A Locally Destructive Mandibular Dentinogenic Ghost Cell Tumor Mimicking Ameloblastoma

Dentinogenic ghost cell tumor (DGCT) is a rare odontogenic neoplasm. The central form is uncommon but clinically important because it can infiltrate bone and recur.¹ Cross-midline growth has also been reported in mandibular DGCT.² Calcified or dentinoid foci may be subtle on imaging. The preoperative differential diagnosis often includes ameloblastoma, calcifying odontogenic cyst, odontoma-associated lesions, and ghost cell odontogenic carcinoma.^{3, 4} Accurate diagnosis is important because limited curettage may leave residual tumor in central lesions with cortical perforation.¹

A 63-year-old man presented with painful swelling of the anterior mandible that had persisted for more than 1 year. He had not received any previous treatment. Physical examination revealed firm expansion of the anterior mandible with tenderness and eggshell crepitus.

Panoramic radiography and computed tomography demonstrated a 65.2 × 40.8 × 38.2 mm expansile osteolytic lesion crossing the mandibular midline. Extensive cortical destruction and loss of anterior mandibular continuity initially suggested ameloblastoma (Figure 1a-c).

Figure 1.

(a-d) A panoramic radiograph shows a large anterior mandibular radiolucency crossing the midline (a). Axial computed tomography shows expansile osteolysis, internal septation, and cortical destruction (b). Three-dimensional reconstruction shows loss of anterior mandibular continuity (c). Hematoxylin-eosin staining shows odontogenic epithelium, ghost cells, and dentinoid material (d).

Histopathological examination demonstrated odontogenic epithelial nests containing ghost cells and dentinoid, without malignant cytologic features, confirming the diagnosis of central DGCT (Figure 1d). Because of the extensive structural destruction, the patient underwent segmental mandibulectomy with immediate fibular free-flap reconstruction. At the 2-year telephone follow-up, he reported no swelling, pain, or other symptoms suggestive of clinical recurrence. Surveillance imaging was unavailable.

The primary diagnostic challenge was the discrepancy between the ameloblastoma-like imaging findings and the histopathological diagnosis of DGCT. Although the marked cortical destruction indicated aggressive local behavior, it was not specific to the tumor type; therefore, histopathological confirmation was essential before definitive treatment. The diagnosis was established by identifying odontogenic epithelial nests containing ghost cells and dentinoid, without malignant cytologic features, consistent with central DGCT.⁴ Previous reports have described recurrence after conservative treatment and have supported resection for large central tumors when local control or preservation of jaw continuity is at risk.^{1, 5} In patients with destructive odontogenic jaw lesions, biopsy specimens should be carefully evaluated for ghost cells, dentinoid, and malignant features. Although DGCT is histologically benign, extensive cortical destruction and loss of mandibular continuity may necessitate radical surgical resection.