Objectives: Ameloblastoma originates from odontogenic epithelium, which involves tooth germ structure, and is well known as an odontogenic tumor. Histopathologically, it is mainly classified into follicular and plexiform types from distribution pattern of tumor parenchyma and stroma. However, there has been few reports concerning about the mechanism of morphological growth pattern in this tumor. Cell to cell adhesion is mediated through various cell adhesion molecules and plays important roles in maintaining the tissues as well as in organ genesis and morphogenesis. Methods: To clarify the involvement of cell adhesion molecules in this tumor, expression of cell adhesion molecules (E-cadherin, P-cadherin a-catenin, b-catenin and ZO-1) were examined by immunohistochemical analysis on 35 ameloblastomas (follicular 12 cases, plexiform 23 cases). Results: Immunohistochemically, E, P-cadherin and ZO-1 expressed in parenchyma cells of the plexiform type. In the follicular type, basal and spindle cells, which line outer side of tumor parenchyma, expressed those adhesion molecules. However, stellate reticulum like cells (SLLC), which locate inner side of tumor parenchyma, were absent from those molecules, and it different from plexiform type one. a and b-catenin expressed in all parenchyma cells of both types ameloblastoma. Thus, SLLC of plexiform type might have more tight adhesion potential than SLLC of follicular one. Conclusions: These results suggested that the difference of E, P-cadherin and ZO-1 expression in SLLC mediates the morphological growth pattern in ameloblastoma.

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