Kiuchi Misa, Yamamura Takashi, Okudera Michisato, Souksavanh Vongsa, Ishigami Tomohiko, Iwase Takashi, Warnakulasuriya Saman, Komiyama Kazuo
Department of Partial Denture Prosthodontics, Nihon University School of Dentistry, Tokyo, Japan.
J Oral Pathol Med. 2014 Jan;43(1):53-60. doi: 10.1111/jop.12072. Epub 2013 Apr 30.
The pathogenesis of denture-induced fibrous hyperplasias has not been examined in detail to explain how tissue injury results in fibrous hyperplasia of the oral mucosa.
We examined the presence of mast cells and myofibroblasts in 33 denture-induced fibrous hyperplasias (DIFH) compared with 10 healthy gingival tissues. The parameters examined included mast cell numbers, tissue distribution, degranulation, and cell subtypes using immunohistochemistry. The presence of myofibroblasts and their likely origin was also examined by double immunofluorescense staining. Furthermore, we investigated the synthesis of osteopontin and TGF-β, considered to be involved in the transformation of a fibroblast to a myofibroblast.
The results demonstrated that the mast cell numbers are significantly increased in the DIFH compared with non-disease controls. The mast cell localization in lesions was higher in the superficial areas with inflammatory cell infiltration compared with the deep fibrotic area (P < 0.01). The number of tryptase-positive mast cells was significantly higher compared with chymase-positive ones. The TGF-β- or osteopontin-positive cell infiltration into the lesion was found in high numbers. The presence of myofibroblasts was identified in 14 of 33 cases (42%), and some of these cells showed apoptosis when assessed by the TUNEL assay. On the survey of the origin of myofibroblasts, results showed αSMA and vimentin positivity indicating these transformed from fibroblasts.
These results are the first to show that mast cells and myofibroblasts can be detected in DIFH, indicating important roles of these cells in the pathogenesis of this lesion.
义齿性纤维增生的发病机制尚未得到详细研究，以解释组织损伤如何导致口腔黏膜纤维增生。
我们检查了33例义齿性纤维增生（DIFH）中肥大细胞和成肌纤维细胞的存在情况，并与10例健康牙龈组织进行比较。检查的参数包括肥大细胞数量、组织分布、脱颗粒情况以及使用免疫组织化学检测细胞亚型。还通过双重免疫荧光染色检查了成肌纤维细胞的存在及其可能的来源。此外，我们研究了骨桥蛋白和转化生长因子-β（TGF-β）的合成情况，它们被认为与成纤维细胞向肌成纤维细胞的转化有关。
结果表明，与非疾病对照组相比，DIFH中的肥大细胞数量显著增加。与深部纤维化区域相比，病变中肥大细胞在有炎性细胞浸润的浅表区域的定位更高（P < 0.01）。色氨酸酶阳性肥大细胞的数量显著高于糜蛋白酶阳性肥大细胞。发现大量TGF-β或骨桥蛋白阳性细胞浸润到病变中。在33例中的14例（42%）中鉴定出成肌纤维细胞，通过TUNEL检测评估时，其中一些细胞显示出凋亡。关于成肌纤维细胞的来源调查，结果显示α平滑肌肌动蛋白（αSMA）和波形蛋白呈阳性，表明这些细胞由成纤维细胞转化而来。
这些结果首次表明在DIFH中可检测到肥大细胞和成肌纤维细胞，表明这些细胞在该病变的发病机制中起重要作用。
