muramidase and Ameloblastoma

Apoptotic cell death in granular cell ameloblastomas was examined by immunohistochemistry using anti-single-stranded DNA (ssDNA) antibody and transmission electron microscopy. Routinely prepared sections of granular cell ameloblastomas showed various quantities of granular cells with some apoptotic nuclear fragments. Immunoreactivity for ssDNA was higher in granular cells than in other neoplastic cells. Ultrastructural examination revealed abundant lysosomes in the cytoplasm of granular cells. Numerous apoptotic cell fragments with condensed nuclei in granular cell clusters were phagocytosed by adjacent granular cells. On immunohistochemical characterization of cellular differentiation, granular cells were positive for cytokeratin, CD68, lysozyme and alpha-1-antichymotrypsin, but negative for vimentin, desmin, S-100 protein, neuron-specific enolase and CD15, indicating epithelial origin and lysosomal aggregation. These features suggest that the cytoplasmic granularity in granular cell ameloblastomas might be caused by increased apoptotic cell death of neoplastic cells and associated phagocytosis by neighboring neoplastic cells.

Topics: Adult; alpha 1-Antichymotrypsin; Ameloblastoma; Antibodies; Antigens, CD; Antigens, Differentiation, Myelomonocytic; Apoptosis; Cell Differentiation; Cell Nucleus; Cytoplasm; Cytoplasmic Granules; Desmin; DNA, Single-Stranded; Female; Humans; Immunohistochemistry; Keratinocytes; Keratins; Lewis X Antigen; Lysosomes; Macrophages; Male; Microscopy, Electron; Middle Aged; Muramidase; Phagocytosis; Phosphopyruvate Hydratase; S100 Proteins; Vimentin

Six cases of oral granular cell lesions were studied with respect to intermediate-sized filaments (IF), peanut lectin binding (PNL) and muramidase activity by means of the peroxidase antiperoxidase technique. The tumours included three granular cell myoblastomas of the tongue (GCM) two cases of congenital gingival granular cell tumour (CGGT) and one granular cell ameloblastoma (GCA). Every tumour studied showed intracytoplasmic PNL binding whereas muramidase was negative in all cases. Vimentin expression was demonstrated in the CGGT and to a lesser extent in the GCM, but was absent in the GCA which was positive for keratin. Desmin and glial fibrillary acidic protein (GFAP) were not present in any of the lesions. These data demonstrate that PNL binding might be considered to be a common feature of granular cells regardless of their histogenesis. Lysosomes are supposed to represent the intracellular binding sites for this marker. Moreover it is shown that histomorphological identity between the granular cells of CGGT and GCA does not signify identity in histogenesis since the former are of mesenchymal derivation while the latter, from their intermediate filament protein types appear to originate from epithelium.

Topics: Ameloblastoma; Arachis; Gingival Neoplasms; Histocytochemistry; Humans; Intermediate Filament Proteins; Mouth Neoplasms; Muramidase; Neoplasms, Muscle Tissue; Receptors, Mitogen; Tongue Neoplasms; Vimentin