Chapter 13 OUTCOME OF ENDODONTIC TREATMENT AND RE-TREATMENT

John I. Ingle, James H. Simon, Pierre Machtou, and Patrick Bogaerts

A question that should be asked of any discipline or technique in dentistry is, What degree of success should be expected? Success, in turn, should be measured longitudinally in timelong-range success as opposed to short-term success. The beautiful resin restoration turning an ugly yellow in 1 year is not an unqualied success. By the same token, the denture worn in the bureau drawer is far from successful, nor is the well-tting partial denture successful if it leads to clasp caries in 6 months. Moreover, the endodontically treated tooth with a large periradicular lesion that does not show signs of healing 2 years after treatment cannot be considered a success. To answer the question, How successful is endodontic therapy? a study was undertaken at the University of Washington School of Dentistry to evaluate endodontically treated teeth to determine their rate of success. More important to the study, the rate of failure was also established, and the causes of failure were carefully examined. Analysis of the failures led to modications in technique and treatment. Finally, the entire discipline of endodontic therapy was re-examined, and denitive improvements were made as a result. The improvements in treatment are reected in the improvement in success, which increased to 94.45% from a former success rate of 91.10%, an improvement of 3.35 percentage points. In other words, nearly 95% of all endodontically treated teeth were successful. There was also a hidden agenda to the Washington studyto prove ourselves to a profession that, at that time, was skeptical of root canal therapy. In light of todays knowledge, the project had some design aws and misinterpretations and was not that well controlled, even though each phase was subjected to statistical analysis. The null hypothesis was ignored in an effort to prove a point: root canal therapy could be successful if properly done. On the other hand, the gures of the Washington study compared favorably with other reports of success.113

A group at Temple University, for example, reported a 95.2% success rate at the end of 1 year with 458 canals lled by the gutta-percha-euchapercha method.5 They found that teeth that started with vital inamed pulps had more success (98.2%) than teeth with nonvital pulps (93.1%). Contrary to other reports, however, they were far less successful with short-lled canals (71.1%) than with ush-lled or overlled canals (100%). (Reports of 100% success must be questioned.) South African researchers enjoyed a success rate similar to that of the Temple University group: 89% success at the end of 1 year.6 Also, as with the Temple group, they were successful 92% of the time in teeth lled to the apex and 91% of the time if the canals were overlled. Filling short of the apex reduced their success rate to 82%.6 The poorest reported rate of success dealt with 845 Dutch military servicemen.7 After 17 years, 45% of the endodontically treated teeth had failed in nonaviators, whereas only 7% had failed in aviator patients. There is a simple explanation for this wide discrepancy in failure rate. The aviators were usually treated with gutta-percha or silver point llings, whereas the nonaviators were more frequently treated by therapy with special chemical compounds. Furthermore, the aviators teeth were more frequently crowned.7 Hession, a highly respected endodontist in Australia, reported the highest rate of success: 98.7% of 151 teeth.8 Nelson reported lower rates in England: 81.9% of 299 teeth. With re-treatment, however, Nelson salvaged 11 of the treatment failures, raising the success rate to 85.6%.9 Kerekes and Tronstad, using the standardized technique recommended in this text, had a success rate similar to the Washington study,10 as did Sjgren and his associates from Sweden.11 Their remarkable study of 356 endodontic patients, re-examined 8 to 10 years later, reported a 96% success rate if the teeth had vital pulps prior to treatment. The success

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rate dropped to 86% if the pulps were necrotic and the teeth had periradicular lesions and dropped still lower to 62% if the teeth had been re-treated. They concluded by stating that teeth with pulp necrosis and periradicular lesions and those with periradicular lesions undergoing re-treatment constitute major therapeutic problems They surmised that bacteria in sites inaccessible might be the cause of increased failure.11 Worldwide, most controlled studies seem to agree that a lower success rate is associated with overlled canals, teeth with preexisting periradicular lesions, and teeth not properly restored after root canal therapy.1115 A Swedish group reported a high failure rate if canals were not totally obturated.13 Sjgren et al., quoted above, also noted a direct correlation between success and the point of termination of the root lling.11 As Figure 13-1 shows, teeth lled within 0 to 2 mm from the apex enjoyed a 94% success rate, which fell to 76% if the teeth were overlled and fell further to 68% if they were lled more than 2 mm short. In reported re-treatment of initial endodontic failures, success gures have been unacceptably low. Only 50% of the overlled teeth were acceptable (Figure 132). Similarly, a Japanese group reported a much higher failure rate if root llings were overextended.14 Surprisingly, a Dutch group enjoyed as high a healing rate whether or not the canals were lled.16 The Dutch report was only a 2-year study. Unlled canals had not been followed over a long period of time (such as 10 to 20 years). Most endodontically treated teeth should last as long as other teeth. Vire examined 116 root-lled teeth that were extracted because of failure and found that only 8.6% failed for endodontic reasons compared with 59.4% restorative failures and 32% periodontal failures.17

Figure 13-2 Results of re-treatment of previously lled roots with apical periodontitis with regard to the level of the nal root lling in relation to the root apex. Number of healed lesions/number of preoperative lesions. Reproduced with permission from Sjgren U.11

The Washington Study The gures above from the University of Washington are only a few from an exhaustive study encompassing many aspects of endodontic therapy. The modications in treatment mentioned above were instituted following a pilot study of endodontic success and failure. Even with the limited number of patients in the pilot study, the causes of failure became apparent. Clinical techniques were then changed in an effort to overcome failure. Patients were recalled for follow-up at 6 months, 1 year, 2 years, and 5 years, and the recall radiographs were carefully evaluated for improvement or lack of improvement. Teeth included in the success group were those that demonstrated decided periradicular improvement (Figures 13-3 and 13-4) and those with continuing periradicular health (Figure 13-5). The failures were made up of those teeth that initially demonstrated periradicular damage and that had not improved (Figure 13-6), as well as those that had deteriorated since treatment (see Figure 13-6). As soon as a statistically signicant group of cases built up in the le, the material was ready to be analyzed. The 2-year recall series was found to be ideal for this study because a statistically signicant sample developed within this group. The 5-year recall sample was also analyzed but in understandably smaller, though signicant, numbers. The study did not take into consideration any illnesses or systemic differences between patients. Two-Year Recall Analysis. Of a total population of 3,678 patients who could have returned for 2 years, 1,229 actually did return, a recall rate of 33.41%a statistically signicant cohort. Before improvements in technique and case selection were instituted, there was

Figure 13-1 Outcome of treatment according to the level of the root lling in relation to the root apex in cases with preoperative pulp necrosis and apical periodontitis. Number of healed lesions/number of preoperative lesions. Reproduced with permission from Sjgren U.11

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Figure 13-3 Special mount for radiographs taken of each case. Note that recall lms are exposed at 6 months, 1 year, 2 years, and 5 years following therapy. Figures at the top of the card indicate that complete healing had occurred at 6 months and was maintained for 5 years.

a 91.10% success rate104 failures of 1,067 cases. After these improvements were instituted, the success rate rose to 94.45%9 failures of 162 cases. Five-Year Recall Analysis. From the beginning of the study, enough 5-year recalls had returned to make a statistically valid analysis of these cases. Of the 302 5-

year recalls, 281 teeth were successfula success rate of 93.05%; 21 teeth were considered failuresa failure rate of 6.95%. These gures compare favorably with the 2-year recall analysis. Two-Year Recall Analysis by Age of Patient. Reference is frequently made to age as a criterion for

Figure 13-4 A, Before radiograph, with large periradicular lesion. B, Treatment radiograph immediately following periradicular surgery. Also note the fractured root tip of a central incisor (arrow) that tests vital. C, Two-year postoperative radiograph of successfully treated case. Lack of total periradicular repair (moderate repair) is related to extensive surface of lling material over which cementum cannot grow. Also note fracture repair (arrow) of vital central incisor.

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Figure 13-5 A, Pulpless mandibular lateral incisor with no periradicular lesion. B, Constant periradicular health is revealed in a 2-year postoperative radiograph, a successful case.

Figure 13-6 Two failure cases demonstrated in a single radiograph. Curved arrow (right) points to a lesion that has failed to heal 2 years following endodontic treatment. Straight arrow (left) points to a lesion that has grown worse 2 years following therapy. Lack of total obturation of canals is revealed by the fuzzy appearance of root canal llings. Defective amalgam restoration (open arrow) contributes to an interproximal periodontal lesion.

endodontic treatment. The youngest patient treated in the study was 212 years old; the oldest patient was 92 years old. There was a fairly consistent rate of success and failure according to age as shown by statistical analysis (2 = 2.72; p > .09). Age, of course, has a great deal to do with the size and shape of the canal. It was found that older teeth, with more restricted canals, were more successfully obturated than very young teeth with large-diameter canals. It also became obvious that the size and shape of the lumen of the canal, as well as the direction of root curvature, play an important part in the successful completion of a root canal lling. Analysis of success, by individual tooth, will demonstrate these points. Two-Year Recall Analysis by Individual Tooth. No signicant difference in failure existed between any of the teeth in either arch ( 2 = 2.45; p > .10). Thus, no particular tooth can be considered a higher endodontic risk, although there was a wide discrepancy between the mandibular second premolar with a failure rate of 4.54% and the mandibular rst premolar with a failure rate of 11.45%. Canal anatomy might account for the greater increase in failure in the rst premolar. Pucci and Reig, in their monumental work Conductos Radiculares, pointed out the great anatomic differences

Outcome of Endodontic Treatment and Retreatment between the two mandibular premolars.18 Whereas the mandibular second premolar has two canals and two foramina 11.5% of the time, the mandibular rst premolar has branching canals, apical bifurcation, and trifurcation 26.5% of the time.18 Others have found similar discrepancies between mandibular premolars, most recently Trope et al. at the University of Pennsylvania.19 These researchers conrmed one of Pucci and Reigs ndings almost exactly: 23.2% of the mandibular rst premolars examined had two canals. They also found that 7.8% of second premolars had two canals, a gure differing from Pucci and Reigs 11.5%. This discrepancy could well be explained on an ethnic basis: the researchers at Pennsylvania reporting on a US African American population and Pucci reporting on a Uruguayan population containing some aborigines. The Pennsylvania study also conrmed the notion that African American patients more frequently have two canals in lower premolars than white patients. In the rst premolars, 32.8% had two canals, compared with 13.7% of whites. In the second premolars, 7.8% of African Americans had two canals, compared with 2.8% of whites. Nearly 40% of the African Americans in the study had at least one premolar with two canals and 16% of the time presented two separate roots in mandibular rst premolars.19 Failures in the maxillary lateral incisor may also be explained by anatomic differences. Pucci and Reig showed extensive distal curvature of the maxillary lateral incisor root 49.2% of the time.18 Here again, poor judgment and preparation frequently prevent adequate instrumentation and obturation, with root perforation at the curvature a common occurrence (Figure 13-7). Increased failure rate in the maxillary lateral incisor is also related to continuing root resorption following treatment, a nding peculiar to these teeth. The overall failure rate, mandible to maxilla, is striking but not statistically signicant. Failure in the mandibular arch was encountered 6.65% of the time and 9.03% of the time in the maxilla. Two-Year Recall Analysis: Nonsurgical versus Surgical Intervention. The degree of success achieved by surgical intervention in treated endodontic cases has long been a contentious point. The Washington study demonstrated that although nonsurgical treatment appears to be slightly more successful than surgical treatment, differences are not statistically signicant (2 = 3.44; p > .05). It is tempting to indict case selection as the basis for increased failure of surgical treatment. One of the indications for surgical intervention has been the grossly

751

Figure 13-7 Root tip biopsy from the curved apex of a maxillary lateral incisor. Severe inammatory reaction surrounding the root end is related to perforation as well as failure to dbride and obturate the curved portion of the canal. Reproduced with permission from Luebke RG, Glick DH, Ingle JI. Oral Surg 1964;18:97.

involved periradicular lesion, where a lower rate of repair might be expected. Although the 10 to 12 mm periradicular lesion appears to heal as readily, if not quite as rapidly, as the 2 mm lesion (Figure 13-8), this may not always be true. Others have shown that larger lesions, or cases with lesions versus those without, are less successful. Nelson reported that the failure rate was three times higher if a periradicular lesion existed before treatment.9 In another study, the failure rate was the same.16 The Dutch study, interestingly enough, found that teeth with periradicular granulomas tend to heal less successfully than teeth showing cysts.12 Similarly, Japanese researchers reported a wide discrepancy in success between treated teeth that had no periradicular rarefaction (88%) and those with a 5.0 mm or greater rarefaction (38.5%).14 For those teeth without periradicular lesions, Sjgren et al. reported a 96% success rate, but this rate dropped to 86% if periradicular lesions were present.11 Two-Year Recall Analysis of Endodontic Failures. The nal and most important portion of the Washington study dealt with 104 failure cases as a group. Careful analysis of these particular cases is most revealing. Arrangement of Failures by Frequency of Occurrence. As Table 13-1 shows, the most striking nding is the 58.66% of the failures caused by incomplete obturation of the canal (Figure 13-9). This is a highly signicant gure. This most common cause of failure is almost 50 percentage points ahead of the next greatest cause of failure, root perforation, which

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Figure 13-8 Large periradicular lesion (left) has healed completely (right) within 6 months in a patient 20 years of age.

Table 13-1 Distribution of Failures of Treated Endodontic Cases: Two-Year Recall by Frequency of Occurrence
Causes of Failure Number of Failures % Failures

Incomplete obturation Root perforation External root resorption Coexistent periodontalperiradicular lesion Canal grossly overlled or overextended Canal left unlled Developing apical cyst Adjacent pulpless tooth Silver point inadvertently removed Broken instrument Accessory canal unlled Constant trauma Perforation, nasal oor Total failures

61 10 8 6 4 3 3 3 2 1 1 1 1 104

58.66 9.61 7.70 5.78 3.85 2.88 2.88 2.88 1.92 0.96 0.96 0.96 0.96 100.00

Distribution of 104 endodontic failures 2 years following therapy. When arranged by frequency of occurrence, note that incomplete obturation accounts for almost 60% of all failures, followed by root perforation, which accounts for nearly 10% of 104 failures. Cause of failure includes infrequently encountered conditions that occur less than 1% of the time.

accounts for 9.61% of the failures. Thus, the two greatest causes of failure stand revealed: inadequate cleaning and shaping and incomplete obturation. In other words, over two-thirds of all of the endodontic failures in the study were related to inadequate performance of two points of the endodontic triad, canal instrumentation and canal obturation. This alone would call for improved technique and attention to detail. Categorical Arrangement of Causes of Failure. The 13 causes of endodontic failure may be arranged in three general categories of causes leading to failure: (1) apical percolation, (2) operative errors, and (3) errors in case selection (Table 13-2). Actually, a clear-cut delineation of the agents of failure is difficult; apical percolation into the canal accounts for almost all of these failures, as Table 13-2 shows. Apical Percolation. Three of the causes of failure shown in Table 13-2 lead to apical percolation and subsequent diffusion stasis into the canal (Figures 13-10 and 13-11). Factor in the bacteria lurking in the region and these three causes together account for 63.47% of all of the endodontic failures in the study and demonstrate how vital careful therapy is to success. One must also consider the potential of microleakage under and around coronal restorations: bacteria penetrating from the crown to the periapex alongside poorly obturated canals. Operative Errors. A category made up of errors in coronal cavity preparation and canal preparation accounts for almost 15% of the failures (root perforation, 9.61%; broken instrument, 0.96%; and canal grossly overlled, 3.85%; total, 14.42% of all of the failures).

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Figure 13-9 Left, Careful examination of an initial radiograph reveals internal resorption and widening of the canal apical to the curved arrow. Right, In a 2-year recall radiograph, periradicular lesion persists owing to failure to totally obliterate the root canal space (arrow).

Table 13-2 Distribution of Failures of Treated Endodontic Cases: Two-Year Recall by Category of Cause of Failure
Causes of Failure Number of Failures % Failures

Apical percolationtotal Incomplete obturation Unlled canal Ag point inadvertently removed Operative errortotal Root perforation Canal grossly overlled or overextended Broken instrument Errors in case selectiontotal External root resorption Coexistent periodontalperiradicular lesion Developing apical cyst Adjacent pulpless tooth Accessory canal unlled Constant trauma Perforation, nasal oor Total failures

66 61 3 2 15 10 4 1 23 8 6 3 3 1 1 1 104

63.46 58.66 2.88 1.92 14.42 9.61 3.85 0.96 22.12 7.70 5.78 2.88 2.88 0.96 0.96 0.96 100.00

Distribution of 104 endodontic failures 2 years following therapy. Causes of failure may be categorized into three general groupings: apical percolation, which accounts for 63.46% of failures; operative errors, which account for 14.42% of failures; and errors in case selection, which account for 22.12% of the 104 failures.

These operative errors are all related to inadequate coronal cavity preparation, improper use of endodontic instruments and lling materials, and lack of standardization of endodontic equipment and material as it arrives from the manufacturer. The latter problem has now been reduced through instrument standardization. On the other hand, delicate root canal instruments must not be mistreated by the inexperienced, and one of the common complaints of the neophyte is instrument breakage. Also, improper use of the instruments causing root perforation and apex perforation accounted for 14 of the 104 failures in the study. Penetrating through the side of a curved root ultimately leads to incomplete instrumentation and incomplete obturation (Figure 13-12). Opening wide the apical foramen during instrumentation illustrates that this is also a form of perforation and leads to gross overlling or overextension. Healing is delayed and often incomplete around the grossly overlled areas that may be caused by foreignbody reaction. Moreover, the perforated apical foramen has destroyed the apical stop and does not allow compaction during canal lling. Although the canal may appear overlled, it is actually incompletely obturated, with resulting percolation and failure (Figure 13-13). The paucity of failures in this study owing to broken instruments illustrates that this is not as desperate a situation as it is often considered to be. In analyzing the University of Washington caseload, Crump and Natkin found that failure following instrument fragmentation was the same as in other endodontic cases.20 Broken instruments, however, are not favored any more than overlling and underlling are favored, but, occasionally, both accidents may occur. Surgical treatment is recommended in operable teeth if the instrument is broken off in the apical one-third of the canal

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Figure 13-10 A, Although the root canal lling appears to be overextended, the fuzzy appearance indicates a lack of density necessary for total obturation. Apical perforation destroyed the apical constriction necessary for compaction of the root canal lling. B, Root end biopsy of this failure case shows root canal cement and cellular debris rather than well-condensed gutta-percha lling. Constant percolation into the root canal space provides media for bacterial growth.

Figure 13-11 A, Constantly draining sinus tract opposite the mesiobuccal root of a maxillary rst molar (arrow) was thought to be related to an advanced periodontal lesion. Total amputation of the mesiobuccal root is indicated. B, Amputated root reveals an error in diagnosis. The reamer is in an undetected second canal, whereas the arrow points to an obturated primary canal. Secondary canals in mesiobuccal roots of rst permanent molars occur about 60% of the time.

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Figure 13-12 Failure owing to root perforation accompanied by incomplete dbridement and imperfect obturation. Note the break in the lamina dura opposite the perforation (arrow).

and is loose in the canal and cannot be removed or bypassed. Surgery may also be the approach if the canal is grossly overlled with irretrievable gutta-percha and

cement. Broken instruments may often be retrieved by oating out the piece with an ultrasonically powered instrument. Broken instruments, loose in the canal, have also been seen to rust out. Failures associated with underlled canals can usually be remedied by retreatment rather than surgery (see Chapter 14). All of these errors of operation may be prevented by careful cavity preparation and canal obturation. For example, if the operator is unsure of the instrument position in the canal, a radiograph should be taken. Also, more accuracy in tting the primary or initial lling point will lead to less overlling. In the nal analysis, operative error is the simplest cause of failure to control and requires more patience, care, and understanding to overcome. Errors in Case Selection. Errors in case selection are not as easily overcome as operative errors and may often be listed as the bad breaks of the game rather than errors in judgment. Who could predict, for example, that external root resorption would continue, an apical cyst would develop following treatment, an adjacent tooth would become pulpless, or an associated periodontal

Figure 13-13 A, Although this incisor appears to be grossly overlled, careful examination (arrow) reveals failure to totally obturate the canal. B, Tissue reaction to overlling and underlling in a single biopsy specimen from this failure case. Curved arrows direct attention to a mass of cement forced into periradicular tissue. Heavy black arrow (right) indicates noninammatory tissue capsule that has developed as foreign-body reaction. Open arrow (bottom) points to a violent inammatory reaction and an abscess related to bacterial products percolating from the unlled canal.

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Endodontics lar lingual grooves extending to the apex24 (Figure 1314) or the resorptive invasion from one endodontic lesion causing the necrosis of an adjoining tooth25 (Figure 13-15). There are, of course, multiple causes of failure not revealed in the Washington study: retrolling failures, root tip and foreign bodies left in surgical sites, root fenestration following surgery (Figure 13-16), cracked or split roots, or carious destruction unrelated to the root canal treatment (Figure 13-17). Ultimately, in all of these situations, bacteria are the nal cause of failure. One must also recognize that one of the most frequent causes of failure of the treated pulpless tooth is fracture of the crown. The tooth must be carefully protected by an adequate restoration. The Washington study has been faulted by some for being only a radiographic study. As Brynolf pointed out in her classic punch biopsy study of root-lled teeth in cadavers, histologic evaluation is a much more accurate method of determining if inammation remains at the apex than is radiologic evidence.26 But her research was done on cadavers, proving the impracticality of punch biopsy on live patients. Green and Walton followed up on Brynolf s approach, comparing histologic and radiographic ndings on cadavers, and also found that 26% of the teeth with no radiolucencies showed chronic inammation histologically.27 But that is not to say that these teeth were uncomfortable or contributing to the patients poor health. How successFigure 13-14 Developmental defect, invagination, and radicular lingual groove, resulting in an unattached periodontal ligament tract to the apex. The defect at the cingulum probably communicated with the pulp. Endodontic and periodontic therapy were to no avail. Reproduced with permission from Simon JHS, Glick DH, Frank AL. Oral Surg 1971;37:823.

lesion would lead to failure?21 These are all factors that led to some of the failures in the Washington study, factors that constitute 22.12% of the total failures. Some could well have been predicted at the time of therapy, but others were entirely unpredictable. As Table 13-2 shows, there were also minor causes of failure: constant occlusal trauma from bruxism,22 perforation of the nasal oor, and unlled accessory or lateral canals. The low incidence of failure associated with unlled accessory canals came as a surprise considering the degree of emphasis placed by some on the absolute necessity of totally obliterating these lateral canals. Returning to some of the greater causes of failure, one should note that all eight cases of continuing root resorption were in maxillary lateral incisors. So one should be wary in evaluating the future of these teeth if they exhibit extensive apical resorption prior to treatment. Most external apical root resorption stops in response to successful root canal treatment! Endodontic failure associated with periodontal pockets is usually the fault of the dentist for not recognizing the pockets existence. One stumbles ahead with the endodontics before careful probing reveals the presence of an associated pocket and that concurrent periodontal/endodontal therapy will be necessary.23 In some cases, concurrent treatment may not solve an unsolvable problem. Witness the destructive and irreparable nature of some dens invaginatus or radicu-

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Figure 13-15 A, No radiolucency is apparent on a 4-year recall radiograph following root canal lling of a rst premolar. Note the anatomic defect on the canine (arrow). B, Radiograph taken 6 years after the lesion was rst noticed. Failed root canal lling in the premolar led to periradicular lesions, inammatory external resorption of canine, and ultimately necrosis of the canine pulp. Reproduced with permission from Frank AL.25

ful is success? Better yet, what are the criteria of success? Comfort and function? Radiographic? Histologic? Since histologic evaluation is impractical, if not illegal, one would have to go with comfort and function and the radiographic ndings. There are well over 50 studies attempting to delineate how successful our treatment procedures are and what the prognosis is for a particular form of treatment.28 All in all, the studies that have been done suggest the following generalizations: 1. The more extensive and severe the endodontic pathosis, the poorer the prognosis. In other words,

the highest percentage of success is with teeth with vital pulps and the worst prognosis is for those with large, long-standing periradicular lesions. 2. The more dental treatment that is done, the poorer the prognosis. In other words, good nonsurgical endodontic treatment has the best prognosis. The worst prognosis lies with teeth that have been retreated nonsurgically and then re-treated surgically once or twice more. MICROBES To further elaborate on the role bacteria play in pulpal and periradicular disease, one must turn to the classic research by Kakehashi and his associates at the National Institute of Dental Research.29 They were able to show, in a gnotobiotic study, that microorganisms alone cause pulpal inammation and necrosis as well as periradicular infection.29 It follows that inadequate removal of microbes (ie, bacteria, fungi, and viruses) from the canal leads to continued infection and inammation30 and that all of the defects listed in the Washington study are ultimately reduced to bacterial invasion and/or colonization. But what happens when everything is done right (ie, cleaning, shaping, and obturation), yet failure still occurs?3134 Can bacteria still be present after adequate endodontic treatment? There is strong evidence that bacteria may not be completely eliminated after thorough cleaning, shaping, and disinfection.3537 Moreover, when obturation is postponed, bacteria may be able to recolonize in the canal.38 Furthermore, try as one might, no preparation

Figure 13-16 Severe bony and soft tissue dehiscence extending to the periapex of a traumatized incisor. Postoperative defects of this type may develop following surgery in an area of osseous fenestration. Reproduced with permission from Luebke RG, Glick DH, Ingle JI. Oral Surg 1964;18:97.

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Figure 13-17 Postoperative failure owing to extension of dental caries rather than endodontic therapy per se. Loss of these abutment teeth led to full denture in this case.

technique can totally eliminate the intracanal irritants, and a critical amount can sustain periradicular inammation (Figure 13-18).39,40 In addition, as stated previously, the obturated canal may be recontaminated from coronal leak-

age.41 Indeed, gutta-percha root canal llings do not resist salivary contamination.42,43 As Ray and Trope have been able to show, long term prognosis of treatment seems to correlate directly with the quality of the coronal seal.44

Figure 13-18 A, The radiograph shows a mandibular cuspid that appears well obturated with a well-tting coronal restoration. B, A sinus tract is traced with a gutta-percha point to the apical lesion that has not responded to treatment. C, Surgical resection of the root end. D, High-power photomicrographs show bacteria containing plaque on the external root surface.

Outcome of Endodontic Treatment and Retreatment There are also times when an irritant, such as infected dentin chips, is packed at the apex or pushed through the apex, there to serve as a continuing irritant45,46 that overwhelms the bodys defense system. As stated before, the periapical tissue could become colonized by periodontal contamination,47 the virulence of the bacteria, or extrusion by overaggressive instrument action.4850 In most cases, the hosts immune system can overcome these antigens.51 On the other hand, some bacteria possess mechanisms to resist phagocytosis such as encapsulation or the production of proteases aimed against the immune system.52,53 Bacteria may also bury themselves in a thick matrix that acts as a sort of apical plaque (see Figure 13-18, D).5456 Many organisms can survive in periradicular lesions: Actinomyces, Peptostreptococcus,5760 Propionibacterium,61,62 Prevotella and Porphyromonas, 6365 Staphylococcus,66,67 and Pseudomonas aeruginosa.35 Barnett, in fact, has stated that Pseudomonas refractory periradicular infection could be cured only by heavy doses of metronidazole (Flagyl) following the failure of re-treatment and apicoectomy.68 FOREIGN BODIES In spite of what has been stated above, foreign-body giant cell reaction can occur without the presence of bacteria, but no fulminating infection will develop without the bacteria. A number of foreign bodies have been reported: lentil beans,69 other vegetables,70 popcorn kernels71 (Figure 13-19), paper points, cellulose, and a variety of unidentied materials.72 Human body defense cells are unable to digest cellulose or cotton pellets.72,73 In addition, various lipids, cholesterols, and crystals have also been implicated as periradicular irritants. By their very presence, these intrinsic factors are capable of sustaining an apical lesion despite correct endodontic treatment.74 Root canal sealers can also act as a foreign body and thus sustain a lesion, although, over time, extruded sealers (and gutta-percha) may be phagocytized by macrophages.75 The cytotoxicity of freshly mixed and unset sealers is well documented.76 In the long term, however, obturation materials are far less irritating than microbes.75 It can be concluded that an overll may cause a delay in healing but will not prevent it.77 EPITHELIUM The role of epithelium must also be taken into account when reviewing failure to heal periapically. If the resting cells of Malassez remain in the region, they may

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respond to the irritants and inammation and proliferate into a cyst-like attempt to wall off the irritants.78 It has been suggested that these latent epithelial cell rests could be activated by the epidermal growth factor present in saliva that contaminates canals left open for drainage.79,80 In the absence of treatment, or in the presence of persistent bacteria, epithelium continues to proliferate to become a bay (pocket) cyst and eventually a true cyst.81,82 The distinction between a bay (pocket) cyst (Figure 13-20) and a true cyst is important from a clinical standpoint. Since root canal therapy can directly affect the lumen of the bay (pocket) cyst, the environmental change may bring resolution of the lesion. There is a controversy over whether cysts heal after nonsurgical endodontic treatment. The true cyst is independent of the root canal system, so conventional therapy may have no effect on it. The prevalence of true cysts is less than 10%. 65,66 Most practitioners now realize that true cysts, as well as some bay (pocket) cysts, probably do not heal with nonsurgical therapy. In spite of good cleaning, shaping, and lling, these lesions have to be surgically removed to effect healing. The dangers delineated above emphasize the point initially stressed: if the case is carefully selected before treatment, if the canal is correctly instrumented and obturated, and if the crown is properly restored, the ultimate outcome should be successful.

Figure 13-19 Biopsy of what was thought to be a root tip reveals columnar-like cells (arrow) of the outer husk of a popcorn kernel that was trapped in a fresh surgical area and served as a severe irritant.

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Figure 13-20 A, Periradicular lesion persisting 2 years following endodontic therapy appears to be either an apical cyst or chronic apical periodontitis. B, Biopsy of the periapex demonstrated the epithelial lining of an apical cyst (arrow). Persistence of development of apical cysts led to failure in three cases in study.

Measures to be Employed to Improve Success. One may draw certain conclusions from this study and nally list a number of procedures to improve the rate of success of treated endodontic cases. These are the Ten Commandments of Endodontics: 1. Use great care in case selection. Be wary of the case that will be an obvious failure, but, at the same time, be daring within the limits of capability. 2. Use greater care in treatment. Do not hurry; maintain an organized approach. Be certain of instrument position and procedure before progressing. 3. Establish adequate cavity preparation of both the access cavity, which can be improved by modications of the coronal preparation, and the radicular preparation, which can be improved by more thorough canal dbridementcleaning and shaping. 4. Determine the exact length of tooth to the foramen and be certain to operate only to the apical stop, about 0.5 to 1.0 mm from the external orice of the foramen. 5. Always use curved, sharp instruments in curved canals, and especially remember to clean and reshape the curved instrument each time it is used. This applies to stainless steel instruments.

6. Use great care in tting the primary lling point. One must be certain to obliterate the apical portion of the canal. Be more exacting in the total obturation of the entire root canal. Always use a root canal sealer cement. 7. Use periradicular surgery only in those cases for which surgery is denitely indicated. 8. Always check the apical density of the completed root canal lling of the patient undergoing periradicular surgical treatment, and this should be done by using a sharp right-angled explorer. If found wanting, the apical foramen is prepared and retrolled. 9. Properly restore each treated pulpless tooth to prevent coronal fracture and microleakage. 10. Practice endodontic techniques until the procedures are as routine as the placement of an amalgam restoration or the extraction of a central incisor. Practice on extracted teeth mounted in acrylic blocks is especially recommended. Careful attention to details in following the Ten Commandments of Endodontics will ensure a degree of success approaching 100%.

Outcome of Endodontic Treatment and Retreatment PROGNOSIS All of this having been said, it should be possible to predict the outcome of endodontic treatment. With the benet of education and experience and some plain luck, one should be able to choose the proper cases for endodontic treatment and reject those that will obviously fail. But it is not quite that simple. The practicing dentist should not be cited for faulty judgment when even the experts tend to disagree on prognosis. A North Carolina group, for example, found considerable disparity in treatment choice between general practitioners and endodontists who were shown seven controversial cases.83 In another instance, Holland and his collaborators reviewed 17 prognosis studies dealing with success or failure of teeth with and without periradicular lesions.84 In the with lesion column, successful outcome ranged from a low of 31.8% to a high of 85%. On the other hand, there was general agreement among these 17 experts that a greater success rate may be enjoyed if there is no initial periradicular lesion present. This is not to say that teeth with periradicular lesions should be shunned. On the contrary, respectable success rates have been reported by many who have treated teeth with radiolucent lesions. All in all, one must ultimately develop condence in ones own abilities. Being able to practice using a variety of techniques and not being married to a single approach in every case greatly enhances ones capabilities. This is the basis of good prognosis, the result of skill, knowledge, and self-condence. On the other hand, if a treated tooth does fail, it may be resurrected by skillful re-treatment! SUCCESSFUL RE-TREATMENT One must recognize that the patients in the Washington study were all controlled university clinic or specialty practice patients, as were the patients in many of the other success and failure reports, an important consideration in evaluating these outcomes. In marked contrast, worldwide reports of endodontic success and failure in a cohort of general practice patients is an entirely different matter.44,85103 To make matters worse, the periradicular lesions in these reports were associated with previously treated endodontic general practice cases and were much higher (24.5 to 46%) than the periradicular lesions in nontreated teeth (1.4 to 10%) (Table 13-3). There is also a very disappointing nding in a general survey by Buckley and Spngberg at the University of Connecticut; they noted that periradicular lesions are found 5 to 10 times more often in endodontically treated teeth than for teeth without root llings.101

761

Mactou pointed out that the quality of treatment plays a decisive role in the successful outcome of endodontic therapy (Figure 13-21) (personal communication, April 2000). Fortunately, treated root canals with inadequate results may be re-treated to improve the quality of the treatment and heal any apical lesion. (Figure 13-22) Bergenholtz et al., for example, reported on 556 retreatment cases in which 50% completely healed after 2 years, and in an additional 30%, the lesions were signicantly reduced in size.104 In a 2-year follow-up study, Bergenholtz et al. also reported a 94% success rate for re-treatments done for one reason only, to improve root canal lling quality prior to prosthodontic therapy.105 Friedman et al. claimed a 100% success rate in retreatment of endodontic cases presenting without periradicular lesions, which suggests that if infection is not present, and re-treatment is performed by skilled clinicians, the success rate can be expected to be very high (Table 13-4). On the other hand, if periradicular lesions are present before re-treatment, the success rate can be expected to fall to around 70% (Table 13-5).28 As many as 22 factors have been listed to affect the prognosis of endodontic re-treatment, the preoperative

Figure 13-21 Apical perforation through overinstrumentation leads to loss of the apical stop, gross overextension, and failure to compact the canal lling. Notice that instrumentation has resulted in a canal that is short of the apex. (Courtesy of Dr. Pierre Mactou.)

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Endodontics

Figure 13-22 A, Failure case with apical and lateral periradicular lesions. B, Re-treatment eliminates bacterial infection through extensive recleaning, reshaping, and canal medication. Obturation by vertical compaction lls the lateral canal as well. C, Complete healing 1 year later. (Courtesy of Dr. Pierre Mactou.)

state of the tooth (as above) obviously being a key factor in outcome.106 Stabholz et al.107 and Friedman108 have noted that causes of endodontic failure fall into three categories: preoperative, intraoperative, and postoperative causes. Of these three, intraoperative, that is, iatrogenic, causes are the most prevalent but the most easily controlled.109 For example, Nair has pointed out that refractory periradicular infections are found in

acute symptomatic teeth.110 At the same time, others have noted that these bacteria may have been planted there as contaminants during previous endodontic treatment.110116 As previously stated, infected dentin chips, extruded from overinstrumentation, may also be the root cause of refractory infections.103 Bergenholtz has stated thatroot lling material [per se] was not the immediate cause of the unsuccessful cases, but that

Table 13-3 Cross-sectional Studies on the Presence of Periapical Periodontitis (PAP) in Nontreated and Endodontically Treated Teeth and Quality of Treatment
Lead Author Country Teeth with PAP (%) Endodontically Treated Teeth (%) Endodontically Treated Teeth with PAP (%) Technically Inadequate Treatment (%)

Bergenholtz, 1973 Hansen, 1976 Petersson, 1986 Allard, 1986 Eckerbom, 1987 Eriksen, 1988 Odesjo, 1990 Imfeld, 1991 De Cleen, 1993 Buckley, 1995 Soikkonen, 1995

Sweden Norway Sweden Sweden Sweden Norway Sweden Switzerland Netherlands United States Finland

6 1.5 6.9 10 5.2 1.4 2.9 8 6 4.1 4

12.7 3.4 12.4 18 13 3.4 8.6 20.3 2.3 5.5 21

31 46 31 27 26.4 34 24.5 31 38 31.3 16

> 60 69 55 59 70 64 50.6 58 75

Outcome of Endodontic Treatment and Retreatment Table 13-4 Nonsurgical Endodontic Re-treatment Outcome in Pulpless Teeth without Periapical Periodontitis
Authors Cases Success (%)

763

Table 13-5 Nonsurgical Endodontic Re-treatment Outcome in Teeth with Periapical Periodontitis
Authors Cases Success Failure (%) Uncertain (%)

Strindberg, 1956 Grahnon and Hansson, 1961 Engstrom et al., 1964 Bergenhotz et al., 1979 Molven and Halse, 1988 Allen et al., 1989 Sjgren et al., 1990 Friedman et al., 1995
From Friedman.28

64 323 (roots) 68 322 (roots) 76 (roots) 48 173 (roots) 42

95 94 93 94 89 96 98 100

Strindberg, 1956 Grahnen and Hansson, 1961 Engstrom et al., 1964 Bergenhotz et al., 1979 Molven and Halse, 1988 Sjgren et al., 1990 Friedman et al., 1995 Sundqvist et al., 1998
From Friedman.28

123 118 (roots) 85 234 (roots) 98 (roots) 94 (roots) 86 50

84 74 74 48 71 62 56 74

30 34

16 26 26 22 29 38 10 26

unsuccessful cases were causedby a reinfection in the apical areas favored by overinstrumentation105 (Figure 13-23). Mactou has laid out the important factors that must be adhered to if re-treatment is to be successful: rst of all, complete recleaning and reshaping of the canals. This should be carried out in a step-down fashion: early coronal enlargement and canal body shaping prior to apical preparation (personal communication, April 2000).

Figure 13-23 A, Failed endodontic treatment caused by overinstrumentation and failure to totally obturate the canal. Note the gross overextension of sealer and that the nal 6 mm of the canal are sealer only. B, Re-treatment by complete recleaning, reshaping, and canal medication before nal obturation. C, Twelve-year recall shows total healing. Note recurrent decay at the distal margin of the crown (arrow) that can lead to microleakage and potential failure. (Courtesy of Dr. Pierre Mactou.)

764

Endodontics in the rst place. One is warned that these cases are challenging, and this is probably not the occasion for one-appointment therapy. Continuing failure is undoubtedly owing to remaining bacteria, and their elimination calls for extra effort. New data regarding failed root canals indicate that these microora120122 differ from those of untreated necrotic teeth. Enterococci, for example, are quite prevalent in previously root-lled teeth and are quite difficult to eliminate. Enterococcus faecalis is the most frequent strain and, as a monoinfection, is found in 33% of the cases.123 Entercocci are quite resistant to calcium hydroxide, so Safaui et al. have recommended the addition of iodine potassium iodide in these cases.124 Heling and Chandler have recommended a mixture of 3% hydrogen peroxide and 1.8% chlorhexidine as an alternative against E. faecalis.125 Staphylococcus aureus and Pseudomonos are also notorious refractory contaminants and may require a prescription of metronidazole and amoxicillin to rid the periapex of these bacteria.126128 OBTURATION AND RESTORATION It goes without saying that total obturation is the sine qua non of successful re-treatment.

The canal should be cleaned segment by segment through a coronal reservoir of 2.5% of sodium hypochlorite. Working length at the radiographic terminus is established late in treatment, when the remainder of the canal has already been cleaned and shaped. Maintenance of apical potency and constant recapitulation with ne les avoids canal blockage with dentin debris. It also allows the sodium hypochlorite to reach this area. Great care must be exercised when removing the previous lling material, particularly when solvents such as chloroform are used. It is very difficult to remove all of the sealer and gutta-percha from the canal walls. Wilcox et al. contended that the last remnants of sealer can be removed only by vigorous reinstrumentation and reshaping of the canal117,118 but cautioned that overenlargement may result.119 It would appear that sealer removal is most important since bacteria can easily hide under previous sealer. CANAL MEDICATION Re-treatment cases are notorious for continued failure! In all probability this is caused by the failure to remove or kill the refractory bacteria responsible for the lesions

B
Figure 13-24 A, Pretreatment radiograph reveals failed endodontic treatment and a periradicular lesion. B, Re-treament by total recleaning, reshaping, and canal medication. Final obturation by vertical compaction lls the lateral canal as well. C, Six-year followup. (Courtesy of Dr. Pierre Mactou.)

Outcome of Endodontic Treatment and Retreatment

765

Figure 13-25 A, Pretreatment radiograph reveals failed root canal treatment and the presence of two posts. B, Re-treatment showing complete obturation of the canals including apical branching in the mesial canals. C, One-year follow-up. (Courtesy of Dr. Pierre Mactou.)

For this, the reader is referred to chapter 11. Furthermore, since many failures are believed to be related to microleakage from around coronal restorations, it is imperative that the re-treated tooth be properly restored, at once, not weeks later (Figure 13-24). Molven and Halse have said it best: Success depends on the elimination of root canal infection present when treatment starts, and the prevention of both contamination during treatment and re-infection later. So success rates reect the standard of the cleaning, shaping and lling of root canals129 (Figure 13-25). REFERENCES
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5. Morse DR, et al. A radiographic evaluation of the periradicular status of teeth treated by the gutta-percha-eucapercha endodontic method: a one year follow-up study of 458 root canals, Part III. Oral Surg 1983;56:190. 6. Barbakow FH, et al. Endodontic treatment of teeth with periradicular radiolucent areas in a general dental practice. Oral Surg 1981;51:552. 7. Meeuwissen R, Eschen S. Twenty years of endodontic treatment. JOE 1983;9:390. 8. Hession RW. Long-term evaluation of endodontic treatment: anatomy, instrumentation, obturationthe endodontic practice triad. Int Endodont J 1981;14:179. 9. Nelson IA. Endodontics in general practicea retrospective survey. Int Endodont J 1982;15:168. 10. Kerekes K, Tronstad L. Long-term results of endodontic treatment performed with a standardized technique. JOE 1979;5:8. 11. Sjgren U, et al. Factors affecting the long-term results of endodontic treatment. JOE 1990;16:498. 12. Mikkonen M, et al. Clinical and radiologic re-examination of apicoectomized teeth. Oral Surg 1983;55:302. 13. Peterson K, et al. Technical quality of root llings in an adult Swedish population. Endodont Dent Traumatol 1986;2:99. 14. Matsumoto T, et al. Factors affecting successful prognosis of root canal treatment. JOE 1987;13:239. 15. Swartz DB, Skidmore AE, Griffin JA Jr. Twenty years of endodontic success and failure. JOE 1983;9:198.

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63. Barnett F, Stevens R, Tronstad L. Demonstration of Bacteroides intermedius in periapical tissue using indirect immunouorescence microscopy. Endod Dent Traumatol 1990;6:153. 64. Haapsalo M, Ranta K, Ranta H. Mixed anaerobic periapical infection with sinus tract. Endod Dent Traumatol 1987;3:83. 65. Van Winkelhoff AJ, Van Steenbergen JM, de Graaff J. Porphyromonas (Bacteroides) endodontalis: its role in endodontic infections. JOE 1992;18:431. 66. Reader CM, Boniface M, Bujanda-Wagner S. Refractory endodontic lesion associated with Staphylococci aureus. JOE 1994;20:607. 67. Tronstad L, Barnett F, Riso K, Slots J. Extraradicular endodontic infections. Endod Dent Traumatol 1987;3:86. 68. Barnett F. Question and answer session. Palm Springs Seminars, Palm Springs, California, January 18, 1992. 69. Simon JHS, Chimenti R, Mintz G. Clinical signicance of the pulse granuloma. JOE 1982;8:116. 70. Yang ZP, Barnett F. Hyaline bodies and giant cells associated with a radicular cyst. Endod Dent Traumatol 1985;1:85. 71. Ingle JI. Endodontics. Baltimore: Williams & Wilkins; 1994. 72. Koppang H, Koppang G, Solheim T, et al. Cellulose bers from endodontic paper points as an etiologic factor in postendodontic periapical granulomas and cysts. JOE 1989;15:369. 73. Sedgley CM, Messer HH. Long-term retention of a paper point in the periapical tissues: a case report. Endod Dent Traumatol 1993;9:120. 74. Nair PNR, Sjgren U, Schumacher E, Sundquist G. Radicular cyst affecting a root-lled human tooth: a long-term posttreatment follow-up. Int Endod J 1993;26:225. 75. Brynolf I. A histological and roentgenological study of the periapical region of upper incisors. Odont Revy 1967;18:1. 76. Arenholt-Bindsley D, Hrsted-Bindsley P. A simple model for evaluating relative toxicity of root lling materials in cultures of human oral broblasts. Endod Dent Traumatol 1989;5:219. 77. Malooley J, Patterson SS, Kafrawy A. Response of periapical pathosis to endodontic treatment in monkeys. Oral Surg 1979;6:545. 78. Simon JHS. Periapical pathology. In: Cohen S, Burns R, editors. Pathways of the pulp. 6th ed. St. Louis: CV Mosby; 1994. p.337. 79. Torres JOC, Torabinejad M, Matiz RAR, Mantilla EG. Presence of secretory IgA in human periapical lesions. JOE 1994;20:87. 80. Lin LM, Wang SL, Wu-Wang C, et al. Detection of epidermal growth factor receptor in inammatory periapical lesions. Int Endod J 1996;29:179. 81. Simon JHS. Incidence of periapical cysts in relation to the root canal. JOE 1980;6:845. 82. Nair PNR. New perspectives on radicular cysts: do they heal? Int Endod J 1998;31:155. 83. Smith JW, et al. A survey: controversies in endodontic treatment and retreatment. JOE 1981;7:47. 84. Holland R, Valle GF, Taintor JF, Ingle JI. Inuence of bony resorption on endodontic treatment. Oral. Surg 1983;55:191. 85. Bergenholtz G, Malmcrona E, Milthon R. Endodontisk behandling och periapikalstatus. 1Rntgenologisk underskning av frekvensen endodontiskt behandlade tnder och frekvensen periapikala destruktioner. Tandlakartidningen 1973;65:64.

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86. Bergenholtz G, Malmcrona E, Milthon R. Endodontisk behandling och periapikalstatus. 2Rntgenologisk bedmning av rotfyllningens kvalitet stlld i relation till frekomst av periapikala destruktioner. Tandlakartidningen 1973;65:269. 87. Hansen BF, Johansen JR. Oral roentgenologic ndings in a Norwegian urban population. Oral Surg 1976;41:261. 88. Allard U, Palmqvist S. A radiographic survey of periapical conditions in elderly people in a Swedish county population. Endod Dent Traumatol 1986;2:103. 89. Petersson K, Petersson A, Hakansson J, et al. Endodontic status and suggested treatment in a population requiring substantial dental care. Endod Dent Traumatol 1989;5:153. 90. Petersson K, Lewin B, Olsson B, et al. Technical quality of root llings in an adult Swedish population. Endod Dent Traumatol 1986;2:99. 91. Petersson K, Hakansson R, Hakansson J, et al. Follow-up study of endodontic status in an adult Swedish population. Endod Dent Traumatol 1991;7:221. 92. Petersson K. Endodontic status of mandibular premolars and molars in Swedish adults. A repeated cross-sectional study in 1974 and in 1985. Endod Dent Traumatol 1993;9:185. 93. Eckerbom M, Andersson E, Magnusson T. Frequency and technical standard of endodontic treatment in a Swedish population. Endod Dent Traumatol 1987;3:245. 94. Eckerbom M, Andersson JE, Magnusson T. A longitudinal study of changes in frequency and technical standard of endodontic treatment in a Swedish population. Endod Dent Traumatol 1989;5:27. 95. Eriksen HM, Bjertness E. Prevalence of apical periodontitis and results of endodontic treatment in an urban adult population in Norway. Endod Dent Traumatol 1988;4:122. 96. Eriksen HM, Bjertness E, rstavik D. Prevalence and quality of endodontic treatment in middle-aged adults in Norway. Endod Dent Traumatol 1991;7:1. 97. Eriksen HM, Berset GP, Hansen BF, Bjertness E. Changes in endodontic status 19731993 among 35-year-olds in Oslo, Norway. Int Endod J 1995;28:129. 98. Odesjo B, Hellden L, Salonen L, Langeland L. Prevalence of previous endodontic treatment, technical standard and occurrence of periapical lesions in a randomly selected adult general population. Endod Dent Traumatol 1990;6:265. 99. Imfeld TN. Prevalence and quality of endodontic treatment in an elderly urban population of Switzerland. JOE 1991;17:604. 100. De Cleen MJH, Schuurs AHB, Wesselink PR, Wu MK. Periapical status and prevalence of endodontic treatment in an adult Dutch population. Int Endod J 1993;26:112. 101. Buckley M, Spngberg LSW. The prevalence and technical quality of endodontic treatment in an American subpopulation. Oral Surg 1995;79:92. 102. Soikkonen KT. Endodontically treated teeth and periapical ndings in the elderly. Int Endod J 1995;28:200. 103. Marques MD, Moreira B, Eriksen HM. Prevalence of apical periodontitis and results of endodontic treatment in an adult Portuguese population. Int Endod J 1998;31:161. 104. Bergenholtz G, Lekholm U, Milthon R, et al. Retreatment of endodontic llings. Scand J Dent Res 1979;87:217. 105. Bergenholtz G, Lekholm U, Milthon R, Engstrom B. Inuence of apical overinstrumentation and overlling on re-treated root canals. JOE 1979;5:310. 106. Gutmann JL, Pitt-Ford TR. Problems in the assessment of success and failure. In: Gutmann JL, Dumsha TC, Lovdahl PE, Hovland EJ, editors. Problems solving in endodontics. 2nd ed. St. Louis: Mosby-Year Book; 1992; p.111.

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