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作 者:于西佼[1] 唐开亮[1] 薛兰德[1] 李纾[2]
机构地区:[1]济南市口腔医院口腔内科,济南250001 [2]山东大学口腔医院牙周科,济南250001
出 处:《中国实用口腔科杂志》2012年第1期37-40,共4页Chinese Journal of Practical Stomatology
摘 要:目的探讨吸烟对牙龈上皮棘层细胞凋亡的影响及可能的机制。方法本研究于2004年12月至2010年12月在济南市口腔医院和山东大学口腔医院进行。选取52例具有不同吸烟史、无严重系统疾病且行牙冠延长术或智齿拔除术的患者,根据吸烟史、日平均吸烟支数和总吸烟支数将患者分为轻度吸烟组(吸烟史<5年或日平均吸烟≥2~10支,且总吸烟支数约1.5万支以下)21例、重度吸烟组(吸烟史≥5年或日平均吸烟≥10支,且总吸烟支数约1.5万支以上)31例。另取无吸烟史的10例患者作为对照组。采用原位末端标记(TdT-mediated-dUTP nickendlabeling,TUNEL)法检测各组患者牙龈上皮棘层细胞的凋亡情况;Student-Newman-Keuls(SNK)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;PV免疫组化法对凋亡抑制基因Bcl-2的表达进行组织定位。结果各吸烟组患者牙龈上皮棘层细胞凋亡阳性的表达与对照组患者间差异均有统计学意义(P<0.01);轻度吸烟组和重度吸烟组患者间差异也有统计学意义(P<0.01)。Bcl-2在吸烟者牙龈上皮的基底层和棘层表达较对照组减弱。结论吸烟可能通过降低促Bcl-2的表达,促进牙龈上皮棘层细胞凋亡的发生,干扰牙龈上皮的正常代谢。Objective To explore the influence of smoking on apoptosis of gingival epithelium and its possible mecha nism. Methods Totally 52 smoking patients with crown lengthening surgery or extraction of impacted teeth were en rolled. According to smoking history(SH),averaged cigarette per day(ACD)and total smoke number(TSM),52 smokers were divided into group I(SH〈5 years or 2≤ACD〈10 and TSM〈15 thousand,n=21)and group II(SH≥5 years or 10≤ACD and 15 thousand ≤ TSM ,n=31). Another 10 non-smoking patients were chosen as control. Apopto sis 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 sig nificance were accepted at the probability level(P〈0.05). SP immunohistochemical method was used to detect the ex pression of Bcl-2 protein. Results Apoptosis in human gingival epithelium was significantly different between smokers and non-smokers(P〈0.01),and between group I and group II(P〈0.01). The expression of Bcl-2 was weaker in gingi val epithelium of smokers. Conclusion Exposure to cigarette smoke may increase apoptosis by decreasing the expres sion of Bcl-2 in gingival epithelium,hence interfere with normal metabolism.
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