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CLINICAL TECHNIQUES IN ENDODONTICS


Issue: May 2006
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Clinical Update on Root Canal Disinfection

The primary goal of endodontic therapy is the prevention or resolution of periradicular periodontitis (PP). Microorganisms are the primary agents responsible for PP, and if they could be removed or prevented from entering the root canal system, PP would not develop.

Many strategies have evolved to achieve a microorganism-free root canal system. These can be categorized into cleaning and shaping the canal, chemical disinfection, and restoring the treated tooth during and after endodontic treatment. This article will examine these 3 categories as they relate to root canal disinfection.

Cleaning and Shaping the Canal
Historically, to prevent or treat PP dentists have used canal enlargement with hand files, irrigation with sodium hypochlorite, various intracanal medicaments, and canal obturation with gutta-percha and sealer. The removal of microorganisms was considered paramount to a successful long-term result. Practitioners used a variety of phenolic or formaldehyde-based products to reduce microbial growth, but the scientific evidence is convincing that the use of these agents is to be discouraged. These intracanal dressings are tissue irritants and ineffective antibacterial preparations.1

To demonstrate that canal "sterility" had been achieved before canal obturation, microbiologic culturing was performed. Research and advancements in endodontic microbiology have since demonstrated that the aerobic culturing techniques used were inadequate in their ability to inform the operator about the true presence or absence of microorganisms within the root canal system.2

Robert E Averbach, DDS
Professor of Endodontics
Division of Endodontics
University of Colorado School of
Dentistry
Aurora, Colorado
Donald J Kleier, DMD
Professor of Endodontics
Division of Endodontics
University of Colorado School of
Dentistry
Aurora, Colorado

Today, the role of microorganisms in PP is well documented. In their landmark study on conventional and germ-free animals, Kakehashi and colleagues showed that without microorganisms, PP did not occur.3 Several studies have since shown that when a periapical radiolucency persists in spite of endodontic therapy, it is almost universally accompanied by bacteria within the root canal system or in the periapical lesion.4,5The basic historical pre­cepts in preventing or treating PP remain the same, but there are more choices for canal cleaning, shaping, and disinfecting than before.

Cleaning and shaping of the root canal system is the primary method for removing the tissue and bacteria responsible for endodontic disease. Canal instrumentation con­cepts have gradually evolved, with the introduction of rotary nickel-titanium (Ni-Ti) systems providing a leap in technology. The "crown down" technique, enlarging the coronal aspect of the canal first, followed by the middle third and then the apical third, has been shown to promote deeper penetration of irrigants resulting in enhanced canal debridement.6


Rotary Ni-Ti instrumentation improves the predictability of maintaining canal shape compared with the use of stainless steel hand in­struments. In addition, the flexibility of Ni-Ti allows greater enlargement of the apical portion of the canal, removing more bacterial substrate and infected apical dentin.7The improved canal shaping by rotary Ni-Ti files encourages the apical distribution of irrigating solutions, providing tissue dissolution and disinfection.

While the cleaning and shaping process has been shown to remove the bulk of pulp tissue and bacteria-laden necrotic debris from the root canal space, chemical agents are a critical adjunct to tissue removal and canal disinfection.6 Products such as Pro-Lubea and RC Prepb are adjuncts to cleaning and shaping. These agents are used to facilitate canal enlargement through lubrication, chelation, and hydration mechanisms. Although the direct cidal activity on microorganisms is limited, these agents can increase the efficiency of canal debridement when used in combination with frequent sodium hypochlorite irrigation.8

Chemical Disinfection
The use of sodium hypochlorite as a root canal irrigant remains the most widely used solution in current endodontic therapy. Con­centrations ranging from 0.5% to 5.25% have been advocated in the past. Contemporary evidence encourages the use of 2.5% to 5.25% to maximize the tissue-dissolving and antimicrobial effects of sodium hypochlorite.9 The authors support diluting household bleach with water in a ratio of 1:1, resulting in 2.5% active sodium hypochlorite.10 This concentration balances possible tissue toxicity with antimicrobial and tissue dissolution efficacy. Canal instrumentation removes the bulk of tissue and bacteria, but it cannot clean the internal intricacies of canal anatomy because of the recognized fins, cul-de-sacs, and other irregularities that are present. Copious flushing of the canal space is a critical element in canal debridement. High volumes of irrigating solution have been demonstrated to produce a cleaner canal space compared with lower volumes.11During the cleaning and shaping process, the canal should be flooded with irrigating solution to synergistically debride the dentin and remaining tissue. The sodium hypochlorite should be constantly replenished to keep the available chlorine level high. The use of canal lubricants containing urea peroxide followed by sodium hypochlorite liberates oxygen and produces effervescence. This "bubbling" in the canal preparation encourages debris to float to the surface where it can be evacuated by suction, improving canal cleaning and disinfection.

The use of a narrow gauge, side-delivery irrigating needle (Figure 1) has been shown to benefit the flushing process, especially in the apical third of the canal preparation. This needle design enhances irrigating solution streaming in the canal with better debridement12 (Figure 2). The needle should be moving in and out of the canal constantly with only passive pressure. The side-delivery needle also reduces the possibility of creating undue apical irrigation pressure, lowering the likelihood of pushing irrigating solution beyond the tooth apex. Expressing sodium hypochlorite into the periapical region can result in pain, swelling, and tissue necrosis, often called hypochlorite accident.13

Calcium hydroxide as an intracanal medi­ca­ment has been found to be an effective antibacterial agent when left in the prepared canal space for at least 1 week.14 This occurs because it imparts a high pH to its surrounding environment, limiting bacterial growth or survival. It also has the ability to alter bacterial lipopolysaccharides, which reduces their pathogenicity.15 However, calcium hydroxide needs time to kill resistant organisms such as Enter­o­-c­o­­ccus faecalis. The ability of intracanal agents to kill E faecalis is important because this patho­gen is a persistent organism that plays a major role in the etiology of root canal failures.16 Re­cently, studies have demonstrated that calcium hy­droxide may be limited in its ability to eliminate E faecalis.16 There is also evidence that long-term (> 4 weeks) use of calcium hydroxide may weaken dentin, making teeth more susceptible to vertical root fractures.17These factors bring into question calcium hydroxide as the ultimate root canal disinfectant.

Chlorhexidine gluconate (CHX) has been used in dentistry as a broad spectrum antiseptic mouthrinse. Laboratory studies have indicated that in higher concentrations than found in mouth rinses CHX may have a place as a final rinse prior to root canal obturation. Its effectiveness lies in its ability to kill or inhibit growth of oral bacteria.18 The use of CHX, especially when combined with cetri­mide, an antiseptic with surfactant properties, has been shown to be an effective agent against E faecalis, even in the presence of dentin powder or bovine serum albumin.19 More research on chemical combinations that will enhance our ability to disinfect the root canal system is needed.

Reducing or eliminating endodontic patho­­­gens in vivo is more difficult than killing them as pure cultures in a petri dish. It is known that some endodontic microbes can penetrate into dentinal tubules or form biofilms in the root canal or on the root periradicular surfaces.20This penetration, combined with the smear layer produced by hand and rotary instrumentation, may reduce the cidal action of disinfectants within the root canal system.

Removing the smear layer at the completion of the cleaning and shaping phase of treatment is a concept that is widely supported (Figures 3A and 3B). The residual smear layer on the prepared root canal walls is composed of dentinal grindings and soft-tissue debris and may harbor residual bacteria. Removal of this layer enhances final canal cleanliness and allows improved adaptation of canal obturating materials.21 Solutions such as EDTA, Smear Clearc, and BioPurea have been advocated for smear layer removal before obturation.22

Smear Clear is a combination of EDTA and a surfactant to enhance flotation. MTAD, a mixture of tetracycline isomer, acid, and detergent, with the trade name BioPure, is composed of an aqueous solution of 3% doxycycline, 4.25% citric acid, and 0.5% polysorbate 80 detergent. MTAD has been shown to rapidly kill E faecalis.23This was also true in the presence of dentin or serum. Both MTAD and CHX impart substantively to their antimicrobial action; they attach to dentin and continue to be released for a period of time after the liquid solution is removed and the canal ob-turated. This attribute is thought to extend their disinfecting properties. Ultimately, controlled clinical studies are needed to compare long-term success rates in cases with PP to determine what clinical protocols should be implemented.

The use of lasers in endodontic therapy has been evaluated for both the cleaning and shaping phase of treatment and for canal disinfection. While current laser systems have demonstrated an ability to remove dentin and smear layer, the devices leave canal walls irregular and rough.24

High-powered lasers have demonstrated an ability to disinfect root canal systems, but concerns remain about thermal injury to the periodontal ligament and other supporting structures. A new laser system agitates a water irrigant with an erbium chromium laser energy source, helping to mitigate the adverse temperature increases inherent in other systems. A recent study, however, has cast doubt on this system's ability to completely disinfect the canal space.25

Restoring the Treated Tooth
Recently, much attention has been focused on the final restoration or coronal seal of endodontically treated teeth. If bacteria are allowed to enter the coronal portion of the root canal, they will eventually penetrate the interface between root canal dentin and the final obturation material. This penetration will result in recontamination of the canal space and periradicular inflammation. In addition to the quality of the endodontics performed, consideration must be given to the timely and proficient placement of a final restoration.26,27

Summary
Endodontic disease is mediated by bacteria. Treatment goals should be directed to reducing the critical concentration of microbial irritants to the lowest level possible. Thorough canal instrumentation, with either stainless steel hand files or Ni-Ti rotary files, removes the bulk of tissue and microbial con­tamination, but adjunctive chemical agents are needed to optimize debridement. Current concepts support the following approaches:

• lubricating and chelating agents during cleaning and shaping
• copious irrigation during all phases of instrumentation with 2.5% sodium hy­po­chlorite, constantly refreshed
• deep penetration of a side port, narrow gauge irrigating needle, constantly moving in and out of the canal space during each irrigation
• removal of residual smear layer at completion of instrumentation prior to obturation

References
1. Spangberg L, Rutberg M, Rydinge E. Biologic effects of endodontic antimicrobial agents. J Endod. 1979;5:166-175.

2. Cohen S, Hargraves K. Pathways of the Pulp. 9th ed. Phila­delphia, Pa: Mosby, 2006.

3. Kakehashi S, Stanley HR, Fitzgerald RJ. The effects of surgical exposures of dental pulps in germ-free and conventional laboratory rats. Oral Surg Oral Med Oral Pathol. 1965;20:340-349.

4. Sunde PT, Olsen I, Lind PO, Tronstad L. Extraradicular infection: a methodological study. Endod Dent Traumatol. 2000;16: 84-90.

5. Gatti JJ, Dobeck JM, Smith C, et al. Bacteria of asymptomatic periradicular endodontic lesions identified by DNA-DNA hybridization. Endod Dent Traumatol. 2000;16:197-204.

6. Gutman J, Dumsha T, Lovdahl P. Problem Solving in Endo­dontics: Preventing, Identification, and Management. 4th ed. Philadelphia, Pa: Mosby, 2005.

7. Kleier D, Averbach R. Comparison of clinical outcomes using a nickel titanium rotary or stainless steel hand file instrumentation technique. Compendium Contin Educ Dent.2006;27:87-91.

8. Anderson DN, Joyce AP, Roberts S, et al. A comparative photoelastic stress analysis of internal root stresses between RC Prep and saline when applied to the Profile/GT rotary instrumentation system. J Endod.2006;32:222-224.

9. Siqueira JF Jr, Batista M, Fraga RC, et al. Antibacterial effects of endodontic irrigants on black-pigmented gram-negative anaerobes and facultative bacteria. J Endod. 1998;24: 414-416.

10. Walton R, Torabinejad M. Principles and Practice of Endodontics. 3rd ed. Philadelphia, Pa: W B Saunders, 2002.

11. Baker NA, Eleazer PD, Averbach RE, et al. Scanning electron microscopic study of the efficacy of various irrigating solutions. J Endod.1975;1:127-135.

12. Kahn FH, Rosenberg PA, Gliksberg J. An in vitro evaluation of the irrigating characteristics of ultrasonic and subsonic handpieces and irrigating needles and probes. J Endod.1995;21: 277-280.

13. Mehra P, Clancy C, Wu J. Formation of a facial hematoma during endodontic therapy. J Am Dent Assoc. 2000;131:67-71.

14. Sjögren U, Figdor D, Spångberg L, et al. The antimicrobial effect of calcium hydroxide as a short-term intracanal dressing. Int Endod J. 1991;24:119-125.

15. Siqueira JF Jr, Lopes HP. Mechanisms of antimicrobial activity of calcium hydroxide: a critical review. Int Endod J. 1999;32:361-369.

16. Stuart CH, Schwartz SA, Beeson TJ, et al. Enterococcus faecalis: its role in root canal treatment failure and current concepts in retreatment. J Endod.2006;32:93-98.

17. Andreasen JO, Farik B, Munksgaard EC. Long-term calcium hydroxide as a root canal dressing may increase risk of root fracture. Dent Traumatol.2002;18:134-137.

18. Fardal O, Turnbull RS. A review of the literature on use of chlor­hexidine in dentistry. J Am Dent Assoc. 1986;112:863-869.

19. Portenier I, Waltimo T, Orstavik D, et al. Killing of Enterococcus faecalis by MTAD and chlorhexidine digluconate with or without cetrimide in the presence or absence of dentin powder or BSA. J Endod.2006;32:138-141.

20. Leonardo MR, Rossi MA, Silva LA, et al. EM evaluation of bacterial biofilm and microorganisms on the apical external root surface of human teeth. J Endod.2002;28:815-818.

21. Torabinejad M, Khademi AA, Babagoli J, et al. A new solution for the removal of the smear layer. J Endod. 2003;29:170-175.

22. Cobankara Fk, Adanr N, Belli S. Evaluation of the influence of smear layer on the apical and coronal sealing ability of two sealers. J Endod. 2004;30:406-409.

23. Torabinejad M, Shabahang S, Aprecio RM, Kettering JD. The antimicrobial effect of MTAD: an in vitro investigation. J Endod.2003;29: 400-403.

24 Ebihara A, Majaron B, Liaw LH, et al. Er:Yag laser modification of root canal dentine: influence of pulse duration, repetitive irradiation, and water spray. Lasers Med Sci. 2002;17:198-207.

25. Jha D, Guerrero A, Ngo T, Helfer A, et al. Inability of laser and rotary instrumentation to eliminate root canal infection. J Am Dent Assoc.2006;137:67-70.

26. Tronstad L, Asbjornsen K, Doving L, et al. Influence of coronal restorations on the periapical health of endodontically treated teeth. Endod Dent Traumatol. 2000;16:218-221.

27. Salehrabi R, Rotstein I. Endodontic treatment outcomes in a large patient population in the USA: an epidemiological study. J Endod. 2004;30:846-850.


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