OBJECTIVE: The aim of the present study was to investigate the association between the expression of cyclooxygenase-2 (COX-2) in keratocystic odontogenic tumors (KCOT) and more commonly used markers, such as p53 and Ki-67. STUDY DESIGN: Expression of cyclooxygenase-2 (COX-2) in 20 biopsy specimens of keratocystic odontogenic tumors (KCOT) has been analyzed and compared with the expression of previously reported markers Ki-67 and p53. Formalin-fixed, paraffin-embedded blocks were sectioned and used for hematoxylin-eosin (H&E) staining and incubated with anti-cox-2, anti-ki-67, and anti-p53 monoclonal antibodies for immunohistochemical examination. Detection of the COX-2 antibody was performed with the EnVision kit. Cellular staining pattern was cytoplasmatic for COX-2 and nuclear for both Ki-67 and p-53. Molecular expressions were semiquantitatively evaluated as negative (-), mild (±) or strong (+). RESULTS: Mild to strong expression of COX-2 was observed in 20 (100%) of the cases. Fifteen (75%) of the KCOTs stained positive for p53 and 18 (90%) stained positive for Ki-67. There was no statistically relevant difference between the expressions of COX - 2, Ki-67, and p53. CONCLUSIONS: Although COX-2 has rarely been used to assess the biological activity of the KCOT, the results portrayed in the current study and the current knowledge of the overall role known to be played by COX-2 in tumorigenesis suggest that COX-2 may be an important marker involved in the biological behavior of the KCOT. Larger studies are required to improve our knowledge of the possible role of COX-2 in the pathogenic mechanism involved in KCOT.
OBJECTIVE: The aim of the present study was to investigate the association between the expression of cyclooxygenase-2 (COX-2) in keratocystic odontogenic tumors (KCOT) and more commonly used markers, such as p53 and Ki-67. STUDY DESIGN: Expression of cyclooxygenase-2 (COX-2) in 20 biopsy specimens of keratocystic odontogenic tumors (KCOT) has been analyzed and compared with the expression of previously reported markers Ki-67 and p53. Formalin-fixed, paraffin-embedded blocks were sectioned and used for hematoxylin-eosin (H&E) staining and incubated with anti-cox-2, anti-ki-67, and anti-p53 monoclonal antibodies for immunohistochemical examination. Detection of the COX-2 antibody was performed with the EnVision kit. Cellular staining pattern was cytoplasmatic for COX-2 and nuclear for both Ki-67 and p-53. Molecular expressions were semiquantitatively evaluated as negative (-), mild (±) or strong (+). RESULTS: Mild to strong expression of COX-2 was observed in 20 (100%) of the cases. Fifteen (75%) of the KCOTs stained positive for p53 and 18 (90%) stained positive for Ki-67. There was no statistically relevant difference between the expressions of COX - 2, Ki-67, and p53. CONCLUSIONS: Although COX-2 has rarely been used to assess the biological activity of the KCOT, the results portrayed in the current study and the current knowledge of the overall role known to be played by COX-2 in tumorigenesis suggest that COX-2 may be an important marker involved in the biological behavior of the KCOT. Larger studies are required to improve our knowledge of the possible role of COX-2 in the pathogenic mechanism involved in KCOT.