Abstract
BackgroundCD166 is a glycoprotein of an immunoglobulin super family of adhesion molecules that has been associated with aggressive characteristics and high recurrence rate of tumors. Different odontogenic lesions exhibit considerable histological variation and different clinical behavior. In an attempt to clarify the mechanisms underlying this different behavior, the present study investigates the immunohistochemical expression of CD166 in these lesions.Material and MethodsIn this study 69 formalin-fixed, paraffin embedded tissue blocks of odontogenic lesion consist of 15 unicystic ameloblastoma (UA), 17 solid ameloblastoma (SA), 18 keratocystic odontogenic tumors (KCOT), and 19 dentigerous cysts (DC) were reviewed by immunohistochemistry for CD166 staining.ResultsIn this study, CD166 immune staining was evident in all specimen groups except dentigerous cyst. In positive cases, protein localization was cytoplasmic and/or membranous. CD166 expression was seen in76.5% (13) of SA, 73.5% (11) of UA, and 66.7% (12) of KCOTs. Statistical analysis showed that CD166 expression levels were significantly higher in ameloblastoma (SA and UA) and KCOTs than dentigerous cyst (P <0.001), but there was no statistically significant difference between CD166 expression in the other groups (P>0.05).ConclusionsThis data demonstrates that overexpression of CD166 may have a role in the pathogenesis of ameloblastoma and KCOT. Key words:CD166, ameloblastoma, dentigerous cyst, odontogenic keratocyst.
Highlights
Cell junctions connect epithelial cells to one another and consist of various proteins, generically called adhesion molecules, which are keys to the regulation of cell growth and differentiation [1].Adhesion molecules are involved in tumor cell-tumor cell adhesion, tumor cell-endothelial cell adhesion, and tumor cell-matrix adhesion, all of which are necessary for primary tumor formation or metastasis [2]
This result indicates that CD166 may play a role in the pathogenesis of ameloblastomas and keratocystic odontogenic tumors (KCOT) but not in dentigerous cysts (DC)
The difference in CD166 expression observed in the present study might explain the variable behavior of these lesions, the highly aggressive and invasive behavior of ameloblastomas and KCOTs, and it supports the concept that KCOT has a neoplastic potential
Summary
Cell junctions connect epithelial cells to one another and consist of various proteins, generically called adhesion molecules, which are keys to the regulation of cell growth and differentiation [1].Adhesion molecules are involved in tumor cell-tumor cell adhesion, tumor cell-endothelial cell adhesion, and tumor cell-matrix adhesion, all of which are necessary for primary tumor formation or metastasis [2]. Keratocystic odontogenic tumor (KCOT) has recently been recommended to describe the lesion previously named odontogenic keratocyst [15] KCOT is a developmental cyst which is locally aggressive and rapidly proliferating and shows a high recurrence rate after removal [16]. Previous studies disclose the role of different adhesion molecules in the pathogenesis and aggressive behavior of odontogenic lesions [19,20]. In view of the distinct clinical behavior of KCOT, dentigerous cyst, and ameloblastoma, the objective of the present study was to investigate the immunohistochemical expression of CD166 in these lesions. CD166 is a glycoprotein of an immunoglobulin super family of adhesion molecules that has been associated with aggressive characteristics and high recurrence rate of tumors. Conclusions: This data demonstrates that overexpression of CD166 may have a role in the pathogenesis of ameloblastoma and KCOT
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