ABSTRACT
OBJECTIVE: To ascertain histology changes of hereditary gingival fibromatosis (HGF) and the location of HGF gene. METHODS: A pedigree analyses of HGF; and the ultrastructure of gingival overgrowth tissue was observed with electron microscopy. The overgrowth of the HGF gene was defined with microsatellite markers. RESULTS: The connective tissue of HGF consisted of coarse collagen bundles and several kinds of cells arranged abnormally, such as: epithelial cells, smooth muscle cells and so on; the HGF locus had been mapped to chromosome 5q13-q22. CONCLUSIONS: The gingival pathologic changes resemble "hamartoma"; the findings has implications for identification of the underlying genetic basis of HGF.
Subject(s)
Fibromatosis, Gingival/pathology , Child , Chromosome Mapping , Chromosomes, Human, Pair 5/genetics , Family Health , Female , Fibromatosis, Gingival/genetics , Fibromatosis, Gingival/ultrastructure , Genetic Predisposition to Disease/genetics , Gingiva/metabolism , Gingiva/pathology , Gingiva/ultrastructure , Humans , Male , Microsatellite Repeats , Microscopy, Electron , PedigreeABSTRACT
Gingival fibromatosis is a rare disease characterized by enlargement of the gingiva. The purpose of this study was to analyze a case of idiopathic gingival fibromatosis, using histochemical and immunohistochemical staining and transmission electron microscopy. The patient was a 39-year-old Japanese man, in whom the gingiva was enlarged throughout the entire mandible and maxilla. Specimens of gingival fibromatosis exhibited epithelial hyperplasia and increased amounts of collagen fiber bundles in the connective tissue light-microscopically. Well-developed collagen bundles were strongly stained with Azan and Masson trichrome staining. Immunohistochemically, the gingival connective tissue was specifically stained by type I collagen and vimentin antibodies. Ultrastructurally, the lesion consisted of fibroblasts and mature collagen fibers running in all directions. No myofibroblasts were detected histochemically, immunohistochemically, or ultrastructurally. These findings suggested that this disease may be the result of an increase in collagen synthesis by the fibroblasts and/or that it may be associated with one of the findings of histologic heterogeneity.
