Pathfiles
Clinical Tips, Endodontic Preparation Techniques

Faster, Easier, Safer Rotary Endo? Get Your Glide Path On.

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Well, I don’t know if I’m going to help you improve the speed of your preparations, but I do want to make some comments about some files that I’ve recently had the opportunity to try (they may not be new to everyone, I work in China and things take a little longer to become available here). I’d like to make the point now that I’m not tied in any way to these files or the companies that sell them. In general, debates over what file system is best usually leave me a little bored and I’m not here to promote a particular brand or system. Everyone has their own favourite system and when you have experience with one type of file, then that is probably the one that will provide the best results for you. I also think it’s often quite difficult to take to a new file system as they all have a learning curve, a different feel within the canal and certainly different tolerances when it comes to fracture resistance.

Pathfiles

Thin files for narrow canals.

Anyway… The Pathfile NiTi files are only designed to prepare the glide path through the canal, and then you can use whatever system you prefer to complete the preparation. Want to know what I think is the key to quality rotary NiTi preparations? You guessed it, it’s the glide path. Most rotary Ni Ti files are designed to follow a path, not create one. It’s quite well accepted that if you can resist the temptation to pick up your initial NiTi file until your glide path is well and truly established, then you’ll find preparations are easier, smoother and probably faster. So, a rotary file system designed to create a glide path is a novel concept which challenges the assertion I just made.

There’s not much research around regarding these files other than an article that showed novice users could produce smoother glide paths in plastic blocks than endodontists can with stainless steel hand files. (Berutti et al, 2009) Sounds promising right? Well, I must admit to being a little hesitant when I first saw these files, because they are really narrow and well, you’re not creating a proper glide path before you put them in the canal. In my head, this meant susceptibility to breakage.

There are three files. A #13 (Purple), #16 (white) and #19 (yellow). The files are 2% taper, so they really are  quite narrow, but I guess that’s what makes them useful for preparing glide paths. The idea is to use a #10 stainless steel hand file to scout the canal (and confirm initial working length with EAL if possible), then use the #13, #16 and #19 to create the glide path. Working length is confirmed after this step. In practice, I found that they do a really good job of preparing the glide path, especially in narrow and curved canals e.g. MB2. The glide path that is produced is generally very smooth and makes the subsequent cleaning and shaping procedure easier and dare I say it faster. I don’t think you necessarily need to use all three files in all canals. Overall, you’re probably not going to prepare the canals any faster as you are now adding additional files to the process, and there is obviously going to be an increase in cost. But, if you are new to rotary NiTi, or looking to improve the consistency with which you can create a smooth tapered prep all the way to the apical foramen, then it might be worth giving these files a try. To be honest, these are the first products I’ve tried in some time that have had any sort of “wow” factor for me.

Using these files won’t be for everyone and more experienced practitioners probably have less need for them, but The Endospot is all about sharing information and helping others to improve their endodontics, so when I find something that I think might be worth discussing, then it will appear in your inbox. So, if you feel inclined to do so, get your friendly local rep (I think will be Dentsply in most places around the world) to drop a few samples off to you and grab some extracted teeth to get the feel of the file before diving into a live case. And remember to be gentle, these files are thin and going into narrow canals. If you do a search for Pathfile on youtube, you’ll find a couple of videos worth watching as well. If any readers have experience with these files and want to contribute some tips, then please leave a comment below.

References:

BERUTTI E, CANTATORE G, CASTELUCCI A, CHIANDUSSI G, PERA F, MIGLIARETTI G, PASQUALINI D. 2009. Use of nickel-titanium rotary pathfile to create the glide path: comparison with manual pre-flaring in simulated root canals. J Endod, 35, 408-412

Aetiology of Apical Periodontitis, Endodontic Surgery

Choosing your battles – Apicoectomy

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I had a patient present to me this week complaining of pain and swelling associated with a lower molar. She had previously had root canal therapy and then apicoectomy performed by her dentist about 8 months ago. She was disappointed that symptoms had recurred as she had seen the dentist in her home country one month ago and he had told her the treatment had been successful, healing was proceeding well and that a crown could be placed. She told me that her dentist had told her prior to the surgery that she had a large lesion and that the actual surgical procedure had been very painful.

apicectomy

Tenderness to percussion or palpation, pain or fistula formation may indicate failure of an apicectomy.

This case is a good one to base a discussion on case selection for apicoectomy. The first thing to note is that the quality of the original RCT is inadequate. One mesial canal is filled well short of the appropriate length. Additionally, the distal canal is poorly filled. There is also evidence that the composite resin restoration may be leaking. It’s reasonable to assume that the root canal was failing due to infection within the canals, and it has been clearly shown that this is the case for the vast majority of root canal treatment failures.

So from a purely endodontic point of view (disregarding alternative options or the influence of prosthetic factors), we have two main options. First, we treat the infection in the canal by undertaking RCT re-treatment. Secondly, we “entomb” the microorganisms in the canal and prevent them and their products reaching the periapical area by undertaking periapical surgery with retrofill.

In this case, we can see that periapical surgery has been undertaken, but no retrofill has been placed. Given the (very safe) assumption that infection remains within the canal, then simply resecting the apical portion of the root will not achieve anything of use. The canal will remain open and the microorganisms will continue to thrive within the canal continue to release products that induce an immune response in the periapical tissues. Unfortunately for this patient, their dentist has shown a lack of understanding of the cause of periapical pathology and needlessly put the patient through a surgical procedure. There may have been some healing of the lesion sue to the surgical procedure, but complete healing could not be expected.

A recent randomized clinical trial compared the outcome of apical surgery where either an MTA retrofilling was placed or the GP filling of the resected root was smoothed and no retrofill placed (Christiansen et al. 2009). The outcome was quite clear that placement of MTA retrofill provides a superior rate of healing compared to just leaving the GP intact. The study didn’t really go into detail as to the quality of the orthograde root fillings in the teeth, but in a situations such as the case discussed above, a retrofill is a necessary part of the procedure. For those of you who don’t have experience with preparing and placing retro fills, it is a skill that requires some practice and specialised equipment. This is especially so once you start to treat molars and teeth with isthmuses.

Without seeing the initial radiographs, I’d have to say that from a purely endodontic point of view, RCT re-treatment should have been considered prior to any surgery. This may have been successful in treating the infection alone, but if not, it provides a better chance of the canals being cleared of infection prior to the surgical procedure, and this then improves the chances of success of the subsequent  surgery. Alternatively, apical surgery with retrofill performed by a skilled clinician might have been successful in this case.

Reference:

Christiansen R, Kirkevang L-L, Hørsted-Bindslev P, Wenzel A. Randomized clinical trial of root-end resection followed by root-end filling with mineral trioxide aggregate or smoothing of the orthograde gutta-percha root filling – 1-year follow-up. Int Endod J, 42, 105–114, 2009.

Diagnosis of Pulpal Pathology, Endodontic Radiography, General Updates

Simple Guide to Pulpal and Periapical Diagnosis Part 1

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In this post, we discuss a simple and practical method of classifying pulpal pathology that can be used in practice on a daily basis. For the new and updated Endospot Podcast, go to the Podcast Page.

Endodontic diagnosis

How do you classify the pulp in this tooth?

Listen to the episode here (12 minutes):The Endospot Episode 2 | Simple Guide to Pulpal and Periapical Diagnosis Part 1

References Referred to in This Episode:

BARBAKOW F, CLEATON-JONES P, FRIEDMAN D. Endodontic treatment of teeth with periapical radiolucent areas in a general practice. Oral Surg Oral Med Oral Pathol 1981. 51, 552–559.

BENDER IB. 2000 Pulpal Pain Diagnosis. A Review. J Endod 2000. 26, 175-179

BENDER IB. 2000. Reversible and irreversible painful pulpitides: diagnosis and treatment. Aust Endod J 2000. 26, 10–14.

MILES TS. Dental pain: self-observations by a neurophysiologist. j Endod 1993. 19, 613-5.

SELTZER S, BENDER IB, ZIONTZ M. The dynamics of pulp inflammation: correlations between diagnostic data and actual histologic findings in the pulp. Oral Surg Oral Med Oral Pathol 1963. 16, 846-71 and 1963. 16, 969-77.

SIGURDSSON A. 2003. Pulpal Diagnosis. Endodontic Topics. 5, 12-25.

Transcript:

Welcome to the Endospot Episode 2.

My Name’s Pat Caldwell and today we’re coming to you from Shanghai, China. On our website we have the complete list of references discussed in this episode, so go to www.endospot.com and remember you can sign up online to receive the Endospot directly to your inbox.

In this episode, we’ll be discussing the classification of pulpal pathology. This will be the first in a series of three episodes looking at the issue of diagnosing pulpal and periapical pathology and in this episode we’ll go through a useful classification system which will help you deliver appropriate treatment to your patients. I’ve broken it up into three episodes because diagnosing and therefore treating appropriately is just so important. I think that often not enough time and thought goes into the initial diagnosis and that is when errors are made and our patients suffer. As endodontists we often see cases where an incorrect diagnosis has been made and treatment either withheld or provided when it wasn’t required and as professionals we owe our patient more than that.

When we look at the pulp and periapical classification systems, there are many out there, but in my opinion the simplest and most useful is the one proposed by Asgir Sigurdsson (Sigurdsson 2003). He published an excellent journal review article on this particular topic in everyone’s favourite journal, Endodontic Topics and that’s the classification system I’ll be discussing today. This classification is very much designed to give a clear indication of the treatment requirement according to the diagnosis, and when it comes down to it, that’s what we’re really looking to achieve out of our diagnosis.

Now when I’m faced with a new patient, whether they are presenting in pain or not, I will still conduct a complete history and examination and make both a pulpal and periapical diagnosis. I split the diagnosis into pulpal and periapical because it helps me have clear in my mind exactly what I’m dealing with, how we should proceed and what follow up’s required. It will also give us clues as to what problems we might run into, such as if the tooth will be difficult to anaesthetise, or if there’s likely to be a high level of post-operative pain. To be fair it will most often be the pulpal diagnosis that is driving your treatment decisions and that’s another reason to spend an episode on going through the various diagnoses.

Now if you think about it, the only way we can definitively diagnose the state of a pulp is to extract the tooth and slice it up and look at it through a microscope. So, our clinical diagnosis is always going to include an element of a guess and I can assure you that it will not always be straightforward. But I dIgress, we’ll get onto how to diagnose in a future episode so now let’s get back to the topic at hand. The classification system we are going to be using includes 4 different diagnoses for the dental pulp, and one of them is the healthy pulp. That’s the easiest one so we will start with that one.

A diagnosis of healthy pulp assumes that the pulp is vital and is not inflamed in any way. This tooth will respond normally to pulp testing, that is hot, cold and electric.  It will be asymptomatic and shouldn’t be tender to percussion or palpation unless there is an occlusion issue causing this. We use this classification sometimes when we need to do RCT on a tooth for prosthodontic reasons. So an example might be where there is not a lot of coronal tooth structure remaining in a vital tooth and the restorative dentist feels that an intracoronal restoration is required in order to provide retention for a core.

We’ll now move on to the more complex diagnoses, the ones indicating some sort of inflammatory response. The first of these is Reversible pulpitis. If we looked at this pulp under a microscope, we’d see a vital pulp with areas of localised inflammation. Most commonly this will be associated with a response to caries or possibly microbial leakage of a restoration. It could also be due to exposed dentine or bacterial ingress along a crack. All these things will lead to inflammation in the pulp. Now by definition, this inflamed pulp should heal when we remove the cause of the inflammation, so it’s important not to misdiagnose this pulp with an irreversible pulpitis and initiate RCT when it’s not needed.

A pulp with reversible pulpitis can present with quite a broad range of symptoms. Typically, the patient will describe pain with hot or cold, or with biting in the case of a crack. The pain might be mild, but can sometimes be severe, but probably the key to this diagnosis is that removal of the stimulus will lead to rapid relief of the pain. For example, drink something hot, tooth hurts, swallow the drink, tooth is fine. In general, there should also be no report of spontaneous  pain, and no tenderness to percussion or palpation. The tooth is likely to respond to a pulp test, but the inflammation in the pulp might mean that an exaggerated response is gained.  This in itself isn’t an indication of irreversible pulpitis, if the other indicators are that of reversible inflammation.

When you diagnoses reversible pulpitis and remove the stimulus by removing caries, or covering exposed dentine, it’s important that you review the patient and re-do all the examination procedures. Because if you think about, if you’ve diagnosed reversible pulpitis, say in case where there is a carious lesion and you treat it by removing the caries and placing a restoration, but the symptoms remain then by definition the pulp wasn’t reversibly inflamed.

Choosing between a diagnosis of reversible pulpitis, and it’s for more unpleasant alternative irreversible pulpitis is a critical decision, because the treatment options are very different. Where a pulp is irreversibly inflamed, this means that the inflammation is so severe that the pulp will not be able to heal. It will eventually necrose and become infected, leading to apical periodontitis. The treatment for these teeth is to undertake root canal therapy in order to remove the diseased pulp tissue and prevent infection.

As with reversible pulpitis we see a wide range of presentations. Commonly there is an exaggerated response to hot and cold, but the key here is that this response lingers for some time. It’s hard to say exactly how long it has to linger to be considered irreversible, so here I’ll have to take some licence and say that a pain that lingers for a number of minutes after stimulus is not a healthy pulp. There is a good biological explanation for this lingering pain but I’ll go through that with you in the diagnosis episode. Sigurdsson tells us to be careful when interpreting this symptom as if you put an intense stimulus even on a healthy pulp the resulting pain will linger somewhat.

Another indicator that we’re dealing with an irreversibly inflamed pulp is where the pain has been severe, and the longer it has been present, the more likely it is to be irreversible in nature (Bender 2000). When pulp testing this tooth, there will often be an exaggerated response and the dull lingering pain experienced before will be induced by the procedure. Tenderness to percussion is often also present. The level of inflammation in these teeth will often lead to neurogenic pain and nerve sprouting which results in inflammation in the periapical tissues. This can occur well before the pulp starts to die and therefore even in a vital, inflamed pulp, tenderness to percussion is often present.

Probably the biggest indicator of an irreversibly inflamed pulp is spontaneous pain. So the patient will report moderate to severe pain that suddenly occurs, and often remains as a dull lingering pain for minutes or hours. They might even report being woken by the pain. I often find that patients with irreversible pulpitis have resorted to over the counter painkillers such as ibuprofen and report that these drugs will help relieve the pain until they wear off of course.
There is an excellent article published by Timothy Miles, who is a neurophysiologist who had previously trained as a dentist (Miles 1993). In the article he explains in detail his not only the physiological response he personally experienced due to a dying pulp, but also the emotional response. It has a grand total of 6 references which it probably could have done without and yet was published in the Journal of Endodontics. It’s probably essential reading for any dentist who has never experienced toothache, and I’ll put the reference in the show notes. If you ever sit the examinations for the Royal Australasian College of Dental Surgeons, then I believe he still lectures on the primary orientation course, and you can have the pleasure of hearing the story in person.

Our final diagnosis is pulpal necrosis. This covers both partial and complete necrosis of the pulp. Consider the progression from reversible pulpitis to irreversible pulpitis and on to pulpal necrosis. At some point the inflammation builds to a level where the vital tissue dies. This necrosis over time then spreads throughout the whole pulp space. There isn’t a lot of information on exactly how quickly the process occurs and I imagine that there is a great variation in the length of that process, but when it comes down to it, some form of Root canal therapy is required.

Most of the time when a pulp is necrotic, it will also be infected. There are a few situations where a pulp can necrose and remain uninfected, mostly after physical trauma to a tooth, but on the whole, a dead pulp lacks a blood supply and therefore lacks the ability to protect itself against microorganisms. These bugs will get into the pulp space through cracks or infected dentine, or possible exposed dentinal tubules and rapidly take over the necrotic space.

When dealing with a patient presenting in pain, there is a strong correlation between the following factors and pulpal necrosis. First is a history of moderate to severe pain. Second is tenderness to percussion, third is a history of spontaneous pain and fourth is a negative pulp test. Seltzer and Bender conducted some of the most useful research we have on this topic way back in 1963 (Seltzer et al. 1963). Basically, they examined patients who presented with pain and then the tooth was extracted and examined histologically. There is a nice summary of their findings in a paper published by IB Bender in 2000 in the JOE which you should read if you are a postgraduate student (Bender 2000).

It’s important to note here though that very often the progression from vital to necrotic pulp is painless, or the level of pain is minimal and no help is sought for the problem. Often patients are completely unaware that they have a chronic infection in their jaw. Two studies reported this happening in 26-60% of cases. (BARBAKOW ET AL. 1981, BENDER 200) In my experience these teeth may be completely asymptomatic. They can be slightly tender to percussion but often don’t even present with this. Usually, they are identified due to a lucency on a PA or OPG Xray. The key for these though is that they will not respond to a pulp test and can be entered without local anaesthetic.

OK, I think that’s enough for this episode. Next episode we’ll be discussing the various periapical diagnoses that we can make. In the meantime, I recommend you have a look at the references, and next time and every time you work on a tooth, have a think about what diagnosis you have for the pulp. If you’re placing large restoration or crown think about whether you’re completely confident of your diagnosis before doing the work.

Also, if you’ve got a comment, or you disagree with something that was said here, please keep it nice, but I’d love you to go to the blog and leave a comment.

Clinical Tips, Endodontic LA, General Updates

The Endospot Episode 1 | Preventing Local Anesthetic Failure in Endodontics

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Problems with Local Anaesthesia?

In this, post, we discuss practical techniques for preventing failure of LA for endodontics, especially when dealing with irreversible pulpitis. Listren to the audio file below:

Preventing Local Anesthetic Failure in Endodontics

For the new and updated podcast, go to the podcast page.

References referred to in this podcast:

Meta Analyisis on Artciaine V lidocaine:
KATYAL V. 2010. The efficacy and safety of articaine versus lignocaine in dental treatments: A meta-analysis.  J dent: 38: 307-317

Intraossesous Injections:
READER A, NUSSTEIN J. 2002. Local anesthesia for endodontic pain. Endodontic Topics: 3: 14–30

Use of Articaine for buccal infiltration:
MATTHEWS R, DRUM M, READER A, NUSSTEIN J, BECK M. 2009. Articaine for Supplemental Buccal Mandibular Infiltration Anesthesia in Patients with Irreversible Pulpitis When the Inferior Alveolar Nerve Block Fails. J Endod: 35(3): 343-346
AGGARWAL V, JAIN A, KABI D. 2009. Anesthetic Efficacy of Supplemental Buccal and Lingual Infiltrations of Articaine and Lidocaine after an Inferior Alveolar Nerve Block in Patients with Irreversible Pulpitis. J Endod: 35(7). 925-929

PSA Block Link –
Information on the PSA Nerve: http://en.wikipedia.org/wiki/Posterior_superior_alveolar_nerve
Video: You Tube Video on the PSA Nerve Block

Show Transcript:
Welcome to the Endospot Episode 1.
In today’s podcast I’ll be discussing my techniques for managing local anaesthetic failure and specifically how to manage teeth diagnosed with irreversible pulpitis.

On the site we have references and show notes for this episode, so head to www.endospot.com and remember you can sign up and receive the Endospot blog posts directly into your inbox.

So let’s get on with the podcast.

On the topic of failed LA, it’s important to recognise situations where complete anaesthesia is likely to be difficult to obtain. In general terms, the mandibular molar teeth are the most difficult to anaesthetise, and this is where you’re likely suffer the most failures.
The issue with mandibular molar teeth is compounded where we have an irreversible pulpitis. The inflamed pulp is always going to more difficult to anaesthetise. You’ll often have a slightly distressed patient in this situation, so it’s important to get it as right the first time. Once you’ve begun treatment on an anxious patient and they’ve suffered a level of pain due to failed LA, it can be quite difficult to win back their faith in you.

Now it’s certainly my experience that where the pulpitis has been long standing and is becoming more and more acute, this will be the most difficult tooth to get numb. A good example might be a case of cracked tooth syndrome where the tooth has been manageably painful to bite for months, but is now becoming more and more sensitive to thermal stimuli and spontaneous pain has begun to occur. I suggest you hit these ones with every trick in the book.

Abscessed teeth don’t normally represent a huge problem for anaesthesia in terms of being able to instrument the canals, but sometimes the surrounding tissues will be difficult to anesthetise and the patient will still respond to things like pressure. One caveat here though. Just because you’ve made a diagnosis of abscess, don’t assume that there is no vital tissue in the canal. Some vital tissue can remain in the canal even in the presence of pus and swelling, and attempting to debride this canal can result in high levels of pain. So, I always assume the worst when dealing with patients in pain and provide complete anaesthesia

In my previous last post, I covered the reasons for LA failure in pulpitis cases, so if you want more details and references, go to the blog post at endospot.com and review those there. The main points that are worth considering though, are that a numb lip after IANB does not necessarily equal pulpal anaesthesia. This is the case even when dealing with an uninflamed pulp, but is especially so where you are dealing with an inflamed pulp. Research generally tells us that if we are dealing with an irreversible pulpitis and we give an IAN block which is apparently successful as the patient’s lip is numb, then , we’ll still only be successful in completely anaesthetising the tooth nerve about 55% of the time. Now, that’s obviously unacceptable, so we’re going to need to use supplementary LA for these cases.

The second point to note is that LA takes time to work. Again, research tells us that in 19-27% of cases, complete anaesthesia doesn’t occur until 15 minutes after the injection. So, next time your LA fails, it may simply be that the LA hasn’t had time to work. Supplemental techniques such as the PDL and intraosseous injection tend to work much faster than IADB, and should have you removing that inflamed pulp much faster.

As to which type of LA you should use, this will to a certain extent come down to personal preference, and obviously the medical profile of the patient. In general terms though, I would recommend using articaine. There’s been plenty of research in recent years devoted to articaine with some conflicting results. But, a recent meta-analysis concluded that articaine was more effective than lidocaine for anaesthetising mandibular molars. The article is by an Australian and so refers to lignocaine, but I assure you it’s the same drug.
So now I’ll go through my standard technique for dealing with hot pulps. Wherever not contraindicated, I’ll prescribe ibuprofen as soon as possible prior to treatment. There is some evidence that this alone may assist in achieving complete anaesthesia in inflamed pulps, but even if it doesn’t let’s remember that  these patients are presenting with pain, and therefore are at risk for post-operative pain. In this case, Ibuprofen (unless contraindicated) would be part of my pain management regime anyway.

When faced with a hot mandibular molar, I’ll start with a regular IAN Block and follow this with a buccal and lingual infiltration. The buccal infiltration ensures that a rubber dam clamp can be placed comfortably, but more importantly, I think that combining the block of the nerve with the local infiltration simply means that we have two sites along the nerve trunk that are blocked and this will lead to improved anaesthesia. This makes a lot of sense to me and is backed up by a number of studies which show that in cases of irreversible pulpitis, the infiltration significantly improves success rates. These studies have also shown the improved effect of articaine over lidocaine for this purpose.

After the buccal and lingual infiltrations, we take a minute’s break to ensure they are active and then move onto the PDL injection. There are a number of specialised equipment kits for PDL injections available, but they can be done successfully with a standard syringe. The first step is to bend the needle with some haemostats so that you are able to place pressure on the needle as it is forced into the PDL. The needle is inserted into the gingival crevice and with the bevel facing away from the root surface. Press hard and inject for 10s. There should be back pressure, if there isn’t, then the solutions wont’ be forced through the cribriform plate into the cancellous space and won’t be effective. I’ll perform the PDL injection at the four corners of the tooth.

The PDL injection is not really a PDL injection. I mentioned that the solution is forced into the cancellous space and as such It’s really an intraosseous injection. Therefore, there may be cardiovascular effects and this should be taken into account when selecting the LA. If an adrenaline containing LA is contraindicated, then you can use a non-adrenaline containing LA for this purpose.

The rate of onset of a PDL injection is fast, but the duration is short compared to IAN block, so at this point I’ll get a rubber dam on to the tooth and start access almost immediately. Once the pulp space is penetrated, and if vital tissue is found, then I’ll perform an intrapulpal injection. This injection relies on backpressure, so can only be used if only a small perforation is made into the pulp chamber.
For maxillary molars, I’ll start with a buccal and palatal infiltration, injecting most of the cartridge bucally. The palatal injection allows the rubber dam clamp to be placed comfortably, but might also anaesthetise the palatal root where a buccal infiltration could fail. After this, I perform a posterior superior alveolar block. I’ve placed a link in the show notes so you can have a look at this technique if you’re not familiar with it. I think that in the same way that the buccal infiltration in the mandible works with the IAN block to improve anaesthesia by blocking two points along the nerve trunk, combining a SPAN block with infiltrations should do the same. I then move onto PDL injections and perform an intrapulpal once the pulp chamber is entered.

The vast majority of cases, these procedures will allow you to enter the pulp space and remove most of the inflamed pulp tissue. If you are unable to even enter the pulp space, then your only real option is to perform an intraosseous injection. This does require specialised equipment. A good review of this technique can be found in the endodontic topics article referred to in the show notes. If you are comfortable with intraosseous injections, then these can be substituted for the PDL injections in the standard routine. My practical experience though is that if you follow the techniques described you really should have a very high level of success.

One point to note though is that infiltrations and PDL injections won’t make up for a failed IANB, so if there is any doubt that the block has been successful, then it’s worth repeating the block. If you want to be certain, it might make sense for you to perform the block and then wait until there are significant signs of lip and tongue anaesthesia before going onto the infiltrations and PDL injections. Obviously these injections can cause lip numbness also and so can mask a failed IAN block.

After entering the pulp chamber, you may find that you can remove some or most of the pulp tissue but attempting to pass a file to length in the canal elicits pain. In this case, I don’t see any reason to persist as the process of removing the bulk of the pulp tissue will result in resolution of the patient’s symptoms. I’ll dress the tooth with a corticosteroid containing dressing such as ledermix or odontopaste and send the patient home with assurances that the symptoms will resolve and the tooth will be easier to treat at the subsequent visit as the inflammation in the pulp will have resolved greatly. If you persist when complete anaesthesia isn’t achieved, you’re likely to put your patient and yourself through a lot of unnecessary pain, and the patient will be sure to be more anxious and will probably be one of those people that for the rest of their life tells their friends how agonising root canal treatment is.

So that is my routine for dealing with hot pulps. I’m aware there will be many different techniques out there and I’d love to hear some feedback. For those listeners who are just beginning their career, I’d recommend getting into the habit of using block and infiltration anaesthesia for all endodontic cases, and adding the PDL and intrapulpal injections when required.

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Failed Anaesthesia
Clinical Tips, Endodontic LA, General Updates

The Endospot Guide to Understanding Local Anesthetic Failure

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Failed Anaesthesia

The patient with a hot pulp spells trouble when it come to anaesthesia

Every dentist has had the unfortunate experience of being unable to achieve anesthesia, especially when dealing with an irreversibly inflamed dental pulp. You find yourself filled with self-doubt and feeling helpless, especially where the patient has presented in pain and you feel you need to remove that inflamed pulp!

But, LA failure is a bit more complex than I think most of us realise. Most of the information that follows is taken from an excellent review of the topic by Ken Hargreaves & Karl Keiser, so grab that if you want in depth analysis (Hargreaves et al. 2002). I’m going to cover what I think is important for most of us.


There are a number of reasons for LA Failure, but the first thing I think we should consider is this:
1.    Complete pulpal anesthesia is not achieved 100% of the time in normal pulps;
2.    Complete pulpal anesthesia has a slower onset than most of us would expect .

The simple fact is that a well administered inferior alveolar nerve block does not provide complete pulpal anesthesia 100% of the time. Bou Dagher conducted IAN block on 30 subjects and achieved 100 numbness of the lip, but only 50-75% of these patients demonstrated complete molar anesthesia when measured by electric pulp tester (Bou Dagher 1997). For most dentists, the majority of LA is given for restorative procedures, and often, anesthesia may be sufficient to prepare a cavity for restoration without problem. I think this probably lulls us into a false sense of security as to how successful our techniques are.

The next point to make is that the onset of complete pulpal Anesthesia takes time, most commonly up to 15 minutes. It’s fair to say that we would often not wait that long before attempting a procedure. In studies, onset was longer than 15 minutes in 19-27% of cases and longer than 30 minutes in 8% of cases. Complete lip numbness occurred much faster, within 5-7 minutes.
On this topic, It has been shown that injecting a second cartridge of LA injected after an apparently successful IAN block does not improve the onset time (Vreeland et al. 1989). In those situations where we have an apparently failed IAN block (despite profound lip numbness), and we inject a second cartridge and we then achieve anesthesia, it’s probably just that we’ve allowed more time for the initial injection to work.

The key points here are:
1.    Lip numbness does not confirm pulpal anesthesia;
2.    Onset takes time
3.    IAN blocks are unreliable when it comes to achieving pulpal anesthesia even in uninflamed pulps

What happens when we have an inflamed pulp? Things are even more dire. Two studies that evaluated pulpal anesthesia after IAN where the pulp was inflamed reported an average of only 55%, despite 100% numbness of the lip (Cohen et al. 1993, Nusstein et al. 1998).
Theories on failure of LA

It is my recollection from reading textbooks at dental school that IAN blocks failed because of the increased pH in the region of an inflamed pulp which prevented dissociation from the acid form of the LA to the base form. The base form was then unable to diffuse across the cell membrane in order to block the sodium channel. This never sat well with me because I couldn’t understand why inflammation at the site of a lower canine tooth would affect the dissociation of an LA molecule deposited near the mandibular foramen.  The truth is that while this theory remains a possibility, it is unlikely that this is a real explanation for the failure of LA. Firstly, the change in pH in inflamed tissues is not large, and inflamed tissues possess a greater buffering ability than normal tissues. Secondly, any change in tissue pH is also likely to be very localised (Punnia-Moorthy, 1988).  So, given our clinical results of reduced anesthesia of mandibular teeth after IAN blocks, we can consider this explanation to have some, but probably limited clinical relevance.

The second reason I recall from dental school for failure of IAN blocks was accessory innervation from the myelohyoid nerve. The lingual, buccal and transverse cervical nerve have also been implicated, however there is limited evidence for these mechanisms. Potentially, however, they could contribute to LA failure.

A third possible method mentioned in the literature is resistance or tachyphylaxis. According to Kenneth Hargreaves (who by the way is an extraordinary speaker and you should make an effort to see him speak) there is little evidence for this, and I think we should be happy to take his word for it.

The next possible mechanism of failure of LA is through the increased blood flow that occurs in inflamed tissues. This could potentially result in increased removal of LA from a site. Again, this is likely to be a localised issue and should not affect regional block anesthesia. Theoretically, increasing the concentration of vasoconstrictor in LA should counteract this mode of failure, but to date there have been few studies (I couldn’t find any) comparing different concentrations of adrenaline in pulpitis cases. In normal pulps, the results have been a little contradictory with some studies showing equivalent results for different concentrations of adrenaline (Epinephrine). One study however has shown a dose dependant effect on onset and duration of infiltration anesthesia with 2% lidocaine and 1:200000, 1:100000 and 1:50000 adrenaline.

OK, now we get into the important stuff – the real reasons why we have trouble convincing inflamed pulps to be quite while we operate on them. In the presence of inflammation, a number of changes occur to the actual nociceptors, or pain receptors. The receptors become both activated and sensitized. For example, when bradykinin is released, this will cause the neuron to fire, causing pain.
Sensitization of nociceptors occurs due to other inflammatory mediators, such as prostaglandin E2 (PGE2).  This results in the threshold for the nerve firing reducing. The result is that the nociceptors will activate with a much milder stimulus. It has been shown that both activation and sensitization result in a level of resistance to anesthetics (Rood et al. 1981).

Another thing that occurs in response to inflammation that might surprise you is nerve sprouting. Inflammatory mediators actually cause nerves to grow into the inflamed are and this has been shown to happen in human dental pulp (Byers et al. 1999). This simply means there are far more nociceptors to block and results in an increased receptive field. Check out work by Byers for some great microscope images showing the vast increase in nociceptors in inflamed rat pulps.

Inflammation also causes an increase in the production of proteins by nociceptors, such as substance P and calcitonin gene related peptide. These proteins play a role in the regulation of inflammation in the pulp, and may have some role to play in LA failure.
Another interesting concept relates to a specific type of sodium channel on neurons which is resistant to tetrodotoxin (TTX), funnily enough called the TTX-resistant sodium channel. These channels are less sensitive to lidocaine, about one quarter as sensitive as normal sodium channels and are present on human pulp nociceptors under normal conditions. Expose a nerve to PGE2, and their activity doubles (gold et al. 1996).  Therefore, this represents a mechanism whereby LA could fail. My thoughts are that the prostaglandin might only operate on these channels locally, and this theory might suffer from the same argument as the pH change theory, that is that it might only occur locally, so shouldn’t necessarily effect block anesthesia.

Central Nervous System (CNS) Sensitization may contribute to LA failure. When inflammation and pain occur for an extended period of time, this results in an increased excitability of the CNS. In basic terms this means that a lesser stimulus will result in a higher level of pain being experienced. Central sensitization is a blog post all by itself and as an endodontists, we are particularly careful of pain control in any patient who presents with a history of chronic pain. Hargreaves feels that the excited CNS may be responsible for otherwise innocuous stimulus presenting as anesthetic failure. For example, we may treat a patient who feels some minor discomfort but tolerates it for the procedure. In a patient who has been subject to central sensitisation, the discomfort may present as pain.

So there you go, and I hope this makes you feel a bit better the next time you can’t anaesthetize a “hot” pulp. It’s probably a bit more complicated than you previously thought, and it’s probably a bit less your fault than you previously felt. I’ll be discussing my methods for dealing with LA failure and inflamed pulps in a separate blog post.

BYERS MR, NARHI MVO. 1999. Dental injury models: Experimental tools for understanding neuro-inflammatory interactions and polymodal nociceptor functions. Crit Rev Oral Biol
Medical . 104–139.

BOU DAGHER F, YARED G, MACHTOU P. 1997. An evaluation of 2% lidocaine with different concentrations of epinephrine for inferior alveolar nerve block. J Endod. 23: 178–180.

COHEN HP, CHA BY, SPANGBERG LS. 1993. Endodontic anesthesia in mandibular molars: a clinical study. J Endod. 19: 370–373.
GOLD M, REICHLING D, SHUSTER M, LEVINE JD. 1996. Hyperalgesic agents increase a tetrodotoxin-resistant Na¹ current in nociceptors. Proc Nat Acad Sci: 93: 1108.

KENNETH M. HARGREAVES & KARL KEISER. 2002. Local anesthetic failure in endodontics:
Mechanisms and Management. Endodontic Topics 2002, 1, 26–39

KNOLL-KOHLER E, FORTSCH G. 1992. Pulpal anesthesia dependent on epinephrine dose in 2% lidocaine. Oral Surg Oral Med Oral Pathol. 73: 537–540.

NUSSTEIN J, READER A, NIST R, BECK M, MEYERS WJ. 1998. Anesthetic efficacy of the supplemental intraosseous injection of 2% lidocaine with 1: 100,000 epinephrine in irreversible pulpitis. J Endod. 24: 487–491.

PUNNIA-MOORTHY A. 1988. Buffering capacity of normal and inflamed tissues following the injection of local anesthetic solutions. Br J Anaesth. 6: 154–159.

ROOD JP, PATEROMICHELAKIS S. 1981. Inflammation and peripheral nerve sensitisation. Br J Oral Surg 19: 67–72.

VREELAND D, READER A, BECK M, MEYERS W, WEAVER J .1989. An evaluation of volumes and concentrations of lidocaine in human inferior alveolar nerve block. J Endod 1989: 15: 6–
12.

Clinical Tips, Endodontic Preparation Techniques, Endodontic Re-treatment

How to Simply Remove GP for Endodontic Retreatment

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Endodontic retreatment, remove GP

How are you going to remove the GP from this tooth?

Below is a video of a demonstration I gave at the Jiao Tong University Dental School in Shanghai. I was demonstrating a method for removal of GP from treated canals. The method that I describe is only one of many methods, but I think it is a good way to begin re-treating. Please watch the video and share your thoughts:

httpv://www.youtube.com/watch?v=D5SeDNOusV4

Clinical Tips, Endodontic Radiography

How to Improve Your Endodontics in 30 Seconds Flat

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Endodontic radiography

Same Tooth, Very Different Images. Taking an Additional Radiograph Provides A Whole Lot More Information

A simple way to improve your endodontics is to simply take two radiographs where you might previously take one. I routinely take two radiographs with differing horizontal angulations when treating potentially multi-rooted teeth (basically everything apart from maxillary incisors) unless there is a reason not to. When dealing with root canal anatomy we’re dealing with a very three dimensional issue, yet a lot of what we plan and assess our treatment on is two dimensionally based. There are so many reasons to take additional views, and in the long run it can make your life easier and improve your endodontics.

The process of taking an additional radiograph adds 30 seconds or less to the radiograph time. You already have the rubber dam folded back and the x-ray tube in place. Developing two radiographs instead of one does not take any longer (especially with digital). More importantly though, you simply have far more information to work with. Additional canals that might not be visible on a standard radiograph will often be visible on a mesial tube shifted radiograph. Where roots that lie close together have differing lengths, this may not be obvious with a radiograph that superimposes the two roots.  Similarly, two radiographs will allow you to determine more accurately which root a lesion is associated with.

Taking an additional radiograph when measuring working lengths is essential, as often files will superimpose on a radiograph and thus, the information on where the file ends relative to the root tip can be lost. This applies for obturation radiographs also.

The image on the right appears to show one distal canal, but the mesial tube shift reveals two separate canals.

The image on the right appears to show one distal canal, but the mesial tube shift reveals two separate canals.

Let’s not also forget that occasionally, we may take a radiograph that is not of diagnostic value. For example when the apex of the tooth in question has been missed on the radiograph. The second radiograph may have sufficient information to save you having to re-take the radiographs.

The negative aspect of additional radiographs is the increased radiation exposure for the patient. Obviously, it is important to weigh up the benefits versus risks of taking the additional radiograph, and in my opinion, the potential to improve the endodontic outcome makes the taking of these radiographs imperative.

I was recently sent an x-ray by a referrer who had root filled a vital upper pre-molar, however the patient complained of ongoing discomfort associated with the tooth. The radiograph showed a well condensed root filling that appeared slightly off centre from the middle of the canal. I advised taking a mesial shift of the tooth and the presence of a second canal was obvious. After treatment of the missed palatal canal, the tooth was asymptomatic and ready for restoration. It would have saved quite some trouble, as well as time had the mesial tube shift radiograph been taken prior to, and during treatment.

Untreated Canal

This tooth remained symptomatic after treatment. Note the obturated canal appears slightly off-centre.

Untreated Palatal Canal

A radiograph taken with a mesial tube shift clearly shows a palatal canal which has not been prepared or filled.

Resolution of symptoms

Upon cleaning and shaping of the palatal canal, the symptoms resolved.

I’d love to hear reader’s thoughts on this topic, or case examples where tube shift radiographs have assisted to improve the quality of endodontic treatment. Please leave a comment with your thoughts.

Aetiology of Apical Periodontitis, Microbiology, Study Guides

The Lazy Man’s Guide to Persistent Apical Periodontitis

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Poorly Prepared, Obturated and Missed Canals All Contribute to Persistent Apical Periodontitis

Persistent Apical Periodontitis (AP) refers to AP that is associated with a tooth that has had root canal therapy (RCT).  As with primary AP, bacteria are the most common cause of the inflammatory response (Sudqvist et al. 1998). Previously there has been a large body of evidence that persistent infections are commonly composed of a single species, however recent evidence points to the presence of a mixed biofilm (Siqueira et al. 2009a, Chavez de Paz 2007).”]

There are also non microbial causes of AP, including foreign body reactions, cystic formation, endogenous cholesterol crystals and scar formation. These will be discussed later.

The microbes that cause persistent AP are more commonly located intraradicularly (inside the root). Occasionally, these microbes will also be located extraradicularly. We’ll discuss the far more common intraradicular microbes first.

Intraradicular Microbes

The key study for referencing the presence of microbes within the root in cases of persistent AP is Nair et al. 1990a. When considering the cause of the persistent infection, consider that the microbes were either present prior to RCT being initiated (primary infection ) or they entered during or after treatment (secondary infection) (Siquiera 2008).  When thinking about those microbes that have survived from the primary infection, consider how they might have achieved this. They may have been resistant to the chemicals used in the disinfection process (e. feacalis for example has some mechanisms to survive calcium hydroxide), or they may have been located in a portion of the canal that was not instruments nor cleaned via chemical means.

When considering the secondary infection, these microbes may have gained access to the canal during treatment or after treatment. Think about this also. They may have been carried into the canal on a contaminated instrument or perhaps a leaking rubber dam may have allowed saliva to contaminate the root canal. Alternatively, a poorly placed temporary restoration may have allowed leakage into the root canal system in between visits. If caries have not been completely removed, or a previous restoration which is subject to microleakage is left in place, then this can also be a source of secondary infection. Alternatively, these microbes may have entered a previously clean  root canal system after the completion of RCT. This could be due to a leaking restoration, or through caries or a crack in the tooth. It’s important to understand the microbial nature of AP, and to have this foremost in our minds when undertaking treatment.

Which microbes are present in secondary in persistent AP?

When we look at the composition of the infection in AP, we find a significantly different microflora than that found in primary infections (Figdor et al. 2007, Molander et al. 1998). Generally in persistent AP, there are only 1-5 species.  These are predominantly gram-positive and there is an equal amount of obligate and facultative anaerobes. (Figdor et al. 2007, Sundqvist et al. 1998, Siqueira et al. 2009b). Due to the fact that obligate anaerobes are easier to kill, it may be that facultative anaerobes are more likely to persist within the root canal system after treatment.

E. Faecalis & c.albicans

Enterococcus faecalis is an opportunist pathogen which is implicated in many general surgery post-operative infections.  It has been identified as an opportunistic pathogen in persistent AP in a number of studies (Sundqvist et al. 1998, Sundqvist et al. 2003, Molander et al. 1998). This particular microbe has been studies extensively. It possesses a “proton pump” on its cell membrane which allows it to regulate its internal pH. This means that it is resistant to calcium hydroxide and this may be one of the ways that it survives and becomes implicated in persistent infections. It is also able to survive by itself and without nutrition for long periods of time. It is rarely found in untreated canals. Candida albicans (a fungus) is also found more commonly in persistent infections than in primary infections. (Sundqvist et al. 1998, Nair et al. 1990a, Waltimo et al. 2004)

Extraradicular Infections

Occasionally, we may find a situation where microbes establish themselves outside the root canal system. The microbes may establish themselves on the external root surface in a biofilm, in association with infected dentine chips that have been displaced into the periapical region, or within a periapical cyst (Abbott 2004, Nair 2008). These microbes must be able to withstand the body’s attempts to kill them and it is likely that biofilm formation allows this (Noiri et al. 2002). Similarly in the periapical cyst situation, it is the cyst itself that protects the microbe from the immune response.

In particular, two microbes have been implicated in extraradicular infections. These are Actonomyces spp. And Proprionibacterium proprionicus (Siqueira 2002). These microbes are able to form cohesive colonies within an extracellular matrix. This helps them to avoid phagocytosis, and so continue to survive and invoke the immune response.

Non-microbial causes of AP – Cysts, Foreign Body Reactions and Cholesterol Crystals

In some cases, AP may not be “maintained” by microorganisms. I say “maintained”, because often the AP is initially caused by microbes, and after endodontic treatment, one of the following factors takes over, maintaining the immune response and thus, AP.

Periapical cysts are an interesting topic. There are a range of studies that attempt to measure the incidence of periapical cysts in examined PA lesions. In simple terms, the lesion is biopsied and then examined under a microscope. If an epithelium lined sack is found, then the lesion is designated a cyst. But…… In 1980 Simon published a paper which included serial sectioning of periapical lesions (Simon, 1980). What he found was that some lesions that appeared as cysts on one section, appeared differently on other sections. Thus, it was deemed that the majority of studies (which don’t use serial sectioning) relating to the prevalence of cysts were subject to error. If you just take a random slice, the effect in two dimensions may be that of a cyst, when in reality the full three dimensional structure of the cyst does not exist. Nair repeated this study 16 years later and confirmed Simon’s findings (Nair, 1996).

Nair studied far more lesions than Simon, and found that 15% could be classified as cysts (including both true and pocket varieties). This is probably the best figure to be quoting. Other studies report figures from 5-55%, but they failed to use serial sections. It is also important to realize that a great number a large proportion of abcesses and granulomas will also contain epithelium. In Nair’s study, 52% of the lesions were epithelialised, but only 15% were cysts.  It is likely that the inflammatory process results in the proliferation of this epithelium, and over time, the epithelium develops into a cyst.

Through both of these studies, Simon and Nair found two distinct types of cysts. Simon called them true cysts, those with a complete epithelial lining, and bay cysts, those whereby the lining is attached to the root surface and the contents of the root canal contiguous with the contents of the cyst. Nair referred to these as true cysts and pocket cysts (equivalent to Simon’s Bay cyst).

Nair contends that these two types of cysts are quite different (Nair 2008). He feels that the true cyst is self sustaining, and will remain independent of efforts to remove the microorganisms from the root canal system. The pocket cyst, on the other hand is being sustained by the microbes within the canal system. Removal of the microbes which are maintaining the inflammatory response may allow the pocket cyst to heal. In reality, it will be very difficult to prove or disprove this theory, but one could say that it makes sense.

Foreign body reactions

When exogenous materials are located in the periapical region, they can induce and maintain an inflammatory response which may be asymptomatic, but will be seen as a radiolucency. Materials may be GP, amalgam, sealants, Calcium hydroxide or cellulose fibres such as those contained in paper points (Nair et al. 1990b).

In practice these lesions are rarely seen but have been reported in the literature, so it is important to understand that this mechanism for the maintenance of AP does exist. It also reminds us to be careful when using paper points not to extend them into the periapical areas, as human cells cannot degrade cellulose and leaving fibres behind may result in a foreign body reaction.

Gutta percha may also induce a foreign body reaction, especially in fine particles (Sjögren et al. 1995). Overextended GP may, as a result cause delayed healing of periapical tissues.

Cholesterol Crystals

Cholesterol crystals are also seen in AP, and are probably released by disintegrating erythrocytes, lymphocytes, macrophages, plasma cells and from circulating plasma lipids (Nair 1999). These collections of cholesterol are referred to as cholesterol clefts and induce a reaction similar to a foreign body reaction as the macrophages and giant cells are unable to remove the cholesterol. Again, this may result in a non-healing lesion, despite well completed endodontic treatment.

The Endospot Easy Study Guide to Persistent AP

  1. Persistent AP is most commonly caused by microbes remaining within the root canal system (sundqvist et al. 1998)
  2. It appears that a mixed biofilm may be responsible, contrary to the previous belief that usually only one microbe was responsible.  (Chavez de Paz 2007)
  3. The microbes are either (Siquiera 2008):
    1. Primary – remained within the canal from the initial infection
    2. Secondary – entered during or after treatment
  4. Significantly different flora to primary AP (Molander et al. 1998)
    1. 1-5 species per canal
    2. predominantly gram positive
    3. equal number of obligate and facultative anaerobes
  5. E. faecalis – opportunist pathogen which has been identified more commonly in persistent AP (Sundqvist 1998)
    1. Posesses a “proton pump” which allows it to survive in high pH (i.e. can survive calcium hydroxide)
    2. Can survive in mono-infection
    3. can survive long periods of low/no nutrition
  6. Candida Albicans also found more commonly in persistent infections than in primary (Waltimo et al. 2004)
  7. Exraradicular infections can occur in biofilm on the root tip (Noiri 2002), or in the PA area itself (Siquiera 2002)
    1. Proprionibactrium proprionicus and Acinomyces species are able to from adhesive colonies in an extracellular matrix in the PA tissues
  8. Non-microbial causes of AP are:
    1. Periapical cysts – 15% of lesions (Nair 1996)
      1. Serial sectioning indicates two types – true cysts and pocket cysts
    2. Foreign Body Reactions
    3. Cholesterol Clefts

References:

ABBOTT, P. V. 2004. Classification, diagnosis and clinical manifestations of apical periodontitis. Endodontic Topics, 30-54.

CHAVEZ DE PAZ, L. E. 2007. Redefining the persistent infection in root canals: possible role of biofilm communities. J Endod, 33, 652-62.

FIGDOR, D. & SUNDQVIST, G. 2007. A big role for the very small–Understanding the endodontic microbial flora. Australian Dental Journal, 52, 38.

MOLANDER, A., REIT, C., DAHLEN, G. & KVIST, T. 1998. Microbiological status of root-filled teeth with apical periodontitis. Int Endod J, 31, 1-7.

NAIR, P. N., SJÖGREN, U., KREY, G., KAHNBERG, K. E. & SUNDQVIST, G. 1990a. Intraradicular bacteria and fungi in rootfilled, asymptomatic human teeth with therapy-resistant periapical lesions: a long-term light and electron microscopic follow-up study. J Endod, 16, 580-8.

NAIR, P. N., SJÖGREN, U., KREY, G. & SUNDQVIST, G. 1990b. Therapy-resistant foreign body giant cell granuloma at the periapex of a root-filled human tooth. J Endod, 16, 589-95.

NAIR, P. N. 1996. Types and incidence of human periapical lesions obtained with extracted teeth. Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 81, 93-102.

NAIR, P. N. 1999. Cholesterol as an aetiological agent in endodontic failures–a review. Aust Endod J, 25, 19-26.

NAIR, P. N. 2008. Pathobiology of Apical Periodontitis. Essential Endodontology. 2nd ed. Oxford: Blackwell Munksgaard.

NOIRI, Y., EHARA, A., KAWAHARA, T., TAKEMURA, N. & EBISU, S. 2002. Participation of bacterial biofilms in refractory and chronic periapical periodontitis. J Endod, 28, 679-83.

SIMON, J. H. S. 1980. Incidence of periapical cysts in relation to root canal. J Endod, 6, 845-8.

SIQUEIRA, J. F. 2002. Endodontic infections: concepts, paradigms, and perspectives. Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 94, 281-93.

SIQUEIRA, J. 2008. Microbiology of Apical Periodontitis. Essential Endodontology. Oxford: Blackwell Munksgaard.

SIQUEIRA, J. F., JR. & ROCAS, I. N. 2009a. Community as the unit of pathogenicity: an emerging concept as to the microbial pathogenesis of apical periodontitis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 107, 870-8.

SIQUEIRA, J. F. & RÔÇAS, I. N. 2009b. Diversity of endodontic microbiota revisited. Journal of Dental Research, 88, 969-81.

SJÖGREN, U., SUNDQVIST, G. & NAIR, P. N. 1995. Tissue reaction to gutta-percha particles of various sizes when implanted subcutaneously in guinea pigs. European Journal of Oral Sciences, 103, 313-21.

SUNDQVIST, G. & FIGDOR, D. 2003. Life as an endodontic pathogen. Endodontic Topics, 6, 3-28.

SUNDQVIST, G., FIGDOR, D., PERSSON, S. & SJÖGREN, U. 1998. Microbiologic analysis of teeth with failed endodontic treatment and the outcome of conservative re-treatment. Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 85, 86-93.

WALTIMO, T. M. T., HAAPASALO, M., ZEHNDER, M. & MEYER, J. 2004. Clinical aspects related to endodontic yeast infections. Endodontic Topics, 66-78.

Aetiology of Apical Periodontitis, Microbiology, Study Guides

The Lazy Man’s Guide to the Microbial Causes of Primary Apical Periodontitis

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R1This is a dry topic, so we’ll try to cover it as simply as possible. If you just want the outline, check out the study guide at the end of the blog post.

So Microorganisms cause Apical Periodontitis. How do they get into the tooth?

Primary apical periodontitis (AP) occurs when microorganisms (let’s call them bugs) enter the pulp chamber and colonise the pulp tissue. The bugs enter the pulp chamber through a variety of routes such as carious lesions, cracks, traumatic exposure of the pulp and due to dental procedures such as cavity preparation (Nair 1997). As mentioned in the previous post on the aetiology of AP, there is plenty of evidence of bugs being found in teeth that have apparently intact crowns (Bergenholtz 1974). These bugs gain access through accessory canals, exposed dentinal tubules, or microcracks adjacent to the gingival crevice or deep periodontal pockets (Nair 1997). The important message here is that we don’t require an obvious,visible path of entry to the pulp chamber. Bugs can enter through tiny, microscopic spaces such as dentinal tubules.

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Aetiology of Apical Periodontitis, Study Guides

The Lazy Man’s Guide to the Aetiology of Apical Periodontitis

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Lateral Incisor with Apical Periodontitis

What's the Root of This Problem?

Generally, apical periodontitis (AP) is a result of microorganisms entering the root canal system. Of course there are other causes of inflammation in the apical area, such as trauma, traumatic occlusion and foreign body reactions, but if we’re talking about common AP, then “bugs” are the cause (Abbott 2004, Harn et al. 2001).

The classic study on this topic was Kakehashi et al (1965), and this should be the starting point for any essay or exam answer. They took gnotobiotic rats (bacteria free rats) and conventional rats (with bacteria) and exposed the pulps in some teeth. In this study, the germ free rats had food, and in one case a hair forced into their long term exposed pulps, but necrosis did not occur! There was even dentine bridge formation in some cases. Conversely, all the conventional rats developed pulpal necrosis and apical periodontitis. It seems that without bacteria, rat pulps are very hardy indeed.

Sundqvist (1976) was the first to anaerobically culture and taxonomically analyse the constituent bacteria in teeth with necrotic pulps. He concluded that: AP is associated with the presence of bacteria in the root canal and that infected teeth harboured a mixture of bacteria that were predominantly obligate anaerobes (Sundqvist 1976). The significance of obligate anaerobes in endodontic infections are confirmed by a number of independent studies (Bergenholtz 1974, Wittgow et al. 1975, Kantz et al. 1974).

A study by Möller et al. (1981) compared the apical response of inducing pulp necrosis both aseptically and after contamination with indigenous oral flora in monkeys. Basically, they aseptically opened monkey pulps and used a Hedstrom file to mince the pulp. They then closed the pulp chamber so that the necrotic, uninfected tissue was inside, or they infected the tissue with plaque form the monkey’s teeth. In the teeth which contained sterile necrotic tissue, no AP formed. Those with bacteria were associated with AP. At this stage there was still a commonly held belief that necrotic tissue and stagnant tissue contributed to AP formation, but this study helps dispel this theory. In addition, this study showed that there was a variation in the ability of the various bacteria to survive and establish themselves within the root canal environment, and we start to see the concept of bacteria within root canals living in communities, rather than just as one individual strain.

There has been a significant shift away from the concept of one ‘causative pathogen’ and significant evidence exists that specificity seems to be related to the community level as certain species compositions are specifically associated with some forms of apical periodontitis (Siqueira et al. 2009a, Sakamoto et al. 2006). There is a very high level of inter-individual variation of bacterial community profiles, such that 44% of recovered taxa were isolated or detected in only one study (Siqueira et al. 2009b). Microbial ecology differs significantly between different disease forms such as chronic apical periodontitis versus acute apical abscess, suggesting the existence of a pattern associated with each one (Sakamoto et al. 2006, Siqueira et al. 2004). In addition, different magnitudes
of disease, based on intensity of signs and symptoms, may be related to the species composition of the community (Siqueira et al. 2009a).

Siqueira (2002) differentiates the types of endodontic infections into primary, secondary or persistent root canal infections.  Primary infections are those that occur within a root canal system prior to any treatment being applied. A Secondary infection occurs when a root canal (RC) had been treated, and new bacteria enter the RC system.  This can happen when a filling is lost, or micorleakage occurs and the root filling (RF) is exposed to bacteria which then penetrate along the RF. A persistent infection is one that remains in the canal despite treatment. That is the primary infection remains despite RCT.

Primary Apical Periodontitis

This molar exhibits apical periodontitis. It has not been endodontically treated. This is an example of primary apical periodontitis.

Persistant Apical Periodontitis

The first molar exhibits AP associated with both roots. The disease could be persistent (remaining after treatment), or secondary due to coronal microleakage.

An important concept to understand is the formation of biofilms. This relates to the organisation of bacteria into a protected, sessile biofilm comprised of cells embedded in a hydrated exopolysaccharide-complex in microcolonies (Nair 2006). Bacteria in root canals do form biofilms and these are much more difficult for both our immune system and current RCT methods to deal with.

Do you have a reference that should be included in this list, or a comment on what is written? Please share it with our readers.

References:

ABBOTT, P. V. 2004. Classification, diagnosis and clinical manifestations of apical periodontitis. Endodontic Topics, 30-54.

HARN, W. M., CHEN, M. C., CHEN, Y. H., LIU, J. W. & CHUNG, C. H. 2001. Effect of occlusal trauma on healing of
periapical pathoses: report of two cases. Int Endod J, 34, 554-61.

KAKEHASHI, S., STANLEY, H. R. & FITZGERALD, R. J. 1965. The Effects of Surgical Exposures of Dental Pulps in Germ-
Free and Conventional Laboratory Rats. Oral Surg Oral Med Oral Pathol, 20, 340-9.

MÖLLER, A. J., FABRICIUS, L., DAHLÉN, G., OHMAN, A. E. & HEYDEN, G. 1981. Influence on periapical tissues of
indigenous oral bacteria and necrotic pulp tissue in monkeys. Scand J Dent Res, 89, 475-84.

NAIR, P. N. R. 2006. On the causes of persistent apical periodontitis: a review. Int Endod J, 39, 249-81.

SAKAMOTO, M., ROCAS, I. N., SIQUEIRA, J. F., JR. & BENNO, Y. 2006. Molecular analysis of bacteria in asymptomatic and
symptomatic endodontic infections. Oral Microbiol Immunol, 21, 112-22.

SIQUEIRA, J. F. 2002. Endodontic infections: concepts, paradigms, and perspectives. Oral Surg Oral Med Oral Pathol Oral
Radiol Endod, 94, 281-93.

SIQUEIRA, J. F., JR. & ROCAS, I. N. 2009a. Community as the unit of pathogenicity: an emerging concept as to the
microbial pathogenesis of apical periodontitis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 107, 870-8.

SIQUEIRA, J. F. & RÔÇAS, I. N. 2009b. Diversity of endodontic microbiota revisited. Journal of Dental Research, 88, 969-81.

SUNDQVIST G. 1976. Bacteriological studies of necrotic dental pulps. Odontological Dissertations No. 7. Department of Oral Microbiology, Umea° University, Sweden.

The Endospot Easy Study Guide on Aetiology of Apical Periodontitis

  1. Most AP is due to micororganisms within the RC. Other occasional causes include trauma, occlusal trauma, foreign body reaction. (Abbott 2004, Harn et al. 2001)
  2. Exposing pulps in rat teeth lead to AP in conventional rats (bacteria present), but no AP in gnotibiotic rats (no bugs present) (Kakehashi, 1965)
  3. Bacteria in infected necrotic pulps predominately obligate anaerobes. Anaerobic techniques required to culture (Sundqvist thesis, 1976)
  4. Monkey teeth with necrotic, uninfected pulps do not develop AP. If infected, AP develops. Different microorganisms display differing ability to survive in the root canal system. (Mollar, 1981)
  5. It is unlikely one microorganism causes disease in RCs. More likely that a community of mircobes exists. This community varies between people, and between various forms of disease. (Siqueira et al. 2009a, Sakamoto et al. 2006)
  6. Biofilms form in RCs. Biofilms protect bacteria from being destroyed. (Nair 2006)
  7. Primary infections (new in previously unifected RCs), secondary infections (new in previously treated RCs), persistent (remaining after treatment). Siqueira (2002)