Bartake Anirudha R, Sarode Sachin, Krishnapillai Rekha, Sarode Gargi, Narang Bindiya, Hallikeri Kaveri
Department of Oral Pathology and Microbiology, Sinhgad Dental College and Hospital, Pune, Maharashtra, India.
Department of Oral Pathology and Microbiology, Dr. D.Y. Patil Dental College and Hospital, Dr. D.Y. Patil Vidyapeeth, Pune, Maharashtra, India.
J Oral Maxillofac Pathol. 2024 Apr-Jun;28(2):186-191. doi: 10.4103/jomfp.jomfp_417_23. Epub 2024 Jul 11.
It is a well-recognized fact that abnormal cell proliferation plays a crucial role in the development of odontogenic lesions. p53 is a tumour-suppressor gene which assists in cell cycle regulation and p63 is a homolog of p53 responsible for ectodermal differentiation and maintenance of stratified epithelial progenitor-cell. Analysing the tissue expression of p53 and p63 in odontogenic lesions may provide us with an insight into their potential role in the development of these lesions.
The objective is to study the expression of p53 and p63 in selected odontogenic lesions using immunohistochemistry.
Formalin-fixed paraffin-embedded tissues of 15 ameloblastomas, 10 adenomatoid odontogenic tumours (AOT), 15 odontogenic keratocysts (OKCs), 10 dentigerous cysts (DCs) along with 10 cases of normal mucosa were retrieved from the departmental archives. These specimens were then subjected to immunohistochemical staining using p53 and p63 oncoproteins.
p53 and p63 immune-expression showed mainly intranuclear localization. The mean positivity of p53 in ameloblastoma (59.45%) and OKC (26.38%) was significantly higher than AOT (6.77%) and DC (4%). In contrast, there was no significant difference in the positivity of p63 in between ameloblastoma (77.55%), AOT (69.50%), OKC (76.47%), and DC (50.69%).
p53 expression can be correlated with the clinical behaviour of the odontogenic lesions and it can be used as a prognostic marker in odontogenic cysts and tumours. In contrast, p63 expression does not corelate with the biological behaviour of odontogenic lesions.
异常细胞增殖在牙源性病变的发生发展中起关键作用,这是一个公认的事实。p53是一种参与细胞周期调控的肿瘤抑制基因,而p63是p53的同源物,负责外胚层分化和分层上皮祖细胞的维持。分析p53和p63在牙源性病变中的组织表达情况,可能有助于我们深入了解它们在这些病变发生发展中的潜在作用。
采用免疫组织化学方法研究p53和p63在选定牙源性病变中的表达情况。
从科室档案中检索出15例成釉细胞瘤、10例腺样牙源性肿瘤(AOT)、15例牙源性角化囊肿(OKC)、10例含牙囊肿(DC)以及10例正常黏膜的福尔马林固定石蜡包埋组织。然后使用p53和p63癌蛋白对这些标本进行免疫组织化学染色。
p53和p63免疫表达主要定位于细胞核内。成釉细胞瘤(59.45%)和OKC(26.38%)中p53的平均阳性率显著高于AOT(6.77%)和DC(4%)。相比之下,成釉细胞瘤(77.55%)、AOT(69.50%)、OKC(76.47%)和DC(50.69%)之间p63的阳性率无显著差异。
p53表达可与牙源性病变的临床行为相关联,可作为牙源性囊肿和肿瘤的预后标志物。相比之下,p63表达与牙源性病变的生物学行为无关。