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

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

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.

Keywords: Clinical characteristics; Immunohistochemistry; Odontogenic keratocyst; Proliferation markers.

MeSH terms

  • Adult
  • Cyclin D1*
  • Humans
  • Ki-67 Antigen
  • Neoplasm Recurrence, Local
  • Odontogenic Cysts*
  • Retrospective Studies
  • Tumor Suppressor Protein p53

Substances

  • Ki-67 Antigen
  • Tumor Suppressor Protein p53
  • Cyclin D1