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80 例牙源性角化囊肿的临床特征及 p53、Ki-67 和 cyclin D1 的免疫组化分析。

Clinical characteristics and immunohistochemical analysis of p53, Ki-67 and cyclin D1 in 80 odontogenic keratocysts.

机构信息

Charité-Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, Department of Oral and Maxillofacial Surgery, 13353, Berlin, Germany.

Department of Oral and Maxillofacial Plastic Surgery, Martin-Luther-University Halle-Wittenberg, 06120 Halle (Saale), Germany.

出版信息

J Stomatol Oral Maxillofac Surg. 2018 Nov;119(5):359-364. doi: 10.1016/j.jormas.2018.03.002. Epub 2018 Mar 9.

DOI:10.1016/j.jormas.2018.03.002
PMID:29530737
Abstract

OBJECTIVE

The aim of this study was to evaluate clinical parameters and expression patterns of Ki-67, cyclin D1 and p53 in odontogenic keratocysts.

MATERIAL AND METHODS

In this study, fifty-three patients with 80 odontogenic keratocysts were included. The medical records of these patients were reviewed retrospectively. To elucidate the molecular pathogenesis of the disease, the expression of p53, Ki-67 and cyclin D1 was analyzed using immunohistochemistry.

RESULTS

A total of 53 patients (mean age 38 years) with a median follow-up of 4.2 years (ranging from 4 days to 14.4 years) were evaluated. The rates of recurrence and post-operative complications varied depending on the surgical approach: cystectomy and peripheral ostectomy led to manageable low rates of complications and recurrence frequency. Immunohistochemical evaluation revealed that all lesions were positive for Ki-67 and cyclin D1 expression. The expression of Ki-67 was associated with the degree of inflammation. Cyclin D1 was expressed significantly higher in syndrome-associated keratocystic lesions. In contrast to non-syndromal lesions, all syndromal lesions expressed p53.

CONCLUSION

This investigation demonstrates that the pathogenesis of syndromal keratocysts appears to differ from sporadic odontogenic keratocysts. Additionally, the primary and recurrent non-syndromal keratocysts have a similar etiology, as no differences in the expression patterns of Ki-67, p53 and cyclin D1 were observed.

摘要

目的

本研究旨在评估牙源性角化囊肿的临床参数和 Ki-67、cyclin D1 和 p53 的表达模式。

材料与方法

本研究共纳入 53 例 80 个牙源性角化囊肿患者。回顾性分析这些患者的病历。为了阐明疾病的分子发病机制,使用免疫组织化学分析了 p53、Ki-67 和 cyclin D1 的表达。

结果

共评估了 53 例患者(平均年龄 38 岁),中位随访时间为 4.2 年(范围为 4 天至 14.4 年)。手术方法的不同导致复发率和术后并发症的发生率也不同:囊切除术和周围骨切除术导致并发症和复发频率较低。免疫组织化学评估显示所有病变 Ki-67 和 cyclin D1 的表达均为阳性。Ki-67 的表达与炎症程度有关。综合征相关角化囊肿病变中 cyclin D1 的表达明显更高。与非综合征性病变相比,所有综合征性病变均表达 p53。

结论

本研究表明,综合征性角化囊肿的发病机制似乎与散发性牙源性角化囊肿不同。此外,原发性和复发性非综合征性角化囊肿具有相似的病因,因为 Ki-67、p53 和 cyclin D1 的表达模式没有差异。

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