吸烟与口腔癌发生的关系

本文对２８０例口腔癌患者和２８０例非肿瘤患者进行了较详细地全面流行病学调查。清楚的看出，吸烟与患口腔癌有着密切的关系。为了人类的健康，请戒烟。     

口腔癌的细胞和分子遗传学研究进展

近年来，口腔癌的细胞遗传和分子遗传学研究进展很快。已在口腔癌组织或衍化的癌细胞株中发现染色体数目或结构异常，核仁组织区ＡｇＮＯＲｓ数量增强，ＤＮＡ相对含量改变，ｒａｓ，ｃ－ｍｙｃ和ｃ－ｅｒｂＢ等癌基因激活和表达增强，抗癌基因Ｐ５３突变等。     

口腔癌的细胞和分子遗传学研究进展

近年来,口腔癌的细胞遗传和分子遗传学研究进展很快。已在口腔癌组织或衍化的癌细胞株中发现染色体数目或结构异常,核仁组织区AgNORs数量增强,DNA相对含量改变,ras,c-myc和c-erbB等癌基因激活和表达增强,抗癌基因p53突变等。这些研究表明一些遗传变化在口腔癌的发生发展中起重要作用。     

用核酸杂交法研究人类乳头瘤病毒与口腔癌的相关性

以放射性核素￣（３２）Ｐ标记ＨＰＶ１１、ＨＰＶ１６、Ｅ＿６和ＨＰＶ１８ＤＮＡ探针，用核酸斑点杂交法，检测了部分口腔恶性肿瘤组织中的ＨＰＶ相关序列。（１）用ＨＰＶ１１探针检测１２例，其中口腔粘膜鳞状细胞癌（ｓｑｕａｍｏｕｓｃｅｌｌｃａｒｃｉｎｏｍａ，ＳＣＣ）８例，涎腺腺样囊性癌（ａｄｅｎｏｉｄｃｙｓｔｉｃｃａｒｃｉｎｏｍａ，ＡＣＣ）２例，涎腺多形性腺瘤恶变（ｍａｌｉｇｎａｎｔｐｌｅｏｍｏｒｐｈｉｃａｄｅｎｏｎｉａ，ＭＰＡ）１例，软组织胚胎性横纹肌肉瘤（ｅｍｂｒｙｏｉｄｒｈａｂｄＯｍｖｏｓａｒｃｏｍａ，ＥＲＳ）１例；结果阳性５例（５／１２），弱阳性１例，６例为阴性。（２）用ＨＰＶ１６Ｅ＿６探针检测１０例，其中ＳＣＣ６例，ＡＣＣ２例，ＭＰＡ１例，ＥＲＳ１例；结果阳性６例（６／１０），弱阳性１例，３例为阴性。（３）用ＮＰＶ１８探针检测１２例，肿瘤类型及例数同ＨＰＶ１１检测组，结果阳性３例（３／１２），阴性９例（９／１２），非肿瘤对照组共４例（唇、腭裂各２例），除１例唇裂出现了与ＨＰＶ１１和ＨＰＶ１６Ｅ＿６杂交呈弱阳性外，余均为阴性。     

口腔癌发病分子机制的研究新进展

随着分子生物学技术的发展，人们逐渐认识到口腔癌的发生是一个受多因素作用、表现为多阶段的复杂病理过程。与口腔癌发病相关的因素既包括各种理化刺激、致瘤性病毒等外源性因素，又包括机体的免疫状态、遗传易感性以及DNA损伤修复能力等内源性因素。既往许多学者从细胞增殖、细胞凋亡、细胞周期调控、生长因子及其受体等各个方面对口腔癌的发生机制进行了较为深入的研究。下面重点谈谈口腔癌细胞的起源以及发生过程中细胞遗传学研究，即口腔癌的分子发病机制研究新进展。     

下颌骨的口腔癌侵袭

发生于颊、舌、口底、牙龈等部位的口腔癌常常有波及下颌骨的可能。有关口腔癌侵袭下颌骨的病理学过程众说不一；尽管目前对下颌骨的口腔癌破坏采取了一系列有效的影像学诊断，但仍缺乏足够的特异性和准确性。因此，以手术治疗为主的口腔癌治疗中，有关下颌骨的处理问题令临床医师感到很棘手。本文对口腔癌侵袭下颌骨的病变机制、相关影响因素、诊断及治疗方面的研究进展进行了综述。     

临时冠单体释出对颊黏膜上皮细胞DNA损伤的影响

目的研究4种临时冠桥材料戴用后的单体释出对颊黏膜上皮细胞DNA损伤的影响。方法给狗的右侧后牙进行全冠牙体预备后,分别选用4种临时冠桥材料(自凝塑料、热凝塑料、DMG-TEMP树脂、松风SWIFT-TEMP树脂)进行临时冠修复。在牙备前、戴冠时及戴冠后1周、2周、1个月5个时期,收集临时冠对应区域的颊黏膜上皮细胞,应用单细胞凝胶电泳(彗星实验)检测颊黏膜上皮细胞的DNA损伤程度。结果自凝塑料组及热凝塑料组临时冠戴用后,颊黏膜上皮细胞的彗星百分率在戴冠1周>戴冠2周>戴冠1月>牙备前和戴冠时,存在显著性差异(P<0.01)。空白对照组、DMG-TEMP树脂组及松风SWIFT-TEMP树脂组的颊黏膜上皮细胞的彗星百分率在戴冠前、后均维持较低水平,无统计学差异(P>0.05)。颊黏膜上皮细胞的DNA损伤程度(以彗星百分率反应)与临时冠材料中的有机叔胺及MMA单体的释出量呈正相关性。结论自凝塑料及热凝塑料临时冠在戴冠后的早期均有残余单体释出,并导致对应区域颊黏膜上皮细胞的DNA损伤。DMG-TEMP树脂及松风SWIFT-TEMP树脂临时冠戴用后,未有显著的颊黏膜上皮细胞的DNA损伤。     

染色体不稳定的潜在机制及其与口腔癌发生的关系

在口腔癌发生发展的影响因素中，染色体不稳定表现扮演了十分重要的角色．其中包括染色体数目异常和染色体结构改变．前者由于有丝分裂检查点缺陷和中心体异常，导致不正常的染色体分离．染色体结构改变与DNA损伤检查点和DNA双链断裂点修复系统缺陷有关，引起染色体易位或断裂发生。相关研究已证明，染色体不稳定发生的分子遗传学异常改变与口腔癌的发生发展密切相关。     

大蒜对口腔癌前病变及口腔癌影响的实验研究

将６２只Ｗｉｓｔａｒ大白鼠随机分为二组，于实验组大鼠硬腭后份粘膜涂大蒜注射液，对照组涂等量蒸馏水，随后在二组相同部位涂４－硝基喹啉氧化物（４，ｎｉｔｒｏｑｕｉｎｏｌｉｎｅ－１－Ｏｘｉｄｅ，简称４ＮＱＯ）每周三次，共重复１９周。于实验第１０、１３、１９周随机分批处死动物，对其腭粘膜标本进行光镜和透射电镜观察，结果显示，对照组癌变率明显高于实验组，说明大蒜能有效抑制４ＮＱＯ诱发的口腔癌前病变和口腔癌。     

口腔癌分子生物学研究进展

随着分子生物学发展,人们可以从分子水平探讨人类肿瘤发生及进展过程。大量研究表明,口腔 癌与埋化刺激、病毒感染和遗传等因素有关,其本质是一些基因发生变异所致,其中包括H-ras,c-mycc-erbB等癌基因及其产物的异常、抗癌基因P53的突变等。应用分子生物学技术对口腔癌进行DNARNA及蛋白水平的研究将有益于揭示肿瘤发生、发展机制,对肿瘤患者预后判断及治疗有重要意义。     

Single cell gel electrophoresis on peripheral blood leukocytes of patients with oral squamous cell carcinoma

The single cell gel electrophoresis (SCGE) assay, also known as the comet assay, is a cytogenetic technique for measuring and analyzing DNA single stranded breaks (SSB) and/or alkali labile sites within individual cells. Peripheral blood leukocytes of 22 oral squamous cell carcinoma (OSCC) patients were subjected to SCGE and the DNA damage levels (SSB) were quantified with respect to clinical staging and histopathologic grading. Highly statistically significant differences in DNA damage levels were found between normal subjects and patients with OSCC of the same age group. DNA damage levels were altered in all clinical stages and histopathological grades of oral squamous cell carcinoma. The differences were generally significant between all the clinical stages of OSCC. while in histopathologic grading the results were significant only between grades 1 and 111. The results support the concept of a systemic host response in malignancy.     

口腔鳞癌组织与口腔正常黏膜组织蛋白质差异表达的初步研究

目的:筛选口腔鳞癌及正常口腔黏膜组织的差异表达蛋白质,为研究口腔鳞癌发生机制提供实验依据.方法: 收集10 例口腔鳞癌组织及正常口腔黏膜组织,进行二维电泳,选择在表达差异量较大的29 个点进行质谱和生物信息学分析,确定所分析的蛋白质类型. 结果: 口腔鳞癌及相应正常口腔黏膜组织凝胶的平均蛋白质点数分别为2 325±390和2 487±281.双向凝胶电泳图显示,口腔鳞癌及正常口腔黏膜组织的差异表达蛋白质点数为29 个,这29 个点在癌组织中均为低表达,对其进行了质谱(PMF)和生物信息学分析,鉴定了其中的3 个点,它们是:β纤维蛋白(fibrin beta)、磷酸丙糖异构酶(triosephosphate isomerase TIM)、unknown蛋白.结论: β纤维蛋白、磷酸丙糖异构酶、unknown蛋白在口腔鳞癌发生发展过程中发生了改变,其机制尚待进一步阐明.     

吸烟和非吸烟者口腔良恶性肿瘤组织中P53蛋白的表达

目的:研究吸烟与口腔肿瘤组织中P53蛋白表达的关系,探讨吸烟致口腔癌的发病机制。方法:选择22例吸烟及32例非吸烟口腔良恶性肿瘤患者的手术切除标本,良性病变切除后其边缘正常组织设为对照组。应用免疫组化技术SP法结合高温高压组织抗原修复,对P53蛋白表达进行检测,按组织病理类型进行分析。实验所得数据由SAS软件进行统计检验。结果:吸烟组P53阳性表达率为90.91%,非吸烟组为46.88%,2组阳性表达率有显著性差异(P<0.01)。恶性肿瘤的阳性表达率明显高于良性肿瘤和正常组织(P<0.01),良性肿瘤与正常组织的阳性表达率比较无差异(P>0.05),恶性肿瘤中,吸烟者P53表达的染色强度及阳性细胞数均明显高于非吸烟者。结论:吸烟对p53基因可产生损害性作用,烟草的刺激可使p53基因发生突变,这可能是香烟致癌的重要机制。本研究结果表明吸烟是诱发人体遗传物质损伤的重要诱变因素之一。     

螺旋藻对实验性口腔癌预防作用的研究

目的 研究螺旋藻对二甲基苯并蒽(DMBA)诱发的金黄地鼠口腔癌的预防作用。方法选用DMBA诱发金黄色地鼠口腔癌模型,同时用1.0g/kg、0.3g/kg螺旋藻进行预防,进行口腔肿瘤发生率、癌变率、微核细胞率、细胞增殖核抗原(PCNA)和上皮生长因子受体(EGFR)检测。结果螺旋藻高、低剂量组平均瘤负荷抑制率分别为74.2％和59.8%;癌变率、微核细胞率和PCNA标记指数与阳性对照组相比均明显降低,但对EGFR表达没有影响。结论螺旋藻对DMBA诱发的动物口腔癌有预防作用。     

Dental patient awareness of smoking effects on oral health: Comparison of smokers and non-smokers

OBJECTIVES: The negative effects of cigarette smoking on oral health are well established, yet few studies assessed patient awareness of such effects. The aim of this study was to examine differences in dental patient knowledge and awareness of the effects of smoking on oral health between smokers and non-smokers. METHODS: Adult patients from 12 dental centers in Kuwait were asked to complete a 14-point self-administered structured questionnaire on the effects of smoking on oral health in this cross-sectional survey. Significant associations between oral health knowledge, smoking status, and sociodemographic variables were examined with univariate analysis and logistic regression. RESULTS: A total of 1012 subjects participated (response rate = 84.3%). The prevalence of smoking was 29.3%. Fewer smokers than non-smokers thought that oral health and smoking are related (92.2% vs. 95.8%; P = 0.020), and that smoking affected oral cancer (52.4% vs. 66.8%; P < 0.001), periodontal health (72% vs. 78%; P = 0.040), or tooth staining (86.1% vs. 90.9%; P = 0.018). Logistic regression analysis showed smokers to be significantly less aware of the oral health effects of smoking than non-smoking patients (OR=1.51; 95% CI: 1.05-2.16; P = 0.025). CONCLUSION: Smoking dental patients are significantly less aware of the oral health effects of smoking than non-smokers. Comparative studies in other populations may be warranted to ascertain the validity of these results.     

GP—PCR检测口腔粘膜中HPV的研究

为了解口腔粘膜中人乳头瘤病毒的感染情况，诈者采用通用引物介导的聚合酶链反应（GP－PCR）技术，对临床正常口腔粘膜（NOM），口腔扁平苦藓（OLP），口腔鳞状细胞癌（OSCC）中的人乳头瘤病毒（HPV）进行检测。结果：30例口腔粘膜中，HPVDNA阳性率43．3％，其中NOM28％，OLP46．7％、（JSCC57．1％。其结果表明：临床正常和病变口腔粘膜中存在多种型别的HPVDNA．此外，GP可作为普查口腔粘膜HPV的较好方法。     

正常口腔黏膜和口腔鳞癌中人乳头瘤病毒感染率的研究进展

黏膜高危型HPV-16、HPV-18感染是宫颈癌的主要致病因素,且与口腔鳞癌的发生密切相关,但目前对口腔鳞癌中HPV的感染率和亚型的分布尚不十分清楚。作者系统查阅了目前已经发表的有关HPV在正常口腔黏膜或口腔鳞癌中感染率和亚型分布的文献资料,对正常口腔黏膜、口腔鳞癌中人乳头瘤病毒的感染率的研究进展进行了综述。     

Screening methylation of DNA repair genes in the oral mucosa of chronic smokers

ObjectiveThe aim of this study was to evaluate the epigenetic changes in the process of oral carcinogenesis by screening the methylation of repair genes in chronic smokers.DesignTwo groups were formed: Group 1: 16 smokers with consumption of 20 cigarettes/day for at least 10 years; and Group 2: 10 non-smoking. Exfoliative cytology of the tongue was performed, and the extracted DNA was treated by enzymes. The PCR Array System performed methylation screening to evaluate 22 DNA repair genes, and the results were validated by RT-qPCR for each gene with methylation levels ≥10%.ResultsHighest percentages of methylation were observed for MLH3 and XRCC1 genes (11–20% methylation) and in one case for MRE11A and PMS2 (>50% methylation). Statistical analysis showed significant differences in the expression of the genes MRE11A (p = 0.0002), PMS2(p = 0.0068), XRCC1 (p = 0.0080) and MLH3 (0.0057) between the two groups.ConclusionThe effects of chronic smoking on oral mucosa led to the methylation of genes MRE11A PMS2, XRCC1 and MLH3, but resulted in a reduction of gene expression of MRE11A and PMS2, which showed ≥50% methylation. These results provide evidence that smoking cause methylation and reduced expression of repair genes.     

Immunohistochemical expression of Tenascin in embryogenesis, tumorigenesis and inflammatory oral mucosa

Objective

Tenascin is a large extracellular matrix glycoprotein that plays specific role in cell matrix interaction. This protein is mainly attracted because of its oncofetal predominance expression at epithelial–mesenchymal interaction and also been associated with inflammatory response. Thus the aim was to study the expression of Tenascin within the oral cavity in a developing tooth, normal oral mucosa, squamous cell carcinoma and inflammatory mucosa and further to compare its expression in inflammatory mucosa with that of squamous cell carcinoma.

Design

A total numbers of 92 cases were included, with 22 being all morphological stages of developing tooth, 10 cases of normal oral mucosa, 30 cases each of inflammatory gingival hyperplasia and oral squamous cell carcinoma. The intensity and pattern of expression was assessed immunohistochemically using anti-human mouse monoclonal Tenascin antibody.

Results and conclusion

Tenascin expression in developing tooth was seen mainly at epithelial–mesenchymal junctions, but temporally reduced at cap stage. In normal mucosa TN expression was restricted only at basement membrane zone. Inflammatory gingival hyperplasia intensity of expression was enhanced at the juxtraepithelial stroma and showed reticular pattern of expression. In oral squamous cell carcinoma, intensity of expression was seen in superficial front of the stroma and also around tumour islands with intraepithelial expression and predominantly showed fibrillar pattern of expression. Furthermore, Tenascin expression was noticed around neovascularization. Hence, there is a regulatory system in Tenascin expression and plays a vital role in embryogenesis, tumerogenesis and inflammation in remodelling the stroma for cell migration and also for healing.