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Central giant cell granulomas of the jaws: phenotype and proliferation‐associated markers
Author(s) -
O'Mailey Miriam,
Pogrel M. Anthony,
Stewart Jeffery C. B.,
Silva Rebeka G.,
Regezi Joseph A.
Publication year - 1997
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.1600-0714.1997.tb00451.x
Subject(s) - pathology , cd34 , cd68 , peripheral blood mononuclear cell , biology , population , immunohistochemistry , factor xiiia , cell cycle , cell , medicine , microbiology and biotechnology , in vitro , stem cell , biochemistry , genetics , environmental health
Central giant cell granulomas (CGCGs) are jaw tumors of unknown origin that often exhibit an aggressive, though unpredictable, clinical course. The purpose of this study was to determine the immunoprofile of the mononuclear cells that seem to be responsible for the biologic behavior of these tumors. Numbers of cells in cell cycle were also determined and compared in clinically aggressive and non‐aggressive CGCGs. Sixteen aggressive and 12 non‐aggressive CGCGs were immunohistochemically stained with antibodies to CD34, CD6S. factor XHIa, ct‐smooth muscle actin. prolyl 4‐hydroxylase, Ki‐67. and p53 protein. Cell populations and numbers of cells in cell cycle were determined through microscopic quantitative assessment. CD34‐positive ceils were limited to support vessels. CD68‐positive mononuclear cells constituted a small population of cells in ail tumors. With two exceptions, factor XIIIa‐positive cells were rarely seen. Alpha‐smooth muscle actin staining was present in approximately half the tumors, and occasionally large numbers of positive cells were seen. Most mononuclear cells were positive for fibroblast‐associated antigen. No phenotypic differences were detected between aggressive and non‐aggressive tumors. P53 protein did not appear to be overexpressed in CGCGs. Ki‐67 staining showed that only mononuclear cells were in cell cycle, and that there were no differences between aggressive and non‐aggressive tumors. We conclude that CGCGs are primarily fibroblastic (and myofibroblastic) tumors in which macrophages appear to play a secondary role. Tumor cells show no differentiation toward endothelial cells or macrophage‐related dendrocytes (factor XIIIa). Cellular phenotypes and numbers of cells in cell cycle are similar in both aggressive and non‐aggressive tumors.