This article will review what is known about the classification, causes, and treatment of root resorptions that are either internal or external.
Resorption of root surfaces, whether internal or external, occurs by the action of odontoclastic or osteoclastic cells. These osteoclastic cells are multinucleated giant cells with cytoplasmic vacuoles originating from bloodborne leucocytes from the bone marrow.1 These osteoclasts have membranes specific to the attachment of the cell of the hard tissue plus another that is involved in the resorptive process. Cellular components in a resorptive complex include inflammatory cells such as lymphocytes, plasma cells, histiocytes or macrophages, and fibroblasts, along with the multinucleated giant cells.1 This process can occur internally or externally, and it requires some form of stimulus to begin. It is thought that there are anti-resorption factors in the periodontal ligament (PDL) and in the pulp to prevent osteoclastic activity in normal situations. Root resorption after traumatic occurrences or infection is thought to be associated with the wound healing.1
It is thought that, most commonly, continuing trauma by some sort of mechanical, bacterial, or chemical event causes the various forms of root resorption to continue developing.1
The classification of the various types of root resorption is confusing in the literature, with different terminology used to describe the same processes. One of the latest classifications has been proposed by Fuss, Tsesis, and Lin. It is based on the stimulation factors leading to the resorption,3 and is as follows:
• Intrapulpal infection is the stimulation factor in internal root resorption and also in periradicular inflammatory root resorption.
• Periodontal infection root resorption causing external root resorption due to an injury to the pericementum.3
• Pressure from orthodontic movement, impacted tooth, or tumor can cause external root resoption.3
• Impacted tooth or tumor pressure can cause external root resorption adjacent to the area near the stimulation source.3
• Resorption can occur on a luxated tooth that has been replaced in the socket. It is thought the stimulus for the resorption and ankylosis of the tooth is related to damage to the PDL due to too long a time out of the mouth, or lack of adequate storage before replacement.3
• Trauma causing injury to the dentin, cementum, or PDL can bring about a clastic response of cells as a normal part of the scavenging function of cells. This is normally a transient process, but with added stimulation may continue into a chronic inflammatory process, creating external resorption of the root surface.4
Differential Radiographic Diagnosis
Distinguishing internal versus external root resorption by radiographic means often requires the use of two radiographs, the first taken perpendicular to the tooth, the second taken mesial to the perpendicular on the same horizontal plane. This is the mesial buccal distal (MBD) rule, where objects closer to the source of radiation will shift distally in relation to objects further from the source.) If the lesion is an external root resorption, the image will shift, and the root canal system can be clearly seen in the films superimposed on the external lesion. If the lesion is internal resorption, the lesion will not move in relation to the root canal system. In these cases, the root canal system will enlarge at the site of the root resorption.2
If the external resorption lesion is apically placed, the apex will appear shortened, blunted, or square, and the lesion will be ragged or irregular. The lesion may appear superimposed over the root end, and the canal can always be followed in the X-ray the full length of the root. If the lesion is internal resorption, the root canal system has an enlarged area, and the margins of the lesion are sharp, smooth, and clearly defined. The canal is not present in the lesion, and the size is variable. If the lesion is mid-root or higher, it will be sharply defined compared to a carious lesion. Carious lesions progress from the outside in, and their margins are not abrupt. 6
Identifying the source of the trauma will lead to the diagnosis, and it will also direct the form of treatment, because the source of the trauma must be removed to prevent further destruction.
Linking Diagnosis to Treatment
The use of bleaching agents, specifically hydrogen peroxide, in internal tooth bleaching has been linked to cervical resorption, especially when the peroxide is heated to drive it into the dentinal tubules.2,3 This is a direct chemical insult to the attachment tissues on the tooth root, resulting in an inflammatory condition that resembles wound healing. Internal bleaching should be completed using sodium perborate.2
Intrapulpal infection is the stimulation factor in internal root resorption and also in periradicular inflammatory root resorption. The bacterial infection can damage the pulpal tissues and the external cementum and PDL to the extent that they can no longer prevent the osteoclastic activity, leading to internal resorption or external apical resorption.
Periodontal infection can cause root resorption causing external root resorption due to an injury to the pericementum.4 In a significant case involving generalized root resorption due to extensive periodontal infection of 24 teeth supported by a very acidic diet, it is reported that the cervical resorptions were caused by an osteoclastic response presumably because the root-protective role of the junctional epithelium did not develop. The authors felt that the microflora and the acidic environment combined to cause the root resorption over a two-year period.2 In another reported case involving guided tissue regeneration (GTR) two years after the use of GTR therapy around the mandibular central incisors, the right central incisor developed a severe proximal cervical resorption extending into the pulp. When extracted and viewed for histological analysis, it was found that mononuclear and multinucleated cells were present in the resorptive lesion, with no evidence of root caries. The authors stated, “root surface resorption, ankylosis (replacement resorption) and alveolar bone resorption are not uncommon sequellae to periodontal healing...”2
Pressure from orthodontic movement, impacted tooth, or tumor can cause external root resoption.4 In animal and human experiments, continuous orthodontic forces produced by use of pseudo-elastic characteristics produce more resorptions than discontinuous forces. The magnitude of the force up to 200 cN (~200g) probably does not cause significant root resorption.2,3 Periapical replacement resorption (PARR) is a frequent and unpredictable sequellae of orthodontic movement of maxillary incisors, whereby the apical root portion is resorbed and replaced by bone. This seems to occur less in endodontically treated incisors. It is unknown as to what role the vital pulp plays in the resorptive process.2 Orthodontic tooth movement can induce changes in the pulps of teeth with completed apical formation. Release of neurotransmitters — i.e., neuropeptides — can influence both the blood flow and cellular metabolism during tooth movement. These are thought to affect the initiation and perpetuation of root resorptive processes during apical tooth remodeling caused by forced movement.2
Impacted tooth or tumor pressure can cause external root resorption adjacent to the area near the stimulation source.4 The force of eruption (commonly of canines on laterals or third molars on second molars) can cause resorption of the roots. Removal or redirection of these teeth can prevent further resorption. Tumor pressure caused mostly by slow growing tumors such as cysts, ameloblastomas, giant cell tumors, and fiber-osseous lesions, does not affect the pulpal health unless the tumors are located at the apical foramen and disturb blood flow. Removal of the stimulus from the tumor is required to prevent further resorption, and the surgery to remove the tumor may cause a problem for the tooth whose root is being resorbed.4
Resorption can occur on a luxated tooth that has been replaced in the socket. It is thought the stimulus for the resorption and ankylosis of the tooth is related to damage to the PDL due to too long a time out of the mouth, or lack of adequate storage before replacement.2,3 It is thought that there are anti-resorption factors located in the PDL and the pulp which prevent osteoclastic activity. Disruption of these factors by injury, as in a luxated tooth, or infection of the pulp, can result in ankylosis or root resorption. “In evaluating the events where resorption does occur, it appears that the loss of tissue components within the pulp (including odontoblasts) implies a risk of root canal resorption if non-pulpally derived cells gain access to the site.”3 The wound healing that occurs in these sites of trauma to the cells initiate the resorptive process, and because of a lack of the cells preventing octeoclastic activity, the resorptive lesion progresses. Trauma causing injury to the dentin, cementum, or PDL can bring about a clastic response of cells as a normal part of the scavenging function of cells. This is normally a transient process, but with added stimulation may continue into a chronic inflammatory process, creating external resorption of the root surface.2,3
The cause of the resorptive process leads to the treatment recommendation. The source(s) of the trauma must be removed. In the case of tumor and impacted tooth pressure, removal of the impacted tooth or tumor relieves the pressure on the root. In the case of periodontal infections, treatment to eradicate the infection, including scaling, root planing, localized antibiotic therapy, and other indicated periodontal therapy, are used to remove the infection source and stop the root resorption.
Pulpal infections require root canal therapy. There are suggestions that the use of calcium hydroxide in the canal will halt any resorptive process and promote healing.5 The antibacterial properties and high pH promote healing. It is suggested that at least a two-week interim dressing with calcium hydroxide is most effective before obturation of the canal. Calcitonin has been recommended in root canals to treat external root resorptions. Experimentally, it is reported that calcitonin will diffuse through the root to the cementum in six hours and will be released over the next 10 hours. Slower release of the calcitonin can be measured up to nine days later.2
External root resorption in the cervical region can be treated once the gingival tissues are reflected to provide access to prepare and restore the defect. It is not uncommon to find inflammatory tissues growing in the resorptive defect that must be totally removed prior to restoration. Glass ionomer,2,3 composite,2 amalgam, and even castable ceramic2 have been used to restore the defects caused by external resorption. Upon examination, the defect typically has sharp edges; hard, calcified dentin; and at times may show communication with the pulp. Most often, the gingival attachment stays below the external root resorptive defect once it is restored. Post-operative periodontal complications can occur after such restoration.17, 18
Early diagnosis of internal and external resorptions can aid in the retention of the tooth provided the appropriate therapy and the source of the trauma, whether from force, infection, or chemical damage, is eradicated.
1. Bergmans L, Van Cleynenbreugel J, Vergeken E, Wevers M, Van Meerbeck B, Lambrechts P. Cervical external root resorption in vital teeth.
J Clin Periodontol 2002 Jun;29(6):580-5.
2. Toto PD, Restarski JS. The histogenesis of pulpal odontoclasts. Oral Surg, Oral Med & Oral Path. Feb 1967;16(2):172-8.
3. Andreasen JO, Andreasen FM. Root resorption following traumatic dental injuries. Proc Finn Dent Soc 88 (1992), pages 95-114.
4. Fuss Z, Tsesis I, Lin S. Root resorption - diagnosis, classification and treatment choices based on stimulation factors. Dent Traumatol 2003 Aug;19(4):175-82.
5. Gunraj MN. Dental root resorption. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999 Dec; 88(6):647-53.
6. Gartner AH, Mack T, Somerlott RG, Walsh LC. Differential diagnosis of internal and external root resorption. J Endod Nove 1976;2(11):
7. Dahl JE, Pallesen U. Tooth bleaching — a critical review of the biological aspects. Crit Rev Oral Biol Med 2003;14(4):292-304.
8. Tredwin CJ, Naik S, Lewis NJ, Scully C. Hydrogen peroxide tooth-whitening (bleaching) products: review of adverse effects and safety issues. Br Dent J 2006 Apr 8;200(7):371-6.
9. Dahl JE. Tooth bleaching - A critical review of the biological aspects. Crit Rev Oral Biol Med 2003;14(4):292-304 (2003).
10. Beertsen W, Piscaer M, Van Winkelhoff AJ, Everts V. Generalized cervical root resorption associated with periodontal disease. J Clin Periodontol 2001 Nov;28(11):1,067-73.
11. Blomlof L, Lindskog S. Cervical root resorption associated with guided tissue regeneration: a case report. J Periodontol 1998 Mar;69(3):392-5.
12. Owman-Moll P. Orthodopntic tooth movement and root resorption with special reference to force magnitude and duration. A clinical and histological investigation in adolescents. Swed Dent J Suppl 1995;105:1-45.
13. Weiland F. External root resorptions and orthodontic forces: correlation and clinical consequences. Prog Orthod 2006;7(2):156-63.
14. Bender IB, Byers MR, Mori K. Periapical replacement resorption of permanent, vital, endodontically treated incisors after orthodontic movement: report of two cases. J Endod 1997 Dec;23(12):768-73.
15. Hamilton RS, Gutmann JL. Endodontic-orthodontic relationships: a review of integrated treatment planning challenges. Int Endod J 1999 Sept;32(5):343-60.
16. Croll TP, Pascon EA, Langeland K. Traumatically injured primary incisors: a clinical and histological study. ASDC J Dent Child 1987 Nov-Dec;54(6):401-22.
17. Wiebkin OW, Cardaci SC, Heithersay GS, Pierce AM. Therapeutic delivery of calcitonin to inhibit external inflammatory root resorption. I. Diffusion kinetics of calcitonin through the dental root. Endod Dent Traumatol 1996 Dec;12(6):265-71.
18. Heithersay GS. Clinical endodontic and surgical management of tooth and associated bone resorption. International Endod J 1985;18:72-92.
19. Meister F, Haasch GC, Gernstein H. Treatment of external resorption by a combined endodontic-periodontic procedure. J Endod 1986;12:542-45.
20. Culbreath TE, Davis GM, West NM, Jackson A. Treating internal resorption using a syringeable composite resin. JADA 2000 Arp;131($):493-5.
21. Dumfahrt H, Moschen I. A new approach in restorative treatment of external root resorption. A case report. J Periodontol 1998 Aug;69(8):
• Dr. Larson is Asssociate Professor, Department of Restorative Sciences, Division of Operative Dentistry, University of Minnesota School of Dentistry, Minneapolis, Minnesota 555455. Email is firstname.lastname@example.org.