Wright H J, Chapple I L C, Cooper P, Matthews J B
Unit of Oral Biology & Pathology, Periodontal Research Group, School of Dentistry, University of Birmingham, Birmingham, UK.
Oral Dis. 2006 May;12(3):315-23. doi: 10.1111/j.1601-0825.2005.01201.x.
To investigate possible associations between platelet-derived growth factor (PDGF), PDGF receptor expression and macrophages in drug-induced and hereditary gingival overgrowth.
Tissues from patients with drug-induced gingival overgrowth (DIGO) (n = 10) and hereditary gingival fibrosis (n = 10) were studied and compared with 'control' gingiva (n = 10). Expression of PDGF and its alpha and beta receptors was investigated immunohistochemically and by RT-PCR. Macrophages were identified by immunostaining for CD68.
PDGF isoforms and receptors were detected in most cells within all specimens. There were no differences in the numbers of macrophages, or fibroblasts expressing PDGF or receptors, between groups. The level of PDGF expression by fibroblasts, determined by absorbance measurements, was similar between groups for PDGF A. Significantly lower levels of total PDGF and the receptors were detected in drug-induced overgrowth compared to those in hereditary fibrosis (P < 0.004) and control specimens (P < 0.034). All specimens expressed mRNA for PDGF A, PDGF B and alpha and beta receptors.
These data do not support a pivotal role for macrophage-derived PDGF B in the pathogenesis of DIGO. They suggest that fibroblasts in drug-induced lesions have a lowered capacity to produce, and respond to, PDGF, a property not shared by fibroblasts associated with hereditary fibrosis.
研究血小板衍生生长因子(PDGF)、PDGF受体表达与巨噬细胞在药物性和遗传性牙龈过度生长中的可能关联。
对药物性牙龈过度生长(DIGO)患者(n = 10)和遗传性牙龈纤维化患者(n = 10)的组织进行研究,并与“对照”牙龈组织(n = 10)进行比较。采用免疫组织化学和逆转录-聚合酶链反应(RT-PCR)研究PDGF及其α和β受体的表达。通过对CD68进行免疫染色鉴定巨噬细胞。
在所有标本的大多数细胞中均检测到PDGF异构体和受体。各组之间巨噬细胞数量或表达PDGF或受体的成纤维细胞数量无差异。通过吸光度测量确定的成纤维细胞PDGF表达水平,PDGF A在各组之间相似。与遗传性纤维化(P < 0.004)和对照标本(P < 0.034)相比,药物性过度生长中检测到的总PDGF和受体水平显著降低。所有标本均表达PDGF A、PDGF B以及α和β受体的mRNA。
这些数据不支持巨噬细胞衍生的PDGF B在DIGO发病机制中起关键作用。它们表明药物性病变中的成纤维细胞产生和响应PDGF的能力降低,这一特性与遗传性纤维化相关的成纤维细胞不同。