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TGF‐β isoforms and TGF‐β receptors in drug‐induced and hereditary gingival overgrowth
Author(s) -
Wright Helen J.,
Chapple Iain L. C.,
Matthews John B.
Publication year - 2001
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1034/j.1600-0714.2001.300505.x
Subject(s) - ctgf , extracellular matrix , transforming growth factor , fibromatosis , fibroblast , medicine , immunohistochemistry , receptor , transforming growth factor beta , endocrinology , growth factor , pathology , biology , cell culture , microbiology and biotechnology , genetics
Drug therapy and hereditary factors are two of the main causes of gingival overgrowth (GO). Both of these forms of GO are associated with increased extracellular matrix production by fibroblasts. Transforming growth factor beta (TGF‐β) is an important mediator of wound healing and tissue regeneration, which stimulates fibroblasts to produce extracellular matrix materials. The aim of this immunohistochemical study was to determine whether there is any altered expression of TGF‐β isoforms or its receptors in tissue from patients with drug‐induced GO (DIGO; n =10) and hereditary gingival fibromatosis ( n =10) when compared to non‐overgrowth tissue ( n =10). Compared to control tissues, significantly more fibroblasts expressed TGF‐β1 in both DIGO and hereditary gingival fibromatosis tissues ( P <0.03). Cells expressing TGF‐β2 were present at control levels in DIGO but were significantly reduced in hereditary gingival fibromatosis ( P <0.02). By contrast, the number of TGF‐β3‐positive cells was the same in overgrowth tissues and controls. However, because of differences in total fibroblast densities between groups, there was a proportional increase in TGF‐β3 as well as TGF‐β1 expressing cells within both overgrowth populations ( P <0.0001). Furthermore, representation of the TGF‐β2‐positive phenotype was reduced in hereditary gingival fibromatosis ( P <0.01) but increased in DIGO ( P <0.005) compared to controls. Absorbance measurements of the positive cell populations showed that the level of expression was significantly higher for TGF‐β1 in hereditary gingival fibromatosis ( P <0.002) and significantly lower for TGF‐β3 in DIGO ( P <0.03). No significant differences in the numbers of TGF‐βRI‐ or RII‐positive cells were detected between overgrowth tissues and controls. However, there were increases in the proportion of receptor‐positive cells in the total cell population analysed in overgrowth tissues ( P <0.0001). These results indicate qualitative and quantitative differences in TGF‐β isoform and receptor expression by fibroblasts in gingival overgrowth that may contribute to disease pathogenesis.