Ameloblastomas are a rare entity, representing 1% of tumors and cystic lesions of the jaw. A subset of these lesions, termed ameloblastic carcinoma, contain histologic architectural features of ameloblastoma along… Click to show full abstract
Ameloblastomas are a rare entity, representing 1% of tumors and cystic lesions of the jaw. A subset of these lesions, termed ameloblastic carcinoma, contain histologic architectural features of ameloblastoma along with malignant cytological features. Ameloblastic carcinomas were re-classified as a separate diagnostic entity by the WHO in 2005. This re-classification separates ameloblastic carcinoma from malignant ameloblastoma, which refers to metastatic ameloblastomas with benign cytologic features. Primary ameloblastic carcinomas are more common; however, cases arising from a pre-existing ameloblastoma, categorized as secondary ameloblastic carcinoma, have been reported. A 30-year-old man presented with a right-sided parotid mass. His medical history was significant for nodular sclerosing Hodgkin lymphoma, treated with radiation therapy at the age of 20. He subsequently developed ameloblastic carcinoma of the left mandible extending through the mandible to involve surrounding soft tissue. He underwent resection with adjuvant chemoradiation for his initial tumor at age 24 and a for local recurrence at age 27. Five years following initial diagnosis, he experienced right sided facial swelling over the parotid gland. Fine-needle aspiration of the parotid mass was performed. DiffQuik® and Papanicolaou stained smears were hypercellular, consisting of numerous single cells and loosely cohesive fragments and clusters of cells (Figure 1). Most cellular fragments displayed a peripheral palisading. Morphologically, the cells were small to intermediate size, basaloid with high nuclear to cytoplasmic ratio, and appeared cuboidal to tall columnar (Figure 2). Rare large cells with clear cytoplasm were present mingled with basaloid cells. Spindle cells were noted on Papanicolaou stain. The nuclei were round to oval with finely granular chromatin containing one or multiple small nucleoli (Figure 3). Nuclear molding, nuclear overlap, and occasional nuclear grooves were better observed with Diff-Quik stain. The cytoplasm was scant to moderate, delicate, and finely vacuolated with indistinct cell borders (Figure 4). Additional cytomorphologic findings included occasional atypical mitotic figures, apoptotic nuclei, small areas of necrosis, and nuclear streaking artifact. A finely granular, vacuolated, gray, and basophilic matrix was seen in DiffQuik stained smears. These findings, particularly a hypercellular aspirate showing basaloid cells with peripheral palisading, the presence of spindled cells, and nuclear features including molding and fine chromatin, suggest a diagnosis of ameloblastic carcinoma. The differential diagnosis should include lymphoma, small cell carcinoma, HPV-related head and neck squamous cell carcinoma, and a neuroendocrine tumor of the nasopharynx based on the small, loosely cohesive, basaloid cell population seen in this case. Ameloblastic carcinoma lacks the prominent lymphoglandular bodies seen in lymphoma, and has a finer chromatin pattern than the “salt and pepper” chromatin seen in small cell carcinoma. Adenoid cystic carcinoma with a solid pattern could also be considered, particularly given the parotid location; however, the presence of peripheral palisading suggests against this diagnosis, and ameloblastic carcinoma typically does not have the dense, acellular material commonly seen in adenoid cystic carcinoma. The differential would also include a low grade adenocarcinoma of the salivary gland, which would show cuboidal and spindled cells with oval nuclei containing finely
               
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