Comparative immunohistochemical study of Bcl-X in ameloblastoma, keratocystic odontogenic tumor and adenomatoid odontogenic tumor

Abstract

Objectives:Since its recognition as a physiologic process associated with tumor, among molecular mechanisms involved in tumor progression, defects in regulation of apoptosis have generated an accelerating volume of research that has sought to elucidate the role of programed cell death in pathogenesis and treatment of various tumors. Therefore, this study was performed to understand better the diverse biological profile of epithelial odontogenic tumors with the help of immunohistochemical expression of Bcl-X protein.Materials and Methods:We studied Bcl-X protein expression in 45 cases of epithelial odontogenic tumors which included 15 cases each of ameloblastomas, keratocystic odontogenic tumor (KCOT) and adenomatoid odontogenic tumor (AOT) and correlated the expression with their growth pattern.Results:Cytoplasmic staining of Bcl-X revealed overexpression in ameloblastoma when compared to KCOT and AOT. Percentage of positive cells showed a statistically significant difference, P = 0.007 between ameloblastoma and KCOT, whereas P < 0.001 between ameloblastoma and AOT. However, no significance was observed between KCOT and AOT (P = 0.132).Conclusion:The present study supports the fact that epithelial odontogenic tumors show diverse growth profiles. An increased Bcl-X expression was seen in ameloblastoma compared to KCOT and least expression in case of AOT which could be indicative of more aggressive biological behavior and increased cell survival activity of ameloblastoma than KCOT and AOT. This signifies the diagnostic relevance of this biomarker and also could be a possible regulator of the proliferative compartment by contributing in tumor progression and cytodifferentiation of epithelial odontogenic tumors.

BDNF/TrkB/Akt Signaling Pathway Epithelial Odontogenic Tumors and Keratocyst: An Immunohistochemical Study Comparative With Dental Germs

“…In Am, in contrast, BDNF in epithelial cells was significantly higher compared with stromal BDNF, indicating a predominance in autocrine mechanisms of TrkB activation. Previous studies have demonstrated the presence of epithelial expression of other growth factors in Am, such as TGF-β17 and fibroblast growth factor-8 23. Combined, these results suggest that epithelial cells of OL might acquire the capacity to produce and secrete growth factors, triggering autocrine stimulus.…”

“…The final IRS value represents a product of points and ranged from 0 to 12. The IRS system was initially proposed by Remmele and Stegner15 and has been previously used for the study of OLs 16,17…”

“…The IRS system was initially proposed by Remmele and Stegner 15 and has been previously used for the study of OLs. 16,17 The arrangement of positive expression within cystic and tumoral epithelium was also evaluated using previously described expression patterns: (1) prostromal pattern-positivity of peripheral/basal cells and negativity of central/suprabasal cells; (2) antistromal patternnegativity of peripheral/basal cells and positivity of central/suprabasal cells; (3) full pattern-positivity of both peripheral/basal and central/suprabasal cells. 18 Periphery cells were considered as the most external layer of cells in close contact with the ectomesenchymal tissue (basal cells).…”

Immunohistochemical Analysis of Dentigerous Cysts & Odontogenic Keratocysts Associated with Impacted Third Molars: A Systematic Review

“…The treatment landscape for odontogenic lesions, such as odontogenic keratocyst (OKC), adenomatoid odontogenic tumor (AOT), and ameloblastoma (AB), is evolving rapidly due to new discoveries in molecular markers and therapeutic targets like survivin, EGFR, BMP4, FOXN1, and paxillin [127][128][129][130]. These markers are shifting treatment paradigms from traditional surgical interventions to innovative, targeted therapies that address the underlying molecular and genetic drivers of these lesions.…”

“…For instance, the roles of molecules such as survivin and EGFR suggest novel approaches for managing lesion growth. Studies have demonstrated that survivin expression is highest in ameloblastoma, followed by OKC, AOT, and reduced enamel epithelium, suggesting that survivin plays a role in inhibiting apoptosis and influencing the biological behavior of these lesions [127]. Similarly, EGFR and survivin have been shown to play crucial roles in the pathogenesis of ameloblastoma, OKC, and calcifying odontogenic cyst, highlighting the potential of targeting these markers in therapeutic approaches [128].…”