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Ameloblastic fibroma: growth potentiality of odontogenic epithelium and coexpression of intermediate filament proteins in fibromatous cells
Author(s) -
Tatemoto Y.,
Yamamoto N.,
Onojima M.,
Okada Y.,
Mori M.
Publication year - 1988
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/j.1600-0714.1988.tb01519.x
Subject(s) - keratin , desmin , vimentin , intermediate filament , histogenesis , biology , ameloblastoma , pathology , odontogenic tumor , microbiology and biotechnology , immunohistochemistry , cell , cytoskeleton , anatomy , medicine , immunology , odontogenic , biochemistry , maxilla
Four cases of ameloblastic fibroma are described immunohistochemically in terms of intermediate‐sized proteins in both epithelial and mesodermal components. Keratin proteins were demonstrated by polyclonal anti‐keratin antiserum (TK: detecting 41–65 kDa keratins) and 2 monoclonal antibodies to keratin (KL1: 55–57 kDa, PKK1: 44, 46, 52 and 54 kDa), and monoclonal antibodies to vimentin and desmin. Two types of odontogenic epithelial tumour cells were discriminated: undifferentiated odontogenic cells and common ameloblastoma cells. Keratin expression was found to be stronger in undifferentiated cells than in the ameloblastoma cells. Undifferentiated cells were PAS–positive, while ameloblastoma cells were negative. Fibroma cells were strongly positive for vimentin, and negative for desmin. Keratin proteins were also expressed slightly. Thus, coexpression of keratin and vimentin was seen in fibroma cells. Histogenesis is discussed from the standpoint of the distribution patterns of keratin and vimentin, as well as with respect to the histopathology.