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药物性和遗传性牙龈过度增生中的转化生长因子-β亚型及转化生长因子-β受体

TGF-beta isoforms and TGF-beta receptors in drug-induced and hereditary gingival overgrowth.

作者信息

Wright H J, Chapple I L, Matthews J B

机构信息

Unit of Oral Biology & Pathology, School of Dentistry, University of Birmingham, UK.

出版信息

J Oral Pathol Med. 2001 May;30(5):281-9. doi: 10.1034/j.1600-0714.2001.300505.x.

DOI:10.1034/j.1600-0714.2001.300505.x
PMID:11334464
Abstract

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-beta) 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-beta 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-beta1 in both DIGO and hereditary gingival fibromatosis tissues (P<0.03). Cells expressing TGF-beta2 were present at control levels in DIGO but were significantly reduced in hereditary gingival fibromatosis (P<0.02). By contrast, the number of TGF-beta3-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-beta3 as well as TGF-beta1 expressing cells within both overgrowth populations (P<0.0001). Furthermore, representation of the TGF-beta2-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-beta1 in hereditary gingival fibromatosis (P<0.002) and significantly lower for TGF-beta3 in DIGO (P<0.03). No significant differences in the numbers of TGF-betaRI- 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-beta isoform and receptor expression by fibroblasts in gingival overgrowth that may contribute to disease pathogenesis.

摘要

药物治疗和遗传因素是牙龈过度生长(GO)的两个主要原因。这两种形式的GO都与成纤维细胞增加细胞外基质的产生有关。转化生长因子β(TGF-β)是伤口愈合和组织再生的重要介质,它刺激成纤维细胞产生细胞外基质材料。这项免疫组织化学研究的目的是确定与非过度生长组织(n = 10)相比,药物性牙龈过度生长(DIGO;n = 10)和遗传性牙龈纤维瘤病(n = 10)患者组织中TGF-β亚型或其受体的表达是否有任何改变。与对照组织相比,DIGO和遗传性牙龈纤维瘤病组织中表达TGF-β1的成纤维细胞明显更多(P < 0.03)。表达TGF-β2的细胞在DIGO中处于对照水平,但在遗传性牙龈纤维瘤病中明显减少(P < 0.02)。相比之下,TGF-β3阳性细胞的数量在过度生长组织和对照中相同。然而,由于各组间成纤维细胞总密度的差异,两个过度生长群体中表达TGF-β3以及TGF-β1的细胞均成比例增加(P < 0.0001)。此外,与对照相比,遗传性牙龈纤维瘤病中TGF-β2阳性表型的比例降低(P < 0.01),而在DIGO中增加(P < 0.005)。对阳性细胞群体的吸光度测量表明,遗传性牙龈纤维瘤病中TGF-β1的表达水平明显更高(P < 0.002),而DIGO中TGF-β3的表达水平明显更低(P < 0.03)。在过度生长组织和对照之间未检测到TGF-βRI或RII阳性细胞数量的显著差异。然而,在分析的过度生长组织总细胞群体中,受体阳性细胞的比例有所增加(P < 0.0001)。这些结果表明牙龈过度生长中成纤维细胞TGF-β亚型和受体表达在质量和数量上存在差异,这可能有助于疾病的发病机制。

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