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.