AIM: To investigate the presence of myofibroblasts (MFBs) in epithelial odontogenic lesions by immunohistochemistry and to correlate the findings with tumor aggressiveness, as well as to analyze the expression of TGF-β1 and IFN-γ during the differentiation of these cells. METHODS AND RESULTS: Twenty solid ameloblastomas (SAs), 10 unicystic ameloblastomas (UAs), 20 keratocystic odontogenic tumors (KCOTs), and 20 adenomatoid odontogenic tumors (AOTs) were selected. For evaluation of the presence of MFBs, anti-α-SMA-immunoreactive cells were quantified in connective tissue near the epithelium. The expression of TGF-β1 and IFN-γ was evaluated in epithelial and connective tissue by determining the percentage of immunoreactive cells. A higher concentration of MFBs was observed in SAs (mean of 30.55), followed by KCOTs (22.50), UAs (20.80), and AOTs (19.15) (P = 0.001). There was no significant correlation between the immunoexpression of TGF-β1 or IFN-γ and the number of MFBs (P > 0.05). CONCLUSIONS: The larger number of MFBs suggests that these cells are one of the factors responsible for the more aggressive biological behavior of these lesions. The lack of correlation between the number of MFBs and immunoexpression of TGF-β1 and IFN-γ indicates that these proteins are not involved in the differentiation of this type of contractile cell in the lesions studied and that only the use of immunohistochemistry to establish such a correlation is a limiting factor.
AIM: To investigate the presence of myofibroblasts (MFBs) in epithelial odontogenic lesions by immunohistochemistry and to correlate the findings with tumor aggressiveness, as well as to analyze the expression of TGF-β1 and IFN-γ during the differentiation of these cells. METHODS AND RESULTS: Twenty solid ameloblastomas (SAs), 10 unicystic ameloblastomas (UAs), 20 keratocystic odontogenic tumors (KCOTs), and 20 adenomatoid odontogenic tumors (AOTs) were selected. For evaluation of the presence of MFBs, anti-α-SMA-immunoreactive cells were quantified in connective tissue near the epithelium. The expression of TGF-β1 and IFN-γ was evaluated in epithelial and connective tissue by determining the percentage of immunoreactive cells. A higher concentration of MFBs was observed in SAs (mean of 30.55), followed by KCOTs (22.50), UAs (20.80), and AOTs (19.15) (P = 0.001). There was no significant correlation between the immunoexpression of TGF-β1 or IFN-γ and the number of MFBs (P > 0.05). CONCLUSIONS: The larger number of MFBs suggests that these cells are one of the factors responsible for the more aggressive biological behavior of these lesions. The lack of correlation between the number of MFBs and immunoexpression of TGF-β1 and IFN-γ indicates that these proteins are not involved in the differentiation of this type of contractile cell in the lesions studied and that only the use of immunohistochemistry to establish such a correlation is a limiting factor.