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Finding Safe Endodontic Irrigants

Primum non nocere

Endodontic therapy is designed to prevent or eliminate periradicular disease which, as demonstrated by Kakehashi et al, is caused by a variety of microorganisms emanating the root canal.1 By comparing the results of pulp exposures in germ-free rats to those with normal oral biota, these authors have shown that no periradicular disease developed in the absence of microorganisms. Therefore, the goal is to eradicate bacteria from the root canal system by cleansing and shaping the canal, and to prevent the infection or re-infection of the canal by properly obturating it.

This deceptively simple task is made difficult by the complexities of the root canal system (Figure 1). There is no question that endodontic files, despite the superelasticity of nickel-titanium, are unable to mechanically clean and debride these tortuous canals. Although cleansing and shaping significantly reduces bacteria, it is unable to sterilize the canals,2 and leaves bacteria behind that can rapidly multiply to their original numbers. Recent concern about the ability of certain bacteria, particularly Enterococcus faecalis (a species commonly found in teeth with failed endodontic treatment), to remain dormant in dentinal tubules3 increases the need for an irrigant that can eliminate bacteria, and perhaps even pulp tissue, from the inaccessible areas of the canal.


Concerns Regarding Endodontic Irrigants

 The search for such an irrigant is not a new one. Many agents have been tested including sulfuric acid, hydrochloric acid, sodium hydroxide, and others.4 Fortunately, these agents have fallen into disuse, but the most commonly used endodontic irrigant today is still sodium hypochlorite. It is revered by many for its antimicrobial effect, but haunted by the specter of tissue toxicity.5  

When weighing a therapeutic agent for human use, many aspects must be evaluated to determine its cost-to-benefit ratio. For example, if the desired agent is occasionally toxic, it may be worth using if the disease is very dangerous to the patient’s health, if the agent itself is very effective, if the toxic occurrences are rare and not too severe, and if the problem cannot be addressed by some other means. These points must be considered as they relate to sodium hypochlorite. Endodontic disease is a common occurrence, but death from endodontic disease is rare. Hence, it must be concluded that it would be difficult to justify endangering a patient’s health by using a caustic irrigant to treat a tooth that in all likelihood will not threaten the patient’s health as much as a potential adverse reaction to the agent.

Additionally, clinicians must decide whether using a potentially dangerous agent will guarantee success. In the case of sodium hypochlorite for example, “rebound”--a canal that was thought to be sterile after the use of an agent which was later found to be infected at a following visit--is commonplace. Why this happens is not entirely clear. One likely reason may be that, although sodium hypochlorite is a powerful antibacterial and tissue solvent in vitro, when confined to a very small area like the fins and isthmuses of a root canal system, its high surface tension does not allow it to penetrate effectively,6,7 thus leaving these critical areas untouched. It is clear from the literature that the combination of cleansing, shaping, and sodium hypochlorite irrigation routinely leaves viable bacteria in the root canal that could propagate quickly to cause further disease.2

How severe is a sodium hypochlorite accident? Numerous case reports exist in the literature of the sequelae following extrusion of sodium hypochlorite through the apical foramen,8,9 through a perforation,10 when injected into tissue,11 or when dropped into a patient’s eye.12 Common symptoms of these accidents are immediate severe pain with hemorrhage and massive swelling, for which only palliative treatment is available. That treatment usually requires several days of hospitalization and several weeks for recovery. Sequelae can also include paresthesia and facial scarring.

Brown et al13 raise the possibility that smaller amounts of sodium hypochlorite extruded through the apex may not produce a clinical emergency, but may be what cause the flare-ups that occasionally follow endodontic treatment. Perhaps it even contributes to the discomfort of biting that is so often seen postoperatively. These authors demonstrated that even when only the pulp chamber is irrigated, some sodium hypochlorite is extruded periapically during treatment.

Finally, and perhaps most importantly, it is important to consider whether there are alternate agents available for use. Chlorhexidine immediately comes to mind, as it has been shown to be as effective as sodium hypochlorite on tested microorganisms.14 Other agents may also be effective; good efficacy has been found for a povidone-iodine/surfactant combination, for example, and IKI was able to kill 100% of the E. faecalisequestered in dentinal tubules in vitro within a 15-minute contact time.15espite its efficacy, IKI is significantly less toxic than sodium hypochlorite.16 In addition, it was found that chlorine dioxide, which is commonly used in food processing and for water treatment, was as effective as sodium hypochlorite in eliminating E. faecalis from dentin disks in vitro.17



The past two decades have been a golden age in the field of endodontics, thanks to the introduction of ultrasonic instrumentation, the operating microscope, and rotary nickel-titanium instrumentation, each of which has allowed dental professionals to take their procedures to a higher level of excellence. To reach that level, however, we must examine even those irrigants and intracanal medicaments that receive little criticism. Evidence-based practice demands that randomized prospective clinical studies be employed to determine whether the efficacy of caustic irrigants is justified by improved clinical success without attendant morbidity. Above all, the aim must be to “first, do no harm.”


*Professor and Chairman, Department of Endodontics, School of Dentistry, Virginia Commonwealth University, Richmond, VA.



  1. Kakehashi S, Stanley HR, Fitzgerald R. The exposed germ-free pulp: Effects of topical corticosteroid medication and restoration. Oral Surg Oral Med Oral Pathol 1969;27(1):60-67.
  2. Bystrom A, Sundqvist G. Bacteriologic evaluation of the efficacy of mechanical root canal instrumentation in endodontic therapy. Scand J Dent Res 1981;89(4):321-328.
  3. Vivacqua-Gomes N, Gurgel-Filho ED, Gomes BP, et al. Recovery of Enterococcus faecalis after single- or multiple-visit root canal treatments carried out in infected teeth ex vivo. Int Endod J 2005;38(10):697-704.
  4. Weinreb MM, Meier E. The relative efficiency of EDTA, sulfuric acid, and mechanical instrumentation in the enlargement of root canals. Oral Surg Oral Med Oral Pathol 1965;19(2):247-252.
  5. Pashley EL, Birdsong NL, Bowman K, Pashley DH. Cytotoxic effects of NaOCl on vital tissue. J Endod 1985;11(12):525-528.
  6. Senia ES, Marshall FJ, Rosen S. The solvent action of sodium hypochlorite on pulp tissue of extracted teeth. Oral Surg Oral Med Oral Pathol 1971;31(1):96-103.
  7. Baker NA, Eleazer PD, Averbach RE, Seltzer S. Scanning electron microscopic study of the efficacy of various irrigating solutions. J Endod 1975;1(4):127-135.
  8. Becker GL, Cohen S, Borer R. The sequelae of accidentally injecting sodium hypochlorite beyond the root apex. Report of a case. Oral Surg Oral Med Oral Pathol 1974;38(4):633-638.
  9. Sabala CL, Powell SE. Sodium hypochlorite injection into periapical tissues. J Endod 1989;15(10):490-492.
  10. Reeh ES, Messer HH. Long-term paresthesia following inadvertent forcing of sodium hypochlorite through perforation in maxillary incisor. Endod Dent Traumatol 1989;5(4):200-203.
  11. Herrmann JW, Heicht RC. Complications in therapeutic use of sodium hypochlorite. J Endod 1979;5(5):160.
  12. Ingram TA 3rd. Response of the human eye to accidental exposure to sodium hypochlorite. J Endod 1990;16(5):235-238.
  13. Brown DC, Moore BK, Brown CE Jr, Newton CW. An in vitro study of apical extrusion of sodium hypochlorite during endodontic canal preparation. J Endod 1995;21(12):587-591.
  14. Jeansonne MJ, White RR. A comparison of 2.0% chlorhexidine gluconate and 5.25% sodium hypochlorite as antimicrobial endodontic irrigants. J Endod 1994;20(6):276-278.
  15. Baker NE, Liewehr FR, Buxton TB, Joyce AP. Antibacterial efficacy of calcium hydroxide, iodine potassium iodide, betadine, and betadine scrub with and without surfactant against E faecalis in vitro. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2004;98(3):359-364.
  16. Barnhart BD, Chuang A, Lucca JJ, et al. An in vitro evaluation of the cytotoxicity of various endodontic irrigants on human gingival fibroblasts. J Endod 2005;31(8):613-615.
  17. Eddy RS, Joyce AP, Roberts S, et al. An in vitro evaluation of the antibacterial efficacy of chlorine dioxide on E. faecalis in bovine incisors. J Endod 2005;31(9):672-675.
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