Comparison of immunohistochemical expression of CD10 in keratocystic odontogenic tumor and ameloblastoma.

Dent Res J (Isfahan)

Torabinejad Dental Research Center and Department of Oral and Maxillofacial Pathology, School of Dentistry, Isfahan University of Medical Sciences, Isfahan, Iran.

Published: April 2016

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Article Abstract

Background: Odontogenic keratocyst (OKC), also called keratocystic odontogenic tumor (KCOT), is a developmental lesion which should be carefully monitored and it exhibits development mechanisms and biologic behaviors different from those of other more common lesions such as dentigerous and radicular cysts. CD10 antigen is a cell surface metalloendopeptidase, which inactivates various peptides that are physiologically active. Studies have shown that increase in the expression of CD10 in the stromal cells helps the progression of the tumor. Ameloblastoma (AB) is a local invasive tumor and given the role of supporting connective tissue stroma in the aggression and progression. The aim of the present study was to comparatively evaluate the expression of CD10 in the connective tissue stroma of AB and OKC as a KCOT.

Materials And Methods: In this retrospective, cross-sectional study, 14 paraffin blocks of KCOT and 9 of AB (7 multicystic and 2 unicystic) were evaluated with CD10 immunohistochemical expression in the connective tissue stroma of AB and the connective tissue wall of KCOT. The data were analyzed with Fisher's exact test (P < 0.05).

Results: In 8 samples of 9 AB and in 13 samples of 14 KOT lesions, expression of CD10 was shown. Fisher's exact test did not reveal any significant differences between these two lesions in the expression of CD10 (P = 0.64).

Conclusion: The results of this study propose that high expression rate of CD10 might be one of the reasons for the aggressive behavior of AB and high recurrence rate of OKC and reinforce the classification of OKC as an odontogenic tumor.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4810907PMC
http://dx.doi.org/10.4103/1735-3327.178195DOI Listing

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