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An Incidental Finding During Orthodontic Treatment.

The patient was an asymptomatic, 30-year-old, African American woman with no significant past medical or surgical history who presented to the Oral and Maxillo-facial Surgery Department at Henry Ford Hospital, Detroit, Mich, on a referral from her orthodontist. While the patient was undergoing orthodontic treatment for correction of malaligned dentition, routine radiographic examination revealed a unilocular, triangular-shaped, radiolucent lesion between the roots of teeth numbers 22 and 23. The roots exhibited divergence in association with the lesion (Figure 1).

[Figure 1 ILLUSTRATION OMITTED]

Clinically, the patient had no lymphadenopathy, neck masses, or facial swelling. Intraorally, the soft tissue overlying the area in question appeared normal and firm on palpation. There was no buccal or lingual cortical expansion; however, teeth numbers 22 and 23 did have a slightly enlarged cervical embrasure. The lesion was excised as a whole, and the cavity was curetted.

Grossly, the specimen consisted of an irregular, 20 x 10 x 7-mm fragment of firm, pale gray tissue. Microscopically, the lesion was composed of sharply circumscribed squamous nests within a fibrous stroma. The epithelial nests displayed focal acantholysis and lacked any significant cytologic atypia (Figure 2).

[Figure 2 ILLUSTRATION OMITTED]

What is your diagnosis?

Pathologic Diagnosis: Squamous Odontogenic Tumor

Squamous odontogenic tumor (SOT) is a benign but occasionally aggressive epithelial odontogenic tumor first described in 1975 by Pullon et al.[1,2] Squamous odontogenic tumor has 3 clinicopathologic presentations, the most common of which arises within the jaw bones (the subject of this presentation). The other presentations include a so-called mural form (an indolent odontogenic cyst with mural SOT-like proliferations originating from the cyst lining or mural odontogenic epithelial rests) and a rare, extraosseous type (thought to arise from the overlying gingival epithelium, similar to peripheral ameloblastoma).[1,3,4]

The age of incidence varies widely, peaking in the third decade.[4] Leider et al reported multiple lesions in 3 siblings, which implies that a familial distribution may occur in some cases.[4] There is an almost 2:1 male predilection in the solid variant.[3] The lesion may be asymptomatic and incidentally detected in a radiograph, or complaints of tooth mobility, pain, or tenderness (particularly to percussion) may be present.[3] Local swelling and deep pocket formation have been noted.[3,5]

Location is almost equally distributed between the mandible and maxilla, with the former involved somewhat more frequently.[2,4] The incisor-canine segment is more often affected in the maxilla, whereas the premolar-molar region is the more common location in the mandible.[2,4] Typically, the alveolus is affected. Large tumors may involve the body of the mandible or extend into the maxillary sinus -when they arise in the maxilla.[4] Multiple lesions can occur in up to 25% of cases.[4] Squamous odontogenic tumor can have locally aggressive behavior, eroding through the facial or lingual plates of alveolar bone, or extending into the palate, maxillary sinuses, nasal floor, and nasal spine.[2,5] This is especially true of the maxillary lesions.[2,3]

The typical radiographic appearance is that of a triangular or semicircular radiolucency with the narrow part of the lesion toward the alveolar crest, often with a radiodense border, and located within the alveolar process between the roots of teeth.[1-4] Root resorption has been described. [2] Larger lesions have presented as multilocular radiolucencies, some of which are associated with embedded teeth.[4]

Histopathologically, the tumor consists of numerous, variably sized and shaped, sometimes anastomosing islands of stratified squamous epithelium. These islands consist of benign squamous epithelium composed mostly of oval to polygonal nonkeratinized cells surrounded by flattened, round, or focally cuboidal basaloid cells. The cells are generally uniform with no pleomorphism, nuclear hyperchromatism, or mitoses. Intercellular bridges are easily identified. The presence of epithelial vacuolization and microcysts is frequently noted. Individual cell keratinization and keratin or parakeratin pearls may be seen. Additionally, the squamous islands may contain central lamellar calcifications. Intraepithelial globular, hyaline, crystalloid, and periodic acid-Schiff-positive eosinophilic structures have been described.[2] The islands are separated by a collagenous, mildly cellular, fibroconnective stroma containing small blood vessels and, occasionally, laminated calcifications and diffuse or focal chronic inflammatory cell infiltrates.

Most authors favor SOT arising from the rests of Malassez for the following reasons: (1) no periodontal ligament can be seen between the SOT and the root of the tooth, suggesting origin in the periodontal ligament[1]; (2) the usual location in the alveolus[4]; (3) the pattern of bony destruction seems to originate relatively consistently from the tooth roots[2]; and (4) the pattern of cytokeratin expression.[6] Additionally, the SOT-like proliferations associated with chronic periodontitis have been suggested to arise in the rests of Malassez.[2] The cases reported in association with embedded teeth indicate the tumor may also develop from proliferation of epithelial rests in the dental follicle.[4]

Several pathologic entities must be differentiated from SOT. The most important one is well-differentiated squamous cell carcinoma in the jaws, either primary intraosseous or metastatic. The absence of cytologic atypia, increased mitotic activity, desmoplasia, and infiltrative features in SOT allows it to be differentiated from squamous cell carcinoma. It must be noted that pleomorphism, hyperchromatism, and an increased number of mitotic figures may sometimes be seen in SOT of younger patients.[5] Acanthomatous ameloblastoma features squamous islands with a peripheral palisaded layer of columnar polarized cells. Additionally, there are no central epithelial cells resembling stellate reticulum. Finally, central mucoepidermoid carcinoma falls in the differential diagnosis, especially in the presence of microcystic change and periodic acid-Schiff-positive material within the epithelial nests of SOT. The lack of anaplasia, mucus cells, and other cell types typical of mucoepidermoid carcinoma rule out the diagnosis of mucoepidermoid carcinoma.[7]

Squamous odontogenic tumor should be treated by complete surgical excision, and there is low probability of recurrence.[1,2] En bloc resection or hemimaxillectomy may be required to eradicate disease in some cases owing to the extent and involvement of adjacent structures.[2] However, failure to control the tumor has not been reported.[4] Malignant transformation has not been documented, although a case of bilateral maxillary SOT was found to be associated with a primary squamous cell carcinoma of the mandible.[4]

References

[1.] Pullon PA, Shafer WG, Elzay RP, Kerr DA, Corio RL. Squamous odontogenic tumor: report of six cases of a previously undescribed lesion. Oral Pathol. 1975; 40:616-630.

[2.] 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; 54:187.-196.

[3.] Batsakis JG, Cleary KR. Squamous odontogenic tumor. Ann Otol Rhinol Laryngol. 199:1; 102:82-824.

[4.] Baden E, Doyle J, Mesa M, Fabie M, Lederman D, Eichen M. Squamous odontogenic tumor: report of three cases including the first extraosseous case. Oral Surg Oral Med Oral Pathol. 1993;75:733-738.

[5.] Leventon GS, Happonen R-P, Newland JR. Squamous odontogenic tumor: report of two cases and review of the literature. Am J Surg Pathol. 1981;5:671677.

[6.] Tatemoto Y, Okada Y, Mori M. Squamous odontogenic tumor: immunohistochemical identification of cytokeratins. Oral Surg Oral Med Oral Pathol. 1989; 67:63-67.

[7.] McClatchey KD. Tumors of the dental lamina: a selective review. Semin Diagn Pathol. 1987;4:200-204.

Accepted for publication May 4, 2000.

From the Departments of Pathology (Drs Gomez and Zarbo) and Oral and Maxillofacial Surgery (Dr Gulati), Henry Ford Hospital, Detroit, Mich.

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Author:Gomez, Jose A.; Gulati, Arvind; Zarbo, Richard J.
Publication:Archives of Pathology & Laboratory Medicine
Date:Feb 1, 2001
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