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作 者:薛兰德[1] 徐冬梅[1] 路吉坤 于西佼[1] 李纾[2]
机构地区:[1]济南市口腔医院,250001 [2]山东大学口腔医学院
出 处:《中国临床实用医学》2010年第11期38-40,共3页China Clinical Practical Medicine
摘 要:目的对比吸烟者和未吸烟者的牙龈上皮细胞凋亡的情况不同,评价吸烟对牙龈上皮细胞凋亡的影响并探讨其可能机制。方法选择21例行冠延长术的男性患者,年龄为30~45岁,无相关系统疾病和明显的牙龈疾病。无吸烟史10人作对照,切取的牙龈上皮经新鲜配置4%多聚甲醛固定、脱水、石蜡包埋,TUNEL(TdT.mediated—dUTP nick end labeling,TUNEL)法原位细胞凋亡检测牙龈上皮的细胞凋亡情况。Newman—Keuls法计算各吸烟组与对照组及各吸烟组之间的差异,取α=0.05水准。SP免疫组化法对凋亡抑制基因Bcl-2的表达进行组织定位。结果各吸烟组与对照组都存在显著差异(P〈0.01);轻度吸烟组和重度吸烟组间也存在显著性差异(P〈0.01)。Bcl-2在吸烟者的牙龈上皮的表达较对照组减弱。结论吸烟促进牙龈上皮细胞凋亡的发生,干扰牙龈上皮的正常代谢。Objective To compare the different apoptosis in gingival epithelium between smokers and non-smokers. Methods 21 healthy male patients of crown lengthening surgery without systemic or distinct gingival diseases, the age ranged from 30 to 45years old. Ten normal gingival epithelium were chosen as control. Apoptosis was identified by the terminal deoxy-transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL) method. Differences among the three groups were analyzed using Student-Newman-Keuls (SNK). The criteria for statistical significance were accepted at the probability level P 〈 0. 05. SP immunohistochemical method was used to detect the expression of Bcl-2 protein. Results Apoptosis in human gingival epithelium were significant difference between smokers and non-smokers (P 〈 0. 01 ). The expression of Bcl-2 was weaker in gingival epithelium of smokers. Conclusion We conclude that exposure to cigarette smoke can increase apoptosis in gingival epithelium and interfere with normal metabolism.
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