ILK与NOS在SACC中的表达及意义

目的:通过观察整合素连接激酶(Integrin-linked kinase,ILK)与一氧化氮合酶(nitric oxide synthase,NOS)在涎腺腺样囊性癌(salivary adenoid cystic carcinoma,SACC)中的定位及表达,探讨ILK与NOS在SACC中的作用。方法:对2006-2012年吉林医药学院附属医院病理科30例SACC存档蜡块,和25例非肿瘤疾病的正常涎腺组织(对照组)行免疫组化分析,观察ILK与NOS在SACC中的表达分布情况。利用SPSS13.0统计软件分析ILK与NOS的差异性及相关性。结果:在SACC中,ILK阳性率为76.67%,e NOS阳性率为63.33%,i NOS阳性率为80%。ILK实验组与对照组比较,P<0.05;e NOS实验组与对照组比较,P>0.05;i NOS实验组与对照组比较,P<0.05。ILK与e NOS在SACC中的表达不存在相关性;ILK与i NOS在SACC中的表达存在正相关,r=0.512。结论:ILK与i NOS在SACC中的表达存在正性相关,可能通过i NOS信号转导途径启动VEGF的表达,促进肿瘤早期的血管发生和形成。     

涎腺腺样囊性癌中NOS和VEGF的表达与血管生成及临床病理因素的关系

目的：研究血管内皮生长因子（vascular endothelial growth factor,VEGF）、诱导型一氧化氮合酶（induciblenitric oxide synthase,iNOS）和内皮型一氧化氮合酶（endothelial nitric oxide synthase,eNOS）在涎腺腺样囊性癌（salivaryadenoid cystic carcinoma,SACC）中表达的相关性;探讨三者与SACC血管生成和临床病理特征的关系;研究一氧化氮（nitric oxide,NO）和VEGF的相互作用及NO在VEGF促肿瘤生长中的作用机制。方法：应用免疫组织化学方法检测32例SACC手术切除标本VEGF、iNOS和eNOS的表达,CD34血管内皮细胞特异性染色计数肿瘤微血管密度（microvesseldensity,MVD）。结果：①20例SACC组织表达VEGF,22例表达iNOS,25例表达eNOS;②VEGF与iNOS的表达正相关,与eNOS的表达无相关;③VEGF、iNOS的表达与涎腺腺样囊性癌MVD呈正相关,eNOS的表达与涎腺腺样囊性癌MVD的差异无显著性意义;④VEGF的表达与SACC病理类型、淋巴结转移、肿瘤部位及临床分期密切相关;iNOS的表达与病理类型、肿瘤部位及临床分期密切相关;与淋巴结转移未见相关。eNOS表达与以上因素均无关。结论：①iNOS对VEGF的生成和发挥作用的过程有重要影响;②MVD随着VEGF和iNOS表达的增强而增加,说明两者对SACC血管生成具有促进作用.     

VEGF和NOS在涎腺腺样囊性癌中的表达及与细胞增殖的关系

目的研究涎腺腺样囊性癌(salivary adenoid eystic carcinoma,SACC)组织血管内皮生长因子(vascular endothelial growth factor,VEGF)、诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)和内皮型一氧化氮合酶(endothelial nitric oxide synthase,eNOS)的表达与癌细胞增殖的相关性。方法应用免疫组化方法检测32例SACC手术切除标本VEGF、iNOS、eNOS和增殖细胞核抗原(proliferating cell unclear angigen,PCNA)的分布及表达。结果①20例(62.5%)SACC组织表达VEGF,22例(68.75%)表达iNOS;25例(78.13%)表达eNOS;②VEGF与iNOS的表达具有明显相关性,VEGF与eNOS的表达无明显相关性;③表达VEGF的涎腺腺样囊性癌PCNA标记指数(PLI)明显高于不表达VEGF的SACC;表达iNOS的涎腺腺样囊性癌PLI明显高于不表达iNOS的SACC。表达eNOS的涎腺腺样囊性癌PLI与不表达eNOS的SACC无显著性差异(P>O.05)。结论①VEGF与iNOS的表达具有明显相关性,说明iNOS在VEGF的生成和发挥作用过程中起重要作用;②PLI随着VEGF和iNOS表达的增加而增加;说明二者对SACC细胞增殖具有促进作用。     

中期因子和微血管密度在涎腺腺样囊性癌组织中的表达

目的探讨中期因子（MK）、微血管密度（MVD）在涎腺腺样囊性癌（SACC）组织中的表达和意义,以及两者之间表达的相关性。方法 采用免疫组织化学方法（SP法）检测60例SACC组织及26例正常涎腺组织中MK、MVD的表达状况及两者之间的相关性。结果 MK在SACC组织中高表达,阳性表达率为70.0%（42/60）,正常组织中未见MK表达,二者间差异有统计学意义（P<0.05）。SACC中MVD计数为38.73±8.96,正常涎腺组织中MVD计数为11.15±3.33,二者间差异有统计学意义（P<0.05）。MK、MVD的表达与年龄、性别、分型无关（P>0.05）;与肿瘤的大小、淋巴结转移、TNM分期有关（P<0.05）。MK和MVD在SACC中的表达具有正相关性（r=0.560,P<0.05）。结论MK蛋白的表达、MVD计数的增加与SACC的发生有关,可能是SACC早期诊断指标之一。     

涎腺腺癌中NOS和VEGF的表达与血管生成及临床病理分析

目的 研究血管内皮生长因子（VEGF）、诱导型一氧化氮合酶（iNOS）和内皮型一氧化氮合酶（eNOS）在涎腺腺癌中表达的相关性；探讨三者与涎腺腺癌血管生成和临床病理特征的关系；研究一氧化氮（NO）和VEGF的相互作用及N0在VEGF促肿瘤生长中的作用机制。方法 应用免疫组织化学方法检测47例涎腺腺癌手术切除标本VEGF、iNOS和eNOS的表达，第Ⅷ因子相关抗原（FⅧRAg）血管内皮细胞特异性染色计数肿瘤微血管密度（MVD）。结果 ①30例涎腺腺癌组织表达VEGF，31例表达iNOS，33例表达eNOS；②VEGF与iNOS的表达正相关，与eNOS的表达无相关；③VEGF、iNOS的表达与涎腺腺癌MVD呈正相关，eNOS的表达与涎腺腺癌MVD的差异无显著性意义；④VEGF的表达与涎腺腺癌淋巴结转移和肿瘤分化程度正相关，与临床分期无关。iNOS表达与涎腺腺癌的分化程度及临床分期和有无淋巴结转移正相关；eNOS表达与涎腺腺癌临床分期和分化程度及有无淋巴结转移均无关。结论 ①VEGF表达与iNOS表达具有明显的相关性，iNOS对VEGF的生成和发挥作用的过程可能有一定影响；②MVD随着VEGF和iNOS表达的增强而增加，说明两者对涎腺腺癌血管生成具有促进作用。     

涎腺腺样囊性癌组织中ILK和E-cadherin的表达及意义

目的:探讨整合素连接激酶(integrin-linked kinase,ILK)和上皮型钙黏蛋白(E-cadherin)在涎腺腺样囊性癌(salivary adenoid cystic carcinoma,SACC)组织中的表达及其意义。方法:采用免疫组织化学SP法检测ILK和E-cadherin在SACC及正常涎腺组织中的表达。结果:ILK在SACC中表达,ILK的表达与SACC临床病理分型不相关(P>0.05),与TNM分期有关,在发生神经侵犯及远处转移的病例中,ILK的表达明显增加(P<0.05);与正常涎腺组织相比,E-cadherin在SACC中表达下降,差异有统计学意义(P<0.05),E-cadherin表达与不同组织病理学类型有关,且在实体型、发生神经侵犯及远处转移的病例中,E-cadherin表达下降更明显(P<0.05);ILK与E-cadherin的表达呈负相关(r=-0.768,P<0.001)。结论:SACC组织中ILK表达上调而E-cadherin表达降低,有望成为临床判断涎腺腺样囊性癌恶性程度、评估预后的潜在指标。     

整合素连接激酶和基质金属蛋白酶-9在涎腺腺样囊性癌中的表达及意义

目的: 探讨整合素连接激酶(ILK)和基质金属蛋白酶-9(MMP-9)在涎腺腺样囊性癌(SACC)中的表达及意义。方法: 选取59例SACC患者和42例非肿瘤患者正常涎腺组织,利用qRT-PCR技术检测ILK和MMP-9在SACC组织中表达。结果: SACC组织中ILK mRNA和MMP-9 mRNA相对表达量均高于对照组,差异均有统计学意义(P<0.05);ILK和MMP-9在SACC组织中表达均与组织类型、淋巴结转移、TNM分期有关(P<0.05),实体型和管状型SACC组织中ILK mRNA和MMP-9 mRNA相对表达量均高于筛状型(P<0.05);Pearson相关分析显示,SACC组织中ILK mRNA相对表达量与MMP-9 mRNA相对表达量呈正相关(r=0.586,P=0.000)。结论: ILK和MMP-9在SACC组织中呈高表达,可能共同协同参与了肿瘤细胞侵袭、转移过程。     

涎腺腺样囊性癌COX-2表达与肿瘤血管生成的研究

目的：探讨环氧化酶-2（Cycloxygenase-2,COX-2）表达与涎腺腺样囊性癌（salivary adenoid cystic carcino-ma,SACC）血管生成的关系。方法：免疫组化法检测SACC中COX-2、诱导型一氧化氮合酶（inducible nitric oxide synthase,iNOS）、血管内皮生长因子（vascular endothelial growth factor,VEGF）表达,并测定肿瘤微血管密度（microvessel density,MVD）。结果：SACC中COX-2表达与VEGF、iNOS表达密切相关（P〈0.05,P〈0.01）。SACC中COX-2表达阳性组和阴性组MVD有显著差异（P〈0.01）.结论：SACC中COX-2表达和肿瘤血管生成有关,iNOS和VEGF可能参与COX-2对肿瘤血管生成的促进作用。     

Survivin基因在人涎腺腺样囊性癌中的表达

目的：研究survivin基因在人涎腺腺样囊性癌（SACC）中的表达及其临床意义。方法：用免疫组化（S-P法）染色技术对38例SACC组织和8例癌旁正常腮腺组织标本进行survivin基因表达的检测和分析。结果：SACC组织中survivin的阳性表达率为68.4%,而癌旁正常腮腺组织无1例表达。survivin的表达与年龄、性别、部位、病理类型、肿瘤大小、临床分期、淋巴结转移无明显相关（P〉0.05）,但survivin表达阳性组术后5年生存率显著低于表达阴性组（P〈0.05）。结论：survivin基因与SACC的预后有关,其高表达提示SACC预后不良;survivin基因有望成为涎腺腺样囊性癌诊断和基因治疗的新靶点。     

酪氨酸激酶A和血管内皮生长因子受体2在涎腺腺样囊性癌侵袭转移中的作用

目的通过检测酪氨酸激酶A（TrkA）与血管内皮生长因子受体2（VEGFR2）在涎腺腺样囊性癌（SACC）的表达情况,探讨TrkA与VEGFR2在SACC侵袭转移中的作用。方法采用免疫组织化学SP法检测47例SACC患者组织病理切片中TrkA与VEGFR2的表达情况,结合临床资料统计分析,评价TrkA、VEGFR2与SACC侵袭转移特性的相关性。结果TrkA、VEGFR2在SACC组织中的阳性率分别是87.23%（41/47例）和85.11%（40/47例）,在有神经侵袭、有复发/转移的SACC患者组织切片中TrkA和VEGFR2的表达率均高于无神经侵袭、未复发/转移者,且差别有统计学意义（P<0.05）。组织内微血管密度（MVD）计数与VEGFR2的表达率成正相关关系;MVD在神经侵袭组为25.14±2.83,在无神经侵袭组为18.81±1.33,两者差异有统计学意义（P<0.05）;MVD在复发/转移组为26.58±2.38,未复发/转移组为19.06±1.39（P<0.05）。结论TrkA、VEGFR2的表达强弱与SACC的嗜神经侵袭,复发转移成正相关关系,提示该2种受体在SACC的侵袭转移过程中具有重要作用,并据此推测TrkA、VEGFR2可以作为评价涎腺腺样囊性癌患者预后的指标。     

Mood and malignancy: head and neck cancer and depression

Head and neck cancer patients have been reported to show high rates of depression. However, it is important to differentiate between depressive symptoms and a depressive disorder. This review critically examines the relationship between head and neck cancer and depression. There appears to be little evidence for depression leading to an increased risk of developing cancer and although depressive symptoms in head and neck cancer patients are common, very few studies have investigated depressive disorders. The studies that investigated the incidence of a comorbid depressive disorder report a prevalence very close to that of the general population, implying that major depression is not a normal response to cancer. Finally, the evidence suggests that comorbidity of depression with cancer has a negative impact on morbidity and mortality. Both psychosocial and biological factors could account for this. Dysregulation of the stress hormone axis and increased inflammation are common in depressive disorders and have been suggested as underlying pathological mechanisms and are both markers of poor prognosis in cancer. This evidence suggests that a relatively small number of patients develop a depressive disorder following a diagnosis of cancer, but for those that do it may have a substantial impact on their prognosis.     

低氧和自噬与肿瘤的发生发展

自噬作为真核生物的一种应激调控机制,既可以促进肿瘤的发生发展,又可以抑制肿瘤的增殖。在肿瘤局部低氧的微环境下,低氧诱导因子-1α、哺乳动物雷帕霉素靶蛋白信号转导通路抑制、内质网应激均可促进自噬的发生。在肿瘤快速地发生发展过程中,肿瘤的糖代谢功能增强、活性氧族增多、窖蛋白1下调以及上皮间质转化的激活均诱导了自噬的发生并促进肿瘤的局部浸润、侵袭转移和耐药,因此,抑制自噬可能为肿瘤治疗提供一种新的策略。     

补体与牙周炎发生发展及其治疗

在牙周炎这一慢性炎症反应过程中,补体不仅可以调解机体防御反应,保护宿主,还可直接作用于免疫细胞或通过调控信号转导通路,协助病原菌进一步感染和破坏牙周组织,最终导致免疫病理性的损伤反应。在免疫炎症反应中,补体不仅可刺激白细胞分泌白细胞介素、肿瘤坏死因子和粒细胞-巨噬细胞集落刺激因子,调节辅助性T细胞和巨噬细胞,促进细胞免疫和T细胞依赖的抗体分泌,增强免疫效应的调节,提高机体免疫力;亦可引起的炎症反应可对组织造成损伤,引起牙周炎。以补体受体拮抗剂干扰补体受体-Toll样受体信号转导通路,有利于机体清除病原菌,达到防治牙周炎的目的。理解补体在牙周炎发生发展中的作用,可为牙周炎治疗探索新途径。     

VEGF及受体在颌面部血管瘤和血管畸形中表达及意义

目的 检测细胞因子血管内皮生长因子(VEGF),血管内皮生长因子受体(VEGFR/KDR)及VEGF mRNA在颌面部血管瘤和血管畸形中的表达,探讨VEGF及其受体与血管瘤发病机制的关系。方法 采用二步EnVision免疫组织化学方法,分别检测27例血管瘤和15例血管畸形组织中VEGF和VEGF/KDR表达;同时采用原位杂交Gene Point法检测VEGF mRNA的表达。结果 VEGF和VEGFR/KDR在血管瘤中高表达,而在血管畸形组中低表达,两者有显著差异(P<0.01);VEGF和VEGF mRNA在血管瘤细胞及周围间质细胞明显表达,VEGFR/KDR主要表达于血管瘤中内皮细胞膜上。结论 VEGF可通过自分泌和旁分泌的形式影响血管瘤内皮细胞的增殖,可能与血管瘤发生、发展和退化有密切相关。     

Molecular biology and its applications in orthodontics and oral and maxillofacial surgery

Molecular biology is an exciting, rapidly expanding field, which has enabled enormously greater understanding of the biology of diseases and malfunctions in many fields. It chiefly concerns itself with understanding the interactions between the various systems of a cell, including the interrelationship of DNA, RNA and protein synthesis and how these interactions are regulated. Since the introduction of molecular biology into modern science, numerous other fields have been enabled to go ““molecular““. Advanced molecular biological techniques showed us new avenue towards finding answers to the questions asked for decades. The first part of this article described the history of molecular biology. It started as a joined discipline of other areas of biology, i.e. genetics and biochemistry in the 1930s and 1940s, and enjoyed its classical period and became institutionalized in the 1950s and 1960s. Major molecular techniques manipulating proteins, DNA and RNA were introduced and their mechanisms were concisely illustrated. The current knowledge of molecular biology and their applications in orthodontic and oral and maxillofacial surgery, i.e. osteoclast differentiation and function, regulation of tooth movement, mechanotransduction/cell-signalling, bone fracture healing, oral cancer as well as craniofacial/dental anomalies and distraction osteogenesis were discussed. Although the problems of introducing molecular technologies are still substantial, it is anticipated that the future of medicine/dentistry will be ““molecular““: molecular prevention, molecular diagnosis and molecular therapy.     

成釉细胞瘤、颌骨囊肿中E-cadherin、vimentin的表达及意义

目的通过免疫组化双染技术检测成釉细胞瘤(ameloblastomas,AM)、颌骨囊肿中E-cadherin、vimentin的表达情况,探索AM中是否存在上皮间充质转化(epithelial-mesenchymal transition,EMT)现象。方法选择37例不同分型的AM、5例颌骨囊肿为研究对象,用免疫组化双染技术检测E-cadherin、vimentin的表达情况,通过计数分析二者共同表达细胞的分布情况。单因素方差分析AM与颌骨囊肿、实性型与单囊型AM的EMT。结果 AM中存在EMT现象,EMT发生特点在实性型与单囊型AM之间、AM与颌骨囊肿之间均无统计学差异。结论 EMT与成釉细胞瘤的侵袭性生物学行为无相关性,EMT存在于AM中可能为肿瘤组织中间质细胞的来源之一。     

Clinical and microbiological effect of scaling and root planing in smoker and non-smoker chronic and aggressive periodontitis patients

OBJECTIVES: To compare the effects of scaling and root planing (SRP) on clinical and microbiological parameters at selected sites in smoker and non-smoker chronic and generalized aggressive periodontitis patients. MATERIALS AND METHODS: Clinical parameters including probing depth (PD), relative attachment level (RAL), and bleeding upon probing (BOP), and subgingival plaque samples were taken from four sites in 28 chronic periodontitis (CP) and 17 generalized aggressive periodontitis (GAgP) patients before and after SRP. Polymerase chain reaction assays were used to determine the presence of A. actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythensis, Prevotella intermedia and Treponema denticola. RESULTS: Both CP and GAgP non-smokers had significantly greater reduction in pocket depth (1.0+/-1.3 mm in CP smokers versus 1.7+/-1.4 mm in non-smokers, p=0.007 and 1.3+/-1.0 in GAgP smokers versus 2.4+/-1.2 mm in GAgP non-smokers, p<0.001) than respective non-smokers, with a significant decrease in Tannerella forsythensis in CP sites (smokers 25% increase and non-smokers 36.3% decrease, p<0.001) and Prevotella intermedia at GAgP sites (smokers 25% reduction versus 46.9% in non-smokers, p=0.028). CONCLUSION: SRP was effective in reducing clinical parameters in both groups. The inferior improvement in PD following therapy for smokers may reflect the systemic effects of smoking on the host response and the healing process. The lesser reduction in microflora and greater post-therapy prevalence of organisms may reflect the deeper pockets seen in smokers and poorer clearance of the organisms. These detrimental consequences for smokers appear consistent in both aggressive and CP.     

种植体周围炎与牙周炎的类比探究

种植体周围炎症是种植失败的主要原因之一,包括种植体周围黏膜炎和种植体周围炎。种植体周围炎的发生、发展及治疗和预防与牙周炎存在一定的相似性,本文将种植体周围炎和牙周炎的流行病学、组织病理表现、始动因素、危险因素、治疗和预防等方面进行类比,探讨如何更好地预防和治疗种植体周围炎。