CRACKED TEETH: Classification

Cracked teeth can be one of the most complex, confusing and frustrating dental problems we face in every day practice. Its estimated in general practice that at least one patient per week presents with symptoms relating to a cracked or fractured tooth.  Accurate diagnosis and correct management are obviously the crucial steps of successful treatment, but we need to start by defining the various crack types to ensure we are all talking about the same thing at the same time.

It is important for us to have a clear understanding of what is meant by each definition as this allows discussion of the characteristics, prognosis and reliable treatment planning for each crack type. There are many classification systems out there for cracked teeth. Thankfully, the American Association of Endodontists (AAE) has developed a simple classification system for longitudinal tooth fractures based upon their location, direction, and extent. Not everyone out there agrees with this classification, but it’s the best we have and a good starting point when trying to manage.

Craze Lines
Craze lines occur only within enamel. They run parallel to enamel rods and terminate at the DEJ (Bodecker et al. 1951). Craze lines are present in most adult teeth. Various patterns of infraction lines can be seen depending on the direction and location of the impact to enamel, i.e. horizontal, vertical or diverging. Anterior teeth often exhibit vertical craze lines, involving the incisal edge or proximal corners. Posteriorly, craze lines usually cross the marginal ridges and extend along buccal and lingual surfaces.

Fractured Cusp
Fractured cusps occur most frequently in heavily restored teeth, where the marginal ridge is weakened and the affected cusp has insufficient support (Kahler 2008). A fractured cusp involves a complete or incomplete fracture initiated from the crown and extending subgingivally, usually directed both mesiodistally and buccolingually (Rivera & Walton 2008). The fracture usually crosses the marginal ridge, and also tracks down a buccal or lingual groove. It extends to the cervical third of the crown or root.

Fractured Cusp

Cracked Tooth
A cracked tooth is an incomplete longitudinal fracture originating in the crown and extending apically. Often cited as being only in a mesio-distal direction (Rivera & Walton 2008), the literature also reports an significant number of bucco-lingual fracture planes (Seo et al. 2012). It may extend through either or both of the marginal ridges, through the proximal surfaces and onto the root surface. Occlusally, the crack is more centred and apical than a fractured cusp and therefore more likely to cause pulpal and periapical pathosis (Rivera & Walton 2008). A cracked tooth may progress to a split tooth.

Cracked Tooth

Split Tooth
A split tooth is a complete fracture originating in the crown and extending subgingivally, directed most commonly mesiodistally through both marginal ridges and proximal surfaces (Seo et al. 2012). The split root area is often in the middle or apical third and tends towards the lingual. The more centred the crack is on the occlusion, the further apically the split extends. The segments are entirely separate and although it may occur suddenly it may be considered as a continuum from an incompletely cracked tooth (Rivera & Walton 2008).

Split Tooth

Vertical Root Fracture
Vertical root fractures are complete or incomplete fractures initiated from the root (at any level), usually directed buccolingually (Rivera & Walton 2008). Most occur in endodontically-treated teeth although the literature reports occurrences in non-root filled teeth (Yang et al 1995). A VRF may progress coronally and/or apically from the point of origin in any part of the root.

Vertical Root Fracture

Now we’re all on the same page, take a look at the next post in this series: Management of Cracked Teeth for an overview of recommended treatment strategies.

REFERENCES
Bodecker, CF, Gottlieb, B, Orban, B, Robinson, HB, Schour, I,  Sognnaes, RF 1951. Enamel lamellae. Oral Surg Oral Med Oral Pathol, vol. 4, 787-98.
Kahler, W 2008. The cracked tooth conundrum: terminology, classification, diagnosis, and management. American Journal of Dentistry, vol. 21, 275-82.
Rivera, EM,  Walton, RE 2008. Cracking the Cracked Tooth Code: Detection and Treatment of Various Longitudinal Tooth Fractures. Endodontics Colleagues for Excellence, Summer 2008.
Seo DG, Yi YA, Shin SJ, Park JW (2012) Analysis of factors associated with cracked teeth. Journal of Endodontics 38(3), 288-292.
Yang SF, Rivera EM, Walton RE (1995) Vertical root fracture in nonendodontically treated teeth. Journal of Endodontics 21(6), 337-339.

There are a huge number of factors that can affect the outcome of endodontic therapy. Attempting to isolate these individual factors and determine the relative importance of each is something that has proven difficult or impossible in endodontic scientific literature.

Ultimately, our primary aim is to allow our patients to keep their teeth for the rest of their lives. The evidence we have available points to the majority of endodontically treated teeth surviving for long periods of time. (1) Those that are extracted most commonly fail due to non-endodontic reasons. The most common cause of extraction of root filled teeth is crown fracture and periodontal disease.(2)

In terms of crown (and root) fracture, I believe that the conservation of dentine in the crown and in the region a couple of mm just above and below the cervical area is essential to providing ongoing resistance to fracture. In order to have as strong a tooth as possible, we need maximum thickness of tooth structure in this area.

In terms of this, I see that using strategies to limit the amount of tooth structure loss during endodontic access as one of the most important measures that can be taken to ensure the greatest longevity for root filled teeth. Of course, we still need to achieve the aims of endodontic treatment, but this shouldn’t come at the cost of doing irreversible damage to the crown of the tooth that may compromise the tooth’s long term survival.

Endodontic access has been performed which gives good access to the canal orifices. But imagine the thickness of dentine that will remain mesially and distally if a crown was prepared for this tooth. The endodontics can be perfectly performed, but the tooth is compromised due to the excessive loss of tooth structure during access.

This is why we aim to keep access limited and you will sometimes see what appears to be incomplete opening of the pulp chamber. This is by design and allows important tooth structure to be maintained that contributes to the strength and durability of the tooth. Strategies for conserving tooth structure during endodontic access include removing restorations and caries and utilising this space for endodontic access. A good discussion of these strategies, along with examples can be found in articles by Clark and Khademi. (3) (4)

Maintaining the dentine in the peri-cervical region whilst achieving the goals of endodontics give this tooth the best possible chance of survival. Ultrasonics and copious irrigation allow the cleaning of the pulp chamber space and canal spaces without the need for excessive removal of tooth structure.

The restricted access still give good straight line access to the canal orifices. But see how much solid tooth structure remains? It does, however make the job of performing high quality endodontics more difficult. But what’s more important? Us having an easy time of it, or giving the patient the best possible long term outcome?

Limiting tooth destruction becomes a greater challenge when attempting to treat teeth with calcified pulp chambers or canals. When attempting to work through pulp chamber calcification or locate these difficult to find canals it can be easy to remove vitally important dentine.  Assessing the degree of calcification prior to attempting treatment is the key to preventing this iatrogenic damage to teeth. Additionally, if upon access the location of all canals is difficult, it may be better to consider referring at that early stage, rather than to damage the tooth’s long term prognosis in an attempt to locate a difficult to find and prepare canal.

One important aspect of learning to limit the removal of healthy tooth structure for access is that it actually makes endodontic procedures much more difficult (especially in second and third molars) and increases the chances of missing canals, so you need to balance these potential issues with benefits of doing so.

1.    Salehrabi R, Rotstein I. Endodontic treatment outcomes in a large patient population in the USA: An epidemiological study. J Endod. 2004;30(12):846-50.
2.    Vire D. Failure of endodontically treated teeth: classification and evaluation. J Endod. 1991;17:338-42.
3.    Clark D, Khademi J. Modern molar endodontic access and directed dentin conservation. Dent Clin North Am. 2010 Apr;54(2):249-73.
4.    Clark D, Khademi JA. Case studies in modern molar endodontic access and directed dentin conservation. Dent Clin North Am. 2010 Apr;54(2):275-89.

We usually blame bacteria for causing pulpitis but………. This patient complained of severe irreversible pulpitis symptoms for four days, which were only just starting to settle. She couldn’t isolate to either the upper second premolar or molar. Her dentist had extirpated the molar but symptoms hadn’t changed. Pulp testing showed the premolar was also responding negatively.

Take a look at the image below. This presentation is consistent with herpes zoster, commonly referred to as shingles. It is caused by the varicella zoster virus, also responsible for chicken pox. The trigeminal nerve is an unusual location for an outbreak (approximately 1-2% of cases), but when it occurs the virus affects a particular dermatome. If this dermatome also includes teeth, the pulp can also be affected. I can only imagine how painful this would be. Long term follow up is required as multiple teeth may lose vitality.

Notice how the viral outbreak is only affecting the greater palatine nerve distribution. If the nerve innervating the teeth are involved, this can lead to pulpitis and necrosis of the pulp tissues.

Diagnosing this initially may prove difficult, as the lesions on the mucosa don’t show up until a few days after symptoms appear, but some things to look out for include pulpitis symptoms from multiple teeth and a tingling or burning sensation in the distribution of the trigeminal nerve.

Pat Caldwell

In Australia, the average dentist sees at least one patient with cracked tooth syndrome (CTS) per week (Bader et al 1995), so managing this condition is bread and butter work.  When dealing with CTS a good outcome relies on an accurate diagnosis but this can vary from straightforward diagnostic results to complex, inconsistent signs and symptoms that are difficult to distinguish from other dental and non-dental pathologies.

A detailed pain history is a good place to start. First and foremost, look out for pain on biting. Sensitivity to cold/sweet/hot, and symptoms of reversible/irreversible pulpitis may be reported too. Where there is periodontal involvement due to advanced CTS or vertical root fracture, there may also be recurrent swelling, or a feeling of vague pain or pressure. Patients with a cracked tooth often report having made multiple dental visits, with only temporary pain relief achieved.

I think it’s important to distinguish between what we refer to as CTS, and vertical root fracture. CTS usually occurs in a vital tooth. The pain that is felt is a response of the vital pulp and progression of the condition relates to increasing inflammation of the pulp due to bacterial infiltration of the crack. Vertical root fracture occurs most commonly (but not exclusively) in root filled teeth. The pain that is felt is periodontal in nature and relates to infection of the crack.

When it comes to conducting the examination, we’re looking to confirm first the diagnosis of CTS, and secondly diagnose the pulp. These include, in order of importance:

• Bite tests to reproduce the chief complaint. By far the best method is to use a ‘Tooth Slooth’ or ‘FracFinder’. Cotton rolls, rubber wheels etc. can be used, but they can’t as accurately isolate pressure to one part of the tooth.

Note: Though pain on release is considered to be a classic sign of a cracked cusp, one study actually found that 68% of cracked tooth cases had pain only when pressure was applied (Abbott & Leow 2009). That said, if you do find that the pain is significantly worse on release than on biting, you can be comfortable with the diagnosis of CTS.

• Perio probing – presence of a deep, narrow pocket at a single site may indicate a vertical root fracture or endo lesion draining through the periodontium.

In this xray you can see the two molars present with lucencies that surround the coronal portion of the mesial roots. The video below is not the best quality, but you get the drift of how a vertical root fracture presents. A vertical root fracture usually presents as a deep, narrow pocket. Locating a pocket such as this can only be done adequately under local anaesthesia.

Note the lucency surrounding the mesial roots of the first and second molars, yet there is no distinct periapical lucency. This is suggestive or vertical root fracture. The video below shows the periodontal probing pattern.

http://www.youtube.com/watch?v=8P5trYcaNII

• Visual examination (with dental operating microscope and rubber dam for best results). Pay particular attention to marginal ridge areas. Restoration removal is ESSENTIAL to visualise the crack completely.

Removal of the restoration allows the full extent of the crack to be visualised.

• Staining and/or transillumination – staining the crack with methylene blue + transillumination is a good combination to confirm the presence of a crack. (Wright et al. 2004).
• Pulp testing – The pulp is usually vital in CTS and non-vital in vertical root fracture, but you need to confirm this, because the status of the pulp will help determine treatment.
• Palpation, percussion testing, mobility testing as per ususal to confirm pulpal and periapical status.
• Radiographic examination – may not be useful in actually identifying the crack, but it can help to rule out other options during your differential diagnosis stage. In cases of complete vertical root fracture, you may be able to see periradicular bone loss (a ‘halo’ radiolucency). There is plenty of debate as to whether CBCT can confirm the presence of a crack, and I would be wary of relying on this for diagnosis.

I’ll discuss my preferred method of management of CTS in an upcoming post.

References

Abbott, P,  Leow, N 2009. Predictable management of cracked teeth with reversible pulpitis. Aust Dent J, 54, 306-15.

Bader, JD, Martin, JA,  Shugars, DA 1995. Preliminary estimates of the incidence and consequences of tooth fracture. J Am Dent Assoc, 126, 1650-4.

Wright, HM, Jr., Loushine, RJ, Weller, RN, Kimbrough, WF, Waller, J,  Pashley, DH 2004. Identification of resected root-end dentinal cracks: a comparative study of transillumination and dyes. J Endod, 30, 712-5.

This is just a short post to let you know that I will be running a hands-on course for general dentists on October 12 in Brisbane. I wanted to let Endospot followers have the first opportunity to sign up. It should be a great day with a nice mix of useful information, practical advice and hands-on experience.

You can download the course flyer here or sign up here.

I hope to see you there.

Pat Caldwell

I know it’s been a long time since I’ve posted so I thought I’d show a case that caused me some trouble recently. The owner of this tooth had suffered a significant facial swelling and ended up in hospital. Fortunately, the swelling had subsided by the time I saw him and he was keen to save the tooth.

A Wide Canal That Narrows Suddenly is an Indication of a Splitting Canal.

Apical Periodontitis is Apparent. Note the Bulbous Shape of The Root.

The thing to note about this pre-op xray are that the canal appears to split at the mid root level. Even if you can’t see the split, the fact that the canal narrows suddenly is an indication of a split in the canal system. The second telling point that we are dealing with something complex is the bulbous shape of the root, when compared to the first premolar. This alone would tell us that we should be looking for anatomy other than a single canal.

I was able to locate two canals, and confirm that these canals joined apically, but I wasn’t happy with the position of the files in the radiograph. As you can see, the lingual canal was quite centred in the root, while the distobuccal canal is shifted to the distal. It doesn’t look right does it? There must be another canal.

Note the Off-Centre Location of the Second File

So…. I know to look for a third canal, but no matter how hard I looked, I just couldn’t find it. The canal were prepared and obturated, with the result below.

After Preparation and Obturation a Small Squirt of Sealer to the Mesial Confirms the Missed Anataomy

So you can see the squirt of sealer to the mesial at the mid-root point. There is no doubt that some anatomy has not been properly cleaned, and would likely be full of infected tissue. Back in we go. The GP was removed and the access expanded to allow location of the canal to be identified and confirmed with a file.

There it is!

The third canal was then prepared. It too joined the other canals apically. The key to cleaning this sort of anatomy is passive ultrasonic irrigation, which I have discussed previously. The only way to then obturate is with a warm technique such as continuous wave or warm vertical. The tooth, of course needs a crown. In this case persistance paid off and the outcome can be much more certain now that the full anatomy has been cleaned and obturated. In hindsight, a cone beam CT scan may have assisted in locating the full anatomy.

Pat

I Call This Tooth “The Squid”

The Arrow Shows the Spot Where the Missing Canal Was Located

The hard working team that is the Roots Endodontic Community has banded together to organise what will be a wonderful Summit to be held later this year in Foz do Iguaçu in Brazil. The venue looks amazing and there is a world class line-up of speakers.

More information at http://rootssummit2012.com

Waterfalls at Foz Do Iguacu. Looks like a top place for an Endo conference.

Happy New Year from the mountains of Japan where I’m hitting the ski slopes, eating some delicious meals and soaking up some fantastic Japanese hospitality. Last night we were served the traditional midnight meal of Soba Noodles by our hosts at the Sidehill Lodge in Hakuba, Nagano Prefecture.

The skiing Budda accross the road from our lodge in Hakuba

I’m a fan of utilizing passive ultrasonic irrigation (PUI) to improve the effectiveness of our irrgants, and believe that it produces root canals with fewer debris and bacteria than needle irrigation alone. Recently there has been some talk about the use of lasers to activate our irrigants in a similar manner and there is at least some evidence that this may improve the cleanliness. Here is a promotional video to give you a brief overview:

http://www.youtube.com/watch?v=U0dLJWm6LGk

Now, we are still waiting on evidence to prove that any of these methods provide a better outcome in terms of healing or prevention of apical periodontitis, but in the meantime, we should be aiming to produce the cleanest canals we can.

My colleague Mateus Miranda has volounteered to look into the use of lasers to activate irrigants and has produced a nice overview of the available evidence. The key paper so far is probably the one by Ove Peters in the JOE in 2011 showing an improved ability of the technology to reduce, but not remove bacteria from intra-orally infected teeth.

Enter Mateus……….

There has been recently introduced onto the dental market a said “revolutionary” mechanism for cleaning and debriding of root canal systems. The PIPS uses Erbium: Yttrium Aluminium Garnet (Er:YAG) laser energy at sub-ablative power levels which produces wavelengths of 2940nm. PIPS was developed by Dr. Enrico DiVito with assistance from Dr. Mark Colonna.

This non-visible-to-human-eye laser energy is strongly absorbed by water and when activated with specific peak power derived from short pulse duration results in a photomechanical phenomenon or photo-ablation on dentin, allegedly removing smear layer and exposing dentinal tubules.

The Er: YAG laser was tested for the first time in 1988 for preparing dental hard tissues. It was successfully used to prepare holes in enamel and dentine with low ‘fluences’ (energy (mJ)/unit area (cm2)). In 1989, it was demonstrated that the Er: YAG laser produced cavities in enamel and dentine without major adverse side effects (A. HUSEIN 2006).

In 1998 a study performed by TAKEDA FH and colleagues concluded “The root canal walls irradiated by Er:YAG laser were free of debris, with an evaporated smear layer and open dentinal tubules. These results suggested that Er:YAG laser irradiation had an efficient cleaning effect on the prepared root canal walls. FLAVIO SOARES et al (2008) found laser cleanliness in root walls of primary teeth was similar with rotary instruments and superior to manual instrumentation and it required less time for completion. KYOKO INAMOTO et al in 2009 found no smear layer presence following instrumentation of root canal walls using the same laser therapy.

Irrigation wise, ROELAND JG De MOOR et al (2010) showed the efficacy of Laser Activated irrigation (LAI) using Er:YAG for 20 seconds compared to Passive Ultrassonic Irrigation (PUI) for 60 seconds for dentinal debris removal. DIVITO et al (2010) concluded the Er:YAG laser used in this study showed significantly better smear layer removal than traditional syringe irrigation.

Considering thermal effect, studies were performed and were conclusive on the safety of the Er: YAG lasers usage unless proper water cooling and specific power output setting was used (V ARMENGOL et al. 2000, REMI YAMAZAKI et al. 2001, KIMURA et al. 2002, B N CAVALCANTI et al.2003).

Most importantly some studies tested the efficacy of the bactericidal effect of the Er: YAG laser, particularly on Escherichia coli and Enterococcus faecalis and were happy to concluded positively (MORITZ A. 1999, Loma Linda University School of Dentistry.2010). However, a study conducted by OVE A PETERS et al (2011) showed activated disinfection did not completely remove oral bacteria from the apical root canal third and infected dentinal tubules, requiring some further investigation.

But how does PIPS® actually work?
After gaining access to the canal, an instrumentation of the canal is done to ISO #20 only. No further enlargement is necessary thus preserving tooth strength.
This is followed by PIPS® activation delivered from a cone-shaped fiber tip attached to a handpiece within an irrigating solution, either EDTA or NaOCl. The tip is inserted into the coronal third of the canal thus there is no risk of tip breakage from curved canals or undesirable apical extrusion of chemical irrigants possible with other laser endodontic methods (ROY GEORGE et al, 2008). The canal system is finally flushed clean with water and is ready to be obturated.

It is worthy it to check on the images provided by Dr Enrico DiVito and its team related to this new mechanism of root canal debridement. Please follow the link.

To sum up, this new technology seems to be very effective and efficient regarding root canal therapy. The ability to prepare/ instrument canals in a short period of time associated with great reduction of bacterial count (when compared to conventional root canal instrumentation) is absolutely promising.

References:

A. Husein. 2006. Applications of Lasers in Dentistry: A Review.

Takeda FH, Harashima T, Eto JN, Kimura Y, Matsumoto K. 1998. Effect of Er: YAG laser treatment on the root canal walls of human teeth: an SEM study.

Flavio Soares, Claudio H. Varella, Roberta Pileggi, Abi Adewumi, Marcio Guelmann. 2008. Impact of Er,Cr:YSGG Laser Therapy on the Cleanliness of the Root Canal Walls of Primary Teeth.

Kyoko Inamoto, Naoki Horiba, Shinpei Senda, Munetaka Naitoh, Eiichiro Ariji, Akira Senda, Hiroshi Nakamura. 2009. Possibility of root canal preparation by Er: YAG laser.

Roeland J.G. De Moor, Maarten Meire, Kawe Goharkhay, Andreas Moritz, Jacques Vanobbergen. 2010. Efficacy of Ultrasonic versus Laser-activated Irrigation to Remove Artificially Placed Dentin Debris Plugs.

E. DiVito, O. A. Peters, G. Olivi. 2010. Effectiveness of the Erbium:YAG laser and new design radial and stripped tips in removing the smear layer after root canal instrumentation.

V. Armengol, A. Jean, D. Marion. 2000. Temperature Rise During Er: YAG and Nd:YAP Laser Ablation of Dentin.

Reimi Yamazaki, Claudia Goya, Da-Guang Yu, Yuichi Kimura, Koukichi Matsumoto. 2001. Effects of Erbium, Chromium:YSGG Laser Irradiation on Root Canal Walls: A Scanning Electron Microscopic and Thermographic Study.

Yuichi Kimura, Kazuo Yonaga, Keiko Yokoyama, Jun-ichiro Kinoshita, Yoshiko Ogata, Koukichi Matsumoto. 2002. Root Surface Temperature Increase during Er: YAG Laser Irradiation of Root Canals.

Bruno Neves Cavalcanti, José Luiz Lage-Marques, Sigmar Mello Rode. 2003. Pulpal temperature increases with Er:YAG laser and high-speed handpieces.

Moritz A, Schoop U, Goharkhay K, Jakolitsch S, Kluger W, Wernisch J, Sperr W. 1999. The bactericidal effect of Nd:YAG, Ho:YAG, and Er:YAG laser irradiation in the root canal: an in vitro comparison.

Loma Linda University School of Dentistry. 2010. Final Report: Efficacy of Er: YAG Laser on Root Canals Infected with Enterococcus faecalis.

Ove A. Peters, Sean Bardsley, Jennifer Fong, Goldie Pandher, Enrico DiVito. 2011. Disinfection of Root Canals with Photon-initiated Photoacoustic Streaming.

Roy George, Laurence J. Walsh. 2008. Apical Extrusion of Root Canal Irrigants When Using Er: YAG and Er,Cr:YSGG Lasers with Optical Fibers: An In Vitro Dye Study.
Hyperlink: http://www.fotona.com/media/aurora/dokumenti/2010/11/pips_brochure_fotona_web.pdf

Invasive Cervical Resorption can spell disaster for a tooth if not diagnosed early.

The disease process known as Invasive Cervical Resorption (ICR) can be quite devastating for a tooth. The big problem for us as practitioners is that it’s difficult to identify ICR early. By far the most comprehensive article on ICR is by Geoff Hiethersay, (an Australian Endodontic legend) and this is the one article you need to read if you want more information than is contained in this post (Hiethersay 2004).

For dental resorption to occur, we need three things: 1. blood supply; 2. a stimulus; 3. breakdown or loss of the protective layer. When I refer to the protective layer, what I’m referring to is the pre-cementum externally, and the pre-dentine internally. It might seem odd that these seemingly frail tissues are able to protect tooth structure. The reason this protection occurs is that specific peptides named RGD peptides provide binding sites for the resorptive cells. These RGD peptides are bound to calcium salt crystals on mineralised surfaces. So when the resorbing cells reach the unmineralised pre-dentine or pre-cementum, they are unable to bind as no RGD peptides are present and thus, no resorption occurs.

So, it would seem that a lack of pre-cementum on the surface of a root may predispose to the development of ICR. This could happen due to trauma via a number of mechanisms such as scaling/root planing, internal bleaching, physical trauma or perhaps orthodontic movement of teeth. Dental trauma, internal bleaching and orthodontics have been associated with the development of ICR (Heithersay 1990). The condition also occurs without any pre-disposing factors, and it is suggested that a genetic lack of cementum (and therefore pre-cementum) may be present in those cases.

This is the same tooth as seen in the xray above. Invasive cervical resorption is both external and cervical in nature.

ICR is known by a number of other names and one of these is External Invasive Cervical Resorption. The “External” label is a reasonable addition as ICR is always external in nature. The resorption develops from cells in the periodontal ligament in the cervical region. This is the area that is most likely to have an absence of cementum from a developmental point of view at least. I mentioned that pre-dentine is also protective against ICR. The reason we know this is that in extensive cases the external resorption reaches the pulp, but the pulp is spared, protected by the pre-dentine. For this reason, even in extensive cases of ICR, the pulp usually remains vital. The resorptive tissue which invades the tooth seems to resist bacterial invasion. Certainly, you will not usually find a traditional periodontal pocket adjacent to the resorption.

I mentioned the three things that are required for resorption to occur. It’s obvious we have a blood supply and lack of protection, but where does the stimulus come from? The answer is that we don’t know. It has been hypothesised to be either inflammatory due to sulcular infection or a benign proliferative fibrovascular or fibro-ossesous disorder. That’s quite a mouth-full and I’ll leave it up to somebody much smarter than me to work out which one is correct. The cell that does the resorbing is similar in morphology to the osteoclast and may represent a functional variant of the same lineage.

A slight pink discolouration (arrow) is the only symptom from this tooth, which tested positive to pulp testing. This tooth is the same as seen in the xray and CBCT above.

Clincially, the tooth is usually completely asymptomatic. There may be a pink (or sometimes grey) discolouration of the crown but often the radiograph is the only indication that resorption is occuring. Radiographically, a mottled lucency is present and in advanced cases, there is a radiopaque line bordering the pulp chamber. Taking mesial and distal angled images will see the lesion move in relation to the pulp and this will differentiate the resorption from an internal resorption, as well as tell you if it’s positioned buccaly or lingually. Of course cone beam CT will also provide useful information.

Heithersay’s clinical classification is as follows:

Class 1 – small lesion with shallow penetration

Class 2 – well defined lesion close to coronal pulp

Class 3 – Deeper invasion to include the coronal third of radicular dentine

Class 4 – Large invasive lesion extending beyond the coronal third of the root

Class 1 and 2 lesions can be treated predictably, but the success rate in treating class 3 and 4 lesions drops dramatically. Treatment usually consist of using trichloracetic acid (TCA) to attempt to destroy the resorptive tissue via coagulation necrosis. The difficulty comes from the fact that the resorption is not usually confined to a discrete area and can have multiple feeding channels from well below the gingival margin. The lesion can also be treated surgically, but in practice it can be difficult to access and may even require bone removal to gain direct vision of the lesion. This rapidly gets destructive of both tooth structure and periodontal tissues which is why it is important to identify and treat (if indicated) the disease as early as possible. See Heithersay’s article for a description of the use of TCA and also other treatment options.

References:

Hiethersay G. Invasive Cervical Resorption. Endodontic Topics 2004, 7, 73–92

Back when I was working as an Endodontist with the Australian Navy, I often mentored newly graduated dentists. There was an interesting interaction between us that would often occur. The junior dentist would come into my surgery with a question about diagnosis. They would explain a set of symptoms and then show me a radiograph. I would then ask what the pulp test result was. The new grad would then slowly back out of the room in order to return to the patient and conduct the test.

I’m not sure why the pulp testing was left off the list, but I hope I hope that by the time the junior dentist had finished their posting and moved on to a new posting that pulp testing is one of the most important tools allowing us to to diagnose. Unfortunately, there is nothing certain when it comes to pulpal diagnosis, especially when we get to the grey area of reversible/irreversible pulpitis. If we really want to know what’s happening in the pulp and periapical area of a tooth, we need to extract it, section it, and look at it under a microscope. But that’s not practical…….

Pulp testing is not 100% accurate. If it was, then diagnosis would be much easier, but it often gives us essential information that will confirm a clinical diagnosis. When it comes to vital pulps, electric and cold testing gives a positive result 81-86% of the time (Petersson & Kiani-Anaraki, 1999). In a partially or completely necrotic tooth, these modalities will give a negative result on almost all occasions. This is useful infromation to have at hand.

Here is an example from when I was doing my post-graduate training:

Compare these radiographs. The image on the left is the pre-op and the image on the right is the two year review.

In the case above, we can see there is a definite lucency surrounding the lower right canine and central incisor. The lateral incisor may also be involved. Pulp testing with both cold and EPT revealed the canine was testing negative and the incisors were testing positive. As only the canine was testing negative, I only treated the canine. At the two year review, we can see that the lesion has healed and normal periradicular architecture has been re-formed around the vital incisors. If we just worked from the x-rays, we’d probably treat all three teeth, and subject the patient to unnecessary treatment. This is a pretty simple lesson.

Here are the keys to successful pulp testing:

1. Make sure the teeth are completely dry and isolated with cotton wool rolls;

2. Place the tip of the pulp tester on tooth structure, not restoration, and use a small (perhaps half of a) cotton pellet or endo sponge;

3. Start your test with a tooth that you expect will give a normal result and is not involved with the area in question. This will allow the patient to get a feel for what a normal response is;

4. Test with both cold and EPT. If the patient is experiencing symptoms such as a hyper-response to hot foods/liquids, then use hot as well.

In my surgery I have the pulp tester sitting right next to me, along with things like the apex locator and endo motor. We use it that often.

References:

Petersson KS, C. Kiani-Anaraki, M. Evaluation of the ability of thermal and electrical tests to register pulp vitality Endod Dent Traumatol 1999;15:127-131.