人牙髓组织缺氧耐受机制的初步研究

The study on hypoxia preconditioning mechanism in human dental pulp

目的:研究缺氧诱导因子-1α(Hypoxia inducible factor-1α,HIF-1α)和环氧化酶-2(Cyclooxygenase-2,COX-2)在人正常牙髓和炎症牙髓中的免疫定位,探讨缺氧耐受机制在牙髓炎病程中和牙髓自身修复过程中的作用和意义。方法:通过SP法对第1组10例健康牙髓、第2组10例深龋(有过敏症状但无牙髓炎症状)患牙牙髓、第3组15例急性牙髓炎牙髓和第4组15例慢性牙髓炎牙髓进行免疫组化染色,分别对HIF-1α和COX-2进行免疫定位和半定量分析。结果:①HIF-1α在第1组健康牙髓和第2组深龋牙髓标本中,只有个别标本呈弱阳性表达,二组间无显著性差异(P>0.05),但对比其它二组标本则有显著性差异(P<0.001);第3组急性牙髓炎牙髓呈强阳性表达,第四组慢性牙髓炎牙髓亦呈阳性染色与第3组比较总体偏弱,有显著性差异(P<0.05)。②COX-2在第1组牙髓中个别标本呈弱阳性表达;第2组标本绝大多数染色呈弱阳性,与第1组比较有显著性差异(P<0.05);第3组标本染色均呈强阳性,与前两组比较有显著差异性(P值分别为P<0.001,P<0.05);第4组标本亦呈阳性染色,总体上阳性程度明显高于第1组(P<0.001),高于第2组(P<0.05),弱于第3组(P<0.05)。HIF-1α与COX-2的表达关系主要在第3组和第4组牙髓标本中体现明显,在第3组二者的变化大致呈平行关系;在第4组基本呈反向变化关系。结论:HIF-1α和COX-2在牙髓炎病程中可能发挥着重要的生理和病理作用,.在牙髓炎进程中和牙髓自身修复过程中可能存在着缺氧环境和缺氧耐受机制。

The present study was to immunolocalize and assess the quantity of hypoxia inducible factor- lalpha and cyclooxygenase-2 in human normal and inflammatory pulp. Method： Pulpal tissues were obtained from clinical-ly extracted human healthy and inflammatory teeth .The 50 samples include 10 healthy pulps, 10 deep carious cases , 15 chronic pulpitis cases and 15 acute pulpitis cases （Four groups）.The SP Method was employed to immunostain and to eluci-date the localization and distribution of HIF-1α and cox-2. Result： The immunoreactivity was demonstrated in the ceils as following： ① HIF-1α expressing ceils were scarcely found in the former two groups （healthy group and deep carious group） .They were significantly lower than the other two （P〈O.O01） ,The third group were higher than the fourth group （P〈 0.05）.②COX-2 expressing ceils were scarcely found in the first group： The second group mainly demonstrated slight to staining intensity , but higher than the first group （P〈O.O5）.The third group were the highest.The fourth group were higher than the first group （P〈O.OO1）and the second group （P〈0.05） ,but lower than the third group （P〈O.O5）.Conclusion：These findings indicate that HIF-1α and COX-2 may be two important factors in pulpal lesions and there is a significantly hypox- ia condiction in inflamed pulp. The increase of HIF-lα is a possible mechanism for hypoxia preconditioning.