遗传性牙龈纤维瘤发病机制的实验研究

The study of pathogenic mechanism in hereditary gingival fibromatosis

目的研究B细胞特异的莫洛尼白血病病毒插入位点1基因(Bmi1)在遗传性牙龈纤维瘤(HGF)发病中的作用。方法比较22例HGF(HGF组)和15例正常牙龈组织(对照组)的HE形态、Bmi1、增殖细胞核抗原(PCNA)和caspase-3蛋白及mRNA表达的差异。结果与对照组比,HGF组牙龈上皮层增厚,上皮钉突明显伸长,结缔组织体积增大,充满粗大的胶原纤维和成纤维细胞,血管较少,可见轻度炎症增生,牙龈组织的Bmi1及Bmi1 mRNA表达明显增高(P <0.05),caspase-3及caspase-3 mRNA表达明显降低(P <0.05)。两组PCNA及PCNA mRNA表达差异无统计学意义(P> 0.05)。结论 Bmi1基因高表达与HGF发病有一定的关系,可能与Bmi1抑制促凋亡基因caspase-3及mRNA表达相关。

Objective To determine the role of B cell specific moloney leukemia virus insert site 1 (Bmi1)in hereditary gingival fibromatosis(HGF). Methods The HE staining was used to analyze the HGF and normal groups. The protein and mRNA of the Bmi1,PCNA and caspase-3 in 2 groups were detected by immunohis-tochemistry and PCR,respectively. Results In HGF group,the gingival epithelial was incrassation,epithelial spikes was elongation,connective tissue was rich in fibroblast and collagen fibers,aless blood vessels and mild inflammatory hyperplasia. Bmi1 expression was higher(P < 0.05)and caspase-3 expression was lower(P < 0.05) in HGF group than in normal group. There was no difference of PCNA expression in the 2 groups(P > 0.05). Conclusion The Bmi1 might have a role in the pathogenesis of HGF by decreasing caspase-3 and caspase-3 mRNA.