Document Type

Journal Article

Date of this Version

9-2007

Publication Source

Journal of Dental Research

Volume

86

Issue

9

Start Page

888

Last Page

892

DOI

10.1177/154405910708600916

Abstract

Variations in the balance between cell proliferation and apoptosis could contribute to the etiology of gingival overgrowth. The aim of this study was to test the hypothesis that, in fibrotic gingival lesions, fibroblast proliferation is stimulated and apoptosis is decreased. Apoptotic index, caspase 3 expression, the proliferative index, FOXO1 expression, and histological inflammation were measured in situ. Analysis of data showed that apoptosis decreased in all forms of gingival overgrowth examined (p < 0.05), and inflammation caused a small but significant increase compared with non-inflamed tissues (p < 0.05). The greatest decrease of apoptosis occurred in the most fibrotic tissues. Cell proliferation was elevated in all forms of gingival overgrowth tested, independent of inflammation (p < 0.05). To identify potential mechanisms of transcriptional regulation of apoptosis, we assessed FOXO1 and caspase 3 expression levels and found them to correlate well with diminished apoptosis. Analysis of data suggests that increased fibroblast proliferation and a simultaneous decrease in apoptosis contribute to gingival overgrowth.

Comments

At the time of publication, author Dana Graves was affiliated with the Boston University School of Dental Medicine. Currently, he is a faculty member in the Penn Dental School at the University of Pennsylvania.

Keywords

gingival overgrowth, fibrosis, fibroblast, apoptosis, FOXO1

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Date Posted: 02 April 2015

This document has been peer reviewed.