Abstract

The odontogenic keratocyst (OKC) is a controversial lesion that was reclassified as a tumor with the name “keratocystic odontogenic tumor” in 2005. The reclassification was revoked recently in 2017, with a conclusion on the need for further studies on the subject. In this study, the expressions of an important regulatory protein (maspin), an important integral membrane proteoglycan (syndecan-1), and a universal proliferation marker (Ki-67) in the epithelium of the OKC were investigated in comparison with the dentigerous cyst (DC) and ameloblastoma (AB). Twenty-six OKCs, eleven DCs, and ten conventional ABs were immunohistochemically stained for maspin, syndecan-1, and Ki-67. ImageJ was used to analyze the positivity of maspin and syndecan-1. The Ki-67 score was calculated as the percentage of positive nuclei in 5 high power fields. Analysis of variance (ANOVA) test and Student t-test were used as appropriate. Lower expressions of maspin were noted in OKC and DC compared to those in AB, and lower expressions of syndecan-1 were noted in OKC and AB compared to those in DC. The differences, however, did not reach statistical significance (ANOVA and t-test: P > 0.05). The Ki-67 score was significantly higher in OKC than in DC (t-test: P < 0.05), and not significantly different from AB (t-test: P > 0.05). In conclusion, expressions of maspin and syndecan-1 are not strongly representative of differences in behavior between OKC, AB, and DC. However, the expression of Ki-67 indicates comparable proliferative activities of OKC and AB, which are higher than that of DC. Further investigation on the biologic behavior of OKC is still recommended to arrive at more specific conclusions regarding its classification.

Highlights

  • Odontogenic keratocysts (OKCs) comprise a significant proportion of odontogenic cysts. ey are known to show locally aggressive behavior with a tendency to recur following excision

  • Occasional plasma cells used as an internal positive control for syndecan-1 showed strong membranous expression

  • Discussion e WHO reclassification of the OKC in 2005 as a benign odontogenic tumor rather than an odontogenic cyst was a result of its locally aggressive behavior and relatively high recurrence rate, in addition to the studies on genetic and molecular mechanisms involved in its development and progression [5,6,7,8,9,10,11, 20,21,22, 26,27,28,29,30,31]. e debate has culminated recently in the revocation of the reclassification in the 2017 WHO classification of diseases [4]. e consensus panel considered evidence of a neoplastic nature of OKC to be currently lacking or insufficient and concluded that further research on the subject is needed [35, 36]

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Summary

Introduction

Odontogenic keratocysts (OKCs) comprise a significant proportion of odontogenic cysts. ey are known to show locally aggressive behavior with a tendency to recur following excision. E OKC was reclassified as a tumor with the name “keratocystic odontogenic tumor” in 2005 [2]. Higher proliferative activity and more significant or different P53 expression in the OKC compared to other odontogenic cysts have been reported [5,6,7,8,9, 12,13,14, 16,17,18,19,20,21,22, 24]. Mutations or abnormalities of the PTCH, P53, P16, International Journal of Dentistry and MCC tumor suppressor genes have been reported to be associated with the etiology of sporadic and syndromic OKCs [26,27,28,29,30,31,32,33]

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