May 1, 2015
by Craig Bellamy, DDS; Gevik Malkhassian DDS, MSc, FRCD(C)
Resorption can be defined as a condition associated with either a physiologic or a pathologic process resulting in a loss of dentin, cementum and/or bone.1 Imfeld describes resorption as the process of biological degradation and assimilation of substances or structures previously produced by the body.2 Recorded observation of root resorption dates back as early as 1806, when Joseph Fox likened tooth resorptive lesions to a “tumor in bone”.3 Several classifications of resorptive lesions affecting teeth have been described4-11 based largely on:
• Location (e.g. internal, external)
• Etiology (e.g. infection)
• Site (e.g. apical, cervical)
• Type or morphology of the resorptive process (e.g. replacement)
• Combination of the above
Several types of resorption are described in Table 1, including external invasive cervical resorption (EICR). This type of resorption is considered by several authors to be unique in its etiology and presentation compared to other resorptive lesions10,12-16 and has been assigned a subset classification.16
EtiologyRoot resorption can be initiated by many factors acting alone or simultaneously. Commonly described stimulants include pulpal necrosis, trauma, tooth whitening agents, periodontal treatment, and orthodontic treatment.7 Patient remarks combined with clinical and radiographic assessment identifying crown preparations, pulpotomy, removal of impacted teeth, surgical procedures in proximity to the affected roots as well as periodontal disease and its management can all be suggestive of an etiology.7,9,10,17-20 Other possible etiologies may include systemic disturbances such as scleroderma21,22 hormone dysregulation23-25 and viruses.26 Case reports of idiopathic resorption have also been reported.27-30 In the case of more extensive resorptive conditions involving multiple teeth it may be of interest to discuss if the patient has any contact with cats. A disease associated with feline viruses known as feline odontoclastic resorptive lesions (FORL) is common in cats.31 In a case report26 describing four patients presenting with multiple teeth affected by invasive cervical resorption (ICR), all patients reported having had direct (two cases) or indirect (two cases) contact with cats. In addition, blood samples were taken from all patients for neutralization testing of feline herpes virus type 1 (FeHV-1) and the sera obtained were able to neutralize (two cases) or partly inhibit (two cases) replication of FeHV-1, indicating transmission of feline viruses to humans. This may suggest a role of this virus as a co-factor in the etiology of the resorptive lesions in these individuals.26
MechanismDespite the wide range of etiologies, the resorption process is largely considered to be inflammatory in nature.9 Biological mechanisms involving osteoprotegerin, RANKL, and RANK, as well as bioactive neuropeptides such as Substance P, NKA, NPY, VIP, and CGRP play a part in this resorptive process through their vasoactive, chemotactic, and cellular effects.5,25,32,33 The pathophysiology behind resorption centers around osteoclast formation, recruitment and stimulation.34,35 The clastic cell adheres to the mineralized surface, and releases hydrogen ions and proteolytic enzymes creating a localized, acidic microenvironment: this results in dissolution of mineralized tissue.35
Risk Factors: Patient-RelatedPatient-related risk factors may include previous history of root resorption, caries, certain root morphologies, roots with developmental abnormalities, previous trauma, genetic influences, systemic factors including certain drugs, nutritional deficiencies, hormone deficiency, tooth length, hypothyroidism, expanding pathological lesions, hypopituitarism, asthma, tooth impactions, root proximity to cortical bone, alveolar bone density, chronic alcoholism, endodontic treatment, severity and type of malocclusion, patient age, increased periodontal probing depths, reduced crestal bone heights, and increased use of fewer remaining teeth.5,36-39
Risk Factors: Treatment-RelatedTreatment-related risk factors may include sustained high magnitude forces, direction of tooth movement, duration of tooth movement, sustained high temperatures, chemical insult, and iatrogenic physical trauma to the root/PDL through aggressive tissue manipulation.5,12,37
IncidenceThe multitude of risk factors combined with a variety of etiological possibilities foreshadows a wide range of reported incidence. Incidence levels from 0 percent40 to 100 percent41 have been recorded when diagnosis was made using radiographs. Friedman et al.17 reported an incidence of external root resorption to be 6.9 percent after bleaching pulpless teeth. Majorana et al.42 reported an incidence of root resorption to be 17.24 percent after luxation/avulsion injury. A 2010 systematic review37 looking at root resorption associated with orthodontic tooth movement reported an incidence spanning from five percent for severe resorption to over 90 percent for histologically detected resorption. The high level of histologic detection of resorption may be suggestive that resorption is a normal physiologic process in permanent teeth.43
PrevalenceIt is difficult to state a definitive prevalence for root resorption based on epidemiological data. Prevalences from 0 percent to 100 percent have been reported in subjects based on histological reports.44 In their study to determine the frequency of apical root resorption in the permanent dentition of patients who had not been treated orthodontically, Harris et al. reported between seven percent and 10 percent of the 306 patients exhibited obvious apical resorption.39 Vier and Figueardo45 showed that the prevalence of teeth with periapical lesions showing periforaminal or forminal resorption was over 82 percent. In Haapasalo and Endal’s46 report on internal inflammatory root resorption, an estimated prevalence of 0.1 percent to one percent was made acknowledging that the estimate is quite rough and may be wrong. Study methodological differences, pre- and post-treatment image variability, misdiagnoses, and undetectable lesions may be some of the challenges in identifying an overall prevalence. It can also be difficult, in some instances, to determine whether or not missing tooth structure is due to developmental disturbances or resorptive mechanisms.47 Despite this, it is agreed that most resorptive lesions requiring intervention are rare due, in part, to inherent biological mechanisms that include a vital periodontal ligament, healthy cementum, and the extra-cellular predentin layer, all of which are thought to be protective against resorptive processes.20,48-51 Violations in these structures may increase the risk of developing resorptive lesions.
ManagementSuccessful management of resorptive lesions starts with an early diagnosis10,13,18,46,52 as teeth affected by resorption are often asymptomatic. A thorough history along with radiographic and clinical assessments are critical: some cases require minimal intervention (i.e. reduction or cessation of orthodontic forces in some cases of external surface resorption), while other, possibly more aggressive cases may require coordinated, multidisciplinary maneuvers involving root canal treatment, periodontal surgery, orthodontics, and surgical debridement and repair of the root defect. Without a clear diagnosis, however, mismanagement may result in perpetuation of the resorptive process leading to unnecessary and catastrophic tooth destruction leaving extraction as the only option.
Clinical findings p
rompting a more detailed evaluation for resorption may include a red-pink blush in the clinical crown, gross caries, altered percussion or mobility, subgingival cavitation, attachment loss, or pulp necrosis with no apparent cause.16,18,52 Periapical radiographs taken from different mesio-distal angulations and/or cone beam computed tomography (CBCT) will help to identify the site and extent of the lesion. Studies on the use of CBCT in the detection of root resorption are encouraging and may accelerate treatment interventions and improve outcomes by detection of early resorptive lesions.53-55 Undoubtedly, the extent of resorptive lesions can be better appreciated with a three dimensional representation through CBCT. This increased information is very useful for diagnosis and treatment planning, and may improve prognostic determination. However, not unlike conventional radiography, the benefits and risks, including the financial costs and radiation exposure for the patient, must be weighed on a case by case basis.
Once a diagnosis has been made, appropriate management strategies can be formulated. The fundamental principle related to management of any resorptive lesion is to halt the activity of the clastic cell. This may be accomplished by removing the source of stimulation, reducing osteoclastic activity, stimulating repair, or a combination of these methods.7,18,52,56 An overview of possible endodontic management strategies56 can be seen in Table 2.
The clinical examples that follow demonstrate the viability of the endodontic management of root resorptive lesions, helping to retain teeth that may otherwise require extraction.
Three cases are presented: the first two cases belong to the same patient, who was a 41-year-old male with a non-contributory medical history.
Case Report #1, tooth #4.6:The patient was referred to the endodontic practice (GM) one day after pulpotomy was performed and a resorptive defect was suspected by the general practitioner. (Fig. 1) The patient mentioned that, prior to treatment, he had some discomfort only when brushing the area. A composite resin restoration was replaced about one year ago on the same tooth. Endodontic assessment revealed a localized gingival swelling on the buccal aspect of the tooth adjacent to the furcation area. A 7mm pocket was detected and rarefying osteitis was noted in the furcation. Diagnosis of cervical resorption was confirmed. (Fig. 2) Prognosis of the tooth was established as guarded. Treatment options were presented and discussed, including extraction and replacement with an implant-supported crown, or continuation of root canal treatment in an attempt to seal and repair the perforation followed by a coronal restoration. Prior to any treatment attempt the option of CBCT imaging was also discussed. The patient consented to CBCT imaging. After receiving the CBCT report, the patient chose to proceed with root canal treatment being aware of the risk involved and the prognosis.
FIGURE 1. #1: prior to pulpotomy
FIGURE 2. #2: Pre-op
A brief summary of the CBCT report of tooth #4.6 (image CBCT #1, tooth #4.6):
The distal surface of the mesial root of tooth 4.6 exhibited external resorption that extended from the root surface to the root canal. The defect was broad and irregularly shaped. Rarefying osteitis was present in the furcal region, secondary to pulp exposure caused by the external resorption.
The pulp chamber of tooth 4.6 was grossly enlarged and a mesial root perforation was present in the cervical region of the root. Rarefying osteitis was detected in the bone adjacent to the same area. Restorability of the tooth was questioned.
In the first appointment, after proper anesthesia and isolation of the tooth, three root canals were cleaned and shaped using nickel-titanium rotary instruments. All procedures were performed under high magnification using a dental operating microscope. Bleeding was noted from the mesial aspect of the pulp chamber and mesio-lingual canal. During the treatment a significant amount of granulation tissue was removed from inside the pulp chamber and a resorptive perforation was noted. At the end of the first appointment the mesio-buccal canal was filled with gutta-percha and sealer with no complications. Minor bleeding was noted in the distal canal, which was controlled and subsequently filled with ProRoot® MTA (Dentsply, Tulsa Dental, Tulsa, OK, USA). The perforation in the mesial wall of the chamber was also sealed with MTA. However, the mesio-lingual canal, due to excessive bleeding, was filled with calcium hydroxide paste (CH) and the access cavity was sealed with a temporary restoration. The next day the tooth was re-accessed and CH removed. The source of bleeding was located, which corroborated the observations in the CBCT images. The perforation was at the distal aspect of the mesio-lingual canal toward the furcation. The apical third of the canal, below the bleeding spot, was filled with gutta-percha and sealer. The remainder of the canal and chamber floor was filled with MTA. (Fig. 3) At the one-month follow-up appointment the tooth was asymptomatic, the permanent restoration was already in place (Fig. 4) and soft tissue appeared within normal parameters. No probing was attempted at that session. At the three-month follow-up appointment probing depth was considerably reduced and was within normal limits. (Fig. 5) After 10 months, the tooth was restored with a crown and all clinical and radiographic observations were consistent with healing within normal parameters. (Fig. 6) At subsequent 28 and 40 months follow-up, the tooth was asymptomatic, functional and all clinical and radiographic findings were normal. (Figs. 7 & 8)
FIGURE 3. #3: Post-op
FIGURE 4. #4: 1 month Recall
FIGURE 5. #5: 3 month Recall
FIGURE 6. #6: 10 month Recall
FIGURE 7. #7: 28 month Recall
Case Report #2: tooth #3.6:Following endodontic assessment tooth 3.6 was reported as asymptomatic. However, a sinus tract was present at the disto-buccal aspect of the tooth, and a 7 mm periodontal pocket was detected at the disto-buccal corner of the tooth. On periapical radiographs (Figs. 9 & 10) a resorptive defect was suspected in the distal root associated with vertical bone loss at the distal aspect of the root. Both mesial and distal roots also appeared shorter compared to the adjacent teeth. The option of CBCT imaging also was discussed. The patient consented to CBCT imaging. After receiving the CBCT report, the patient chose to proceed with root canal treatment being aware of the risk involved and the prognosis.
FIGURE 9. #9: Pre-op 1
FIGURE 10. #10: Pre-op 2
A brief summary of CBCT report of tooth #3.6, (image: CBCT #2, tooth #3.6):
A severe resorptive defect was present in the distal root of tooth 3.6. The root canal was significantly enlarged and the resorption had extended to the distal surface of the root of tooth 3.6. Rarefying osteitis was present distal to this region secondary to the presence of this resorptive defect.
The region of rarefying osteitis that extended from the resorptive defect on the distal root of tooth 3.6 to the alveolar crest was evident in the sagittal reference slice. Periapical rarefying osteitis was also present. The gross loss of root structure of the distal root of tooth 3.6 was evident.
The remaining osseous and soft tissue structures in the field of view appeared normal.
In the first appointment, after proper anesthesia and isolation of the tooth, three root canals were cleaned and shaped using nickel-titanium rotary instruments along with passive ultrasonic irrigation. All procedures were performed under high magnification using a dental operating microscope. During and after cleaning and shaping of the canals, bleeding was noted in the distal canal. Calcium Hydroxide paste was inserted into the canals and the access cavity was sealed with a temporary restorative material. At the second appointment (two weeks later) it was noted that the sinus tract was closed. The mesio-buccal canal was filled with Gutta-Percha and sealer and the mesio-lingual and distal canals were filled with MTA. (Fig. 11) At the two-month follow-up appointment, the tooth was asymptomatic, soft tissue appeared within normal parameters, and a permanent restoration was already in place. (Fig. 12) After eight months, all clinical and radiographic observations were consistent with healing within normal parameters. No abnormal periodontal probing was noted. (Fig. 13) The tooth was restored with a crown. At subsequent 14, 26 and 38 months follow-up, (Figs. 14-16) the tooth was asymptomatic, functional and all clinical and radiographic findings were normal.
FIGURE 11. #11: Post-op
FIGURE 12. #12: 2 month recall
FIGURE 13. #13: 8 month recall
FIGURE 14. #14: 14 month recall
FIGURE 15. #15: 26 month recall
FIGURE 16. #16: 38 month recall
Case Report #3: tooth #3.4:A 40-year-old healthy male patient with a chief complaint of pain associated with the mandibular left quadrant presented to his periodontist. After assessment, tooth 3.5 was diagnosed with irreversible pulpitis. A resorptive defect was detected on 3.4 and the patient was referred to an endodontist (GM) for reassessment and possible treatment. (Fig. 17) Following endodontic examination tooth 3.5 was diagnosed with symptomatic irreversible pulpitis. Tooth 3.4 was diagnosed with necrotic pulp secondary to cervical root resorption penetrating into the pulp from the lingual aspect of the tooth. An explorer tip could penetrate into the defect from the lingual aspect. The patient’s dental history revealed previous orthodontic treatment approximately seven years ago. There was no recollection of trauma. Tooth 3.5 was treated and CBCT imaging was requested to assess the extension of the resorption in tooth 3.4.
FIGURE 17. #17: Consultation
Summary of the CBCT report, (image: CBCT #3, tooth #3.4):
There was extensive external root resorption extending from the lingual aspect of the cementoenamel junction to the middle third of the root. The resorption extended well into the tooth structure and just reached the pulp canal about half way to the buccal surface. No evidence of periodontal ligament space widening, loss of lamina dura, or other signs of periapical inflammatory disease associated with tooth 3.4 was reported.
FIGURE 18. #18: follow-up After 20 months
After reviewing the CBCT report the tooth was deemed to have a poor prognosis. The pattern of resorption was consistent with Class 4 extensive invasive cervical root resorption. (Table 1) All treatment options as well as the option of no treatment were discussed with the patient. The patient chose not to proceed with any endodontic treatment or extraction of the tooth at that moment being aware of the consequences. Regular follow-ups showed no apparent change radiographically and clinically (Fig. 18). After 20 months, while the tooth was still asymptomatic, the patient chose to proceed with extraction and replacement with an implant-supported crown.OH
Acknowledgement: to Dr. Vipul Shukla for restoration and follow-up hygiene maintenance of the first and second cases.
The authors are grateful to CANARAY specialists in Oral and Maxillofacial Radiology for contributing the CBCT images and report for the first and second cases.
The authors are grateful to the Discipline of Oral and Maxillofacial Radiology at the Faculty of Dentistry, University of Toronto for contributing the CBCT images and report for the third case.
Dr. Craig Bellamy is a second-year resident in the M.Sc. Endodontics Program, University of Toronto.
Dr. Gevik Malkhassian is an endodontist and a fellow member of the RCDC. He is an Assistant Professor in the discipline of Endodontics at the University of Toronto. He maintains a private practice limited to endodontics in Toronto and Mississauga.Oral Health welcomes this original article.
1. AAE. Glossary of Endodontic Terms;2012. 8th Edition.
2. Imfeld T. Dental erosion. Definition, classification and links. Eur J Oral Sci. 1996;104(2 ( Pt 2)):151-5.
3. Fox J. The history and treatment of the diseases of the teeth, diseases of the gums and alveolar process, with the operations which they respectively require. London: James Swan; 1806.
4. Tronstad L. Root resorption—etiology, terminology and clinical manifestations. Endod Dent Traumatol. 1988;4(6):241-52.
5. Darcey J, Qualtrough A. Resorption: part 1. Pathology, classification and aetiology. Br Dent J. 214. England2013. p. 439-51.
6. Kanas RJ, Kanas SJ. Dental root resorption: a review of the literature and a proposed new classification. Compend Contin Educ Dent. 2011;32(3):e38-52.
7. Fuss Z, Tsesis I, Lin S. Root resorption—diagnosis, classification and treatment choices based on stimulation factors. Dent Traumatol. 2003;19(4):175-82.
8. Trope M. Root resorption of dental and traumatic origin: classification based on etiology. Pract Periodontics Aesthet Dent. 1998;10(4):515-22.
9. Andreasen JO. External root resorption: its implication in dental traumatology, paedodontics, periodontics, orthodontics and endodontics. Int Endod J. 1985;18(2):109-18.
10. Discacciati JA, de Souza EL, Costa SC, Sander HH, Barros Vde M, Vasconcellos WA. Invasive cervical resorption: etiology, diagnosis, classification and treatment. J Contemp Dent Pract. 13. India2012. p. 723-8.
11. Shafer WG, Hine MK, Levy BM. A Textbook of Oral Pathology. 3 ed. Philadelphia: W.B. Saunders; 1974.
12. Heithersay GS. Invasive cervical resorption following trauma. Aust Endod J. 1999;25(2):79-85.
13. Heithersay G. Invasive cervical resorption. Endodontic Topics. 2004;7:73-92.
14. Kandalgaonkar SD, Gharat LA, Tupsakhare SD, Gabhane MH. Invasive cervical resorption: a review. J Int Oral Health. 2013;5(6):124-30.
15. Kim Y, Lee CY, Kim E, Roh BD. Invasive cervical resorption: treatment challenges. Restor Dent Endod. 2012;37(4):228-31.
16. Heithersay GS. Clinical, radiologic, and histopathologic features of invasive cervical resorption. Quintessence Int. 1999;30(1):27-37.
17. Friedman S, Rotstein I, Libfeld H, Stabholz A, Heling I. Incidence of external root resorption and esthetic results in 58 bleached pulpless teeth. Endod Dent Traumatol. 1988;4(1):23-6.
18. Trope M. Root resorption due to dental trauma. Endodontic Topics. 2002;1:79-100.
19. Harrington GW, Natkin E. External resorption associated with bleaching of pulpless teeth. J Endod. 5. United States1979. p. 344-8.
20. Andreasen JO, Andreasen FM. Root resorption following traumatic dental injuries. Proc Finn Dent Soc. 1992;88 Suppl 1:95-114.
21. de Figueiredo MA, de Figueiredo JA, Porter S. Root resorption associated with mandibular bone erosion in a patient with scleroderma. J Endod. 34. United States2008. p. 102-3.
22. Rout PG, Hamburger J, Potts AJ. Orofacial radiological manifestations of systemic sclerosis. Dentomaxillofac Radiol. 1996;25(4):193-6.
23. Nissenson RA. Parathyroid hormone-related protein. Rev Endocr Metab Disord. 2000;1(4):343-52.
24. Boabaid F, Berry JE, Koh AJ, Somerman MJ, McCcauley LK. The role of parathyroid hormone-related protein in the regulation of osteoclastogenesis by cementoblasts. J Periodontol. 2004;75(9):1247-54.
25. Kikuta J, Yamaguchi M, Shimizu M, Yoshino T, Kasai K. Notch signaling induces root resorption via RANKL and IL-6 from hPDL cells. J Dent Res. 94. United States: International & American Associations for Dental Research 2014.; 2015. p. 140-7.
26. von Arx T, Schawalder P, Ackermann M, Bosshardt DD. Human and feline invasive cervical resorptions: the missing link?—Presentation of four cases. J Endod. 35. United States2009. p. 904-13.
27. Jiang YH, Lin Y, Ge J, Zheng JW, Zhang L, Zhang CY. Multiple idiopathic cervical root resorptions: report of one case with 8 teeth involved successively. Int J Clin Exp Med. 2014;7(4):1155-9.
28. Kanungo M, Khandelwal V, Nayak UA, Nayak PA. Multiple idiopathic apical root resorption. BMJ Case Rep. 2013;2013.
29. Wu J, Lin L, Yang J, Chen X, Ge J, Sun W. Multiple idiopathic cervical root resorption: a case report. Int Endod J. 2015.
30.Bansal P, Nikhil V, Kapur S. Multiple idiopathic external apical root resorption: A rare case report. J Conserv Dent. 18. India2015. p. 70-2.
31. DeLaurier A, Boyde A, Jackson B, Horton MA, Price JS. Identifying early osteoclastic resorptive lesions in feline teeth: a model for understanding the origin of multiple idiopathic root resorption. J Periodontal Res. 44. Denmark2009. p. 248-57.
32. Tyrovola JB, Spyropoulos MN, Makou M, Perrea D. Root resorption and the OPG/RANKL/RANK system: a mini review. J Oral Sci. 50. Japan2008. p. 367-76.
33. Bender IB, Byers MR, Mori K. Periapical replacement resorption of permanent, vital, endodontically treated incisors after orthodontic movement: report of two cases. J Endod. 23. United States1997. p. 768-73.
34. Pierce AM, Lindskog S, Hammarstrom L. Osteoclasts: structure and function. Electron Microsc Rev. 1991;4(1):1-45.
35. Vaananen HK, Zhao H, Mulari M, Halleen JM. The cell biology of osteoclast function. J Cell Sci. 2000;113 (Pt 3):377-81.
36. Sameshima GT, Sinclair PM. Predicting and preventing root resorption: Part I. Diagnostic factors. Am J Orthod Dentofacial Orthop. 119. United States2001. p. 505-10.
37. Weltman B, Vig KW, Fields HW, Shanker S, Kaizar EE. Root resorption associated with orthodontic tooth movement: a systematic review. Am J Orthod Dentofacial Orthop. 137. United States: Inc; 2010. p. 462-76; discussion 12A.
38. Harris EF, Kineret SE, Tolley EA. A heritable component for external apical root resorption in patients treated orthodontically. Am J Orthod Dentofacial Orthop. 111. United States1997. p. 301-9.
39. Harris EF, Robinson QC, Woods MA. An analysis of causes of apical root resorption in patients not treated orthodontically. Quintessence Int. 1993;24(6):417-28.
40. Dermaut LR, De Munck A. Apical root resorption of upper incisors caused by intrusive tooth movement: a radiographic study. Am J Orthod Dentofacial Orthop. 90. United States1986. p. 321-6.
41. Massler M, Perreault JG. Root resorption in the permanent teeth of young adults. J Dent Child. 1954;21:158-64.
42. Majorana A, Bardellini E, Conti G, Keller E, Pasini S. Root resorption in dental trauma: 45 cases followed for 5 years. Dent Traumatol. 2003;19(5):262-5.
43. Vlaskalic V, Boyd RL, Baumrind S. Etiology and Sequelae of Root Resorption. Seminars in Orthodontics. 1998;4(2):124-31.
44. Henry JL, Weinmann JP. The pattern of resorption and repair of human cementum. J Am Dent Assoc. 1951;42(3):270-90.
45. Vier FV, Figueiredo JA. Prevalence of different periapical lesions associated with human teeth and their correlation with the presence and extension of apical external root resorption. Int Endod J. 35. England2002. p. 710-9.
46. Haapasalo M, Endal U. Internal inflammatory root resorption: the unknown resorption of the tooth. Endodontic Topics. 2006;14:60-79.
47. Newman WG. Possible etiologic factors in external root resorption. American Journal of Orthodontics. 1975;67(5):522-39.
48. Andreasen JO, Kristerson L. The effect of limited drying or removal of the periodontal ligament. Periodontal healing after replantation of mature permanent incisors in monkeys. Acta Odontol Scand. 1981;39(1):1-13.
49. Selvig K, Zander H. Chemical analysis and microradiography of cementum and dentin from periodontally diseased human teeth. J Periodontol. 1962;33:303-10.
50. Wedenberg C, Lindskog S. Experimental internal resorption in monkey teeth. Endod Dent Traumatol. 1985;1(6):221-7.
51. Chambers TJ. Phagocytic recognition of bone by macrophages. J Pathol. 1981;135(1):1-7.
52. Darcey J, Qualtrough A. Resorption: part 2. Diagnosis and management. Br Dent J. 214. England2013. p. 493-509.
53. Patel S, Durack C, Abella F, Shemesh H, Roig M, Lemberg K. Cone beam computed tomography in Endodontics–a review. Int Endod J. 2015;48(1):3-15.
54. Liedke GS, da Silveira HE, da Silveira HL, Dutra V, de Figueiredo JA. Influence of voxel size in the diagnostic ability of cone beam tomography to evaluate simulated external root resorption. J Endod. 35. United States2009. p. 233-5.
55. Durack C, Patel S, Davies J, Wilson R, Mannocci F. Diagnostic accuracy of small volume cone beam computed tomography and intraoral periapical radiography for the detection of simulated external inflammatory root resorption. Int Endod J. 2011;44(2):136-47.
56. Heithersay GS. Clinical endodontic and surgical management of tooth and associate
d bone resorption. Int Endod J. 1985;18(2):72-92.
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