Do procedural errors cause endodontic treatment failure? LOUIS M. LIN, PAUL A.

ROSENBERG and JARSHEN LIN J Am Dent Assoc 2005;136;187-193

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ABSTRACT
Background. This article reviews the effect of endodontic procedural errors, such as underfilling, A D A J overfilling, root perfora tions and separated instruments, on the outcome of endodontic N C U therapy. A ING EDU 4 RT Types of Studies ICLE Reviewed. Filling the root canal more than 2 millimeters from the radiographic apex (underfilling) or beyond the radiographic apex (overfilling), perforations of the root canal system and instrument separation are possible complications of endodontic therapy. Although these procedural errors may have different causes, they all may affect the outcome of treatment. Results. Endodontic procedural errors are not the direct cause of treatment failure; rather, the presence of pathogens in the incompletely treated or untreated root canal system is the primary cause of periradicular pathosis. Procedural errors typically are due to several factors. Among them is a lack of understanding of the root canal anatomy, the principles of mechanical instrumentation and tissue wound healing. Clinical Implications. Procedural errors impede endodontic therapy, thus increasing the risk of treatment failure, especially in teeth with necrotic pulps and periradicular lesions. However, procedural errors often are preventable. Key Words. Endodontic procedural errors; bacteria; treatment outcomes.
CON
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Do procedural errors cause endodontic treatment failure?

LOUIS M. LIN, B.D.S., D.M.D., Ph.D.; PAUL A. ROSENBERG, D.D.S.; JARSHEN LIN, B.D.S., D.D.S.

IO N

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ndodontic periradicular pathosis is the sequela of pulpal infection in the root canal system. The classic study by Kakehashi and colleagues1 showed that periapical inflammation developed in conventional laboratory rats but not in germ-free rats with surgically exposed pulps. In conventional laboratory rats, oral microorganisms entered the pulpal cavity and caused inflammation and necrosis, as well as subsequent periradicular tissue destruction. In germThe primary free rats, even when the canals were cause of packed with sterile food debris, neither periradicular pulpal necrosis nor periradicular inflampathosis is mation developed. In a clinical study, Sundqvist2 showed bacterial infection in the that bacteria could be cultured from the canals of traumatized necrotic teeth root canal with intact crowns if periapical lesions system. were present, but could not be cultured However, from necrotic teeth if periradicular procedural lesions were absent. Many studies have errors impede shown that factors such as pulpal and endodontic periradicular status, underfilling, overfilling, root perforations, separated therapy. instruments and ledge formation affect the prognosis for endodontic therapy. However, only two factorsroot canal infection at the time of root filling and a preoperative periradicular lesionhave been shown clearly to have a direct impact on the outcome of endodontic therapy.3-8 Clinicians generally believe that endodontic procedural errors, such as underfilling, overfilling, separated instruments, root perforations and ledge formation, are the direct cause of endodontic treatment

failure. However, procedural errors by themselves do not jeopardize the outcome of treatment unless a concomitant infection is present. A procedural accident often impedes therapy or makes it impossible for therapy to be completed (for instance, by preventing thorough mechanical dbridement or a bacteriatight seal of the root canal system). An increased risk of failure exists when a procedural accident occurs during treat187

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ment of infected teeth.9 The purpose of this article is to review critically the effect of procedural errors on the outcome of endodontic therapy.
UNDERFILLING OR INCOMPLETE FILLING OF ROOT CANALS

Underfilling or incomplete filling of the root canals (more than 2 millimeters short of the radiographic apex) often occurs as the result of incomplete instrumentation or ledge formation of the root canal during mechanical instrumentation. Incomplete instrumentation commonly is caused by inaccurate measurement of the working length or inadequate irrigation and recapitulation of canal patency and working length during instrumentation, thus leading to the accumulation of dentin filings and canal blockage. Ledge formation can be caused by the following: dinadequate straight-line access to the apical portion of the canal; dinadequate irrigation, lubrication or both; dexcessive enlargement of a curved canal with large files; dpacking of debris in the apical portion of the canal; dskipping of sequential file sizes.10,11 Consequently, the clinician does not remove the infected necrotic tissue remaining in the apical portion of the root canal because of incomplete instrumentation or ledge formation. In teeth with necrotic pulp and a periradicular lesion, bacteria colonize not only within the apical few millimeters of the canal, but also at the apical foramen. A key aspect of endodontic treatment is the elimination of bacteria from the root canal system.12-14 Unless this is done, persistent bacterial infection in the root canal may initiate or perpetuate periradicular inflammation after endodontic therapy.12,13,15 Many studies have shown a poorer prognosis for teeth with underfillings (68 percent success rate), especially those with necrotic pulp and a periradicular lesion, compared with teeth with flush-fillings (94 percent success rate) and overfillings (76 percent success rate).3,4,6 Chugal and colleagues16 reported that a 1-mm loss in working length increased the chance of treatment failure by 14 percent in teeth with apical periodontitis. However, if the unfilled canal does not contain irritants, such as bacteria or contaminated necrotic tissue, underfilling by itself would not cause periradicular inflammation.
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From about 1930 to the early 1960s, clinicians assumed that apical percolation and subsequent diffusion stasis of tissue fluid or blood components in the unfilled canal space could cause persistent periradicular inflammation.17 The socalled hollow tube concept has been disproved.18,19 Studies involving polyethylene tube implants in animals demonstrated clearly that blood components or tissue fluid stagnating inside the lumen of the tubes did not induce persistent inflammation in the tissue at the open ends of the tubes.18,19 In contrast, if the polyethylene tubes contained bacteria from the test animals oral cavity, moderate-to-intense inflammation was observed at the open ends of the tubes.20 Davis and colleagues21 demonstrated that when the canals of vital teeth in dogs were instrumented with a no. 80 file to within 1 mm of the radiographic apex and underfilled by 3 mm, some underfilled canal spaces became filled with viable connective tissue that was continuous with the periodontium one year after endodontic therapy. Similarly, Benatti and colleagues22 reported that when the canals of vital teeth in dogs were instrumented 2 mm beyond the apical foramen with nos. 40, 60 or 80 files and underfilled 1 to 3 mm short of the apex, the unfilled canal spaces exhibited ingrowth of periodontal connective tissue 120 days after endodontic therapy. de Souza Filho and colleagues23 demonstrated that when the canals of teeth in dogs with periradicular lesions were instrumented 2 mm beyond the apical foramen with a no. 60 file and underfilled by 2 to 3 mm, healing and ingrowth of connective tissue into the root canal occurred in 67.8 percent of the animals 90 days after endodontic treatment. This occurred because intracanal bacteria were eliminated. The authors believed that cases in which periradicular healing did not occur were due to persistent root canal infection resulting from incomplete removal of bacteria during instrumentation. Hrsted and Nygaard-stby24 treated patients with vital teeth that were scheduled for extraction. They found that when pulps were extirpated to the apical foramen and the canals were enlarged up to 2 to 4 mm coronally to the radiographic apex, the canal spaces between the root canal fillings and the apical foramen were occupied by connective tissue six to 10 months after endodontic therapy. Several clinical studies also have shown that if the root canals were completely dbrided of necrotic tissue and micro-

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organisms, the diseased periradicular tissues were capable of healing even without root canal fillings, provided that the coronal seal could prevent entry of oral microorganisms into the canal.25-28 These studies illustrate that root canal infectionnot unfilled canal spaceis the cause of periradicular inflammation.1 Studies also have shown that the quality of the root canal seal influences the prognosis for endodontic therapy. Adequate seals (that is, complete root canal obturation) have been associated with a higher success rate than have defective seals.3,4,6 Sjgren and colleagues6 reported that adequate root canal seals resulted in higher success rates (67 percent) than did inadequate seals (31 percent) in re-treatment cases. They conFigure 1. Teeth nos. 30 and 31 underwent endodontic cluded that bacterial infection in the root canal or therapy approximately three years before this radiograph was obtained. The mesiobuccal and mesiolingual canals in the periradicular tissues might be the cause of of tooth no. 31 were ledged and underfilled. The mesial endodontic treatment failure in underfilled or canals of tooth no. 30 also were underfilled. Both teeth were asymptomatic and had no periradicular lesion. inadequately sealed teeth. 16 Chugal and colleagues reported that in teeth with a diseased periapex in which the filling density of the root canal was fair (that is, only a few torily after proper endodontic therapy.6,32,33 The voids) or poor (many voids), 20 percent more response of the periradicular tissues to root canal treatment failures occurred than when the filling filling materials depends on the complex interacdensity was better (no voids). Underfilling per se tion between the properties of materials (that is, does not have a direct effect on the outcome of cytotoxicity, antigeneity and quantity) and the endodontic therapy; rather, it is the hosts immune defenses (innate and remaining infected necrotic tissue adapted). Root canal sealers are in the inadequately instrumented cytotoxic and irritating to the periUnderfilling per and incompletely filled canal that radicular tissues.34-36 Gutta-percha se does not have causes continuing irritation to the may act as a foreign body or hapten, a direct effect on periradicular tissues (Figure 1). but it is more biocompatible with the outcome of the periradicular tissues than are OVERFILLING OF ROOT endodontic therapy. root canal cements.37-40 CANALS However, Sjgren and colOverfilling of root canals (more leagues41 demonstrated that small than 2 mm beyond the radiographic apex) often particles of gutta-percha implanted subcutaoccurs as a result of inflammatory apical root neously in guinea pigs induced intense tissue resorption, an incompletely formed root apex or reaction, characterized by the presence of instrumentation through the apical foramen macrophages and giant cells. Other animal exresulting from inaccurate measurement of the periments also showed that excess root filling working length. In such cases, creating an apical materials extruded into the periradicular tissues stop becomes more difficult, thus leading to overwere capable of inducing periradicular inflammafilling. Numerous clinical studies have shown tion or necrosis of the periodontal ligament.35,42 that overfillings have a negative effect on the It is reasonable to assume that if materials prognosis for endodontic therapy.3,4,6 These accepted for use in endodontic therapy and studies indicate that filling materials might act extruded accidentally into the periradicular tisas a foreign body, causing irritation of the perisues were responsible for treatment failures, radicular tissues.29-31 almost all teeth overfilled with similar materials Nevertheless, not all overfilled teeth are would experience failure. However, clinical finddoomed to treatment failure, because approxiings do not appear to completely support the hismately 76 percent of overfilled teeth heal satisfactologic findings in animal experiments of periJADA, Vol. 136, February 2005 Copyright 2005 American Dental Association. All rights reserved. 189

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Figure 2. Tooth no. 10 underwent endodontic therapy more than 10 years before this radiograph was obtained. The canal was overfilled with silver point. The tooth was asymptomatic and had no periradicular lesion.

radicular inflammation in all overfilled teeth; approximately 76 percent of overfilled teeth heal satisfactorily without clinical signs and/or symptoms after proper endodontic therapy.3,4,6,32 Clinically successful endodontic treatment does not necessarily imply histologic periapical healing.43-45 Extruded root canal filling materials may cause localized periradicular inflammation and a delay in periradicular healing that may not result in treatment failure, as would be manifested by clinical symptoms or signs or by radiographic evidence of periradicular destruction.43-45 In an endodontic re-treatment study, Bergenholtz and colleagues46 reported that root filling material was not the immediate cause of unsuccessful treatment; rather, treatment failures were caused by a persistent root canal infection or by reinfection in the apical area resulting from overinstrumentation. Halse and Molven33 demonstrated that apical overfilling per se had little influence on the healing results of endodontic therapy, regardless of the preoperative periradicular status. They concluded that treatment failures were related closely to infection. Sjgren and colleagues6 also demonstrated that
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slight overfilling (< 2 mm beyond the radiographic apex) appeared to have no influence on the treatment outcome, even in teeth with apical periodontitis. Lin and colleagues47 reported that although the apical extent of root canal fillings had no correlation with endodontic treatment failure, intraradicular infection was a critical factor. Overinstrumentation frequently precedes overfilling, which inevitably poses the risk of forcing infected root canal contents into the periradicular tissues, thereby impairing the healing process.23,46,48 Endodontic treatment failures associated with overfilled teeth usually are caused by concomitant intraradicular infection, extraradicular infection, or both.9,13 Noiri and colleagues49 used the scanning electron microscope to examine extruded guttapercha cones retrieved from teeth that had undergone failed endodontic treatment. They demonstrated that biofilms had formed and attached to the extruded gutta-percha cones. Therefore, they believed that biofilms were the cause of persistent periradicular inflammation. Biofilm is an accumulation of microorganisms embedded in a self-produced extracellular polysaccharide matrix, adherent to a solid organic or inorganic surface.50,51 Biofilms constitute a protected mode of bacterial growth that enables organisms to survive in a hostile environment. Bacteria embedded within biofilms are resistant to both acquired immunological and nonspecific antimicrobial defenses, as well as to antimicrobial therapy.52 Phagocytes are unable to effectively engulf bacteria growing within a complex polysaccharide matrix adhering to a solid surface. Consequently, biofilms are remarkably resistant to phagocytes.53 Overfilling per se is not as irritating to the periradicular tissues as are intraradicular microorganisms (Figure 2). Nonetheless, overfilling is not encouraged, because the filling material may cause foreign-body giant cell reaction31 or may act as a foreign body that supports the formation of biofilms.51
SEPARATED INSTRUMENTS

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Instrument separation or breakage usually is caused by improper use or overuse of the instruments, as well as by excessive force applied to the instruments in curved or calcified canals during instrumentation. A limited number of studies pertain to the influence of instrument separation on

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the outcome of endodontic therapy. Crump and Natkin54 analyzed 53 endodontically treated teeth with separated instruments in the canals. They found no statistically significant difference in failure rates between root-filled teeth that had or had not experienced instrument separation. However, Frostell55 and Strindberg3 showed that rootfilled teeth in which instruments had separated experienced failed endodontic treatment 14 percent more frequently than did those in which instruments had not separated. Seltzer and colleagues56 reported that periapical repair could occur in endodontically treated teeth with separated instruments if vital pulps were present in the teeth before therapy. In contrast, instrument separation in root-filled teeth with necrotic pulps resulted in a less favorable prognosis.3,4,56-58 If a separated instrument can be bypassed and incorporated into the root canal filling, the prognosis for endodontic therapy is favorable.59,60 Torabinejad and Lemon11 suggested that the prognosis is best when separation of a large instrument occurs in the later stages of canal instrumentation close to the working length. The prognosis is poor for teeth with undbrided canals in which a small instrument is separated short of the apex or beyond the apical foramen early in instrumentation, because the prognosis depends on the extent of undbrided infected canal space apical to the separated instrument. Strindberg3 cautioned that instruments separated in the root canals should be considered a serious problem, because the practitioner does not know whether an infection was present apical to the separated instrument at the time of the accident. Accordingly, instrument separation is not the direct cause of endodontic therapy failure; rather, the separated instrument impedes the mechanical instrumentation of the infected root canal apical to the instrument, and that is the primary cause of treatment failure (Figure 3).
ROOT PERFORATIONS

Figure 3. Tooth no. 31 underwent endodontic therapy approximately two years before this radiograph was obtained. An instrument was separated in the canal of the mesial root. The tooth was asymptomatic and had no periradicular lesion.

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Figure 4. Endodontic therapy was performed on tooth no. 30 approximately three years before this radiograph was obtained. The mesiobuccal canal was perforated close to the furcation area and was repaired immediately with mineral trioxide aggregate. The tooth was asymptomatic and had no osteolytic lesion at the perforation site.

Root canal walls may become perforated as a result of iatrogenic causes, resorptive processes or caries. Iatrogenic perforations often are due to a lack of attention to the details of the internal anatomy of the root canal system and a failure to consider anatomical variations.61 Strip perforations (that is, perforation of canal walls resulting from excessive removal of canal dentin) may result from excessive enlargement of the coronal

third of small curved canals, which has been described as a danger zone.62 Perforations also can be caused by an inability to maintain canal curvature because of ledge formation. The prognosis for endodontically treated teeth with root perforations depends on several factors, such as the time that has elapsed before the dentist repairs the defect, the location of the perforation (its proximity to the gingival sulcus), the adequacy of the perforation seal and the size of the perforation.61 All of these factors are related closely to bacterial infection.63-65 Root perforations often prevent negotiation through the canal, as well as treatment of the original root canal apical to the perforations. Although dentists may treat a root perforation as a lateral canal in vital teeth with irreversible pulpitis, the often-neglected bac191

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terial contamination still plays an important role in the prognosis for endodontic therapy. Therefore, root perforations are not the direct cause of endodontic treatment failure. Rather, the primary cause of periradicular inflammation is the remaining infected tissue in the uninstrumented portion of the canal apical to the perforation (Figure 4).
CONCLUSION

The primary cause of periradicular pathosis is bacterial infection in the root canal system.1 Without the presence of bacteria, periradicular inflammation will not develop or persist, unless cytotoxic filling materials have been forced into the periradicular tissues.32,35 Endodontic procedural errors are not the direct cause of treatment failure. Rather, they increase the risk of failure because of the clinicians inability to eliminate intraradicular microorganisms from the infected root canals. s
Dr. Louis Lin is a professor and director of the Advanced Education Program in Endodontics, Department of Endodontics, New York University College of Dentistry, 345 E. 24th St., New York, N.Y. 10010, e-mail lml7@nyu.edu. Address reprint requests to Dr. Lin. Dr. Rosenberg is a professor and chair, Department of Endodontics, and associate dean for graduate programs, New York University College of Dentistry, New York City. Dr. Jarshen Lin is an instructor and a director of the predoctoral endodontic program, Department of Restorative Dentistry and Biomaterials Sciences, Harvard School of Dental Medicine, Harvard University, Boston. 1. Kakehashi S, Stanley HR, Fitzgerald RJ. The effects of surgical exposures in the dental pulps in germ-free and conventional laboratory rats. Oral Surg Oral Med Oral Pathol 1965;20:340-9. 2. Sundqvist G. Bacteriologic studies of necrotic dental pulp [odontological dissertation no. 7]. Ume, Sweden: Ume University; 1976:1-94. 3. Strindberg LZ. The dependence of the results of pulp therapy on certain factors: an analytic study based on radiographic and clinical follow-up examination. Acta Odontol Scand 1956;14(supplement 21):1175. 4. Kerekes K, Tronstad L. Long-term results of endodontic treatment performed with a standardized technique. J Endod 1979;5(3):83-90. 5. Bystrom A, Happonen RP, Sjogren U, Sundqvist G. Healing of periapical lesions of pulpless teeth after endodontic treatment with controlled asepsis. Endod Dent Traumatol 1987;3(2):58-63. 6. Sjgren U, Hagglund B, Sundqvist G, Wing K. Factors affecting the long-term results of endodontic treatment. J Endod 1990;16: 498-504. 7. Sjgren U, Figdor D, Persson S, Sundqvist G. Influence of infection at the time of root filling on the outcome of endodontic treatment of teeth with apical periodontitis. Int Endod J 1997;30:297-306. 8. Chugal NM, Clive JM, Spangberg LS. A prognostic model for assessment of the outcome of endodontic treatment: effect of biologic and diagnostic variables. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001;91:342-52. 9. Siqueira JF Jr. Aetiology of root canal treatment failure: why welltreated teeth can fail. Int Endod J 2001;34(1):1-10. 10. Frank RJ. Endodontic mishaps: their detection, correction, and prevention. In: Ingle JI, Bakland LK, eds. Endodontics. 4th ed. Baltimore: Williams & Wilkins; 1994:816-30. 11. Torabinejad M, Lemon RR. Procedural accidents. In: Walton R, Torabinejad M, eds. Principles and practice of endodontics. 3rd ed. Philadelphia: Saunders; 2002:310-30.

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