Ameloblastoma, calcifying epithelial odontogenic tumor, and glandular odontogenic cyst show a distinctive immunophenotype with some myoepithelial antigen expression.
BACKGROUND
Odontogenic neoplasms have some morphologic overlap with salivary gland neoplasms, many of which show myoepithelial differentiation. In the 1980s, an ultrastructural study identified a population of myoepithelial-like cells in calcifying epithelial odontogenic tumor. Myoepithelial derived tumors have since been shown to have distinct immunohistochemical profiles.


METHODS
We examined a series of odontogenic neoplasms, including 11 ameloblastomas, four calcifying epithelial odontogenic tumors, five glandular odontogenic cysts (GOCs), and five keratocystic odontogenic tumors with a panel of myoepithelial-associated immunohistochemical stains. We also assessed representative control examples of oral mucosa, odontogenic rests, and dentigerous cysts.


RESULTS
All of the neoplastic and non-neoplastic oral epithelium-derived entities share a p63-positive, high molecular weight cytokeratin (CK5/6)-positive immunophenotype. Calponin reactivity was at least focally present in two of four calcifying epithelial odontogenic tumors, three of five GOCs, and 10 of 11 ameloblastomas; the sole completely non-reactive ameloblastoma represents a lung metastasis. One case of calcifying epithelial odontogenic tumor was focally positive for glial fibrillary acidic protein. However, other more definitive markers of myoepithelial differentiation, including S-100 and smooth muscle actin, were negative. Two of three calcifying epithelial odontogenic tumors and five of five GOCs were also positive for a low molecular weight cytokeratin (CK7).


CONCLUSIONS
Ameloblastomas, GOCs, and calcifying epithelial odontogenic tumors show a distinctive immunophenotype which overlaps with that of myoepithelial-derived salivary gland neoplasms but does not provide definitive support for myoepithelial differentiation.
Gratzinger
Dita
D
Department of Surgical Pathology, Stanford University School of Medicine, Stanford, CA 94305-5324, USA. ditag@stanford.edu
Salama
Mohamed E
ME
Poh
Catherine F
CF
Rouse
Robert V
RV
D000564:Ameloblastoma / Q000473:pathology*; D000951:Antigens, Neoplasm / Q000096:biosynthesis; D002135:Calcium-Binding Proteins / Q000096:biosynthesis; D002454:Cell Differentiation; D004847:Epithelial Cells / Q000473:pathology; D015870:Gene Expression; D006801:Humans; D016130:Immunophenotyping; D053531:Keratins, Type II / Q000096:biosynthesis / Q000276:immunology; D008565:Membrane Proteins / Q000096:biosynthesis; D008840:Microfilament Proteins / Q000096:biosynthesis; D032342:Muscle Cells / Q000473:pathology; D009124:Muscle Proteins / Q000096:biosynthesis; D009807:Odontogenic Cysts / Q000473:pathology*; D009808:Odontogenic Tumors / Q000473:pathology*; D012189:Retrospective Studies; D012468:Salivary Gland Neoplasms / Q000473:pathology*; D000096985:Calponins
D000951:Antigens, Neoplasm; D002135:Calcium-Binding Proteins; D053531:Keratins, Type II; D008565:Membrane Proteins; D008840:Microfilament Proteins; D009124:Muscle Proteins; D000096985:Calponins; C081876:CKAP4 protein, human