HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Figures Only Full Text Full Text (PDF) Services Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Häkkinen, L. Articles by Csiszar, A. Search for Related Content PubMed PubMed Citation Articles by Häkkinen, L. Articles by Csiszar, A.

Hereditary Gingival Fibromatosis: Characteristics and Novel Putative Pathogenic Mechanisms

University of British Columbia, Faculty of Dentistry, Department of Oral Biological and Medical Sciences, Laboratory of Periodontal Biology, 2199 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3;

^* corresponding author, lhakkine{at}interchange.ubc.ca

Hereditary gingival fibromatosis (HGF) is a rare condition that can occur as an isolated disease or as part of a syndrome or chromosomal abnormality. In severe cases, the gingival enlargement may cover the crowns of teeth and cause severe functional and esthetic concerns. Histological and cell culture studies have uncovered some of the molecular and cellular changes associated with HGF. However, the pathogenesis of the disease is still largely unknown. Recent studies about the genetic characteristics of HGF have provided novel clues about the potential pathogenic mechanisms. In particular, mutation in the son-of-sevenless (SOS-1) gene has been associated with one form of the disease. However, HGF displays genetic heterogeneity, and mutations in other genes are also likely involved. This review outlines the current knowledge about the histological, cellular, and genetic characteristics of HGF. In addition, the potential role of the SOS-1 molecule and related novel intracellular signaling pathways in the pathogenesis of HGF will be discussed.

KEY WORDS: gingiva • overgrowth • hereditary • pathogenesis • SOS-1