Evaluation of neoplastic nature of keratocystic odontogenic tumor versus ameloblastoma.
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OBJECTIVE
Although most of odontogenic tumors are benign, some of them will show locally destructive behavior, as keratocystic odontogenic tumor (KCOT) is now known as a benign but aggressive odontogenic neoplasm. The neoplastic characteristics in KCOT have been suggested from clinical as well as pathologic aspects. Matrix metalloproteinase-2 (MMP-2) is a gelatinase form of the MMPs family, which is a group of proteolytic enzymes that degrade many types of collagen. Cysteine aspartic acid-specific protease-3 (caspase-3) is the most downstream enzyme in the apoptosis-inducing protease pathway and is probably the most clearly associated with cell death. The aim of this study is to evaluate and compare the extracellular degradation potentiality (MMP-2) and apoptosis (caspase-3) of the epithelial lining in KCOT versus radicular cysts and ameloblastoma, in order to reinforce its classification as an odontogenic tumor.
METHODS
Twenty-six surgical specimens including keratocyst odontogenic tumor (KCOT; n=11), ameloblastoma (AB; n=8) and radicular cysts (RC; n=7) were examined for expression of MMP-2 and caspase-3 using the immunohistochemical method.
RESULTS
For MMP-2 immunoexpression, AB showed the statistically significant highest mean area percentage, followed by KCOT, while RC showed the statistically significant lowest mean area percentage. As for caspase- 3, there was no statistically significant difference between KCOT and AB, while RC showed the statistically significantly lowest mean area percentage.
CONCLUSIONS
Overexpression of MMP-2 protein related to growth and progression of lesions analyzed and may be one of the factors enhancing the recurrence of KCOT and invasion of AB. In addition, the epithelial lining of KCOT showed a high cell turnover reinforcing its classification as an odontogenic tumor.
BACKGROUND
Keratocystic odontogenic tumor (KCOT) - Ameloblastoma (AB) - Radicular cyst (RC) - Matrix metalloproteinase-2 (MMP-2) - Caspase-3.
