Minichromosome maintenance 2 and 5 expressions are increased in the epithelium of hereditary gingival fibromatosis associated with dental abnormalities

Abstract

INTRODUCTION:Gingiva fibromatosis is a relatively rare condition characterized by diffuse enlargement of the gingiva, which is caused by expansion and accumulation of the connective tissue.OBJECTIVE:The aim of the present study was to investigate proliferative and apoptotic biomarker expression in normal gingiva and two forms of gingival fibromatosis.METHODS:Archived tissue specimens of hereditary gingival fibromatosis, gingival fibromatosis and dental abnormality syndrome and normal gingiva were subject to morphological analysis and immunohistochemical staining. The results were analyzed statistically.RESULTS:Proteins associated with proliferation were found in the nuclei of epithelial cells from the basal and suprabasal layers, whereas apoptotic proteins were detected in the cytoplasm of the upper layers of the epithelium. Increased expressions of minichromosome maintenance proteins 2 and 5 were observed in the gingival fibromatosis and dental abnormality syndrome samples. In contrast, geminin expression was higher in normal gingiva samples. No difference in the expression of apoptotic proteins was observed among the groups.CONCLUSION:Our findings support a role for augmented proliferation of epithelial cells within the overgrown tissues associated with gingival fibromatosis or dental abnormality syndrome. However, our data suggest that different biological mechanisms may account for the pathogenesis of different types of gingival fibromatosis.

Possible pharmacotherapy for nifedipine‐induced gingival overgrowth: 18α‐glycyrrhetinic acid inhibits human gingival fibroblast growth

“…We have also previously reported that the pathogenesis of gingival overgrowth involves the inhibition of apoptosis mediated by the down‐regulation of Bax, caspases (3, 8 and 9), p53 and cytochrome c and the overexpression of Bcl‐2 (Takeuchi et al, ). Increased expression levels of minichromosome maintenance (MCM) protein subunits 2 and 5 have been found in cases of gingival fibromatosis and are associated with dental abnormalities (Martelli‐Júnior et al, ). In this study, we investigated the effects of 18α‐GA on the expression of cyclins (A, D1 and E), CDKs (2, 4 and 6), Rb, pRb (ser 780 and ser 807/811 ), p27 Kip1 , Bcl‐xL, Bcl‐2, cytochrome c (total and cytosolic), and p53 and the activities of caspase‐2, caspase‐3, caspase‐8 and caspase‐9.…”

Immunoexpression of α2-integrin and Hsp47 in hereditary gingival fibromatosis and gingival fibromatosis-associated dental abnormalities

“…This heterogeneity can be illustrated by several examples, such as the study of Sullivan et al (20), in which genetic sequencing uncovered a mutation in the gene responsible for amelogenesis imperfecta FAM20A associated with GF. Another example is the increased minichromosome maintenance 2 and 5 expression in the epithelium of hereditary gingival fibromatosis associated with dental abnormalities compared with non-syndromic forms of HGF (21). Studies have addressed the use of Hsp47 as a biomarker in cancer (22) and fibrotic diseases (23,24), given the intimate relationship of this protein with the excessive accumulation of collagen, a feature that is present in HGF.…”

Immunoexpression of Α2-integrin and Hsp47 in hereditary gingival fibromatosis and gingival fibromatosis-associated dental abnormalities

“…This heterogeneity can be illustrated by several examples, such as the study of Sullivan et al (20), in which genetic sequencing uncovered a mutation in the gene responsible for amelogenesis imperfecta FAM20A associated with GF. Another example is the increased minichromosome maintenance 2 and 5 expression in the epithelium of hereditary gingival fibromatosis associated with dental abnormalities compared with non-syndromic forms of HGF (21). Studies have addressed the use of Hsp47 as a biomarker in cancer (22) and fibrotic diseases (23,24), given the intimate relationship of this protein with the excessive accumulation of collagen, a feature that is present in HGF.…”