Idiopathic coronal radiolucencies in unerupted permanent teeth. Case reports Steven Singer, BDSFDS(Glas), MSc(Lond), DOrth(Eng)* Paul V. Abbott, BDSc(WA), MDS(Adel), FRACDS(Endo)t David R. Booth, MDSc(WA), FRACDS, FICDI
Key words: Case reports, idiopathic coronal radiolucencies, unerupted permanent teeth. Abstract The discovery of a radiolucency within an uneruptedtooth is a rare occurrence. One cause is external resorption. The clinical features, the histology, and the management of three cases are described. (Received for publication June 1989. Revised May 1990.Accepted May 1990).
Introduction Detection of a pre-eruptive radiolucency associated with the crown of a permanent tooth is a rare phenomenon. It is usually discovered by chance during a routine radiographic examination as most of these lesions are symptomless. There are three possible causes of a pre-eruptive radiolucency: pre-eruptive caries, a developmental defect and external idiopathic resorption. Pre-eruptive caries has been found in some cases. For this to occur there must be access for oral microorganisms to reach the unerupted tooth. Muhler' observed lesions that radiographically resembled caries in unerupted premolars where the overlying deciduous tooth had a periapical infection. On eruption, the lesions proved to be carious and Muhler proposed that bacteria from the apical lesion *Orthodontist, Perth Dental Hospital. ?Endodontist; Visiting Lerturer, University of Western Australia; Visiting Consultant Endodontist, Perth Dental Hospital. $Senior Lecturer in Oral Pathology, University of Western Australia. 32
initiated the dental caries prior to eruption of the premolar into the oral environment. Baddour and Tilson' and Baab, Morton and Page3reported cases where dental caries did occur in unerupted teeth in an older age group, with the cariogenic organisms gaining access via a sinus tract. Some pre-eruptive radiolucent lesions appear to be developmental in origin and have been attributed either to the inclusion of uncalcified enamel matrix within the developing dentine4.5 or to dentine hypoplasia.6 These lesions tend to be static. External idiopathic resorption has been reported as a cause of pre-eruptive radiolucencies with the lesion being mainly limited to the coronal The overlying enamel often appears intact or only has a small defect even in the presence of extensive destruction of the dentine. Such lesions are progressive and can result in almost complete destruction of the coronal dentine. This paper presents three cases of pre-eruptive coronal radiolucency due to external idiopathic resorption.
Case Reports Case 1 A thirteen-year-old boy attended Perth Dental Hospital for an orthodontic consultation. A panoramic radiograph was taken which revealed a large symptomless radiolucency within the crown of the unerupted mandibular right second molar (47). The lesion was rectangular in shape and appeared to be separated from the pulp by a layer of dentine (Fig. 1). There was no detectable communication between the oral cavity and the affected tooth. As the mandibular right third molar (48) was present and the patient was not willing to undergo Australian Dental Journal 1991;36(1):32-7.
Fig. 1 . - Case 1. Rectangular radiolucency associated with the unerupted 47. The lesion appears to be separated from the pulp by a barrier of dentine.
Fig. 2. -Case 2. A large radiolucency associated with the unerupted 37. Most of the coronal dentine has been destroyed by the lesion.
surgical exposure of the 47 for restoration, the affected tooth was surgically removed and sent for histological examination. Visual examination of the extracted tooth showed that the crown appeared intact although the mesio-occlusal aspect of the crown had a bluish-brown translucency. Case 2 As in Case 1, a fourteen-year-old boy who was referred to Perth Dental Hospital for an orthodontic examination had a panoramic radiograph taken. This revealed a very large symptomless radiolucency in the crown of the unerupted mandibular Australian Dental Journal 1991;36:1.
left second molar (37) (Fig. 2). Radiographically, the lesion appeared to have destroyed most of the coronal dentine. A periapical radiograph suggested that despite the size of the lesion the pulp was separated from the lesion by a thin layer of dentine. There was no visible communication between the unerupted tooth and the oral cavity. Due to the extent of the defect and the presence of the mandibular left third molar (38), the 37 was surgically extracted. On exposure of the tooth, a defect approximately 2 mm in diameter was observed on the buccal surface of the enamel. During the extraction the buccal aspect of the crown fractured away. 33
Fig. 3. - Case 3. A radiolucency present within the crown of the immature and partially erupted 47. The lesion appears to extend to involve the mesial pulp horn.
The tooth was then sent for histological examination. Case 3 A twelve-year-old girl was referred to a private endodontic practice for assessment and treatment of acute symptoms associated with the partially erupted mandibular right second molar (47). The patient reported that the tooth had become sensitive to hot and cold stimuli. This pain had started suddenly and was gradually becoming more severe. Oral examination revealed that the 47 was partially erupted with only the mesial cusps visible. A carieslike defect could be probed in the central pit. A periapical radiograph revealed a medium-size radiolucency within the crown of the 47.This radiolucency extended to and appeared to involve the mesial pulp horns. The tooth roots were quite immature with blunderbuss-shaped apical foramina. A panoramic radiograph (Fig. 3) was taken to exclude the presence of other lesions and to confirm the presence and position of the mandibular right third molar (48). The 47 was then recommended for extraction. Visual examination of the extracted tooth confirmed the clinical findings of a caries-like cavity on the occlusal surface and the lingual aspect of the crown had a grey-black discoloration. The tooth was sent for histological examination.
Histopathology The microscopic sections of the three extracted teeth showed that most of the coronal dentine had 34
been lost (Fig. 4a). The normal pulp of the tooth was separated from the area of resorption by a layer of normal dentine. There was evidence of dentine resorption on the margins of the defect within the crown of the tooth. In Case 1 and 2, the area of tooth loss was filled with loose collagenous connective tissue. Close to the current sites of resorption there was a mild, chiefly lymphocytic, chronic inflammatory cell infiltrate with macrophages and giant cells lying in Howship's lacunae in the dentine (Fig. 4b). In some areas there was evidence of cellular hard tissue deposition within previously resorbed areas (Fig. 4c). This hard tissue had the appearance of cementum which suggests phases of repair following phases of dentine destruction. Case 3 showed necrosis of the soft tissue in the area of resorption, micro-organisms within the dentinal tubules, and a small abscess within the pulp adjacent to the carious dentine. Discussion Histological examination of the extracted teeth showed external resorption to be the cause of the pre-eruptive coronal radiolucencies. In common with other cases in the literature, the resorptive tissue consisted mainly of a loose fibroblastic tissue with a diffuse chronic inflammatory cell infiltrate.'-'' Both macrophages and fibroblasts are thought to play a role in pathological bone resorption. Fibroblasts and antigen-activated macrophages are able to produce interleukin-1, a cytokine capable of stimulating bone resorption." Mundy and coAustralian Dental Journal 1991:36:1.
4a
Fig. 4 (a).-A decalcified section of the tooth from case 2, stained with Haematoxylin and Eosin. The resorbed primary dentine (D) space is filled with connective tissue (T). (b) indicates the site where Fig. 4b was photographed and (c) the site for Fig. 4c. Bar represents 1.4 mm. Fig. 4(b).-The resorbed primary dentine (D) with many Howship’s lacunae (H) along its resorbed edge (E). A multinucleated giant cell (G) lies in one lacuna. Macrophages (M) with indented nuclei can also be identified. Bar represents 60 pm. Fig. 4(c).-An area of replacement resorption. The resorbed edge (E) of the primary dentine (D) contains recalcified areas. These consist of calcified tissue (C) and cementoid substance (P).A resorbed channel (R)deep in the primary dentine can also be seen. Bar represents 60 pm.
workersL2have shown that human bone marrow macrophages are capable of resorbing inorganic bone matrix in vitro without direct contact. It may Australian Dental Journal 1991;36:1.
well be that these cells which were evident in Case 1 and 2 play a role in the pathological resorption of dentine as well as the osteoclast. 35
In Cases 1 and 2, although there was almost complete replacement of the coronal dentine by resorptive tissue, the lesions were symptomless and had no signs of pulp pathology. A thin layer of dentine separated the lesion from the pulp. Yaacoub13 examined 26 cases of idiopathic extracoronal resorption histologically and found this to be a common feature. He suggested that the dentine immediately adjacent to the pulp was resistant to resorption. This has been confirmed clinically by Grundy, Pyle and Adkins.14 The teeth were unerupted in Cases 1 and 2. However, in Case 3 the tooth was partially erupted. This resulted in necrosis of the resorptive tissue plus access by the oral microflora. Caries of the dentine ‘bridge’ developed followed by acute pulpitis. This case is very similar to the one described by De Schepper, Haynes and Sabates.IO When a pre-eruptive radiolucency associated with the crown of a tooth is discovered and the cause is thought to be due to a resorptive process, treatment must be initiated immediately because of the progressive nature of the lesion. One problem encountered is that the lesion is usually symptomless when unerupted and generally is found only by chance during a routine radiographic examination. Because these lesions are so rare, practitioners may omit to look for them. They may also be missed when the lesions are small, especially when the standard radiograph taken to monitor dental development is the panoramic r a d i ~ g r a p hBy . ~ the time they are noticed, extensive tooth destruction has often occurred. A notable diagnostic feature is that the majority of the reported cases have involved lower second permanent molars so these teeth should be carefully examined when viewing such radiographs. A conservative approach in management has been suggested by Grundy, Pyle and Adkins14who surgically uncovered two cases and restored them in a similar manner to a carious tooth. The resorptive tissue was removed by hand instrumentation without causing pulpal involvement. The use of a handpiece in such circumstances is contraindicated since there is a high risk of pulpal expo~ure.’~ Difficulty in access and patient management must also be considered with this approach which may require a general anaesthetic. The histopathologic features of these lesions are similar in several respects to external cervical invasive resorption as described in several reports.16-19 Heithersay16.20has reported the use of a 90 per cent solution of trichloroacetic acid as an adjunct to the surgical curettage of cervical invasive resorptive 36
lesions. The solution is used as a chemical escharotic agent to destroy the resorbing cells. The use of this solution as an adjunct to the conservative management of cases of idiopathic external coronal tooth resorption which are detected at an early stage may be advantageous in that it will help to ensure the destruction of the resorbing cells and may help to reduce the use of instruments near the Pulp. If the lesion is very extensive or is causing symptoms, then removal of the affected tooth may be the treatment of choice, especially if the lesion involves a lower second molar tooth and the third molar is present. Although few lower third molars are ideally positioned for eruption it is a relatively simple orthodontic procedure to upright such a tooth once erupted. The ideal time for extraction is just prior to or just after eruption of the tooth so that the operative procedure is simple and the pulp has not become infected by oral pathogens. Endodontic treatment of a partially erupted tooth with irreversible pulpitis is complicated by several factors, especially in lower second molars. Firstly, in order to gain access to the root canal system, the tooth would require surgical exposure. Secondly, rubber dam isolation of the tooth during treatment would be extremely difficult, if not impossible, to achieve. Not to use rubber dam would seriously compromise the endodontic treatment” and the patient’s safety.22Finally, teeth which are unerupted or partially erupted have immature roots. The resultant open apical foramina and often funnel-shaped canals make it difficult to remove all tissue remnants from the canal walls and to achieve adequate sealing of the root canal. Long-term apexification therapy with calcium hydroxide would be required in order to stimulate formation of a hard tissue barrier against which a root canal filling can be condensed.23 Apexification requires multiple appointments to change the intra-canal medicament and this complicates the above problems of access and isolation. Obturation of the root canal following apexification usually requires the use of specific techniques (for example, heat-softened gutta-percha impression technique, vertical condensation) in order to adapt the root filling material to the unusual apical canal morphology that results. Unless the operator is proficient at such techniques this will also complicate treatment. In addition patient co-operation can further affect such longterm treatment plans, especially in young patients. The initiating factor for external coronal tooth resorption is not known but Blackwood* has suggested that a localized defect in the reduced Australian Dental Journal 1991;36:1.
enamel epithelium would allow access to the underlying enamel by resorptive tissues from the dental follicle. Cells capable of promoting hard tissue resorption, namely the macrophage, fibroblast and osteoclast would be especially active when a tooth starts to erupt. This appeared to be a common feature of the teeth presented in this report and in other reports in the literature. Tooth eruption may therefore provide the stimulus which promotes external coronal tooth resorption. The defect through which the resorptive tissue gains access may be clinically undetectable.8.16 Summary Pre-eruptive radiolucencies associated with the crown of a tooth may be due to external resorption. The majority of reported cases have involved lower second permanent molars. These lesions are progressive and destructive but they are usually symptomless while the tooth is unerupted. Hence these lesions are usually only discovered by chance. The dentine overlying the pulp is incompletely resorbed and the pulp is usually healthy. On eruption into the oral cavity, pathogens inevitably gain access via an enamel defect and eventually cause pulpitis. If the lesion is small the tooth can be surgically exposed and restored as for a carious tooth. In cases of gross destruction of coronal dentine and/or pulpitis, extraction is more appropriate, especially when a third molar is present. References 1. Muhler JC. The effect of apical inflammation of the primary teeth on dental caries in the permanent teeth. J Dent Child 1957;24:209-10. 2. Baddour HM, Tilson HB. A carious impacted third molar. Oral Surg Oral Med Oral Pathol 1980;48:490. 3. Baab DA, Morton TH, Page RC. Caries and periodontitis associated with an unerupted third molar. Oral Surg Oral Med Oral Pathol 1984;58:428-9. 4. Walton JL. Dentine radiolucencies in unerupted teeth: Report of two cases. J Dent Child 1980;47:183-6. 5. Wood PF. Radiolucent lesions resembling caries in the dentine of permanent teeth. A report of sixteen cases. Aust Dent J 1985;30:169-73.
Australian Dental Journal 1991 ;36:1
6. Wooden EE, Kuftinec MM. Decay of unerupted premolar. Oral Surg Oral Med Oral Pathol 1974;38:491-2. 7. Sullivan HR, Jolly M. Idiopathic resorption. Aust Dent J 1957;2:193-9. 8. Blackwood HJJ. Resorption of enamel and dentine in the unerupted tooth. Oral Surg Oral Med Oral Pathol 1958;11:79-85. 9. Grundy GE, Adkins KF. Idiopathic external coronal resorption: a case report. Aust Dent J 1982;27:1-4. 10. De Schepper EJ, Haynes JI, Sabates CR. Pre-eruptive radie lucencies of unerupted teeth: Report of a case and literature review. Quintessence Int 1988;19:157-60. 11. Meikle MC, Heath JK, Reynolds JJ. Advances in understanding cell interactions in tissue resorption. Relevance to the pathogenesis of periodontal disease and a new hypothesis. Oral Path 1986;15:239-49. 12. Mundy GR, Altman AJ, Gondek MD, Bandelin JG. Direct resorption of bone by human monocytes. Science 1977; 196: 1109-10. 13. Yaacoub HB. The resistant dentine shell of teeth suffering from idiopathic external resorption. Aust Dent J 1980;25:73-5. 14. Grundy GE, Pyle RJ, Adkins KF. Intra-coronal resorption of unerupted molars. Aust Dent J 1984;29:175-9. 15. Skaff DM, Dilzell WW. Lesions resembling caries in unerupted teeth. Oral Surg Oral Med Oral Pathol 1978;45:643-6. 16. Heithersay GS. Clinical endodontic and surgical management of tooth and associated bone resorption. Int Endod J 1985;18:72-92. 17. Pindborg JJ. Pathology of the dental hard tissues. Copenhagen: Munksgaard, 1970;137. 18. Rushton MA, Cooke BED, Duckworth R. Oral histology. Edinburgh: Livingstone 1970;86-93. 19. Goldman HM. Spontaneous intermittent resorption of teeth. J Am Dent Assoc 1954;49:522-32. 20. Heithersay GS, Wilson DF. Tissue responses in the rat to trichloracetic acid - an agent used in the treatment of invasive cervical resorption. Aust Dent J 1988;33:451-61. 21. Osetek EM. Case selection and treatment planning. In: Cohen S, Burns RC, eds. Pathways of the pulp. 4th edn. St Louis: CV Mosby 1987:53-62. 22. Schwartz SF. Preparation for treatment. Ibid: 63-82. 23. Heithersay GS. Calcium hydroxide in the treatment of p u l p less teeth with associated pathology. J Br Endod SOC 1975;8:74-93.
Address for correspondenceheprints: P. V. Abbott, Suite 19, 38 Ranelagh Crescent, South Perth, Western Australia, 6 151.
37
Key words: Case reports, idiopathic coronal radiolucencies, unerupted permanent teeth. Abstract The discovery of a radiolucency within an uneruptedtooth is a rare occurrence. One cause is external resorption. The clinical features, the histology, and the management of three cases are described. (Received for publication June 1989. Revised May 1990.Accepted May 1990).
Introduction Detection of a pre-eruptive radiolucency associated with the crown of a permanent tooth is a rare phenomenon. It is usually discovered by chance during a routine radiographic examination as most of these lesions are symptomless. There are three possible causes of a pre-eruptive radiolucency: pre-eruptive caries, a developmental defect and external idiopathic resorption. Pre-eruptive caries has been found in some cases. For this to occur there must be access for oral microorganisms to reach the unerupted tooth. Muhler' observed lesions that radiographically resembled caries in unerupted premolars where the overlying deciduous tooth had a periapical infection. On eruption, the lesions proved to be carious and Muhler proposed that bacteria from the apical lesion *Orthodontist, Perth Dental Hospital. ?Endodontist; Visiting Lerturer, University of Western Australia; Visiting Consultant Endodontist, Perth Dental Hospital. $Senior Lecturer in Oral Pathology, University of Western Australia. 32
initiated the dental caries prior to eruption of the premolar into the oral environment. Baddour and Tilson' and Baab, Morton and Page3reported cases where dental caries did occur in unerupted teeth in an older age group, with the cariogenic organisms gaining access via a sinus tract. Some pre-eruptive radiolucent lesions appear to be developmental in origin and have been attributed either to the inclusion of uncalcified enamel matrix within the developing dentine4.5 or to dentine hypoplasia.6 These lesions tend to be static. External idiopathic resorption has been reported as a cause of pre-eruptive radiolucencies with the lesion being mainly limited to the coronal The overlying enamel often appears intact or only has a small defect even in the presence of extensive destruction of the dentine. Such lesions are progressive and can result in almost complete destruction of the coronal dentine. This paper presents three cases of pre-eruptive coronal radiolucency due to external idiopathic resorption.
Case Reports Case 1 A thirteen-year-old boy attended Perth Dental Hospital for an orthodontic consultation. A panoramic radiograph was taken which revealed a large symptomless radiolucency within the crown of the unerupted mandibular right second molar (47). The lesion was rectangular in shape and appeared to be separated from the pulp by a layer of dentine (Fig. 1). There was no detectable communication between the oral cavity and the affected tooth. As the mandibular right third molar (48) was present and the patient was not willing to undergo Australian Dental Journal 1991;36(1):32-7.
Fig. 1 . - Case 1. Rectangular radiolucency associated with the unerupted 47. The lesion appears to be separated from the pulp by a barrier of dentine.
Fig. 2. -Case 2. A large radiolucency associated with the unerupted 37. Most of the coronal dentine has been destroyed by the lesion.
surgical exposure of the 47 for restoration, the affected tooth was surgically removed and sent for histological examination. Visual examination of the extracted tooth showed that the crown appeared intact although the mesio-occlusal aspect of the crown had a bluish-brown translucency. Case 2 As in Case 1, a fourteen-year-old boy who was referred to Perth Dental Hospital for an orthodontic examination had a panoramic radiograph taken. This revealed a very large symptomless radiolucency in the crown of the unerupted mandibular Australian Dental Journal 1991;36:1.
left second molar (37) (Fig. 2). Radiographically, the lesion appeared to have destroyed most of the coronal dentine. A periapical radiograph suggested that despite the size of the lesion the pulp was separated from the lesion by a thin layer of dentine. There was no visible communication between the unerupted tooth and the oral cavity. Due to the extent of the defect and the presence of the mandibular left third molar (38), the 37 was surgically extracted. On exposure of the tooth, a defect approximately 2 mm in diameter was observed on the buccal surface of the enamel. During the extraction the buccal aspect of the crown fractured away. 33
Fig. 3. - Case 3. A radiolucency present within the crown of the immature and partially erupted 47. The lesion appears to extend to involve the mesial pulp horn.
The tooth was then sent for histological examination. Case 3 A twelve-year-old girl was referred to a private endodontic practice for assessment and treatment of acute symptoms associated with the partially erupted mandibular right second molar (47). The patient reported that the tooth had become sensitive to hot and cold stimuli. This pain had started suddenly and was gradually becoming more severe. Oral examination revealed that the 47 was partially erupted with only the mesial cusps visible. A carieslike defect could be probed in the central pit. A periapical radiograph revealed a medium-size radiolucency within the crown of the 47.This radiolucency extended to and appeared to involve the mesial pulp horns. The tooth roots were quite immature with blunderbuss-shaped apical foramina. A panoramic radiograph (Fig. 3) was taken to exclude the presence of other lesions and to confirm the presence and position of the mandibular right third molar (48). The 47 was then recommended for extraction. Visual examination of the extracted tooth confirmed the clinical findings of a caries-like cavity on the occlusal surface and the lingual aspect of the crown had a grey-black discoloration. The tooth was sent for histological examination.
Histopathology The microscopic sections of the three extracted teeth showed that most of the coronal dentine had 34
been lost (Fig. 4a). The normal pulp of the tooth was separated from the area of resorption by a layer of normal dentine. There was evidence of dentine resorption on the margins of the defect within the crown of the tooth. In Case 1 and 2, the area of tooth loss was filled with loose collagenous connective tissue. Close to the current sites of resorption there was a mild, chiefly lymphocytic, chronic inflammatory cell infiltrate with macrophages and giant cells lying in Howship's lacunae in the dentine (Fig. 4b). In some areas there was evidence of cellular hard tissue deposition within previously resorbed areas (Fig. 4c). This hard tissue had the appearance of cementum which suggests phases of repair following phases of dentine destruction. Case 3 showed necrosis of the soft tissue in the area of resorption, micro-organisms within the dentinal tubules, and a small abscess within the pulp adjacent to the carious dentine. Discussion Histological examination of the extracted teeth showed external resorption to be the cause of the pre-eruptive coronal radiolucencies. In common with other cases in the literature, the resorptive tissue consisted mainly of a loose fibroblastic tissue with a diffuse chronic inflammatory cell infiltrate.'-'' Both macrophages and fibroblasts are thought to play a role in pathological bone resorption. Fibroblasts and antigen-activated macrophages are able to produce interleukin-1, a cytokine capable of stimulating bone resorption." Mundy and coAustralian Dental Journal 1991:36:1.
4a
Fig. 4 (a).-A decalcified section of the tooth from case 2, stained with Haematoxylin and Eosin. The resorbed primary dentine (D) space is filled with connective tissue (T). (b) indicates the site where Fig. 4b was photographed and (c) the site for Fig. 4c. Bar represents 1.4 mm. Fig. 4(b).-The resorbed primary dentine (D) with many Howship’s lacunae (H) along its resorbed edge (E). A multinucleated giant cell (G) lies in one lacuna. Macrophages (M) with indented nuclei can also be identified. Bar represents 60 pm. Fig. 4(c).-An area of replacement resorption. The resorbed edge (E) of the primary dentine (D) contains recalcified areas. These consist of calcified tissue (C) and cementoid substance (P).A resorbed channel (R)deep in the primary dentine can also be seen. Bar represents 60 pm.
workersL2have shown that human bone marrow macrophages are capable of resorbing inorganic bone matrix in vitro without direct contact. It may Australian Dental Journal 1991;36:1.
well be that these cells which were evident in Case 1 and 2 play a role in the pathological resorption of dentine as well as the osteoclast. 35
In Cases 1 and 2, although there was almost complete replacement of the coronal dentine by resorptive tissue, the lesions were symptomless and had no signs of pulp pathology. A thin layer of dentine separated the lesion from the pulp. Yaacoub13 examined 26 cases of idiopathic extracoronal resorption histologically and found this to be a common feature. He suggested that the dentine immediately adjacent to the pulp was resistant to resorption. This has been confirmed clinically by Grundy, Pyle and Adkins.14 The teeth were unerupted in Cases 1 and 2. However, in Case 3 the tooth was partially erupted. This resulted in necrosis of the resorptive tissue plus access by the oral microflora. Caries of the dentine ‘bridge’ developed followed by acute pulpitis. This case is very similar to the one described by De Schepper, Haynes and Sabates.IO When a pre-eruptive radiolucency associated with the crown of a tooth is discovered and the cause is thought to be due to a resorptive process, treatment must be initiated immediately because of the progressive nature of the lesion. One problem encountered is that the lesion is usually symptomless when unerupted and generally is found only by chance during a routine radiographic examination. Because these lesions are so rare, practitioners may omit to look for them. They may also be missed when the lesions are small, especially when the standard radiograph taken to monitor dental development is the panoramic r a d i ~ g r a p hBy . ~ the time they are noticed, extensive tooth destruction has often occurred. A notable diagnostic feature is that the majority of the reported cases have involved lower second permanent molars so these teeth should be carefully examined when viewing such radiographs. A conservative approach in management has been suggested by Grundy, Pyle and Adkins14who surgically uncovered two cases and restored them in a similar manner to a carious tooth. The resorptive tissue was removed by hand instrumentation without causing pulpal involvement. The use of a handpiece in such circumstances is contraindicated since there is a high risk of pulpal expo~ure.’~ Difficulty in access and patient management must also be considered with this approach which may require a general anaesthetic. The histopathologic features of these lesions are similar in several respects to external cervical invasive resorption as described in several reports.16-19 Heithersay16.20has reported the use of a 90 per cent solution of trichloroacetic acid as an adjunct to the surgical curettage of cervical invasive resorptive 36
lesions. The solution is used as a chemical escharotic agent to destroy the resorbing cells. The use of this solution as an adjunct to the conservative management of cases of idiopathic external coronal tooth resorption which are detected at an early stage may be advantageous in that it will help to ensure the destruction of the resorbing cells and may help to reduce the use of instruments near the Pulp. If the lesion is very extensive or is causing symptoms, then removal of the affected tooth may be the treatment of choice, especially if the lesion involves a lower second molar tooth and the third molar is present. Although few lower third molars are ideally positioned for eruption it is a relatively simple orthodontic procedure to upright such a tooth once erupted. The ideal time for extraction is just prior to or just after eruption of the tooth so that the operative procedure is simple and the pulp has not become infected by oral pathogens. Endodontic treatment of a partially erupted tooth with irreversible pulpitis is complicated by several factors, especially in lower second molars. Firstly, in order to gain access to the root canal system, the tooth would require surgical exposure. Secondly, rubber dam isolation of the tooth during treatment would be extremely difficult, if not impossible, to achieve. Not to use rubber dam would seriously compromise the endodontic treatment” and the patient’s safety.22Finally, teeth which are unerupted or partially erupted have immature roots. The resultant open apical foramina and often funnel-shaped canals make it difficult to remove all tissue remnants from the canal walls and to achieve adequate sealing of the root canal. Long-term apexification therapy with calcium hydroxide would be required in order to stimulate formation of a hard tissue barrier against which a root canal filling can be condensed.23 Apexification requires multiple appointments to change the intra-canal medicament and this complicates the above problems of access and isolation. Obturation of the root canal following apexification usually requires the use of specific techniques (for example, heat-softened gutta-percha impression technique, vertical condensation) in order to adapt the root filling material to the unusual apical canal morphology that results. Unless the operator is proficient at such techniques this will also complicate treatment. In addition patient co-operation can further affect such longterm treatment plans, especially in young patients. The initiating factor for external coronal tooth resorption is not known but Blackwood* has suggested that a localized defect in the reduced Australian Dental Journal 1991;36:1.
enamel epithelium would allow access to the underlying enamel by resorptive tissues from the dental follicle. Cells capable of promoting hard tissue resorption, namely the macrophage, fibroblast and osteoclast would be especially active when a tooth starts to erupt. This appeared to be a common feature of the teeth presented in this report and in other reports in the literature. Tooth eruption may therefore provide the stimulus which promotes external coronal tooth resorption. The defect through which the resorptive tissue gains access may be clinically undetectable.8.16 Summary Pre-eruptive radiolucencies associated with the crown of a tooth may be due to external resorption. The majority of reported cases have involved lower second permanent molars. These lesions are progressive and destructive but they are usually symptomless while the tooth is unerupted. Hence these lesions are usually only discovered by chance. The dentine overlying the pulp is incompletely resorbed and the pulp is usually healthy. On eruption into the oral cavity, pathogens inevitably gain access via an enamel defect and eventually cause pulpitis. If the lesion is small the tooth can be surgically exposed and restored as for a carious tooth. In cases of gross destruction of coronal dentine and/or pulpitis, extraction is more appropriate, especially when a third molar is present. References 1. Muhler JC. The effect of apical inflammation of the primary teeth on dental caries in the permanent teeth. J Dent Child 1957;24:209-10. 2. Baddour HM, Tilson HB. A carious impacted third molar. Oral Surg Oral Med Oral Pathol 1980;48:490. 3. Baab DA, Morton TH, Page RC. Caries and periodontitis associated with an unerupted third molar. Oral Surg Oral Med Oral Pathol 1984;58:428-9. 4. Walton JL. Dentine radiolucencies in unerupted teeth: Report of two cases. J Dent Child 1980;47:183-6. 5. Wood PF. Radiolucent lesions resembling caries in the dentine of permanent teeth. A report of sixteen cases. Aust Dent J 1985;30:169-73.
Australian Dental Journal 1991 ;36:1
6. Wooden EE, Kuftinec MM. Decay of unerupted premolar. Oral Surg Oral Med Oral Pathol 1974;38:491-2. 7. Sullivan HR, Jolly M. Idiopathic resorption. Aust Dent J 1957;2:193-9. 8. Blackwood HJJ. Resorption of enamel and dentine in the unerupted tooth. Oral Surg Oral Med Oral Pathol 1958;11:79-85. 9. Grundy GE, Adkins KF. Idiopathic external coronal resorption: a case report. Aust Dent J 1982;27:1-4. 10. De Schepper EJ, Haynes JI, Sabates CR. Pre-eruptive radie lucencies of unerupted teeth: Report of a case and literature review. Quintessence Int 1988;19:157-60. 11. Meikle MC, Heath JK, Reynolds JJ. Advances in understanding cell interactions in tissue resorption. Relevance to the pathogenesis of periodontal disease and a new hypothesis. Oral Path 1986;15:239-49. 12. Mundy GR, Altman AJ, Gondek MD, Bandelin JG. Direct resorption of bone by human monocytes. Science 1977; 196: 1109-10. 13. Yaacoub HB. The resistant dentine shell of teeth suffering from idiopathic external resorption. Aust Dent J 1980;25:73-5. 14. Grundy GE, Pyle RJ, Adkins KF. Intra-coronal resorption of unerupted molars. Aust Dent J 1984;29:175-9. 15. Skaff DM, Dilzell WW. Lesions resembling caries in unerupted teeth. Oral Surg Oral Med Oral Pathol 1978;45:643-6. 16. Heithersay GS. Clinical endodontic and surgical management of tooth and associated bone resorption. Int Endod J 1985;18:72-92. 17. Pindborg JJ. Pathology of the dental hard tissues. Copenhagen: Munksgaard, 1970;137. 18. Rushton MA, Cooke BED, Duckworth R. Oral histology. Edinburgh: Livingstone 1970;86-93. 19. Goldman HM. Spontaneous intermittent resorption of teeth. J Am Dent Assoc 1954;49:522-32. 20. Heithersay GS, Wilson DF. Tissue responses in the rat to trichloracetic acid - an agent used in the treatment of invasive cervical resorption. Aust Dent J 1988;33:451-61. 21. Osetek EM. Case selection and treatment planning. In: Cohen S, Burns RC, eds. Pathways of the pulp. 4th edn. St Louis: CV Mosby 1987:53-62. 22. Schwartz SF. Preparation for treatment. Ibid: 63-82. 23. Heithersay GS. Calcium hydroxide in the treatment of p u l p less teeth with associated pathology. J Br Endod SOC 1975;8:74-93.
Address for correspondenceheprints: P. V. Abbott, Suite 19, 38 Ranelagh Crescent, South Perth, Western Australia, 6 151.
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