ORIGINAL CONTRIBUTIONS

DIAGNOSTIC CHALLENGE 

Triangular radiolucent lesion of the mandible Eugene Ko, DDS, Dipl (Oral and Maxillofacial Pathology)

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THE CHALLENGE

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n December 2014, a 62-year-old man sought care from his general dentist for a bulge on the lingual side of teeth nos. 21 and 22, which the patient could feel with his tongue. Although the specific duration of the lesion was unknown, the patient had been undergoing routine periodontal maintenance for 3 to 4 months during which only bite-wing radiographs were obtained, and clinical expansion was not noted during prior examinations. Periapical and panoramic radiographs of the area obtained in December 2014 revealed a well-defined radiolucent lesion between the apexes of the mandibular left canine and first premolar—teeth nos. 21 and 22 (Figures 1 and 2). Clinical examination revealed a bulge that was soft and compressible involving the buccal and lingual area of teeth nos. 21 and 22; endodontic testing indicated that the teeth were vital, and the teeth were not mobile. The patient did not report pain. A biopsy specimen was submitted for histopathologic analysis, which revealed cystic spaces lined by a thin, keratinized stratified squamous epithelium lacking an inflammatory infiltrate (Figure 3). Higher magnification revealed that the cystic lining was characterized by a palisading basal cell layer with a corrugated, parakeratinized surface and a relatively smooth epithelial–connective tissue interface (Figure 4).

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ORIGINAL CONTRIBUTIONS

Figure 1. Panoramic radiograph showing a well-defined area of radiolucency at the apexes of the mandibular left canine and first premolar.

Figure 3. Cystic lining is characterized by a regular, uniform thickness of 5 to 8 cells and a lack of inflammation in the cyst wall (40 magnification, hematoxylin and eosin stain).

Figure 4. Cystic lining characterized by a palisading basal cell layer and a corrugated, parakeratinized surface. Note the relatively smooth epithelial–connective tissue interface (200 magnification, hematoxylin and eosin stain). Figure 2. Periapical radiograph depicting a well-defined area of radiolucency between the mandibular left canine and first premolar. The darker area of radiolucency within is suggestive of lingual erosion.

CAN YOU MAKE THE DIAGNOSIS? A. squamous odontogenic tumor B. lateral periodontal cyst

C. odontogenic keratocyst D. ameloblastoma

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ORIGINAL CONTRIBUTIONS

THE DIAGNOSIS C. odontogenic keratocyst

Odontogenic keratocysts (OKCs) are developmental odontogenic cysts that are known for locally aggressive potential and high recurrence rate.1 Clinically, they commonly are noted in the posterior mandible as a unilocular or multilocular area of radiolucency. In addition, expansion of the cortical plates does not occur as frequently as it does in ameloblastomas.2-4 In this regard, the differential diagnosis of this case favored an ameloblastoma more than an OKC, given the soft, compressible swelling and the expansion of the buccal and lingual cortices. Histopathologic examination of OKCs classically reveals a cyst with a thin, parakeratinized stratified squamous epithelial lining characterized by a palisaded basal cell layer and surface corrugation.1,3 In 2005, the World Health Organization reclassified OKC as keratocystic odontogenic tumor to reflect the understanding at the time of an odontogenic cyst with potential neoplastic behavior.5 The neoplastic nature of OKCs has been based partly on the consistent detection of a higher level of cell-proliferative activity in the lining epithelium.6 Investigations into the PTCH1 gene have shown that this is the disease-causing gene for nevoid basal cell carcinoma syndrome (Gorlin syndrome), which is characterized by multiple OKCs. Study investigators have shown that more than 85% of syndromic OKCs and nearly 30% of sporadic OKCs harbored PTCH1 mutations.6 With simple enucleation, recurrences rates have been reported anywhere from 2% to 62% for OKCs; the thin, friable epithelial lining that adheres to adjacent bone or soft tissues may lead to incomplete removal of the OKC. However, if the lesion is resected, the recurrence rate can be virtually zero.2,4,6 Treatment remains a controversial topic because there are no randomized controlled experiments in the literature but generally ranges from simple enucleation with or without the use of adjunctive treatment (Carnoy solution, cryotherapy, or peripheral ostectomy) to more aggressive surgical resection.4,7,8 However, for larger mandibular lesions, especially with vital structures at risk of injury, decompression might be the preferred therapy.8 Decompression involves making a small opening into the cyst and inserting a drainage tube that over time results in reduction of the cyst’s size. The cyst shrinks away from vital structures, and the cyst lining appears to become thicker. As a result, decompression allows surgeons to enucleate a smaller cystic lesion with fewer complications.9 Recurrence rates for OKCs treated with decompression before enucleation are lower than those for OKCs treated with simple enucleation used in isolation.10

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DIFFERENTIAL DIAGNOSIS

Squamous odontogenic tumor. Squamous odontogenic tumors (SOTs) are rare tumors thought to arise from the epithelial remnants found within the periodontal ligament. SOTs typically arise intraosseously in association with the lateral root surfaces of teeth.1 The maxillary canine and mandibular premolar regions are sites where SOTs frequently are noted.11 Although the radiographic appearance is not pathognomonic, the SOT commonly manifests radiographically as a unilocular, triangular area of radiolucency between the apexes of adjacent teeth.1,11,12 Although rare, SOTs can share features of periodontitis with respect to deep probing depths and radiographic evidence of bone loss.11,12 Under light microscopic evaluation, SOTs manifest as a proliferation of islands of squamous epithelium within a connective tissue stroma. The islands lack the peripheral columnar epithelial cell layer characteristic of ameloblastoma.13 Treatment by means of conservative surgical excision is usually curative.11 Lateral periodontal cyst. Lateral periodontal cysts (LPCs) are developmental cysts that show a predilection for the canine and premolar regions of the mandible.1,14 Radiographically, LPCs commonly manifest as a unilocular area of radiolucency between the roots of adjacent teeth.1,15 Histologically, LPCs consist of a thin, nonkeratinized, stratified squamous epithelium with focal nodular thickening of the lining.15 Occasionally, histopathologic examination may reveal a related polycystic specimen (that is, botryoid odontogenic cyst) that already may have been suggested by the radiographic manifestation of a multilocular area of radiolucency. Neither LPCs nor the botryoid variant are associated with gingival or periodontal inflammation, so the presence of a heavy inflammatory infiltrate at histopathologic examination may negate any argument for the presence of a developmental cyst.1,16 Ameloblastoma. Ameloblastomas are locally aggressive, benign tumors of odontogenic epithelium.1,17 Clinically, ameloblastomas manifest most commonly as a painless swelling or expansion in the posterior mandible; they may manifest as a unilocular or multilocular area of radiolucency radiographically.17-19 Although ameloblastomas have variable histopathologic morphologies that are classified as various different subtypes, the conventional solid type is represented in approximately 90% of ameloblastomas. The conventional solid type is characterized by invasive nests of odontogenic epithelium with peripheral palisaded, columnar cells with reverse polarization of their nuclei, and within the center of the nests are loosely arranged, stellate reticulate areas of

ORIGINAL CONTRIBUTIONS

differentiation.1,20 Treatment varies from conservative enucleation to wide resection. On rare occasions, radiotherapy has been used for patients with recurrent or incompletely resectable tumors.21 CONCLUSION

In this article, on the basis of the radiographic and clinical information, the clinician can formulate a reasonable clinical differential diagnosis for a unilocular, triangular, mandibular radiolucent lesion. This case underscores the need for additional diagnostic inquiry. After biopsy of the lesion, OKC was diagnosed. As this case shows, a biopsy often is indicated for a definitive diagnosis. n http://dx.doi.org/10.1016/j.adaj.2015.09.008 Copyright ª 2016 American Dental Association. All rights reserved.

Dr. Ko is a clinical assistant professor, Department of Periodontics and Oral Medicine, University of Michigan, School of Dentistry, 1011 N. University Ave., Ann Arbor, MI 48109, e-mail [email protected]. Address correspondence to Dr. Ko. Disclosure. Dr. Ko did not report any disclosures. Diagnostic Challenge is published in collaboration with the American Academy of Oral and Maxillofacial Pathology and the American Academy of Oral Medicine. The author thanks Dr. Thomas Butts, Oral and Facial Surgeons of Michigan, and Dr. Don Restauri Jr, private practitioner. 1. Chi AC. Odontogenic cysts and tumors. Surg Pathol Clin. 2011;4(4): 1027-1091. 2. Pogrel MA. The keratocystic odontogenic tumor. Oral Maxillofac Surg Clin North Am. 2013;25(1):21-30. 3. Bhargava D, Deshpande A, Pogrel MA. Keratocystic odontogenic tumour (KCOT): a cyst to a tumour. Oral Maxillofac Surg. 2012;16(2):163-170. 4. Mendes RA, Carvalho JFC, van der Waal I. Characterization and management of the keratocystic odontogenic tumor in relation to

its histopathological and biological features. Oral Oncol. 2010;46(4): 219-225. 5. Barnes L, Eveson JW, Reichart P, Sidransky D, eds. Pathology and Genetics of Head and Neck Tumours—World Health Organization Classification of Tumours. Lyon, France: IARC Press; 2005. 6. Li TJ. Critical reviews in oral biology & medicine: the odontogenic keratocyst—a cyst, or a cystic neoplasm? J Dent Res. 2011;90(2):133-142. 7. Johnson NR, Batstone MD, Savage NW. Management and recurrence of keratocystic odontogenic tumor: a systematic review. Oral Sur Oral Med Oral Pathol Oral Radiol. 2013;116(4):e271-e276. 8. Kinard BE, Chuang SK, August M, Dodson TB. For treatment of odontogenic keratocysts, is enucleation, when compared to decompression, a less complex management protocol? J Oral Maxillofac Surg. 2015;73(4): 641-648. 9. Pogrel MA. Treatment of keratocysts: the case for decompression and marsupialization. J Oral Maxillofac Surg. 2005;63(11):1667-1673. 10. Blanas N, Freund B, Schwartz M, Furst IM. Systematic review of the treatment and prognosis of the odontogenic keratocyst. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2000;90(5):553-558. 11. Haghighat K, Kalmar JR, Mariotti AJ. Squamous odontogenic tumor: diagnosis and management. J Periodontol. 2002;73(6):653-656. 12. Jones BE, Sarathy AP, Belinda Ramos M, Foss RD. Squamous odontogenic tumor. Head Neck Pathol. 2011;5(1):17-19. 13. Goldblatt LI, Brannon RB, Ellis GL. Squamous odontogenic tumor: report of five cases and review of the literature. Oral Surg Oral Med Oral Pathol. 1982;54(2):187-196. 14. Altini M, Shear M. The lateral periodontal cyst: an update. J Oral Pathol Med. 1992;21(6):245-250. 15. Rasmusson LG, Magnusson BC, Borrman H. The lateral periodontal cyst: a histopathological and radiographic study of 32 cases. Br J Oral Maxillofac Surg. 1991;29(1):54-57. 16. Fantasia JE. Lateral periodontal cyst: an analysis of forty-six cases. Oral Surg Oral Med Oral Pathol. 1979;48(3):237-243. 17. Gomes CC, Duarte AP, Diniz MG, Gomez RS. Current concepts of ameloblastoma pathogenesis: review article. J Oral Pathol Med. 2010;39(8): 585-591. 18. Reichart PA, Philipsen HP, Sonner S. Ameloblastoma: biological profile of 3677 cases. Eur J Cancer B Oral Oncol. 1995;31(2):86-99. 19. Neville BW, Damm DD, Allen CM, Chi AC. Oral and Maxillofacial Pathology. St. Louis, MO: Saunders/Elsevier; 2016. 20. Bachmann AM, Linfesty RL. Ameloblastoma, solid/multicystic type. Head Neck Pathol. 2009;3(4):307-309. 21. Mendenhall WM, Werning JW, Fernandes R, Malyapa RS, Mendenhall NP. Ameloblastoma. Am J Clin Oncol. 2007;30(6):645-648.

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Triangular radiolucent lesion of the mandible.

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