Prospective significance of cyclooxygenase-2 in keratocystic odontgenic tumor: an immunohistochemical study differentiating the tumoral and the cystic nature of odontogenic lesions

Background: Keratocystic odontogenic tumor (KCOT) is a benign intraosseous neoplasm with locally invasive behaviour and a tendency to recur. Dentigerous cyst (DC) is one of the most common type of the developmental odontogenic cysts, having the capability of becoming an aggressive lesion. Both can cause involvement of adjacent soft tissues, infiltration and destruction of the bone. Although the exact etiology and pathogenesis of these two odontogenic lesions remain unclear, recent studies have identified several molecular changes that are attributed to their development and progression of the lesions. Cyclooxygenase-2 (COX-2) is an enzyme involved in prostaglandin synthesis that modulates the formation of neoplasm. With the use of COX-2 our study supports the current neoplastic concept of KCOT highlighting its aggressive and recurrent nature and the non-neoplastic and cystic nature of DC.
Materials and Methods: In this study, the expression of COX-2 in 40 specimens (30 KCOT; 20 primary and 10 recurrent, 10 DC) has been analyzed. Sections of colon carcinoma were used as positive controls. Formalin fixed, paraffin-embedded blocks were sectioned and used for Hematoxylin-eosin (H&E) staining and incubated with an anti-COX-2 monoclonal antibody for immunohistochemical (IHC) examination.
Results: Cellular staining pattern for COX-2 was cytoplasmic, seen mainly in the epithelial lining and were semi-quantitatively evaluated as negative (-), mild (+), strong (++). In KCOT, majority of cases demonstrated intense COX-2 immunostaining whereas in the DC it showed negative to mild immunostaining. Shift in color from negative to strong immunostaining in cases of KCOT and DC was attributed to more aggressive and neoplastic nature of the lesion. Thus results of our study demonstrated that COX-2 plays a key role in the network of molecular pathways of the biologic genetic and epigenetic events that lead to the KCOT’s aggressive behaviour.
Conclusion: The study explains the difference in the pathophysiology of these two odontogenic lesions; KCOT as a neoplasm and DC as a cystic lesion.