Saito K, Mori S, Tanda N, Sakamoto S
Department of Preventive Dentistry, School of Dentistry, Tohoku University, Sendai, Japan.
J Periodontol. 2000 Jan;71(1):44-9. doi: 10.1902/jop.2000.71.1.44.
Hyperplastic gingival tissues show the histopathological characteristics of thick parakeratinized squamous epithelia with acanthosis and rete pegs elongated into the lamina propria. However, the pathogenic factors that contribute to the epithelial morphogenesis of this disease are obscure and remain to be studied.
We immunohistochemically examined the expression of both c-Myc and bcl-2 oncoprotein, which can exert influence on the epithelial morphogenesis and homeostasis, in 12 hyperplastic gingival tissues induced by nifedipine and phenytoin as well as 5 control tissues using avidin-biotin-peroxidase complex methods.
Four specimens out of 5 nifedipine-induced and 5 out of 7 phenytoin-induced hyperplastic gingival tissues revealed the expression of c-Myc oncoprotein, whereas no significant immunostaining of c-Myc oncoprotein was found in 5 control tissues. The c-Myc oncoprotein-positive cells were observed to be localized in the basal and suprabasal cell layers of the hyperplastic gingival epithelia. Although all of the 12 hyperplastic gingival epithelia showed the distribution of bcl-2 oncoprotein in the basal and suprabasal layer cells, in 5 control epithelia the bcl-2 oncoprotein expression was slight and confined to the basal layer cells.
The results of our present study indicate that the synergistic overexpression of c-Myc and bcl-2 oncoprotein may be related to the pathogenesis of gingival hyperplasia induced by nifedipine and phenytoin, especially to the morphogenesis of hyperplastic epithelia.
增生性牙龈组织表现出厚的不全角化鳞状上皮的组织病理学特征，伴有棘层增厚和 rete 钉突延伸至固有层。然而，导致该疾病上皮形态发生的致病因素尚不清楚，仍有待研究。
我们使用抗生物素蛋白-生物素-过氧化物酶复合物方法，对 12 例由硝苯地平和苯妥英诱导的增生性牙龈组织以及 5 例对照组织进行免疫组织化学检查，检测对上皮形态发生和稳态有影响的 c-Myc 和 bcl-2 癌蛋白的表达。
5 例硝苯地平诱导的增生性牙龈组织中有 4 例，7 例苯妥英诱导的增生性牙龈组织中有 5 例显示 c-Myc 癌蛋白表达，而 5 例对照组织中未发现 c-Myc 癌蛋白的明显免疫染色。观察到 c-Myc 癌蛋白阳性细胞位于增生性牙龈上皮的基底层和基底上层细胞中。尽管所有 12 例增生性牙龈上皮在基底层和基底上层细胞中均显示 bcl-2 癌蛋白分布，但在 5 例对照上皮中，bcl-2 癌蛋白表达轻微且局限于基底层细胞。
我们目前的研究结果表明，c-Myc 和 bcl-2 癌蛋白的协同过度表达可能与硝苯地平和苯妥英诱导的牙龈增生的发病机制有关，尤其是与增生性上皮的形态发生有关。
