Resorption may present as a primary diagnostic entity
or as a secondary complication resulting in failure of
endodontically treated teeth. Resorption falls into the
following entities: internal root resorption (IRR), invasive
cervical root resorption (ICRR), external inammatory
root resorption (EIRR), replacement resorption (RR), and
pressure resorption (Fig 10-1). Resorption pathogenesis
varies based on type, although inammation is a compo-
nent of each (Fig 10-2).
Odontoclasts in the pulp and osteoclasts in the peri-
odontal ligament (PDL) cannot adhere to unmineralized
tissue like the predentin and odontoblasts internally and
the precementam and cementoblasts externally. For re-
sorption to occur, Tronstad found that loss or damage of
the protective, unmineralized layers must occur.
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10ResorptionResorption may present as a primary diagnostic entity or as a secondary complication resulting in failure of endodontically treated teeth. Resorption falls into the following entities: internal root resorption (IRR), invasive cervical root resorption (ICRR), external inammatory root resorption (EIRR), replacement resorption (RR), and pressure resorption (Fig 10-1). Resorption pathogenesis varies based on type, although inammation is a compo-nent of each (Fig 10-2). Odontoclasts in the pulp and osteoclasts in the peri-odontal ligament (PDL) cannot adhere to unmineralized tissue like the predentin and odontoblasts internally and the precementam and cementoblasts externally. For re-sorption to occur, Tronstad found that loss or damage of the protective, unmineralized layers must occur. 200Resorption10Internal Root ResorptionFrank rst described internal root resorption in 1974. Tronstad later reviewed the patho-physiologic circumstances crucial to progression of IRR. As a result of pulpal injury, some degree of partial coronal pulp necrosis occurs and induces inammation of the remaining apical vital tissue. This inamed tissue must abut an area of exposed dentinal tubules, sec-ondary to loss of the protective predentin and odontoblastic layer, for resorption to occur. If the apical tissue necroses, the resorptive process stops. In an animal study, Wedenberg and Lindskog discovered a further requirement for in-fection of the necrotic tissue apical to the resorptive lesion. Although transient internal resorption occurs commonly following dental trauma, it will not progress in the absence of infection. Even in cases of pulpal infection, progressive IRR is rare, as vital inamed tissue is necessary for continued resorption. Gabor et al found that IRR, whether stable or pro-gressive, is a common histologic nding in the absence of clinical or radiographic changes. They noted IRR defects in 50% of extracted teeth with a preoperative diagnosis of pulpitis and 77% of those with pulpal necrosis. Fig 10-1 Types of resorption.Invasive cervical root resorptionExternal inammatory root resorptionPressure resorptionInternal root resorptionReplacement resorptionLoss of unmineralized protective layer on rootResorptionInammationFig 10-2 Pathogenesis of resorption (Tronstad). 201Invasive Cervical Root ResorptionPatel et al reviewed potential etiologic factors for IRR, including trauma, caries, peri-odontal infections, excessive heat generated during restorative procedures, calcium hy-droxide procedures such as pulp caps or pulpotomy, vital root resections, anachoresis, orthodontic treatment, cracked teeth, or idiopathic dystrophic changes. Gartner et al described the classic radiographic appearance of IRR as an oval-shaped enlargement of uniform density within the pulp space (Fig 10-3). Clinical symptoms gener-ally do not develop until the lesion expands to create a perforation or pulpal involvement progresses to symptoms of pulpitis or pulpal necrosis with infection. Clinically, a pinkish hue may be observed in cases of coronally located IRR, as described by the classic study by Mummery. However, this is an uncommon nding. Fig 10-3 (a to c) Clinical examples of IRR.a b cIf detected early, treatment of IRR is predictable. Caliskan and Turkun reported a 100% success rate of root canal therapy of nonperforating lesions at 2 to 4 years postopera-tively. In cases of perforating lesions, this success rate dropped to 25%. It is important to note, however, that a very small sample size of only four cases was followed, and the study was performed using long-term calcium hydroxide for remineralization. Failures were approached surgically with limited success. With the introduction of mineral trioxide ag-gregate (MTA) as a repair material, success rates for perforating resorptive defects may improve for both surgical and nonsurgical cases. Although no studies have been published examining MTA’s ability to treat perforating IRR, Mente et al demonstrated that MTA can successfully repair iatrogenic perforations. Invasive Cervical Root Resorption ICRR has been reviewed extensively by Heithersay (1999a). For this type of resorptive de-fect to occur, a developmental or iatrogenic defect must be present in the cementum/cementoid layer of the root, so that the PDL, with the potential for inammatory invasion, is in direct contact with dentin. Clinically, ICRR is generally painless because complete pulpal involvement does not occur except in advanced lesions (Heithersay 1999a). Pulpitis can occur secondary to this late-stage pulpal involvement. Many report that ICRR causes pink coronal discoloration, though Heithersay (1999a) refuted this, as it occurs only in very advanced lesions and may also indicate IRR. 202Resorption10Histologically, Heithersay (1999a) found ICRR is composed of bro-osseous and bro-vascular tissue associated with clastic cells. Multiple tunneling channels into dentin were noted, and these increased in density and extension as the lesions progressed apically. Theories on the potential etiologies of ICRR abound, and the true etiology of ICRR is like-ly multifactorial. Often, an obvious cause is un-known. Heithersay (1999b) investigated the po-tential etiologic factors of 250 teeth with ICRR and found that orthodontics was the most com-monly identied factor, followed by trauma, in-tracoronal bleaching, dentoalveolar surgery, peri-odontal therapy such as deep scaling and root planing, bruxism, developmental defects involv-ing cementum, and intracoronal restorations. No identiable potential etiologic factor was evident in 16% of teeth. The occurrence of more than one of the potential risk factors resulted in an in-creased risk of ICRR. The potential risk factors for ICRR are summarized in Fig 10-5.Although Heithersay (1999b) reported that orthodontics is the most common etiologic factor for ICRR, other research indicates that orthodontic causation of ICRR is relatively infrequent. Thonen et al found a low incidence of ICRR at 0.9% in molars subject to ortho-dontic forces, with increased associations in areas of long-duration or larger movement. Consequently, the likelihood of developing ICRR appears low. As the majority of ICRR lesions are asymptomatic and not clinically apparent, most cases are diagnosed incidentally on routine radiographs. Early lesions may present as subcrest-al radiolucencies resembling class V caries. More extensive lesions present with irregularly shaped radiolucencies at the same location and often extend into radicular dentin. Although lesions will approach the pulp space, the outline of the pulp space usually remains well de-ned. Adjacent alveolar bone is usually intact. Figure 10-4 depicts some examples of ICRR. Fig 10-5 Proposed etiologies of ICRR.TraumaOrthodonticsIntracoronal restorationsNonvital bleachingPeriodontal therapyViral (feline herpes virus)IdiopathicFig 10-4 (a to d) Clinical examples of ICRR. a c db 203Invasive Cervical Root ResorptionHarrington and Natkin rst reported the association between ICRR and intracoronal bleaching. Rotstein et al found that superoxyl and heat were particularly associated with ICRR following intracoronal bleaching, and cemental defects found at the cementoenamel junction provided the likely pathway of irritation. Intracoronal bleaching is often performed on previously traumatized teeth, and Heithersay (1999b) suggested that these two factors might act in concert to increase the risk of ICRR. Periodontal therapy, including deep scaling, root planing, and surgical debridement can theoretically interrupt the protective unmineralized precementum and cementoblastic lay-er on root structure. Tronstad theorized that sulcular bacteria could extend through the S-shaped dentinal tubules to induce ICRR. This nding is relatively infrequent, as the rapid downgrowth of epithelium and re-establishment of the junctional epithelium attachment should prevent its occurrence. Among cases of idiopathic ICRR, several etiologic theories have been proposed. Hei-thersay (1999b) presumed that subclinical factors, such as histologic developmental de-fects in cervical precementum, might play a role. Von Arx et al proposed a viral etiology in his case series of four patients testing positive for feline herpes virus, known to cause a similar clinical entity in wild and domestic cats. Heithersay (1999b) classied ICRR lesions based on their size and extension into root structure as follows (Fig 10-6): • Class 1: Small, well-dened lesion localized to cervical area and involving dentin only. • Class 2: Slightly larger, well-dened lesion localized to cervical area but penetrating further into dentin close to the coronal pulp. • Class 3: Larger, less dened lesion extending into the coronal third of the root. • Class 4: Large lesion extending beyond the coronal third of the root. Fig 10-6 Heithersay’s (1999b) classications of ICRR.Class 1 Class 2 Class 3 Class 4 204Resorption10Treatment of ICRR involves debridement of the resorptive defect, placement of glycerol on the gingival tissues, application of 90% trichloroacetic acid for 1 to 4 minutes, and restoration with glass-ionomer cements (Heithersay 1999c). To access the defect, a surgical ap is often necessary. Root canal therapy is indicated in class 2 and 3 defects because of inevitable pul-pal involvement. Trichloroacetic acid deactivates the resorptive tissue via coagulative necro-sis. Glass-ionomer cements are advised for restoration of resorptive defects because Dragoo demonstrated the ability of periodontal tissue to reattach to these materials. While generally an external approach is recommended for treatment, an internal approach for repair can be undertaken for class 2 lesions and involves the use of intracoronal trichloroacetic acid or mul-tiple applications of calcium hydroxide to assure clearance of resorptive soft tissue. Addition-al potential methods for treating ICRR lesions include the use of guided tissue regeneration, orthodontic extrusion (possibly followed by reintrusion), and intentional replantation. Heithersay (1999c) recommends treatment only for lesions falling into classes 1, 2, and 3 based on poor outcomes of class 4 lesions. At 3 years postoperative, Heithersay (1999c) reported 100% success for treated class 1 and 2 lesions, 78% success for class 3 lesions, and only 12.5% success for class 4 lesions. Recurrence of resorption or development of periradicular pathology were indicators of failure in their study. External Inammatory Root Resorption EIRR is generally endodontic or orthodontic in origin according to Tronstad. Apical resorp-tion secondary to periradicular pathology is generally transient. Vier and Figueiredo found that 86% of cases with apical periodontitis had associated EIRR due to infectious stimuli. As long as endodontic therapy is initiated in these cases, resorption will arrest. Orthodontic resorption can occur apically or laterally, dependent on the vector of force. Cwyk et al showed that nearly 30% of orthodontically treated incisors had some degree of EIRR, compared with less than 5% in controls. Massler and Malone reported some degree of root resorption in 86% of orthodontic patients, related to factors including patient age, sex, and systemic conditions. In a recent systematic review, Zahrowski and Jeske found a high correlation between EIRR and intrusive- and rotation-type orthodontic movements. A predisposition to endodontic disease can also increase the risk of EIRR. Brin et al reported an increased prevalence of resorption following orthodontic movement of previously trau-matized teeth. Following cessation of orthodontic movement, resorption generally ceases. Traumatic dental injuries, including luxation and avulsion injuries, are associated with more extensive injuries to the precementum and cementoblastic layer (Tronstad). This, coupled with pulpal necrosis and infection, can result in more extensive EIRR despite endodontic in-tervention. If vital tissue remains or spontaneous revascularization occurs in the case of avul-sion and replantation of immature teeth, Hammarström et al reported transient EIRR. With persistent inammation or infection, EIRR progresses. Following resolution of the inamma-tory component, osseous replacement occurs with commencement of replacement resorp-tion. Consequently, initiation of endodontic therapy is recommended at the rst signs of EIRR, and preventive measures are indicated in cases where inammation and pulpal necrosis and infection are inevitable, such as avulsive injuries. Minimal extraoral dry time and proper storage media are advised, following the recommendations of the American Association of Endodontists trauma guidelines. On replantation, systemic antibiotics are recommended, 205Replacement Resorptionand prompt endodontic therapy should commence. In cases of prolonged extraoral dry time, a sodium uoride soak should be considered. Examples of EIRR can be seen in Fig 10-7. Further information is available in chapter 9. Fig 10-7 Clinical examples of EIRR, including apical (a) and lateral (b) forms.a bReplacement ResorptionTronstad described RR as a secondary complication of widespread EIRR following exten-sive PDL loss as a result of traumatic dental injuries with resultant loss of the corresponding protective precementum and cementoblastic layer. Direct contact between cementum and bone prevents the odontoclasts from distinguishing between bone and tooth structures, leading to further degradation. Odontoblasts replace the area of degraded cementum and dentin in a progressive manner. According to Andreasen and Kristerson, if less than 20% of the root surface is involved, reversal of resorption may occur and ankylosis may be avoided. With greater involvement, progressive replacement resorption is considered inevitable, and no known interventions halt its progression. Clinically, Tronstad described a pathognomonic metallic tone on percussion and progres-sive infrapositioning of the tooth as the root structure is replaced with bone, particularly in young patients. Figure 10-8 depicts examples of RR. Malmgren recommended decoro-nation once infrapositioning great-er than 1 mm is noted. Decorona-tion involves crown sectioning with splinting to the neighboring teeth for an esthetic temporary, surgical ap and removal of any prior root canal lling material, and close ob-servation until complete replace-ment with bone has occurred. Fig 10-8 (a and b) Clinical examples of RR.a b 206Resorption10BibliographyIntroductionTronstad L. Root resorption—Etiology, terminology and clinical manifestations. Endod Dent Traumatol 1988;4:241–252.Internal Root ResorptionCaliskan MK, Turkun M. Prognosis of permanent teeth with internal resorption: A clinical review. Endod Dent Traumatol 1997;13:75–81.Frank AL. Resorption, perforations, and fractures. Dent Clin North Am 1974;18:465–487.Gabor C, Tam E, Shen Y, Haapasalo M. Prevalence of internal inammatory root resorption. J Endod 2012;38:24–27.Gartner AH, Mack T, Somerlott RG, Walsh LC. Differential diagnosis of internal and external root resorption. J Endod 1976;2:329–334.Mente J, Leo M, Panagidis D, Saure D, Pfefferle T. Treatment outcome of mineral trioxide aggre-gate: Repair of root perforations-long-term results. J Endod 2014;40:790–796.Mummery J. The pathology of “pink-spots” on teeth. Br Dent J 1920;41:301–311.Patel S, Ricucci D, Durak C, Tay F. Internal root resorption: A review. J Endod 2010;36:1107–1121.Tronstad L. Root resorption—Etiology, terminology and clinical manifestations. Endod Dent Traumatol 1988;4:241–252.Wedenberg C, Lindskog S. Experimental internal resorption in monkey teeth. Endod Dent Trau-matol 1985;1:221–227.Invasive Cervical Root ResorptionDragoo MR. Resin-ionomer and hybrid-ionomer cements: Part II, human clinical and histologic wound healing responses in specic periodontal lesions. Int J Periodontics Restorative Dent 1997;17:75–87.Pressure ResorptionPressure resorption occurs in response to direct damage to the precementum. The dental pulp is not involved, and some outside factor must be present to create this physical damage. According to Tronstad, pressure resorption can occur secondary to misaligned tooth eruption, slow-grow-ing tumors or cysts (such as ameloblastomas, giant cell lesions, or bro-osseous disease), and orthodontic movement. Pressure resorption does not generally occur secondary to aggressive or malignant tumors due to their rapid nature of expansion. Orthodontically induced pressure re-sorption is generally limited to the apical third of the roots (Fig 10-9). Although it is not reversible once occurred, progression will cease once orthodontic movement stops (Tronstad). Fig 10-9 (a to d) Clinical examples of pressure resorption attributed to orthodontics. a b c d 207BibliographyHarrington GW, Natkin E. External resorption associated with bleaching of pulpless teeth. J Endod 1979;5:344–348.Heithersay GS. Clinical, radiologic, and histopathologic features of invasive cervical resorption. Quintessence Int 1999a;30:27–37.Heithersay GS. Invasive cervical resorption: An analysis of potential predisposing factors. Quin-tessence Int 1999b;30:83–95.Heithersay GS. Treatment of invasive cervical resorption: An analysis of results using topical ap-plication of trichloracetic acid, curettage, and restoration. Quintessence Int 1999c;30:96–110.Rotstein I, Friedman S, Mor C, Katznelson J, Sommer M, Bab I. Histological characterization of bleaching-induced external root resorption in dogs. J Endod 1991;17:436–441.Thonen A, Peltomaki T, Patcas R, Zehnder M. 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J Dent Res 1984;63:IADR abstract no. 1039.Hammarström L, Pierce A, Blomlöf L, Feiglin B, Lindskog S. Tooth avulsion and replantation—A review. Endod Dent Traumatol 1986;2:1–8.Massler M, Malone A. Root resorption in human permanent teeth: A roentgenographic study. Am J Orthod Dentofacial Orthop 1954;40:619–633.Tronstad L. Root resorption—Etiology, terminology and clinical manifestations. Endod Dent Traumatol 1988;4:241–252.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 2002;35:710–719.Zahrowski J, Jeske A. Apical root resorption is associated with comprehensive orthodontic treat-ment but not clearly dependent on prior tooth characteristics or orthodontic techniques. J Am Dent Assoc 2011;142:66–68.Replacement ResorptionAmerican Association of Endodontists. Recommended Guidelines of the American Association of Endodontists for the Treatment of Traumatic Dental Injuries. http://www.aae.org/clinical-re-sources/trauma-resources.aspx. Accessed 8 January 2016.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;39:1–13.Malmgren B. Ridge preservation/decoronation. Pediatr Dent 2013;35:164–169.Tronstad L. Root resorption—Etiology, terminology and clinical manifestations. Endod Dent Traumatol 1988;4:241–252.Pressure ResorptionTronstad L. Root resorption—Etiology, terminology and clinical manifestations. Endod Dent Traumatol 1988;4:241–252.