directly because now youve got necrosis and its not going to heal. Ok?
[Slide 28] [Host Defense]
[Dr. Adamo] Um, soapical periodontitis is, um, response mounted by the body to
combat microbial invasion from the infected root canal coming out the apex. Here, these
endotoxins and all come out. This is the, supposed to be the apex of the tooth. And, um,
the host defense array is composed of multiple components like you see here. Complex
interactions at the cellular and molecular levels. These consist of cells, intercellular
mediator, metabolites, effector molecules, humoral antibodies.
[Slide 29] [Pulpal Inflammation: Local Response]
[Dr. Adamo] Alright, in the pulp, inflammatory, chronic inflammatory cellular response
is characterized by lymphocytes, plasma cells and macrophages. Thats enough, you
know, thats all you have to know. And, uh, the ratio of T4 to T8 cells increases as pulpitis
progresses from reversible to irreversible. Also, the pulp makes IgG that is specific and
reactive for specific bacteria.
[Slide 30] [Apical Periodontitis: Local Response]
[Dr. Adamo] So as inflammation progresses, uh, we find T4 cells predominate during
the active enlargement of the lesion. Um, as in the pulp. You know, when its going in
that direction, getting worse, its an active T4- they predominate during the active
enlargement of the periapical lesion and stabilize in the chronic phase so that we find
more T8 cells. This might be a board kind of question, you know, thats why I put it in,
because even though its immunology, youre supposed to relate these things, integrate
them so you have a little picture in your mind of how that might- what might be
happening at that level. Cytokines and other mediators also are bound so you get IgG,
IgA, IgM, IgE. And so theyve all been demonstrated in periapical lesions which means
that in addition to the local tissue reaction, this whole process serves as a pathway for
22
sensitization. Immunologic reactions also participate in the development and perpetuation
of periradicular lesions.
[Slide 31] [Theory of Focal Infection]
[Dr. Adamo] So, what about theory of focal infection. This was Dr. Buschs office a few
years ago and I bought it. No, no. Anyways, back in the day, the uh, it was a term coined
by E.C. Rosineau. in 1909. And, uh, it was very publicized by a physician named Dr.
William Hunter up in McGill in Montreal in 1910. And it set off a whole years of
unnecessary extractions. Basically, it refers to the localized or generalized infection
causing- caused by dissemination of bacteria or their toxic products from a distant focus
of infection. Thats how he defined it. Subsequent flawed studies by Rosineau and Price
in the 1920s with inadequate experimental design and not using proper controls helped
fuel the fire. Eventually became popular to remove necrotic teeth and/or teeth that had
undergone RCT to prevent a host of diseases such as rheumatoid arthritis and other
chronic degenerate diseases of the kidney, the GI tract, neurological disease because it
was a convenient scapegoat. Oh, it must be from those nasty teeth. There are bacteria
there. And some of the same kinds of bacteria.
[Slide 32] [Focal Theory]
[Dr. Adamo] Um, actually, it became common in that timeframe to extract perfectly
good teeth that were either treatable or that had had prior dental treatment just to manage
medical conditions. It couldnt be explained rationally at that point in time. This led to the
needless removal of millions of necrotic and root canal filled teeth. Now we know that
surgical manipulation of an infected area or the presence of an untreated acute endodontic
infection can induce a bacteremia that can lead to serious consequences during the acute
phase. But thats when you manage it. The patient sees the doctor, they put him on an
antibiotic. You start RCT, you drain it, you extract the tooth, whatever youre going to do.
The presence of non-vital asymptomatic teeth or teeth that have had successful root canal
therapy does not pose such a danger. The very definition of chronic- its proliferative, it
wants to contain the infection. Thats why granuloma forms and sometimes a cystic
lining, epithelial lining- because its trying to contain it, protect you, slough the tooth out
if anything, bone resorption, get rid of the bag of bugs so that youll be safe. So chronic
isnt really a problem but these guys of this school of thinking try to make chronic
abscesses seem like more than they are. Theyre not completely innocent but more so
than one would be thought- or that they would lead you to believe. If it does indeed have
a role in major distal disease, you know the systemic diseases, it has yet to be
demonstrated in any prospective randomized controlled published studies using
contemporary standards and techniques and peer reviewed. So theres no real current
based- current evidence based rationale for removing such teeth. Here is a tooth, chronic
infection, alright, theres something causing this resorption of this root. Its, why? We
dont know. Maybe its a fracture, who knows? Maybe trauma at one point? Um, root
canal might help to arrest that with CaOH therapy. This tooth was properly treated. Why
take it out? Because there are some bacteria that are retained in a tooth after RCT but
23
theyre also entombed and cut off from their nutritional supply and unless theyre
producing disease which would first be seen locally, youd get a local breakdown. Then it
would spread, then it could be a problem. It might be involved in dissemination of
disease but when its chronic and been treated, its really not doing this stuff. They have
never been able to show that it does. Despite the claims of these guys back in the 20s and
so forth.
[Slide 33] [Quantitation of Circulating]
[Dr. Adamo] So now, what about chronic infected teeth with asymptomatic radiolucent
areas? An interesting study was done by Torabinejad and his group in Loma Linda back
in 1983 where he took the serum concentrations of circulating immune complexes, IgG,
IgM, C3 in 30 patients all of whom had either 1, 2 or 3 large periapical lesions that were
asymptomatic. They measured their circulating immune complexes compared to patients
without endodontic lesions or other infection and was unable to demonstrate you know-
[Slide 34] [chronic periapical lesions]
[Dr. Adamo] there was no statistical difference in the immune complex levels- distal to
the sites of infection anywhere in the blood system. So they found really no statistical
difference between these groups, suggesting chronic periapical lesions can not really act
as a focus to cause systemic diseases as far as via immune- you know, by assessing
immune complexes. That said, acute infections, especially with signs of systemic
involvement are definitely dangerous and require immediate treatment. Whether I&D,
antibiotics, RCT or extraction and teeth with chronic asymptomatic lesions should also be
endodontically treated as W.D. Miller said before they become acute. But in that state,
theyre not posing much of a danger. Now, more recent meta-analysis does include that
there is correlation between AP (apical periodontitis) and higher levels of immune
markers. Ok, so including circulating immune complexes with newer techniques, there
are some but it doesnt address- these studies have not identified whether they are acute
or chronic abscesses. So, you know, what does that tell us? We know that its going to
happen with acute. There are similar findings in the presence of periodontal disease. And
periodontal disease are commonly both acute and chronic at the same time. You have
areas that are bleeding and inflamed and others that are chronic but stabilized. So
treatment intervention did indeed also reduce levels of these inflammatory markers. This
occurred with root canal treatment as well as extraction. This provides reliable evidence
for the necessity to treat, either extract or do RCT on teeth with apical periodontitis. Thats
what it shows you but it doesn't say that youre in any great danger in a chronic state. Just
a time bomb you should deal with.
[Slide 35] [Causing Bacteremia]
[Dr. Adamo] So what are bacteremia? So these guys were extracting teeth to protect
their patients. Braamgardener in 1976 and later Heimdahl in 1990 established that non-
surgical endo treatment is less likely to produce bacteremia than tooth extraction. In fact,
24
tooth extraction produces extensive bacteremia 100% of the time. And bacteremia is
definitely is (couldn't hear if he said is or isnt - sorry) implicated in the dissemination of
disease. So if the treatments worse than the cure, you know, you get a much lesser
bacteremia during RCT. So you could just argue that well its a safer way of managing
even if focal theory were true, its still a safer way of managing it than producing a huge
bacteremia. Alright.
[Slide 36] [The Sterile Human Body???]
[Dr. Adamo] Keep things in perspective. We also cant forget that the entire GI tract is
teeming with enteric anaerobacteria and that skin and external surfaces are covered with
staph and other aerobes and many of these can become pathogens as well under the right
conditions but usually theyre within normal benign cohabitants throughout life. So, you
know, just, anyway.
[Slide 37] [Classification of AP: Acute]
[Dr. Adamo] Let, this is what Dr. Busch was talking about. Lets clarify. Symptomatic
apical periodontitis- sensitive to percussion, sometimes palpation associated with a
lesion. Sometimes. And if its very rapid, you may not. If its been there for a while and
its acute again, you might see the beginnings of an apical lesion.
Acute apical abscess is very sensitive to percussion and palpation. Pain, tenderness,
swelling of adjacent soft tissues and its associated with PARL when its arising out of a
chronic infection. If its a first time and went straight from symptomatic apical
periodontitis, may not have enough time for the bone to resorb. You still get the
symptoms and youll get pus when you open the tooth but it doesnt mean that youll see
an area with an acute apical abscess. It might be too fast for that.
[Slide 38] [Classification of AP: Chronic]
[Dr. Adamo] Otherwise, periodontitis, chronic. It may develop into a chronic
asymptomatic apical periodontitis which we just talked about. An area, patient has no
sensation. Its necrotic. And uh, this is an asymptomatic lesion with apical bone, loss
characterized by PARL on X-ray. And it would contain granulomatous tissue and filtrate
it with lymphocytes, plasma cells and macrophages. Chronic apical abscess may quietly
develop. Its characterized by acute intermittent episodes of pus draining through the
sinus tracts. Apical lesions, uh, may also have an epithelial lining and theyre called cysts
but only the pathologist, you know, histopathological examination can show whether its
a cyst or not.
[Slide 39] [Portals of Entry for Microbes]
[Dr. Adamo] Well, I can go through the portals of entry. Its the last thing, uh, you can
also look at it through the slides but Ill keep talking. If you have to leave, go ahead. I
don't know. Are you free to 4 oclock or 10 to 5? Alright, so you know, but Ill just
quickly go through these. They have to enter as we talked about before. And it can be
25
through direct involvement of the pulp. You know, its usually protected by cementum
and you know by dentin. And the root is protected by, excuse me, enamel and dentin in
the coronal portion and cementum and dentin in, you know, radicular portion. And you do
have accessory lateral canals, congenital developmental defects, fracture lines, coronal
micro leakage by not restoring the tooth properly following RCT.
[Slide 40] [Carious Pulpal Exposure]
[Dr. Adamo] Uh, clinically this would be what happens when you get caries. Direct
extension into a lesion. This is a temporary filling. You can see that it was right at the
pulp chamber. And after treatment, it was fine.
[Slide 41] [Periodontal Source]
[Dr. Adamo] Um, periodontal source. Its unlikely that youre going to have extension
to all the way around with the biofilms that form and going to cure that problem. You
might do the root canal, but its hard to eliminate the biofilms off these deep lesions that
are complex and continuous. So they have a notoriously poor prognosis for long term
management. Sometimes we still have to do it to make, you know, maybe its a terminal
abutment for a bridge. The patient is 75, you want to get some more time out of it.
[Slide 42] [Cracked teeth, Microfractures, and Coronal Microleakage]
[Dr. Adamo] Um, cracks. Bacteria enter through cracks. If its confined to the coronal
portion, you might get away with root canal, core and a crown. If it gets down into the
roots poor prognosis. Bacteria will reinfect. Usually you can probe and theres a deep
probing depth right where the crack is.
[Slide 43] [In Vitro Bacterial Penetration]
[Dr. Adamo] Um, you got to seal teeth
[Slide 44] [Over 50% of the root canals]- SKIP
[Slide 45] [Image]
[Dr. Adamo] These are some slides showing a case which, despite the extension - this is
not the reason why this case is failing. This had been done 20 years ago. But when the
filling broke out and it was untreated, bacteria started to work there way-
[Slide 46] [Images]
[Dr. Adamo] through there causing an exacerbation-
[Slide 47] [Image]
[Dr. Adamo] which responded to normal treatment.
26
[Slide 48] [Dont Blame the Silver Points]
[Dr. Adamo] Um, so its not the silver points.
[Slide 49] [Portals of Entry for Microbes]
[Dr. Adamo] Its, uh, it was just bacteria entering through an unsealed- so the bottom
line is the restoration is just as important as doing good endo, you also have to do a good
restoration or else bacteria are gonna recontaminate. In as little as 19 days, Torabinejad
found there was contamination of half the samples with smaller bacteriolytes- staph
epidermis. They will work their way down a long [adjective] gutta percha, so dont think
youre getting away with it. Gotta seal it within a couple weeks after the endo is the best
time.
[Slide 50] [Perio-Endo/Endo-Perio]
[Dr. Adamo] Um, perio-endo. Again, if its endo or etiology, it looks like this (top
picture) but when you see a tooth that has- I mean, this is perio etiology (top picture), Im
sorry. THIS is endodontic etiology (bottom right picture) when you typically see a lesion
between the fulcra but the crystal bone is up here, then its usually caused by a root canal
process but it can do the same thing. Cause a perio-endo abscess. You can treat it- you get
some healing. But this ones not healing, for instance. So, it has biofilms. Howre you
going to get the biofilms off? Youre not.
[Slide 51] [Images]
[Dr. Adamo] So, um when you see a lesion that looks like two teeth, its usually just
one. But in lower anterior, they superimpose. The area looks like you have 2 or 3 teeth
involved. But when you do the root canal on the tooth that had trauma and tested non-
vital, rather than the tooth that tested vital, you get healing of the tooth that looked like it
had an area before also. Its usually one tooth in other words responsible.
[Slide 52] [Images]
[Dr. Adamo] This was the tooth responsible, even though it looks like there were two
areas. This tooth was vital and it starts to heal after you do the root canal on that.
[Slide 53] [Anachoresis]
[Dr. Adamo] Umm, the last thing is anachoresis. Blood-borne attraction. Positive
attracted blood-borne- bacteria to inflamed or necrotic tissue during bacteremia. Its very
controversial. Uh, in 41, it was first identified as a possibility. In 1968, Gieren Mitchell
demonstrated that it could be positive. In 1976 Sundqvist said that maybe thats why
traumatized teeth get infected. Um, but in more recent studies, researchers were unable to
demonstrate blood borne bacteria in root canals that had been instrumented and left
unfilled. DeLovenas and Finn 1984. So the relative importance of this phenomena is to be
determined. And thats about as far as we have to go today. Thank you guys. I could go
on and on but I think otherwise, we otherwise would have Dr. Vernillo far more in depth
27
with more interesting stuff than I have. Very good Tony, hows it going. Ok, let me turn
this thing off. Im sorry, its just so much-
[Slide 54] [References]- SKIP
[Slide 55] [References]- SKIP
28

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Transcribed by Charles Buchanan Date of the Lecture: 10/06/14

[Diagnosis and Treatment of Oral Diseases] [Lecture 45] [Luxation Injuries:

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Transcribed by Charles Buchanan Date of the Lecture: 10/06/14

[Diagnosis and Treatment of Oral Diseases] [Lecture 45] [Luxation Injuries:

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43/44: Luxation & Micro

43/44: Luxation & Micro