Dental Traumatology 2015; 31: 332–337; doi: 10.1111/edt.12171
Arrest and Calcification Repair of internal root resorption with a novel treatment approach: Report of two cases CASE REPORT Kurt Alois Ebeleseder, Lumnije Kqiku Division of Preventive and Operative Dentistry, Endodontics, Pedodontics, and Minimally Invasive Dentistry, Department of Dentistry and Maxillofacial Surgery, Medical University, Graz, Austria
Key words: internal root resorption; calcium hydroxide; mineral trioxide aggregate; healing of internal root resorption Correspondence to: Lumnije Kqiku DDS, MS, Division of Preventive and Operative Dentistry, Endodontics, Pedodontics, and Minimally, Invasive Dentistry, Auenbruggerplatz 4/6, A-8036 Graz, Austria Tel.: ++43 316 385 12213 Fax: ++43 316 385 13375 e-mail: [email protected]
Abstract – Aim: We report a novel treatment option for teeth with internal root resorption (IRR) in which the lesion had perforated to the PDL and was located in the coronal aspect of the root. Arrest and calcification of IRR can be achieved by local application of calcium hydroxide without further intracanal instrumentation. Case Report: Two cases of severe IRR without periapical inflammation were treated with a novel technique: The vital pulp including the granuloma was left in place and subjected to longterm disinfection with application of calcium hydroxide in the coronal aspect of the IRR. In both cases, the radiolucent areas were reduced and showed progressive calcification. Solid barriers were found in the coronal layers of the IRRs, and mineral trioxide aggregate (MTA) was placed as definitive fillings. No apical periodontitis was seen during the follow-up period of 6 years. The root canals appeared to gradually be narrowed. The results were similar to those obtained after successful cervical pulpotomy. Thus, the biological outcome was improved in comparison with pulp extirpation and conventional root canal treatment. Key learning points of this article: A treatment option for internal root resorption without periapical inflammation.
Accepted 12 February, 2015
Internal root resorption (IRR) is a rare, but serious pathologic process. In the absence of timely treatment, it is an irreversible continuous process involving resorption of root dentin and enlargement of the root canal with perforation into the periodontal space. The tooth is eventually lost due to irreparable spontaneous fracture. Histologically the condition is associated with loss of odontoblasts, predentin, and adjacent dentin. The defect is colonized by multinucleated giant cells and pulpal granulation tissue (1, 2). The etiology of IRR is not fully understood. Traumatic injuries, chronic pulpitis, heat caused by tooth preparation, and tooth restorations in general have been implicated as possible causes (1–3) affecting the protective predentin layer (4). One important stimulus for root resorption is bacterial infection of dentin (5). It has been speculated that IRR is triggered by necrotic and infected pulp tissue in the coronal aspect of the resorption zone (6). The treatment of choice has been extirpation of the pulp together with the granulomatous tissue in the area of resorption. After disinfection, the root canal and the resorption defect are obturated with a permanent root canal filling (7). The resorption is thus arrested. However, in cases of a large IRR located in the coronal part of the root canal, the tooth remains susceptible to fracture. 332
If IRR is a result of a bacterial stimulus located in the coronal aspect of the resorption zone, it must be susceptible to disinfection in the zone without removal of pulp and granulation tissue. Subsequent calcification is likely to occur in the formerly inflamed area because this is a standard reaction of healing pulp tissue. This calcification would probably provide greater fracture resistance in the resorbed zone. Calcium hydroxide appears to be suitable for this disinfection procedure because of its strong antibacterial effect as well as its ability to dissolve necrotic tissue, inhibit clastic cells, and promote the formation of hard tissue (8). Two cases of large IRR, treated according to this alternative approach, are presented here. Case reports Case 1
Medical history and clinical features In September 2004, a 38-year-old woman presented for routine examination at the division of conservative dentistry at the University Hospital of Graz. The clinical examination included digital radiographic evaluation (Sirona Dental Systems GmbH, Bensheim, Germany), which showed an irregular radiolucent oval area in the coronal aspect of the internal root canal © 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Treatment of internal root resorption
333
Fig. 2. Clinical presentation of case 1. There was no pink discoloration on the labial surface of tooth 22.
Fig. 1. Case 1, radiographic examination: irregular radiolucent oval area in the coronal third of the root canal of the left lateral maxillary incisor.
wall of the maxillary left incisor (tooth 22) (Fig. 1). The resorptive lesion did not change its central position in an eccentric radiograph which is an indication of IRR. It was marked by perforation of the mesial root canal wall into the periodontal ligament (PDL). The tooth was not sensitive to percussion or thermal stimulus. The patient had no history of dental trauma. An old composite restoration was seen in the mesiopalatal region. No ‘pink spot’ was observed (Fig. 2). Management and outcome The patient was informed that conventional treatment according to the current state of the art (pulp extirpation and root canal filling) was not likely to be successful. The alternative approach of long-term disinfection was explained to her and she consented to the treatment. A dental dam was applied and an access cavity on the palatal side of the crown was made without anesthesia. The pulp chamber was empty, as was a short part of the coronal root canal, which bled slightly. The empty space was irrigated with 3.5% sodium hypochlorite, then with physiologic saline, and finally, with 0.1% chlorhexidine (ChlorhexamedÒ, GlaxoSmithKline Pharma GmbH, Vienna, Austria). A mixture of calcium hydroxide powder and 0.1% chlorhexidine in suitable consistency for plugging (CH/ CHX) was placed in the coronal part of the canal for 3 months. Mechanical compaction of the CH/CHX was slightly painful to the patient. The access cavity was closed with glass ionomer cement (Fuji IX, Fuji, Tokyo, Japan). To prevent spontaneous fracture of the tooth, teeth 22 and 23 were splinted with a TTS (Med© 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Fig. 3. Splinting with TTS to prevent spontaneous root fracture.
Fig. 4. Radiographic and clinical examination at follow up after 2½ years.
artis, Switzerland) and composite (Fig. 3). The splint was placed labially to prevent it from being debonded during mastication. The dressing procedure with calcium hydroxide was repeated 3 and 6 months after initial treatment and then every 6 months. Radiographs
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taken after two-and-a-half years showed no pathological periapical changes; calcification was seen in the area of resorption (Fig. 4). At the 4-year follow up, the tooth was still asymptomatic. The radiograph showed no pathological changes in the tooth or in surrounding tissue. The granuloma appeared to be undergoing calcification (Fig. 5). A brown-colored hard tissue barrier was found in the cervical third of the root canal. After a last irrigation in the described manner, the accessible remainder of the root canal was filled with white MTA (Pro Root, Dentsply, Switzerland). The pulp chamber was filled with glass ionomer cement (Fuji IX, Fuji, Tokyo, Japan) and the access cavity with light-cured composite (Artemis Enamel A2, Vivadent, Schaan, Liechtenstein). The splint was removed. As the mechanical properties of the formerly resorbed zone could only be surmised, a wire-composite retainer was fixed on the palatal side. Calcification of the resorption defect continued even 1 year after definitive treatment. Six years after initial treatment, the tooth showed no pathological changes on clinical or radiographic investigation (Fig. 6). Case 2
Medical history and clinical features A 28-year-old man presented to the private medical office of the author K.A.E. with a referral from a den(a)
tist for endodontic management of the left central maxillary incisor (tooth 21). Radiographs showed an irregular radiolucent oval area in the coronal third of the root canal (Fig. 7). The patient’s dental history was characteristic for IRR: He reported trauma to the upper anterior teeth 10 years earlier. Intra-oral examination showed that the tooth was not sensitive to percussion or thermal stimulus. No restoration was present. The situation was determined to be the same as in patient 1. Patient 2 also agreed to pulp-preserving treatment. Management and outcome After the application of a dental dam, the pulp chamber was accessed without local infiltration anesthesia. During preparation, a cylindrical piece of necrotic tissue about 2 mm long and 1 mm thick was washed out and was lost in the dental aspirator. Bleeding occurred from the root canal into the empty pulp chamber and was controlled by rinsing with saline for 2–3 min. Without further preparation, the disinfection and dressing procedure was performed in the same manner as in case 1. The filling was removed and replaced every 6 months for an additional 2 years (Fig. 8). At the 2year follow up, the radiographic examination showed no pathologic changes in the tooth or surrounding tissue. As in case 1, calcification was seen in the formerly radiolucent area. The tooth was filled definitively with
(b)
Fig. 5. Radiographic (a) and clinical examination (b) after 4 years of treatment with calcium hydroxide filling. (a)
(b)
Fig. 6. Radiographic examination 1 year after definitive treatment of the tooth (a). Radiographic examination 2 years after definitive treatment and 6 years after initial treatment (b). © 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Treatment of internal root resorption
Fig. 7. Initial radiographic examination of case 2: irregular oval radiolucent area located in the coronal third of the root canal of the left central maxillary incisor.
MTA, Fuji IX, and composite as in case 1. One year after definitive treatment, the patient was still free of clinical symptoms and the radiographs showed no pathologic changes in the tooth or in surrounding tissues (Fig. 9). Another examination was scheduled after an additional 2 years. At this time as well, no pathological symptoms were found in the tooth. The resorption process was arrested and the calcification process continued (Fig. 10). Discussion
The formation of calcified tissue after inflammatory resorption is a common dental phenomenon. It has
(a)
335
Fig. 9. Radiographic examination 1 year after definitive treatment with MTA, glass ionomer cement, and composite filling.
been described in alveolar bone (healing of periapical inflammation after root canal disinfection), in the cementum (spontaneous repair after trauma), in healing of infection-related external root resorption after root canal disinfection (9), and in the pulp [internal root resorption and subsequent spontaneous hard tissue repair in horizontal root fractures (10)]. Based on this potential, therapies were developed to initiate the formation of new dental hard tissue. This includes pulp capping and pulpotomy with subsequent dentin bridging of vital exposed pulp, apexification and the formation of an apical cementum barrier, as well as so-called revascularization with apposition of hard tissue to the
(c)
(d)
(b)
Fig. 8. Case 2 after treatment with calcium hydroxide dressing as follows: (a) 6 months, (b) 12 months, (c) 18 months, and (d) 24 months after initial treatment. © 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
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Fig. 10. Radiographic examination 7 years after initial treatment and 5 years after definitive treatment. The resorption has been completely filled by dental hard tissue.
walls of a formerly infected root canal (2). Continuous inflammatory hard tissue resorption has been explained by the constant presence of bacteria in the root canal [periapical inflammation before endodontic therapy, endodontic treatment failures (11), infection-related external root resorption (12)], or in dentinal tubules (external cervical root resorption) (13). Not surprisingly, bacterial infection has also been cited as the main etiological factor responsible for IRR (10). According to Andreasen and Lǿvschall (14), a dental granuloma is an arrested wound healing module consisting of macrophages, capillaries, and fibroblasts. It contains fibroblast-like stem cells for the production of dental hard tissues that, however, are unable to differentiate because of the persistent disturbing effect of bacteria. Thus, the elimination of bacteria in the surroundings of the granuloma should promote the formation of hard tissue within the granuloma, as has been seen in periapical lesions. Both cases show that this concept is also applicable to IRR. Continuous disinfection of the supposedly infected site with calcium hydroxide resulted in calcification of the granulomatous area. The physical properties of this area remain unclear. All that can be said is that, despite excessive loss of root substance, neither tooth has yet developed a fracture. This leads to the question as to whether a conventional root canal filling would have strengthened the root. Apart from root substance loss during instrumentation and brittleness after a longer period of dressing with calcium hydroxide (15), there is little evidence to suggest that root canal fillings strengthen a weak root. Tanalp et al. (16) found that root canal fillings with various sealers or MTA were unable to substantially increase the fracture resistance of roots with thinned walls. Zamin et al. (17) showed that root canal fillings failed to mechanically compensate for the loss of hard substance in root canal walls. This confirms the authors’ previous doubts as regards the use of conventional therapy in both cases
and retrospectively justifies conservative treatment deviating from current common treatment options in these situations. To the authors’ knowledge, this type of treatment has not been described so far for large IRR lesions. Although the exact etiology of IRR remains unknown, the successful treatment of both cases supports the theory that it is caused by bacteria located in the coronal aspect of the resorbing lesion. The apical pulp survived and was able to react with a granulomatous process coronally. It should be noted that this treatment is by no means a generally applicable option because it depends on the presence of vital apical pulp tissue. Positive thermal sensitivity cannot be expected because the relevant part of the pulp is missing. Pulp vitality can only be inferred by indirect signs, such as lack of periapical radiolucency, bleeding after rinsing of the coronal portion of the root canal, and sensitivity to direct mechanical stimulation. For this reason, the initial access was made without anesthesia. One further potential disadvantage of the treatment presented here is the development of pulp canal obliteration (PCO). In combination with the calcified zone in the former area of resorption, PCO may be a serious obstacle to subsequent root canal treatment, which may be required due to further bacterial infection or trauma. Endodontic surgery would probably be needed in these cases. The indication will again depend on indirect signs, such as apical radiolucency, pain, or sinus tract. In cases of complete pulp necrosis prior to the granuloma receiving vascular support from the adjacent periodontium, conventional root canal treatment and filling with standard or thermoplasticized gutta-percha would be the treatment of choice (4, 7, 18, 19). Conclusions
Pulp-conserving treatment of teeth with IRR is possible when it eliminates the causal factor (bacteria), interrupts the progressive resorption mechanism, and stimulates hard tissue repair in the zone of resorption. These three goals can be achieved with calcium hydroxide as a long-term filling from the empty part of the root canal in the coronal aspect of the zone of resorption. This may obviate the need to sacrifice vital pulp as part of conventional root canal treatment in cases of IRR without periapical inflammation. References 1. Tronstad L. Root resorption: etiology, terminology and clinical manifestations. Endod Dent Traumatol 1988;4:241–52. 2. Trope M. Root resorption of dental and traumatic origin: classification based on etiology. Pract Periodontics Aesthet Dent 1998;10:515–22. 3. Weine FS, Potashnick SR. Endodontic–orthodontic relationships. In: Weine FS, editor. Endodontic therapy, 5th edn. St. Louis, MO: Mosby; 1996. p. 674–8. 4. Trope M. Root resorption due to dental trauma. Endod Topics 2002;1:79–100. 5. Andreasen FM, Andreasen JO. Textbook and color atlas of traumatic injuries to the teeth, 3rd edn. St. Louis, MO: Mosby; 1994. p. 563. © 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Treatment of internal root resorption 6. Fuss Z, Tsesis I, Lin S. Root resorption-diagnosis, classification and treatment choices based on stimulation factors. Dent Traumatol 2003;19:175–82. 7. American Association of Endodontists. Treatment Options for the Compromised Tooth. A Decision Guide: www.aae.org 2011; p. 4. 8. Nerwich A, Figdor D, Messer HH. pH changes in root dentin over a 4-week period following root canal dressing with calcium hydroxide. J Endod 1993;19:3026. 9. Cvek M. Endodontic management and the use of calcium hydroxide in traumatized permanent teeth. In: Andreasen JO, Andreasen FM, Andersson L, editors. Textbook and color atlas of traumatic injuries to the teeth, 4th edn. Oxford: Blackwell 2007; p. 598–657. 10. Andreasen FM, Andreasen JO. Resorption and mineralization processes following root fracture of permanent incisors. Endod Dent Traumatol 1988;4:202–14. 11. Gulabivala K. Biological and clinical rationale for root canal treatment. In: Stock C, Walker R, Gulabivala K, editors. Endodontics, 3rd edn. Oxford: Elsevier Mosby; 2004. p. 25–66. 12. Ehnevid H, Jansson L, Lindskog S, Weintraub A, Bloml€ of L. Endodontic pathogens: propagation of infection through patent dentinal tubules in traumatized monkey teeth. Endod Dent Traumatol 1995;11:229–34.
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13. Heithersay GS. Treatment of invasive cervical resorption: an analysis of results using topical application of trichloroacetic acid, curettage and restoration. Quintessence Int 1999;30:96– 110. 14. Andreasen JO, Løvschall H. Response of Oral Tissues to Trauma. In: Andreasen JO, Andreasen FM, Andersson L, editors. Textbook and color atlas of traumatic Injuries to the teeth, 4th edn. Oxford: Blackwell; 2007. p. 62–113. 15. Andreasen JO, Farik B, Munksgaard EC. Long-term calcium hydroxide as a root canal dressing may increase risk of root fracture. Dent Traumatol 2002;18:134–7. € Ersev H, G€ 16. Tanalp J, Dikbas I, Malkondu O, ung€ or T, Bayirli G. Comparison of fracture resistance of simulated immature permanent teeth using various canal filling materials and fiber posts. Dent Traumatol 2012;28:457–64. 17. Zamin C, Silva-Sousa YTC, Souza-Gabriel AE, Messias DF, Sousa-Neto MD. Fracture susceptibility of endodontically treated teeth. Dent Traumatol 2012;28:282–6. 18. Keinan D, Heling I, Stabholtz A, Moshonov J. Rapidly progressive internal root resorption: a case report. Dent Traumatol 2008;24:546–9. 19. Rossi-Fedele G, Figueiredo JA, Abbott PV. Teeth with double internal inflammatory resorption: report of two cases. Aust Endod J 2010;36:122–9.
Arrest and Calcification Repair of internal root resorption with a novel treatment approach: Report of two cases CASE REPORT Kurt Alois Ebeleseder, Lumnije Kqiku Division of Preventive and Operative Dentistry, Endodontics, Pedodontics, and Minimally Invasive Dentistry, Department of Dentistry and Maxillofacial Surgery, Medical University, Graz, Austria
Key words: internal root resorption; calcium hydroxide; mineral trioxide aggregate; healing of internal root resorption Correspondence to: Lumnije Kqiku DDS, MS, Division of Preventive and Operative Dentistry, Endodontics, Pedodontics, and Minimally, Invasive Dentistry, Auenbruggerplatz 4/6, A-8036 Graz, Austria Tel.: ++43 316 385 12213 Fax: ++43 316 385 13375 e-mail: [email protected]
Abstract – Aim: We report a novel treatment option for teeth with internal root resorption (IRR) in which the lesion had perforated to the PDL and was located in the coronal aspect of the root. Arrest and calcification of IRR can be achieved by local application of calcium hydroxide without further intracanal instrumentation. Case Report: Two cases of severe IRR without periapical inflammation were treated with a novel technique: The vital pulp including the granuloma was left in place and subjected to longterm disinfection with application of calcium hydroxide in the coronal aspect of the IRR. In both cases, the radiolucent areas were reduced and showed progressive calcification. Solid barriers were found in the coronal layers of the IRRs, and mineral trioxide aggregate (MTA) was placed as definitive fillings. No apical periodontitis was seen during the follow-up period of 6 years. The root canals appeared to gradually be narrowed. The results were similar to those obtained after successful cervical pulpotomy. Thus, the biological outcome was improved in comparison with pulp extirpation and conventional root canal treatment. Key learning points of this article: A treatment option for internal root resorption without periapical inflammation.
Accepted 12 February, 2015
Internal root resorption (IRR) is a rare, but serious pathologic process. In the absence of timely treatment, it is an irreversible continuous process involving resorption of root dentin and enlargement of the root canal with perforation into the periodontal space. The tooth is eventually lost due to irreparable spontaneous fracture. Histologically the condition is associated with loss of odontoblasts, predentin, and adjacent dentin. The defect is colonized by multinucleated giant cells and pulpal granulation tissue (1, 2). The etiology of IRR is not fully understood. Traumatic injuries, chronic pulpitis, heat caused by tooth preparation, and tooth restorations in general have been implicated as possible causes (1–3) affecting the protective predentin layer (4). One important stimulus for root resorption is bacterial infection of dentin (5). It has been speculated that IRR is triggered by necrotic and infected pulp tissue in the coronal aspect of the resorption zone (6). The treatment of choice has been extirpation of the pulp together with the granulomatous tissue in the area of resorption. After disinfection, the root canal and the resorption defect are obturated with a permanent root canal filling (7). The resorption is thus arrested. However, in cases of a large IRR located in the coronal part of the root canal, the tooth remains susceptible to fracture. 332
If IRR is a result of a bacterial stimulus located in the coronal aspect of the resorption zone, it must be susceptible to disinfection in the zone without removal of pulp and granulation tissue. Subsequent calcification is likely to occur in the formerly inflamed area because this is a standard reaction of healing pulp tissue. This calcification would probably provide greater fracture resistance in the resorbed zone. Calcium hydroxide appears to be suitable for this disinfection procedure because of its strong antibacterial effect as well as its ability to dissolve necrotic tissue, inhibit clastic cells, and promote the formation of hard tissue (8). Two cases of large IRR, treated according to this alternative approach, are presented here. Case reports Case 1
Medical history and clinical features In September 2004, a 38-year-old woman presented for routine examination at the division of conservative dentistry at the University Hospital of Graz. The clinical examination included digital radiographic evaluation (Sirona Dental Systems GmbH, Bensheim, Germany), which showed an irregular radiolucent oval area in the coronal aspect of the internal root canal © 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Treatment of internal root resorption
333
Fig. 2. Clinical presentation of case 1. There was no pink discoloration on the labial surface of tooth 22.
Fig. 1. Case 1, radiographic examination: irregular radiolucent oval area in the coronal third of the root canal of the left lateral maxillary incisor.
wall of the maxillary left incisor (tooth 22) (Fig. 1). The resorptive lesion did not change its central position in an eccentric radiograph which is an indication of IRR. It was marked by perforation of the mesial root canal wall into the periodontal ligament (PDL). The tooth was not sensitive to percussion or thermal stimulus. The patient had no history of dental trauma. An old composite restoration was seen in the mesiopalatal region. No ‘pink spot’ was observed (Fig. 2). Management and outcome The patient was informed that conventional treatment according to the current state of the art (pulp extirpation and root canal filling) was not likely to be successful. The alternative approach of long-term disinfection was explained to her and she consented to the treatment. A dental dam was applied and an access cavity on the palatal side of the crown was made without anesthesia. The pulp chamber was empty, as was a short part of the coronal root canal, which bled slightly. The empty space was irrigated with 3.5% sodium hypochlorite, then with physiologic saline, and finally, with 0.1% chlorhexidine (ChlorhexamedÒ, GlaxoSmithKline Pharma GmbH, Vienna, Austria). A mixture of calcium hydroxide powder and 0.1% chlorhexidine in suitable consistency for plugging (CH/ CHX) was placed in the coronal part of the canal for 3 months. Mechanical compaction of the CH/CHX was slightly painful to the patient. The access cavity was closed with glass ionomer cement (Fuji IX, Fuji, Tokyo, Japan). To prevent spontaneous fracture of the tooth, teeth 22 and 23 were splinted with a TTS (Med© 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Fig. 3. Splinting with TTS to prevent spontaneous root fracture.
Fig. 4. Radiographic and clinical examination at follow up after 2½ years.
artis, Switzerland) and composite (Fig. 3). The splint was placed labially to prevent it from being debonded during mastication. The dressing procedure with calcium hydroxide was repeated 3 and 6 months after initial treatment and then every 6 months. Radiographs
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taken after two-and-a-half years showed no pathological periapical changes; calcification was seen in the area of resorption (Fig. 4). At the 4-year follow up, the tooth was still asymptomatic. The radiograph showed no pathological changes in the tooth or in surrounding tissue. The granuloma appeared to be undergoing calcification (Fig. 5). A brown-colored hard tissue barrier was found in the cervical third of the root canal. After a last irrigation in the described manner, the accessible remainder of the root canal was filled with white MTA (Pro Root, Dentsply, Switzerland). The pulp chamber was filled with glass ionomer cement (Fuji IX, Fuji, Tokyo, Japan) and the access cavity with light-cured composite (Artemis Enamel A2, Vivadent, Schaan, Liechtenstein). The splint was removed. As the mechanical properties of the formerly resorbed zone could only be surmised, a wire-composite retainer was fixed on the palatal side. Calcification of the resorption defect continued even 1 year after definitive treatment. Six years after initial treatment, the tooth showed no pathological changes on clinical or radiographic investigation (Fig. 6). Case 2
Medical history and clinical features A 28-year-old man presented to the private medical office of the author K.A.E. with a referral from a den(a)
tist for endodontic management of the left central maxillary incisor (tooth 21). Radiographs showed an irregular radiolucent oval area in the coronal third of the root canal (Fig. 7). The patient’s dental history was characteristic for IRR: He reported trauma to the upper anterior teeth 10 years earlier. Intra-oral examination showed that the tooth was not sensitive to percussion or thermal stimulus. No restoration was present. The situation was determined to be the same as in patient 1. Patient 2 also agreed to pulp-preserving treatment. Management and outcome After the application of a dental dam, the pulp chamber was accessed without local infiltration anesthesia. During preparation, a cylindrical piece of necrotic tissue about 2 mm long and 1 mm thick was washed out and was lost in the dental aspirator. Bleeding occurred from the root canal into the empty pulp chamber and was controlled by rinsing with saline for 2–3 min. Without further preparation, the disinfection and dressing procedure was performed in the same manner as in case 1. The filling was removed and replaced every 6 months for an additional 2 years (Fig. 8). At the 2year follow up, the radiographic examination showed no pathologic changes in the tooth or surrounding tissue. As in case 1, calcification was seen in the formerly radiolucent area. The tooth was filled definitively with
(b)
Fig. 5. Radiographic (a) and clinical examination (b) after 4 years of treatment with calcium hydroxide filling. (a)
(b)
Fig. 6. Radiographic examination 1 year after definitive treatment of the tooth (a). Radiographic examination 2 years after definitive treatment and 6 years after initial treatment (b). © 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Treatment of internal root resorption
Fig. 7. Initial radiographic examination of case 2: irregular oval radiolucent area located in the coronal third of the root canal of the left central maxillary incisor.
MTA, Fuji IX, and composite as in case 1. One year after definitive treatment, the patient was still free of clinical symptoms and the radiographs showed no pathologic changes in the tooth or in surrounding tissues (Fig. 9). Another examination was scheduled after an additional 2 years. At this time as well, no pathological symptoms were found in the tooth. The resorption process was arrested and the calcification process continued (Fig. 10). Discussion
The formation of calcified tissue after inflammatory resorption is a common dental phenomenon. It has
(a)
335
Fig. 9. Radiographic examination 1 year after definitive treatment with MTA, glass ionomer cement, and composite filling.
been described in alveolar bone (healing of periapical inflammation after root canal disinfection), in the cementum (spontaneous repair after trauma), in healing of infection-related external root resorption after root canal disinfection (9), and in the pulp [internal root resorption and subsequent spontaneous hard tissue repair in horizontal root fractures (10)]. Based on this potential, therapies were developed to initiate the formation of new dental hard tissue. This includes pulp capping and pulpotomy with subsequent dentin bridging of vital exposed pulp, apexification and the formation of an apical cementum barrier, as well as so-called revascularization with apposition of hard tissue to the
(c)
(d)
(b)
Fig. 8. Case 2 after treatment with calcium hydroxide dressing as follows: (a) 6 months, (b) 12 months, (c) 18 months, and (d) 24 months after initial treatment. © 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
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Fig. 10. Radiographic examination 7 years after initial treatment and 5 years after definitive treatment. The resorption has been completely filled by dental hard tissue.
walls of a formerly infected root canal (2). Continuous inflammatory hard tissue resorption has been explained by the constant presence of bacteria in the root canal [periapical inflammation before endodontic therapy, endodontic treatment failures (11), infection-related external root resorption (12)], or in dentinal tubules (external cervical root resorption) (13). Not surprisingly, bacterial infection has also been cited as the main etiological factor responsible for IRR (10). According to Andreasen and Lǿvschall (14), a dental granuloma is an arrested wound healing module consisting of macrophages, capillaries, and fibroblasts. It contains fibroblast-like stem cells for the production of dental hard tissues that, however, are unable to differentiate because of the persistent disturbing effect of bacteria. Thus, the elimination of bacteria in the surroundings of the granuloma should promote the formation of hard tissue within the granuloma, as has been seen in periapical lesions. Both cases show that this concept is also applicable to IRR. Continuous disinfection of the supposedly infected site with calcium hydroxide resulted in calcification of the granulomatous area. The physical properties of this area remain unclear. All that can be said is that, despite excessive loss of root substance, neither tooth has yet developed a fracture. This leads to the question as to whether a conventional root canal filling would have strengthened the root. Apart from root substance loss during instrumentation and brittleness after a longer period of dressing with calcium hydroxide (15), there is little evidence to suggest that root canal fillings strengthen a weak root. Tanalp et al. (16) found that root canal fillings with various sealers or MTA were unable to substantially increase the fracture resistance of roots with thinned walls. Zamin et al. (17) showed that root canal fillings failed to mechanically compensate for the loss of hard substance in root canal walls. This confirms the authors’ previous doubts as regards the use of conventional therapy in both cases
and retrospectively justifies conservative treatment deviating from current common treatment options in these situations. To the authors’ knowledge, this type of treatment has not been described so far for large IRR lesions. Although the exact etiology of IRR remains unknown, the successful treatment of both cases supports the theory that it is caused by bacteria located in the coronal aspect of the resorbing lesion. The apical pulp survived and was able to react with a granulomatous process coronally. It should be noted that this treatment is by no means a generally applicable option because it depends on the presence of vital apical pulp tissue. Positive thermal sensitivity cannot be expected because the relevant part of the pulp is missing. Pulp vitality can only be inferred by indirect signs, such as lack of periapical radiolucency, bleeding after rinsing of the coronal portion of the root canal, and sensitivity to direct mechanical stimulation. For this reason, the initial access was made without anesthesia. One further potential disadvantage of the treatment presented here is the development of pulp canal obliteration (PCO). In combination with the calcified zone in the former area of resorption, PCO may be a serious obstacle to subsequent root canal treatment, which may be required due to further bacterial infection or trauma. Endodontic surgery would probably be needed in these cases. The indication will again depend on indirect signs, such as apical radiolucency, pain, or sinus tract. In cases of complete pulp necrosis prior to the granuloma receiving vascular support from the adjacent periodontium, conventional root canal treatment and filling with standard or thermoplasticized gutta-percha would be the treatment of choice (4, 7, 18, 19). Conclusions
Pulp-conserving treatment of teeth with IRR is possible when it eliminates the causal factor (bacteria), interrupts the progressive resorption mechanism, and stimulates hard tissue repair in the zone of resorption. These three goals can be achieved with calcium hydroxide as a long-term filling from the empty part of the root canal in the coronal aspect of the zone of resorption. This may obviate the need to sacrifice vital pulp as part of conventional root canal treatment in cases of IRR without periapical inflammation. References 1. Tronstad L. Root resorption: etiology, terminology and clinical manifestations. Endod Dent Traumatol 1988;4:241–52. 2. Trope M. Root resorption of dental and traumatic origin: classification based on etiology. Pract Periodontics Aesthet Dent 1998;10:515–22. 3. Weine FS, Potashnick SR. Endodontic–orthodontic relationships. In: Weine FS, editor. Endodontic therapy, 5th edn. St. Louis, MO: Mosby; 1996. p. 674–8. 4. Trope M. Root resorption due to dental trauma. Endod Topics 2002;1:79–100. 5. Andreasen FM, Andreasen JO. Textbook and color atlas of traumatic injuries to the teeth, 3rd edn. St. Louis, MO: Mosby; 1994. p. 563. © 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
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