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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:

Diagnosis and Treatment] by Dr. Busch

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an extra bit of work on your course load, but it is helping to keep a service running that

you actually use. You dont have to commit to transcribing a whole lecture either. Youcan split it and take 30 minute blocks with others. We all need to study and it would

definitely help to lighten the load of the current scribes. Thanks!

[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 ofthe 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 aproblem. 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 ormobility. 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 onlysymptom 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 youhave 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 canget 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 whyit 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 animmature 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 twotypes 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, temporaryfilling, 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 amouth 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 uphigh, 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 hasthe 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 thatsthe 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 thepalate. 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 andback. 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 topercussion 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 apexis-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 thetooth 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-positionit 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 aretreatments 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 somethinghappened 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 whereeverything 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 havea 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

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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 withresorption 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 ifits 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 completelycalcified.

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 youyesterday, 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 theliterature 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 dontgenerally 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 anX-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 alreadywould 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 timeany 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 pulpalpathology 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 whichbacteria.

[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.

[Slide 8] [Anaerobic Bacteria][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 toelucidate 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 yousee Peptostreptococcuswhich 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 littlesymbiosis, a little microecologystarting 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 exactbacteria 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.

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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 thenext 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 underdark 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 quietasymptomatic 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

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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 strainsand 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, itcould 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 ischaracterized 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

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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 havecharacteristically 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 factorsassociated 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

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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 isporphyromonas 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 theyaffect 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 teethwith 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 whichstands 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 asa 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 secondarycolonizers 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 peptidesmade 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 precedethe 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 dentistexcavated. 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 becomesinflamed, 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 alreadythere, 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

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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 goingto 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 responseis 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 findmore 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

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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 coinedby 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 bacteriathere. 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 anantibiotic. 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 bedemonstrated 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

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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 thatthere 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. Thatswhat 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,

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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 itsa 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

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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 termmanagement. 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

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