Apoptosis and cell cycle aberrations in epithelial odontogenic lesions: An evidence by the expression of p53, Bcl-2 and Bax

Abstract

BackgroundAmeloblastoma (AMB), odontogenic keratocyst (OKC) and adenomatoid odontogenic tumor (AOT) are epithelial odontogenic lesions with diverse biologic profiles. Defects in regulation of apoptosis and cell cycle may be involved in the development and progression of those lesions, therefore we aimed to investigate the expression of Bcl-2, Bax and p53 to better understand the possible role of these proteins in AMBs, OKCs and AOTs.Material and MethodsThe studied sample consisted of 20 AMBs, 20 OKCs and 20 AOTs. Immunohistochemistry technique was performed for the antibodies p53, Bcl-2 and Bax. Immunoreactivity was observed in the epithelial component and positive cells were counted in five fields (100x magnification). Statistical analysis was performed with Kruskal-Wallis and Spearman tests (p<0.05).ResultsAll lesions exhibited staining for the three studied proteins. There was no statistically significant associations between the expression of proteins and the lesions, however we identified a positive correlation between the expression of p53 and Bcl-2 (r = 0.200) and a negative correlation between p53 and Bax expressions (r = -0.100). In addition, p53 and Bax were similarly expressed between AMBs and OKCs. Bcl-2 was similarly expressed in AMBs and AOTs.ConclusionsApoptosis regulatory proteins, as well as cell cycle proteins, are differently expressed in epithelial odontogenic lesions and their expression is possibly related to the biological behavior of AMB, OKC and AOT. Key words:Odontogenic tumors, apoptosis, apoptosis regulatory proteins, p53 tumor suppressor protein, immunohistochemistry.

A Rare Case of an Aggressive Clear Cell Variant of Calcifying Epithelial Odontogenic Tumor in the Posterior Maxilla

“…In a study conducted by Carvalhais and coworkers, 36 positivity for p53 was not observed in 51 cases of odontogenic cysts and tumors assessed, and even though a relationship between p53 positivity and a more aggressive behavior had been suggested, their cases of clear cell odontogenic lesions were negative for p53. In contrast, Tenório et al 37 observed that p53 protein was expressed in all cases of ameloblastomas, OKCs, and AOTs. The expression of this tumor suppression infers that there is a greater dysregulation in cell cycle control in lesions with a more aggressive biological behavior, such as ameloblastoma and OKC, reinforcing the possible neoplastic phenotype of some odontogenic lesions.…”

“…The expression of this tumor suppression infers that there is a greater dysregulation in cell cycle control in lesions with a more aggressive biological behavior, such as ameloblastoma and OKC, reinforcing the possible neoplastic phenotype of some odontogenic lesions. 37 In minor salivary gland intraductal MEC, no p53 overexpression was demonstrated. 38 The p63 was also positive in the case presented, in accordance with other cases of CEOTs reported elsewhere.…”

The role of oxidative stress-mediated apoptosis in the pathogenesis of uric acid nephropathy

“…p53 can control the occurrence of apoptotic gene expression. On the one hand, p53 promotes the apoptotic protein expression, such as Bad, Bax, Bak, and so forth, and on the other hand, it reduces the expression of apoptotic protein [14], such as the Bcl-2, the Bcl-xl. The relative ratio of Bax/Bcl-2 determines the occurrence of apoptosis [15].…”

Decompression induces inflammation but do not modify cell proliferation and apoptosis in odontogenic keratocyst

“…In contrast, Tenorio et al . ( 23 ) and Rangiani et al . ( 25 ) reported in OKCs a low expression of Bcl-2 extended to the basal cell layer of the epithelial lining, while Bax showed a diffuse weak labeling.…”