Single-visit endodontics

How many people would like to finish the above case in one visit?

Or the case below, for that matter.

I think the first point of consideration is not how many visit endo should be finished in?

Technical quality of endo treatment is of paramount importance. First consideration is, therefore, whether you can achieve adequate technical quality of endo treatment?

By adequate technical quality I mean;
Diagnosis and treatment plan properly formulated? Rubber dam used and properly applied? All root canal located? Working length correctly determined? Antibacterial irrigant used? MAF large enough? Radiographically, your root filling appears in appropriate length, density and taper? and so on…

If you could achieve all those, but it needs more than one visit to achieve it, then why on earth would you want to finish endo in one visit and, of course, with technical inadequacy.


Now, assume that adequate technical quality can be achieved in one visit. Is there any reason why the treatment shouldn’t be completed?
If you wanted to kill bacteria with calcium hydroxide dressing, it would take at least a week for calcium hydroxide to work effectively (Sjogren et al. 1991). That means you can’t complete the case in one visit.

Is calcium hydroxide dressing necessary?
To answer this question, one more issue needs to be clarified.

There are two separate entities in endodontics. A tooth WITH and WITHOUT apical periodontitis (apical radiolucency).

To make it short, I need to simplify it a bit. A tooth without apical periodontitis (normal vital tooth (elective endo) or irreversible pulpitis) is considered not infected. Or infection hasn’t been established, at least, at the apical part of the canal in case of irreversible pulpitis. There’s no bacteria in the canal at the first place, therefore, endo tx shouldn’t be aiming to reduce a number of bacteria. Make sense? So calcium hydroxide dressing is not necessary in these cases and, as a result, one visit endo could be done, provided that adequate technical quality could be achieved.

A tooth with apical periodontitis is infected (Sundqvist 1976). Apical periodontitis is caused by bacteria (Kakehashi et al. 1965; Moller et al. 1981), so endo tx in this case should be aiming to reduce as much a number of bacteria as possible.

The higher the number of canals that can be rendered bacterial negative, the higher the chance of healing (Sjogren et al. 1997).

Mechanical instrumentation + NaOCl irrigant = 40-60% of the treated teeth bacteria-negative (Bystrom et al. 1983; Shuping et al. 2000).

Mechanical instrumentation + NaOCl irrigant + calcium hydroxide dressing for at least a week = roughly around 70% (weighted average of the following five studies) of the treated teeth bacteria-negative (Orstavik et al. 1991; Peters et al. 2002a; Shuping et al. 2000; Sjogren et al. 1991; Yared et al. 1994)

By extrapolation, including calcium hydroxide dressing between appointments should provide a higher healing rate, because bacteria are further reduced.

In conclusion, one visit can be done in a tooth without apical periodontitis (there’s no controversy about it). Calcium hydroxide dressing should be included in the treatment of a tooth with apical periodontitis (or a tooth with established infection), so one visit endo is biologically and logically not possible (there’re some controversies surrounding this case, though).

Controversial issue:
Even though, it does make biological sense to include calcium hydroxide to the treatment of teeth with apical periodontitis as I outlined the logical step above. Randomized controlled clinical trials (the best design of clinical study to test treatment effectiveness) have failed to show the clinical benefits of calcium hydroxide dressing in terms of healing rate (Peters et al. 2002b; Trope et al. 1999; Weiger et al. 2000).

Why have benefits of calcium hydroxide not been shown in these studies?
Endodontic treatment is skill-dependent procedure (as with any surgical procedures). Operator skill and/or settings could affect treatment outcome (healing rate) to some extent. It has been conjectured that these researchers (Peters, Trope, and Weiger) are experienced endodontists, their treatment technical qualities must be high.

Therefore, the additional benefits of calcium hydroxide are small in comparison to the rest of the treatment and could not be easily shown statistically. On the other hand cleaning, shaping, and obturation by novice operators (low skill level expected) could well be benefited from calcium hydroxide medication as another layer of antibacterial process. In this scenario multiple-visit endodontics with inter appointment calcium hydroxide medication might significanly show better results than single-visit endodontics.

Reference:

Bystrom A, Sundqvist G (1983) Bacteriologic evaluation of the effect of 0.5 percent sodium hypochlorite in endodontic therapy Oral Surgery, Oral Medicine, Oral Pathology 55, 307-12.

Kakehashi S, Stanley H, Fitzgerald R (1965) The effect of surgical exposures of dental pulps in germ-free and conventional laboratory rats. Oral Surgery Oral Medicine Oral Pathology Oral Radiology & Endodontics 20, 340-9.

Moller AJ, Fabricius L, Dahlen G, Ohman AE, Heyden G (1981) Influence on periapical tissues of indigenous oral bacteria and necrotic pulp tissue in monkeys Scandinavian Journal of Dental Research 89, 475-84.

Orstavik D, Kerekes K, Molven O (1991) Effects of extensive apical reaming and calcium hydroxide dressing on bacterial infection during treatment of apical periodontitis: a pilot study International Endodontic Journal 24, 1-7.

Peters LB, van Winkelhoff AJ, Buijs JF, Wesselink PR (2002a) Effects of instrumentation, irrigation and dressing with calcium hydroxide on infection in pulpless teeth with periapical bone lesions International Endodontic Journal 35, 13-21.

Peters LB, Wesselink PR (2002b) Periapical healing of endodontically treated teeth in one and two visits obturated in the presence or absence of detectable microorganisms International Endodontic Journal 35, 660-7.

Shuping GB, Orstavik D, Sigurdsson A, Trope M (2000) Reduction of intracanal bacteria using nickel-titanium rotary instrumentation and various medications. Journal of Endodontics 26, 751-5.

Sjogren U, Figdor D, Persson S, Sundqvist G (1997) Influence of infection at the time of root filling on the outcome of endodontic treatment of teeth with apical periodontitis International Endodontic Journal 30, 297-306.

Sjogren U, Figdor D, Spๅngberg L, Sundqvist G (1991) The antimicrobial effect of calcium hydroxide as a short-term intracanal dressing International Endodontic Journal 24, 119-25.

Sundqvist G (1976) Bacteriological Studies of Necrotic Dental Pulps. Umea Sweden: Umea University Odontological Dissertations no. 7.

Trope M, Delano EO, Orstavik D (1999) Endodontic treatment of teeth with apical periodontitis: single vs. multivisit treatment. Journal of Endodontics 25, 345-50.

Weiger R, Rosendahl R, Lost C (2000) Influence of calcium hydroxide intracanal dressings on the prognosis of teeth with endodontically induced periapical lesions. International Endodontic Journal 33, 219-26.

Yared GM, Dagher FE (1994) Influence of apical enlargement on bacterial infection during treatment of apical periodontitis Journal of Endodontics 20, 535-7.

MTAD: endodontic irrigant?

What is MTAD?
It is an irrigant consisting of tetracycline (to kill bacteria, so to speak), citric acid (to get rid of smear layer increasing the likelihood of killing bacteria), detergent (to reduce surface tension again increasing the likelihood of getting to bacteria in fin, ramification and all hard to reach region of the root canal system)

Why has MTAD been developed?
I guess it could have something to do with an ineffectiveness of current root canal disinfection protocol (instrumentation+0.5%NaOCL irrigation+EDTA+1wk of calcium hydroxide dressing) especially in retreatment of fail cases. A study has shown that with the above protocol, around 17% of their retreatment cases remained culture positive (Sundqvist et al. 1998). Another clinical study looked into the effects of instrumentation and 0.5% NaOCL on E. faecalis (Peciuliene et al. 2001) in retreatment cases. Despite the facts that 0.5%NaOCL is very effective in killing E. faecalis in vitro, this clinical study showed that 30% of the cases remained E. faecalis positive. It clearly demonstrated that 0.5%NaOCL cannot predictably eliminate E. faecalis clinically. This article also suggested that alternative irrigant in retreatment of a fail cases might be needed.

Also it could be a process gearing towards single-visit endodontics.

How should MTAD be used?
First as a replacement of current irrigating protocol (NaOCl+EDTA). Personally, I don’t think it should be used in this way for the simple reason that MTAD doesn’t have tissue dissolving property as NaOCl does.
Second MTAD can be used as an adjunct (as a final flush) additional to either NaOCl+EDTA or NaOCl alone. To me, this way is more logical. And I will explore further based on this premises, OK?

I’m trying not to muck around and just cut to the chase here.

Can MTAD improve treatment outcome?
Short answer would be “don’t know” long answer can be long……really long.

Logic
Now let’s look at it logically. Tetracycline is bacteriostatic meaning it only stops bacteria from growing but does not kill bacteria per se. It works as systemic antibiotic because body defense mechanism can get to bacteria and destroy it. Basically tetracycline helps tip the balance in favor of body immune response. However, in root canal, where immune system is in complete absence (necrotic->no blood supply->no defense mechanism), how can it kill bacteria????

Evidence
Now before any innovations (MTAD included) should be adopted, wouldn’t it be prudent (as a health care provider) to demand to see evidence showing their benefits?

High level evidence
Is there any clinical evidence showing improvement in treatment outcome because of MTAD? So far there’s none and I can tell you now that there will never be. In well executed endodontic treatment, the success (healing) rate is in the area of 90% (Friedman 2002). Suppose MTAD can improve healing rate to 95% (this considered to be very very small difference from epidemiological perspective). To show that it is significant statistically (at 80% power, p = 0.05), a sample size of 870 is required (Sokal & Rohlf 1995). I can tell you (again) that the trial of this size will extremely unlikely to be conducted in our field.
So where evidence does not exist and will never exist, should we be using that thing on our patients??

Low level evidence
There are plenty of laboratory studies around supporting the benefit of MTAD. Many studies showed a high smear layer removal property of MTAD (Torabinejad et al. 2003). I couldn’t care less if it removes smear layer. EDTA has done a great job with half the price (in fact it’s much less ;). Many showed other points (Machnick et al. 2003a, Machnick et al. 2003b, Park et al. 2004). Again I couldn’t care less if MTAD does any of those.

What I want to see (but haven’t seen so far) is that (NaOCl+MTAD) or (NaOCl+EDTA+MTAD) can reduce bacterial load to a greater extent than NaOCl+EDTA. Basically, even the low level evidence, it is still far from conclusive.

Conclusion
There’s nothing replacing high level of professionalism, accepting to nothing but the highest treatment standard and to persevere in cultivating the utmost clinical dexterity.
As I mention earlier, well-executed endodontic treatment has a very high healing rate. Technical quality of the treatment has, probably, much higher impact on treatment outcome than one single irrigant.
Unfortunately there’s no magic bullet or magic wand here.

References:
Friedman S (2002) Prognosis of initial endodontic therapy Endodontic Topics 2, 59-88.

Machnick TK, Torabinejad M, Munoz CA, Shabahang S (2003a) Effect of MTAD on flexural strength and modulus of elasticity of dentin J Endod 29, 747-50.

Machnick TK, Torabinejad M, Munoz CA, Shabahang S (2003b) Effect of MTAD on the bond strength to enamel and dentin J Endod 29, 818-21.

Park DS, Torabinejad M, Shabahang S (2004) The effect of MTAD on the coronal leakage of obturated root canals J Endod 30, 890-2.

Peciuliene V, Reynaud AH, Balciuniene I, Haapasalo M (2001) Isolation of yeasts and enteric bacteria in root-filled teeth with chronic apical periodontitis. International Endodontic Journal 34, 429-34.

Sokal RR, Rohlf FJ (1995) Biometry: the principles and practice of statistics in biological research, 3rd edn. New York: W.H. Freeman.

Sundqvist G, Figdor D, Persson S, Sjogren U (1998) Microbiologic analysis of teeth with failed endodontic treatment and the outcome of conservative re-treatment Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, & Endodontics 85, 86-93.

Torabinejad M, Cho Y, Khademi AA, Bakland LK, Shabahang S (2003) The effect of various concentrations of sodium hypochlorite on the ability of MTAD to remove the smear layer J Endod 29, 233-9.

Cultures and clinical endodontics

Why do we culture?

It’s a general fact by now that cause of endo disease is bacteria. Therefore, getting rid of bacteria is one of treatment objectives. If bacterial eradication can be achieved (negative culture), successful treatment should then ensued. Was that making sense? Historically, that’s a rationale for culture (Bender et al. 1964).

The confusion arises because we now know better. We have now known that the dominant endodontic bacteria is anaerobic (Sundqvist 1976; Sundqvist 1992), which merely impossible to be cultured with the simple technique we normally use. So if aerobic culture technique is being employed in dental school, so what are we doing? Negative culture cannot mean no bacteria and higher success rate then.

Why do we still culture in dental school?

The argument I usually heard is to teach dental student about sterile technique, maintaining field of operation sterile, which I think it’s a legitimate argument. Even though, we can’t be certain of what are actually inside the canals with the simple culture technique, we can be certain that we did not inoculate new bacteria into the canals by poor sterile technique. In dental school, the students do not only require to do endo but also require to LEARN how to do it right. I think culture technique can be part of that learning process.

Why is culture not being practiced in the real world?

As a matter of fact negative culture does mean higher healing rate (Sjogren et al. 1997) (94% healed in negative culture group, while 68% healed in positive culture group) their culture technique was state of the art, though.

Practicality issue: to make culture results informative, it has to be anaerobic culture technique, which is time consuming and costly obviously it’s not practical. Cost effective, and cost benefit analysis might have shown that it’s not worth it.

If the culture result was negative after proper treatment i.e. antibacterial irrigants were used, canals prepared to reasonable size, they’ve been dressed with calcium hydroxide for at least one week, what could be done to change culture results? The answer is nothing, that’s why we don’t culture in the real world.

References

Bender IB, Seltzer S, Turkenkopf S (1964) To Culture or Not to Culture? Oral Surgery Oral Medicine and Oral Pathology 18, 527-40.

Sjogren U, Figdor D, Persson S, Sundqvist G (1997) Influence of infection at the time of root filling on the outcome of endodontic treatment of teeth with apical periodontitis International Endodontic Journal 30, 297-306.

Sundqvist G (1976) Bacteriological Studies of Necrotic Dental Pulps. Umea Sweden: Umea University Odontological Dissertations no. 7.

Sundqvist G (1992) Ecology of the root canal flora Journal of Endodontics 18, 427-30.

Antibiotic cocktails and endodontics

อยากทราบวิธีทำ endo ที่เรียกว่า LSTR ที่ใช้ในฟันน้ำนมและฟันแท้ รวมถึง NIET หลักการมันเป็นอย่างไรคะ ขอบคุณค่ะ หรือสามารถหาอ่านรายละเอียดได้ที่ไหน

Basically, it is an antibiotic cocktail dressed in canal for certain period of time to eliminate bacteria, which is the cause of disease. This concept is not new, it was proposed dating back to the 50’s (Bender et al. 1952), it was, however, depopularized later on because of the concern regarding allergic reactions and its ineffectiveness of antibiotics at the time.

The concept resurfaced because of the push from Dr Hoshino’s group (Sato et al. 1996) and also new development of antibiotics. You are right about the components of this cocktail.

Two case reports demonstrated a successful treatment without mechanical instrumentation of a necrotic immature premolar with periapical involvement (apical radiolucency). The treatment involved intraradicular medication with combination of antibiotics instead of conventional apexification. Follow up showed complete closure of the apex and thickening of the root canal wall indicating revitalization of intraradicular tissue. In addition, normal response to thermal and electric pulp test also returned (Banchs et al. 2004; Iwaya et al. 2001).

One case series (87 cases) utilized the similar concept but apply to primary teeth also reported the excellent outcomes (Takushige et al. 2004).

The concept and findings are undeniably exciting. However, I don’t think adopting this concept to daily clinical practice is warranted, at this stage (in the not-too-distant future, probably does??). It is for the simple reason that the above papers are “reports” and not “studies”. There was no control group in these papers, so the favorable outcomes could well be entirely coincidental. I believe the formal study with a better study design is ongoing and its results should be out soon.

References:

Banchs F, Trope M (2004) Revascularization of immature permanent teeth with apical periodontitis: new treatment protocol? Journal of Endodontics 30, 196-200.

Bender IB, Seltzer S (1952) Combination of antibiotics and fungicides used in treatment of the infected pulpless tooth. Journal of the American Dental Association 45, 293-300.

Iwaya SI, Ikawa M, Kubota M (2001) Revascularization of an immature permanent tooth with apical periodontitis and sinus tract Dental Traumatology 17, 185-7.

Sato I, Ando-Kurihara N, Kota K, Iwaku M, Hoshino E (1996) Sterilization of infected root-canal dentine by topical application of a mixture of ciprofloxacin, metronidazole and minocycline in situ Int Endod J 29, 118-24.

Takushige T, Cruz EV, Asgor Moral A, Hoshino E (2004) Endodontic treatment of primary teeth using a combination of antibacterial drugs International Endodontic Journal 37, 132-8.

Chlorhexidine irrigant

Why CHX?
Because we want to get rid of E. faecalis.

Why E. faecalis?
This bacteria have attracted a lot of attention since first two articles published in 1998 (Molander et al. 1998, Sundqvist et al. 1998). It was found that 30% of endodontically-well-treated teeth with persistent disease (failed despite well-performed treatment) have E. faecalis. Because of this finding, E. faecalis has been (rightly or wrongly) implicated as a potential pathogen in failed cases. Since then many aspects of E. faecalis have been investigated.

Endodontically speaking, is E. faecalis overrated?
My gut feeling said YES a few years back and unfortunately it still IS overrated even now. The only different is that I have more evidence to back up my suspicion.

Why do I think E. faecalis overrated?

1. Generally, well-executed endodontic treatment achieves around 90% success (healing) (Friedman 2002). Statistically speaking, only 10% we are talking about here. In this 10%, some are responsible by extraradicular infection, some by true cyst, some by foreign body reaction and some by vertical root fractures (Nair 2006). Realistically, how many percent of failed cases is E. faecalis directly responsible? It must be negligibly small.

2. In the first two articles which give E. faecalis stardom in endodontics, prevalence of this bacteria wasn’t that high. It’s only 30%. Even we had some antibacterial strategy which could effectively eradicate E. faecalis, it wouldn’t do anything to the rest of the failed cases any way because they didn’t harbor E. faecalis. And that was a big chunk i.e. 70%.

3. This point was troubling me the most. We, endodontic community, have mixed up association with causation. None of these articles (Molander et al. 1998, Sundqvist et al. 1998, Peciuliene et al. 2000, Hancock et al. 2001, Siqueira & Rocas 2004, Fouad et al. 2005) (and many more) could prove that E. faecalis is causative of failure, they could only show the presence of E. faecalis in small portion of failed cases. Yet the endodontic community has swiftly accepted the idea that E. faecalis is responsible for failure and global efforts were started finding the way to kill every single E. faecalis in the root canals. Back then I strongly suspected that E. faecalis could only well be an innocent bystander because Koch’s postulates (Theilade 2003) had not been fulfilled. In fact evidence seemed to emerge supporting my suspicion. Using epidemiological concept and odd ratio (these are another way to establish causation without getting tangled in complexity of Koch’s postulates), two recent articles showed quite clearly that E. faecalis is exceedingly unlikely to be the culprit of failed cases (Kaufman et al. 2005, Zoletti et al. 2006).

Apparently, Spångberg wrote a very interesting editorial in triple O about this (November 2006 issue, hot from the press :); it was elegantly titled “Infatuated by enterococci”. I read it with overwhelming joy…

If (and only if) E. faecalis is not causative of failure, then what a big fuss of CHX then???? My strong conviction is that proof of E. faecalis causation is sine qua non for any attempts of targeting and eradicating such species.

The really important question i.e. E. faecalis and its causation has been asked, the less important question can now be explored then.

Can CHX really get rid of E. faecalis?
Laboratory studies seemed to suggest so but so does the NaOCL.
The trouble is that resistance of E. faecalis to standard antibacterial measures in endodontics (MI+NaOCl+calcium hydroxide) is well established clinically (Peciuliene et al. 2001, Evans et al. 2002). It has been shown in bench top studies that NaOCl is really effective against E. faecalis (Siqueira Jr et al. 1997, Siqueira et al. 2002), but why it fails dismally in clinical settings as shown by Peciuliene et al. 2001. I believe there must be some marked differences between laboratory and clinical conditions. And if NaOCl effectiveness against E. faecalis differs greatly between laboratory and clinical settings, why CHX will be any different? If I’m not mistaken (admittedly, I haven’t closely followed literature in this area), there has not been any one single clinical study showing CHX effectiveness against E. faecalis. All we have are scattered in vitro reports showing that CHX can kill E. faecalis effectively.

See? From academic standpoint, with all these questions in my head, it’s far from logical to incorporate CHX into endodontic antibacterial strategy and I have troubles convincing myself to do so.
Having said that, from practicality perspectives, I couldn’t see any harm in incorporating this chemical in to our practice, even though strong evidence is not yet available. It could simply be just a waste of time (a few seconds) and money (a few bath), that’s all. In other words, the risks of incorporating CHX are negligible, the benefits are far more remote (to me anyway).

References:
Christen AG (1967) Accidental swallowing of an endodontic instrument. Report of a case Oral Surgery, Oral Medicine, Oral Pathology 24, 684-6.

Evans M, Davies JK, Sundqvist G, Figdor D (2002) Mechanisms involved in the resistance of Enterococcus faecalis to calcium hydroxide Int Endod J 35, 221-8.

Fouad AF, Zerella J, Barry J, Spangberg LS (2005) Molecular detection of Enterococcus species in root canals of therapy-resistant endodontic infections Oral Surgery Oral Medicine Oral Pathology Oral Radiology & Endodontics 99, 112-8.

Friedman S (2002) Prognosis of initial endodontic therapy Endodontic Topics 2, 59-88.

Hancock HH, 3rd, Sigurdsson A, Trope M, Moiseiwitsch J (2001) Bacteria isolated after unsuccessful endodontic treatment in a North American population Oral Surgery Oral Medicine Oral Pathology Oral Radiology & Endodontics 91, 579-86.

Kaufman B, Spångberg L, Barry J, Fouad AF (2005) Enterococcus spp. in endodontically treated teeth with and without periradicular lesions Journal of Endodontics 31, 851-6.

Molander A, Reit C, Dahlén G, Kvist T (1998) Microbiological status of root-filled teeth with apical periodontitis. International Endodontic Journal 31, 1-7.

Nair PN (2006) On the causes of persistent apical periodontitis: a review International Endodontic Journal 39, 249-81.

Peciuliene V, Balciuniene I, Eriksen HM, Haapasalo M (2000) Isolation of Enterococcus faecalis in previously root-filled canals in a Lithuanian population. Journal of Endodontics 26, 593-5.

Peciuliene V, Reynaud AH, Balciuniene I, Haapasalo M (2001) Isolation of yeasts and enteric bacteria in root-filled teeth with chronic apical periodontitis. International Endodontic Journal 34, 429-34.

Siqueira JF, Jr., Rjcas IN, Santos SR, Lima KC, Magalhaes FA, de Uzeda M (2002) Efficacy of instrumentation techniques and irrigation regimens in reducing the bacterial population within root canals Journal of Endodontics. 28, 181-4.

Siqueira JF, Jr., Rocas IN (2004) Polymerase chain reaction-based analysis of microorganisms associated with failed endodontic treatment Oral Surgery Oral Medicine Oral Pathology Oral Radiology & Endodontics 97, 85-94.

Siqueira Jr JF, Machado AG, Silveira RM, Lopes HP, de Uzeda M (1997) Evaluation of the effectiveness of sodium hypochlorite used with three irrigation methods in the elimination of Enterococcus faecalis from the root canal, in vitro International Endodontic Journal 30, 279-82.

Sundqvist G, Figdor D, Persson S, Sjogren U (1998) Microbiologic analysis of teeth with failed endodontic treatment and the outcome of conservative re-treatment Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, & Endodontics 85, 86-93.

Theilade E (2003) The microbiology of the necrotic pulp. In G Bergenholtz, P Hörsted-Bindslev, C Reit eds. Textbook of endodontology, 1st edn; pp. 111-29. Oxford; Malden, MA: Blackwell Munksgaard.

Zoletti GO, Siqueira Jr JF, Santos KRN (2006) Identification of Enterococcus faecalis in root-filled teeth with and without periradicular lesions by culture-dependent and – independent approaches. Journal of Endodontics 32, 722-6.