ABSTRACT
OBJECTIVE: The aim of this study was to investigate the presence of CD1a-positive Langerhans cells and their relationship with E-cadherin in minor salivary gland tumors. METHODS: Twenty-seven minor salivary gland tumors were investigated using immunohistochemistry for CD1a and E-cadherin. RESULTS: A significant difference regarding the mean density of CD1a-positive Langerhans cells was observed between pleomorphic adenomas and malignant tumors studied (P = 0.001). No CD1a-positive cells were detected in most cases (n = 5) of cystic adenoid carcinomas. CD1a-positive cells were detected in one mucoepidermoid carcinoma case, and six low-grade polymorphous adenocarcinomas cases. Comparison of the mean density of CD1a-positive cells between the three malignant tumors showed no significant difference (P = 0.127). No significant difference was observed in the presence of E-cadherin between tumors (P = 0.73), but it was detected in 24 cases. CONCLUSIONS: The lack of CD1a-positive in malignant salivary gland tumors facilitates the neoplastic development and suggests that these cells might be useful as auxiliary diagnostic and prognostic tool in minor salivary gland tumors. Furthermore, it is suggested that E-cadherin mediates cell adhesion in these tumors although we did not demonstrate significance.
Subject(s)
Antigens, CD1/analysis , Cadherins/analysis , Langerhans Cells/pathology , Salivary Gland Neoplasms/pathology , Salivary Glands, Minor/pathology , Adenocarcinoma/pathology , Adenoma, Pleomorphic/pathology , Carcinoma, Adenoid Cystic/pathology , Carcinoma, Mucoepidermoid/pathology , Cell Count , Coloring Agents , Dendritic Cells/pathology , Epithelium/pathology , Female , Humans , Image Processing, Computer-Assisted/methods , Immunohistochemistry , Langerhans Cells/immunology , Male , Middle AgedABSTRACT
AIM: To investigate the immunohistochemical expression of Ki-67, p53 and p63 in Keratocyst Odontogenic Tumours (KOTs) in order to contribute to the biological profile of this tumor. METHODS: Immunohistochemical technique was performed using the EnVision System in 37 cases of KOTs. RESULTS: Ki-67- and p53-immunostained cells were mainly located in the suprabasal layers. p63-positive cells were found throughout the lining cystic epithelium. No difference in the immunostaining for these proteins was observed between primary and recurrent KOTs (Ki-67: P = 0.5591; p53: P = 0.9847; p63: P = 0.9127), or between KOTs associated with Nevoid Basal Cell Carcinoma Syndrome (NBCCS) and sporadic KOTs (Ki-67: P = 0.7013; p53: P = 0.3197; p63: P = 0.2427). CONCLUSIONS: It is possible that biological behavior of KOTs may be related to suprabasal proliferative compartment in the cystic epithelium as observed by high levels of Ki-67, p53 and p63. In addition, p63 immunostaining may represent immaturity of keratinocytes in KOTs, and suggests that this protein may participate in the regulation of epithelial cell differentiation. Taken together, these data may favor tumorigenesis on KOTs.
