Journal of Conservative Dentistry

: 2013  |  Volume : 16  |  Issue : 1  |  Page : 4--8

Tooth resorption part I - pathogenesis and case series of internal resorption

Marina Fernandes1, Ida de Ataide1, Rahul Wagle2,  
1 Department of Conservative Dentistry and Endodontics, Goa Dental College and Hospital, Bambolim, Goa, India
2 Consulting Endodontist, Ex faculty, Goa Dental College and Hospital, Bambolim, Goa, India

Correspondence Address:
Marina Fernandes
Department of Conservative Dentistry and Endodontics, Goa Dental College and Hospital, Bambolim, Goa


Resorption is a pathologic process that often eludes the clinician with its varied etiologic factors and diverse clinical presentations. The key cells involved in tooth resorption are odontoclasts which are multinucleated cells that produce resorption lacunae. Resorption can be classified as internal and external resorption. Internal resorption has been described as a rare occurrence as compared to external resorption. This article describes the pathogenesis of tooth resorption and various forms of internal resorption along with some clinical cases. Early diagnosis is the key factor in the successful management of resorptive lesions.

How to cite this article:
Fernandes M, de Ataide I, Wagle R. Tooth resorption part I - pathogenesis and case series of internal resorption .J Conserv Dent 2013;16:4-8

How to cite this URL:
Fernandes M, de Ataide I, Wagle R. Tooth resorption part I - pathogenesis and case series of internal resorption . J Conserv Dent [serial online] 2013 [cited 2021 Sep 18 ];16:4-8
Available from:

Full Text


According to the Glossary of the American Association of Endodontists, resorption is defined as a condition associated with either a physiologic or a pathologic process resulting in loss of dentin, cementum or bone. [1] Physiologic resorption is seen in primary teeth that results in their exfoliation and allows eruption of their permanent successors. [2],[3] Pathologic resorption can occur following traumatic injuries, orthodontic tooth movement, or chronic infections of the pulp or periodontal structures. [1] Pathologic resorption if untreated will result in the premature loss of the affected teeth. [4]

Root resorption may be classified based on its location in relation to the root surface: Internal or external. [3] Internal resorption may be classified as internal inflammatory resorption and internal replacement resorption. External resorption is further classified into external surface resorption, external inflammatory resorption, external replacement resorption, external cervical resorption and transient apical breakdown. [1],[3]


Osteoclasts are multinucleated giant cells that are responsible for bone resorption. They are formed by fusion of mononuclear precursor cells [Figure 1]a that arrive at the resorption site through the blood stream. [1],[4] Their differentiation is under the control of factors produced by bone marrow stromal cells or found on the mature osteoblast. Two such factors are RANK (receptor activator of nuclear factor kappa B) ligand (RANKL) and osteoprotegerin (OPG). The receptor of RANKL is RANK and is localized on the surface of the progenitor osteoclast [Figure 1]b. Therefore, physical contact between the osteoblast or stromal cells and the progenitor osteoclast is essential for a direct interaction of RANKL and RANK for osteoclast formation and activation. [2] OPG acts as a decoy receptor that can bind to RANKL and interferes with its ability to bind to RANK receptors, thus inhibiting osteoclast formation. Thus, both RANKL and OPG play an important role in osteoclastinogenesis. [4]{Figure 1}

The cell organelles of an osteoclast consists of many nuclei, multiple Golgi complexes, mitochondria, rough endoplasmic reticulum and numerous vesicular structures. [5] The cell membrane of the osteoclast adjacent to the tissue surface has a series of finger-like projections called as the ruffled border. [4] At the periphery of this ruffled border, the plasma membrane is apposed closely to the bone surface, and the adjacent cytoplasm, devoid of cell organelles, is enriched in actin, vinculin, and talin, fibrillar contractile proteins. [5] This is called as a clear or sealing zone which comprises the peripheral non-resorptive area of adhesion of osteoclasts to bone (i.e. it helps to attach the cells to the bone). [6] Extracellular matrix proteins like osteopontin present on the surface of bone serve as binding sites for the osteoclasts. The osteopontin molecule contains different domains, with one domain binding to bone and another domain binding to integrin receptors in the plasma membranes of osteoclasts. [4] A microenvironment [Figure 1]c is thus created between the ruffled border of the osteoclast and the hard tissue in which resorption takes place. [1] Odontoclasts (tooth resorbing cells) are morphologically analogous to osteoclasts and have similar enzymatic properties and resorption patterns. However, odontoclasts are smaller in size, have fewer nuclei and form smaller resorption lacunae than osteoclasts. [1],[2]

The resorption process occurs in two stages: Degradation of the inorganic mineral structure followed by disintegration of the organic matrix. [7] Degradation of the inorganic crystal structure is brought about by enzymes like acid phosphatase and carbonic anhydrase II present in the osteoclasts. These enzymes are synthesized in the rough endoplasmic reticulum, transported to the Golgi complexes and moved to the ruffled border in transport vesicles where they release their content into the sealed compartment adjacent to the bone surface. [5] The carbonic anhydrase II enzyme catalyses the intracellular conversion of CO 2 to H 2 CO 3 , which provides a readily available source of H + ions to be pumped into the subosteoclastic region via the proton pump associated with the ruffled border [Figure 1]d. The disintegration of the organic matrix is brought about by cysteine proteinase, collagenase and matrix metalloproteinase enzymes. The cysteine proteinase enzymes act at an acidic pH closer to the ruffled border, while collagenase and matrix metalloproteinase enzymes are active at the resorbing bone surface where the pH is closer to neutral due to the buffering capacity of the dissolving bone salts. [1] The inorganic and organic degradation products then undergo endocytosis at the ruffled border. They are then translocated in transport vesicles and their extracellular release occurs along the membrane opposite the ruffled border (transcytosis). [5]

Internal resorption

Internal resorption has been associated with chronic inflammation of the pulp following caries, trauma or a cracked tooth. [8] Two types of internal resorption can occur: Internal inflammatory resorption and root canal replacement resorption. While both types involve a progressive loss of dentin, root canal replacement resorption involves subsequent deposition of hard tissue that resembles bone or cementum but not dentin. [1] Internal inflammatory resorption can be transient or progressive. [1],[9] It has been hypothesized that internal resorption once initiated can progress only if the dentinal tubules have an unexpected course from an area of necrotic tissue to an area of vital pulp tissue. [9],[10] This perhaps explains why it is reported as a rather rare occurrence as compared to external root resorption. [11]

Inflammatory non perforating internal resorption

Case 1

A 49-year-old female patient undergoing periodontal therapy was referred from the department of Periodontics for management of internal resorption in tooth #8 that was evident on a routine periapical radiograph. The patient's medical history was non-contributory. No episode of pain was reported by the patient in tooth #8. The patient gave a history of trauma to her anterior teeth about 15 years back. On clinical examination, tooth #8 was discoloured and displayed an Ellis class IV fracture. It failed to respond to thermal and electric pulp testing while the adjacent teeth responded within normal limits. Tooth #8 on a periapical radiograph revealed a well delineated oval enlargement of the pulp space in the apical third of the root, which was continuous with the root canal walls [Figure 2]a. The diagnosis was inflammatory non perforating internal resorption.{Figure 2}

Following access cavity preparation, the canal was negotiated. The root canal system was debrided using stainless steel K- files to a master apical file (MAF) size 40 under 5.25% sodium hypochlorite (NaOCl) irrigation. Since the tooth was nonvital, there was no bleeding evident from the root canal that is typical of active resorptive tissue. However, to facilitate thorough debridement of the resorptive defect ultrasonic activation of NaOCl was carried out. The canal was dried with paper points and calcium hydroxide (Ca(OH) 2 ) paste was placed as an intracanal medicament for 1 week. At the next appointment, the Ca(OH) 2 paste was flushed out; the canal was dried and obturated with warm vertical compaction technique using gutta-percha [Figure 2]b. The post endodontic restoration was completed at a later date and the patient was referred back to the department of Periodontics.

The case report exemplifies inflammatory internal resorption which was probably self-limiting as tooth #8 was nonvital. For internal resorption to progress, the pulp tissue apical to the resorptive lesion must have viable blood supply that provides clastic cells whereas the infected necrotic coronal pulp tissue provides stimulation for those clastic cells. [1],[4] Bacteria probably entered the pulp space through the fracture site thus infecting the coronal pulp tissue which served as a stimulus for the resorption process resulting in the damage to the odontoblast layer and predentin. Wedenberg and Lindskog reported that damage to both these layers results in exposure of the underlying mineralized dentin to odontoclasts. [12] The resorptive defect that forms is filled with inflammatory connective tissue. Failure to intervene at this stage could result in further progress of the resorption in the defect laterally resulting in a perforation or the resorption may progress apically and the pulp tissue apical to the resorptive defect may undergo necrosis, [13] the later consequence being evident in this case. The management of internal resorption is intended to remove all the vital and non vital pulpal remnants and to disinfect and obturate the root canal. [14] NaOCl an effective antimicrobial irrigating solution, aids in dissolving necrotic tissue. [15] Ultrasonic activation of irrigants has also proved to be an effective method to remove debris lodged in inaccessible resorptive sites. [16],[17] However, some amount of debris may still persist within the resorption niche thus necessitating the placement of an intracanal medicament like Ca(OH) 2 [8],[9],[18],[19] that has a pronounced antimicrobial effect due to its alkaline pH. [20],[21] Placement of Ca(OH) 2 has been recommended for 1 to 2 weeks that provides sufficient time to necrotize the residual pulp tissue. [22] The obturation of internal resorption defects can be difficult due to their shape and lack of adequate access. The warm vertical compaction and thermoplasticized gutta-percha techniques have proved beneficial in this regard as they seal the defects satisfactorily. [23]

Inflammatory perforating internal resorption

Case 2

A 31-year-old male patient reported to the department of Conservative Dentistry and Endodontics for esthetic rehabilitation of his anterior teeth. The patient complained of occasional pain in tooth #10. The medical history was non-contributory. Clinically, unsightly restorations were present on teeth #7, 8, 9 and 10. A periapical radiograph revealed radiolucent lesions in relation to the apices of teeth #7, 8, 9 and 10. An oval radiolucency indicative of internal resorption was evident in the middle third of the radicular portion of tooth #10 [Figure 3]a. The radiolucency appeared to be continuous with the distal radicular surface, suggestive of a perforating resorptive defect. Teeth #7, 8, 9, 10 failed to respond to thermal and electric pulp testing. The diagnosis was inflammatory perforating internal resorption.{Figure 3}

Following access cavity preparation, the coronal pulp in tooth #10 was nonvital while profuse bleeding was induced on probing the middle third of the canal space. Coronal flaring of the canal was done with Gates Glidden drills to facilitate entry of an endodontic spoon excavator to remove granulation tissue from the resorption site under copious 5.25% NaOCl irrigation. The apical third of canal space was negotiated to the working length with hand K- files and debridement of the canal system was carried out. Ultrasonic activation of the resorptive defect was carried out with NaOCl. The canal was dried with paper points and Ca(OH) 2 paste was placed as an intracanal medicament. After 1 week, Ca(OH) 2 was flushed out of the canal with NaOCl. Residual Ca(OH) 2 from the resorptive defect was removed out with the help of the endodontic spoon excavator. The canal was dried and sectional cone obturation with gutta- percha was carried out in the apical third of canal [Figure 3]b. The resorptive defect was then repaired with Mineral trioxide Aggregate (MTA) [Figure 3]c. Post endodontic restoration was then carried out with composite resin. The patient was asymptomatic for a period of 3 months following which he has failed to report for a follow up.

In contrast to the case 1, the resorption was active in case 2 evident by the presence of granulation tissue in the resorption site and vital apical tissue. The progress of resorption laterally possibly led to the distal perforation. Numerous studies have proven the superior sealing ability of MTA as a perforation repair material. [24],[25],[26],[27] MTA when placed in direct contact with human tissues forms Ca(OH) 2 that releases calcium ions for cell attachment and proliferation, creates an antibacterial environment by its alkaline pH, modulates cytokine production, encourages differentiation and migration of hard tissue producing cells and forms hydroxyapatite on the MTA surface and provides a biologic seal. [28] Reparative tissue barrier formation through use of Ca(OH) 2 has been tried [29],[30] but this method is time consuming, requiring several months. It has also been reported that the tissue barrier that forms is usually incomplete, displaying voids or porosity. [31] Surgical repair of the defect may also be considered [32] but if the resorption is extensive or occurs on the proximal or lingual surface of the root, it is often impossible. [8] If the resorption is quite extensive, the first presentation may be root fracture, which may manifest as a sudden increase in mobility of the tooth. [22],[33]

Internal replacement resorption

Case 3

A 27-year-old male patient with a non-contributory medical history presented with a palatal swelling in relation to teeth #9 and 10, which were discolored. Patient reported trauma to the teeth about 12 years back. A large radiolucency was evident on a periapical radiograph relative to the apices of teeth #9 and 10. The apices of the teeth showed irregular ragged edges with loss of lamina dura. The pulp canal space of tooth #9 appeared enlarged and exhibited the presence of a less radiopaque material partially obscuring the continuity of the canal space while tooth #10 displayed total obliteration of the canal space [Figure 4]a. A diagnosis of internal replacement resorption along with external inflammatory resorption was made.{Figure 4}

Following access cavity preparation, canal space of tooth #9 was negotiated and the radiograph revealed the deviation of the file towards the mesial aspect [Figure 4]b. Cleaning and shaping of the canal was performed using hand K-files along with 5.25% NaOCl irrigation followed by placement of Ca(OH) 2 intracanal medicament into the canal space. But a periapical radiograph displayed an uneven flow of the intracanal medicament, confirming the presence of metaplatic tissue [Figure 4]c. Hence, the Ca(OH)2 was flushed out of the canal and the metaplastic tissue was scrapped off the canal with the aid of hand H-files [Figure 4]d providing an unhindered flow of the medicament [Figure 4]e, which was refreshed at regular intervals of 15 days. Pulp canal space of tooth #10 was negotiated at a later appointment and the endodontic therapy of both the teeth was completed in next few scheduled visits [Figure 4]f. Further follow-up of the patient could not be done due to relocation to a different state.

This type of resorption results from a low-grade irritation of pulpal tissues such as chronic irreversible pulpitis or partial necrosis that is usually localized to a small area of the root canal system. [34] The resorption process starts once the odontoblast layer and predentin are disrupted. [1],[35] Metaplastic tissue could resemble bone or cementum. [36] Though teeth with internal replacement resorption displaying metaplastic changes often present a challenge to the clinician, management is not always impossible. Careful negotiation of the pulp canal space will usually reveal narrow pathways in between the metaplatic tissue, which usually lead to the apical foramen. Rarely will cul de sacs be encountered. The canal can then be enlarged using hand K- files, taking care to apply less pressure towards the canal wall to avoid thinning of the wall. Once the canal is sufficiently widened a stiff H-file (e.g. No.35/40) can be used in a push-pull motion to scrap the metaplastic tissue off the canal. It is in the opinion of the authors that use of Nickel Titanium rotary files is questionable for such cases as the metaplastic tissue may present varied intricacies that may prove detrimental to the files. They probably could be used only after sufficiently enlarging the canal with hand files and after ensuring a smooth glide path.


Internal resorption is typically asymptomatic and is usually discovered during routine radiographic examination. Lesions that are perforating in nature are more difficult to manage than nonperforating lesions and may even necessitate extraction due to poor prognosis.


1Ne RF, Witherspoon DE, Gutmann JL. Tooth resorption. Quintessence Int 1999;30:9-25.
2Harokopakis-Hajishengallis E. Physiologic root resorption in primary teeth: Molecular and histological events. J Oral Sci 2007;49:1-12.
3Patel S, Kanagasingam S, Pitt Ford T. External cervical resorption: A review. J Endod 2009;35:616-25.
4Patel S, Ricucci D, Durak C, Tay F. Internal root resorption: A review. J Endod 2010;36:1107-21.
5Nanci A, Whitson WS, Bone BP. In: Nanci A, editor. Ten Cate's Oral Histology: Development, Structure, and Function. 6 th ed. St. Louis: C.V. Mosby; 2003. p. 122-30.
6Seltzer S. Endodontology. 2 nd ed. Philadelphia: Lea and Febiger; 1988.p. 170-94.
7Bhaskar SN. Orban's oral histology and embryology. 10 th ed. St. Louis: C.V. Mosby; 1986. p. 206-8.
8Hovland EJ, Dumsha TC. Problems in the management of tooth resorption. In: Gutmann JL, Dumsha T, Lovdahl P, Hovland E, editors. Problem solving in endodontics. 3 rd ed. St. Louis: C.V. Mosby; 1997. p. 253-76.
9Tronstad L. Clinical endodontics. 2 nd ed. NewYork: Thieme; 2003. p. 146-56.
10Tronstad L. Root resorption-etiology, terminology, and clinical manifestations. Endod Dent Traumatol 1988;4:241-52.
11Levin L, Trope M. Root resorption. In: Hargreaves KM, Goodis HE, editors. Seltzer and Bender's dental pulp. Chicago, IL: Quitessence Publishing Co Inc; 2002. p. 425-48.
12Wedenberg C, Lindskog S. Experimental internal resorption in monkey teeth. Endod Dent Traumatol 1985;1:221-7.
13Ricucci D. Apical limit of root canal instrumentation and obturation: Part I-literature review. Int Endod J 1998;31:384-93.
14European Society of Endodontology. Quality guidelines for endodontic treatment: Consensus report of the European Society of Endodontology. Int Endod J 2006;39:921-30.
15Harrison JW. Irrigation of the root canal system. Dent Clin North Am 1984;28:797-808.
16Martin H. Ultrasonic disinfection of the root canal. Oral Surg Oral Med Oral Pathol 1976;42:92-9.
17Burleson A, Nusstein J, Reader A, Beck M. The in vivo evaluation of hand/rotary/ultrasound instrumentation in necrotic, human mandibualr molars. J Endod 2007;33:782-7.
18Bystrom A, Claesson R, Sundqvist G. The antibacterial effect of camphorated paramonochlorophenol, camphorated phenol and calcium hydroxide in the treatment of infected root canals. Endod Dent Traumatol 1985;1:170-5.
19Siqueira JF, Rôças IN, Santos SR, Lima KC, Magalhães FA, de Uzeda M. Efficacy of instrumentation techniques and irrigation regimens in reducing the bacterial population within root canals. J Endod 2002;28:181-4.
20Han GY, Park SH, Yoon TC. Antimicrobial activity of calcium hydroxide containing pastes with enterococcus faecalis in vitro. J Endod 2001;27:328-32.
21Buck RA, Cai J, Eleazer PD, Staat RH, Hurst HE. Detoxification of endotoxin by endodontic irrigants and calcium hydroxide. J Endod 2001;27:325-7.
22Kaiwar A, Ranjini MA, Ashwini P, Pasha MF, Meena N. Internal resorption managed by root canal treatment: Incorporation of CT with 3D reconstruction in diagnosis and monitoring of the disease. J Int Oral Health 2010;2:86-94.
23Gencoglu N, Yildirim T, Garip Y, Karagenc B, Yilmaz H. Effectiveness of different gutta-percha techniques when filling experimental internal resorptive cavities. Int Endod J 2008;41:836-42.
24Lee SJ, Monsef M, Torabinejad M. Sealingability of a mineral trioxide aggregate for repair of lateral root perforations. J Endod 1993;19:541-4.
25Holland R, Filho JA, de Souza V, Nery MJ, Bernabé PF, Junior ED. MTA repair of lateral root perforations. J Endod 2001;27:281-4.
26Daoudi MF, Saunders WP. In vitro evaluation of furcal perforation repair using mineral trioxide aggregate or resin modified glass ionomer cement with and without the use of the operating microscope. J Endod 2002;28:512-5.
27Hardy I, Liewehr FR, Joyce AP, Agee K, Pashley DH. Sealing ability of One-Up Bond and MTA with and without a secondary seal as furcation perforation repair materials. J Endod 2004;30:658-61.
28Parirokh M, Torabinejad M. Mineral trioxide aggregate: A comprehensive literature review-Part III: Clinical applications, drawbacks, and mechanism of action. J Endod 2010;36:400-13.
29Frank AL, Weine FS. Nonsurgical therapy for the perforative defect of internal resorption. J Am Dent Assoc 1973;87:863-8.
30Dumsha TC, Gutmann JL. Clinical techniques for the placement of calcium hydroxide. Compend Contin Educ Dent 1985;6:482-3,486,488-9.
31Goldberg F, Massone EJ, Spielberg C. Evaluation of the dentinal bridge after pulpotomy and calcium hydroxide dressing. J Endod 1984;10:318-20.
32Hsien HC, Cheng YA, Lee YL, Lan WH, Lin CP. Repair of perforating internal resorption with mineral trioxide aggregate: A case report. J Endod 2003;29:538-9.
33Gulabivala K, Searson LJ. Clinical diagnosis of internal resorption: An exception to the rule. Int Endod J 1995;28:255-60.
34Benenati FW. Root resorption: Types and treatment. Gen Dent 1997;45:42-5.
35Wedenberg C, Zetterqvist L. Internal resorption in human teeth: A histological scanning electron microscopic and enzyme histochemical study. J Endod 1987:13:255-9.
36Lindskog S, Blomlöf L, Hammarström L. Repair of periodontal tissues in vivo and vitro. J ClinPeriodontol 1983;10:188-205.