增殖细胞核抗原和p53蛋白在涎腺肿瘤中的表达

为了研究增殖细胞核抗原（ｐｒｏｌｉｆｅｒａｔｉｎｇｃｅｌｎｕｃｌｅａｒａｎｔｉｇｅｎ，ＰＣＮＡ）和ｐ５３在涎腺肿瘤中的表达，作者用抗ＰＣＮＡ及ｐ５３单克隆抗体对良、恶性混合瘤及粘液表皮样癌组织标本进行了免疫组化染色。结果表明，恶性混合瘤ＰＣＮＡ增殖指数较高，与混合瘤细胞生长活跃型及混合瘤相比差异有极显著性（Ｐ＜０．０１）；低分化粘液表皮样癌的ＰＣＮＡ阳性表达明显高于高分化型（Ｐ＜０．０１）。ｐ５３在恶性混合瘤中阳性表达率高（６０．０％），与粘液表皮样癌（２０．０％）相比差异有显著性（Ｐ＜０．０５）。另外，我们观察到ｐ５３阳性表达的肿瘤组织ＰＣＮＡ增殖指数较高。结论：ＰＣＮＡ增殖指数可以作为支持诊断恶性混合瘤的指标；是粘液表皮样癌组织学分级的重要参数。ｐ５３蛋白是恶性混合瘤的有效标记物；ｐ５３蛋白参与ＰＣＮＡ表达的调节。     

口腔鳞癌细胞增殖核抗原和P53免疫组化的比较研究

本文运用ＡＢＣ免疫组化结合图象分析，定量分析了ＰＣＮＡ（细胞增殖核抗原）和Ｐ５３在口腔鳞癌中的表达。探讨了两者在口腔鳞癌的临床病理、肿瘤侵龚和转移等方面的异同点。结果表明：ＰＣＮＡ的表达强度和阳性率与肿瘤的病理分级有关，与肿瘤细胞的侵龚转换无关。而Ｐ５３和肿瘤细胞的侵龚有关密切的关系（Ｐ〈０．０５）。Ｐ５３阳性者，淋巴结转移率较高（８０％）。结果表明在口腔鳞癌的临床行为恶性，预后等方面定量分析上述     

口腔鳞癌增殖细胞核抗原表达及其临床意义

目的：检测口腔鳞状细胞癌中增殖细胞核抗原（ＰＣＮＡ）的表达，探讨与鳞癌预后相关的因素。方法：采用免疫组化的方法，利用ＰＣＮＡ的单克隆抗体检测４４例口腔鳞癌组织中ＰＣＮＡ的表达。结果：低分化鳞癌较高分化鳞癌ＰＣＮＡ的表达明显增强（Ｐ＜０．０５）；晚期鳞癌中ＰＣＮＡ阳性细胞百分率比早期鳞癌显著增高（Ｐ＜０．０５）；ＰＣ－ＮＡ高表达者的淋巴结转移倾向大于ＰＣＮＡ低表达者。结论：ＰＣＮＡ标记可以作为判断鳞癌预后的参考指标。     

增殖细胞核抗原和抑癌基因P53在粘液表皮样癌中的表达

为对粘液表皮样癌中增殖细胞核抗原（ｐｒｏｌｉｆｅｒａｔｉｎｇｃｅｌｎｕｃｌｅａｒａｎｔｉｇｅｎ，ＰＣＮＡ）和Ｐ５３蛋白的表达及分布特点进行分析，作者采用免疫组织化学过氧化物酶法对４１例粘液表皮样癌进行了研究。所有病例均有ＰＣＮＡ阳性表达，ＰＣＮＡ表达指数和染色强度与肿瘤组织学分级呈正相关。根据ＰＣＮＡ阳性细胞分布情况可分为３种类型，分布类型与肿瘤组织学分级相一致。Ｐ５３蛋白总阳性率为４１．５％，除外偶见Ｐ５３阳性细胞９例，阳性率为１９．５％。结果提示：Ｐ５３蛋白在粘液表皮样癌中表达率较低。ＰＣＮＡ表达指数和染色强度可作为评价粘液表皮样癌分化程度的生物学指标。ＰＣＮＡ阳性细胞分布类型有助于粘液表皮样癌的病理学分级诊断     

口腔鳞状细胞癌增殖细胞核抗原的研究

作者采用抗增殖细胞核抗原单克隆抗体，对５２例标本进行了免疫组化染色。结果显示：正常口腔粘膜基底细胞具有少量的ＰＣＮＡ阳性细胞，其阳性分级为１级；而Ｉ级鳞癌ＰＣＮＡ阳性分级为３级为主，随着鳞癌组织学分级的升高，ＰＣＮＡ阳性分级有增高趋势，ＩＩＩ级鳞癌的ＰＣＮＡ阳性分级以４级为主，经统计学分析：除鳞癌Ｉ级与ＩＩ级间无显著差异外（Ｐ＞０．０５），其余各组间均有显著差异（Ｐ＜０．０５）。提示：ＰＣＮＡ表达     

DMBA诱导的金黄地鼠颊囊癌变粘膜中增殖细胞核抗原表达

实验采用抗增殖细胞核抗原单克隆抗体对１０９例金黄地鼠颊囊粘膜标本作免疫组化染色及网格计数和形态学观察，发现正常的金黄地鼠颊囊粘膜基底层有少量增殖细胞核抗原（ＰＣＮＡ）阳性细胞，而上皮异常增生以及癌变时，随着病变程度的加重，ＰＣＮＡ阳性细胞率也相应增加。统计学分析显示：正常粘膜各级上皮异常增生以及癌变各组间ＰＣＮＡ阳性细胞率有显著差异（Ｐ＜０．０５），轻度上皮异常增生组中涂ＤＭＢＡ６周与７周的ＰＣＮＡ阳性分级有显著性差异（Ｐ＜０．０５）；涂ＤＭＢＡ７周，８周，９周之间，其ＰＣＮＡ阳性分级无差异（Ｐ＞０．０５），提示ＰＣＮＡ可作为动态观察癌前病变过程中细胞增殖程度的一种检测指标，它的敏感性强于光镜形态学观察。     

nm23基因在涎腺腺样囊性癌中的表达及其与肺转移的关系

为探讨肿瘤转移抑制基因ｎｍ２３与涎腺腺样囊性癌（ａｄｅｎｏｉｄｃｙｓｔｉｃｃａｒｃｉｎｏｍａ，ＡＣＣ）的关系，应用ＬＳＡＢ免疫组化染色方法，研究ｎｍ２３表达产物二磷酸核苷激酶（ｎｕｃｌｅｏｓｉｄｅｄｉｐｈｏｓｐｈａｔｅｋｉ－ｎａｓｅ，ＮＤＰＫ）在ＡＣＣ中的表达。结果：ＮＤＰＫ／ｎｍ２３在ＡＣＣ中有较高表达，阳性率为６４．０％（１６／２５）；其中，有肺转移者阳性率为１２．５％（１／８），无肺转移者阳性率为８８．２％（１５／１７），差异有极显著性（Ｐ＜０．０１）；ＮＤＰＫ表达与临床分期有关，分期越高，阳性率越低，差异有显著性（Ｐ＜０．０５），与病理分型差异无显著性（Ｐ＞０．０５）。结论：ｎｍ２３基因在人ＡＣＣ肺转移过程中起到抑制转移的作用，可作为临床颈侧ＡＣＣ患者转移和预后的指标。     

颊癌中肿瘤转移抑制基因nm23mRNA的表达 Ⅱ.定量逆转录多聚酶链反应检测

采用定量逆转录多聚酶链反应（Ｑ－ＲＴ－ＰＣＲ）技术检测ｎｍ２３－Ｈ１和ｎｍ２３－Ｈ２ｍＲＮＡ在４７例组织标本中的表达情况，发现ｎｍ２３－Ｈ１和ｎｍ２３－Ｈ２ｍＲＮＡ在颊癌原发灶、癌旁粘膜、正常颊粘膜、颌下腺、白斑、正常淋巴结和有转移的淋巴结中均有不同程度的表达。ｎｍ２３－Ｈ１在肿瘤转移组颊癌原发灶中的表达低于无转移组（Ｐ＜０．０５），ｎｍ２３－Ｈ２在颊癌有、无转移中的表达无差异（Ｐ＞０．０５）；ｎｍ２３－Ｈ１和ｎｍ２３－Ｈ２表达与临床病理参数间均无关（Ｐ＞０．０５）。结果提示：ｎｍ２３－Ｈ１ｍＲＮＡ表达下降与颊癌转移关系密切，而ｎｍ２３－Ｈ２ｍＲＮＡ表达与颊癌转移无关；通过Ｑ－ＲＴ－ＰＣＲ检测ｎｍ２３－Ｈ１ｍＲＮＡ的表达水平可为临床预测颊癌的转移提供有价值的指标。Ｑ－ＲＴ－ＰＣＲ技术的主要优点在于通过少量组织提取的总ＲＮＡ即可检测ｎｍ２３ｍＲＮＡ的表达。     

口腔鳞癌组织超氧化物歧化酶免疫组化定位观察

作者对７０例口腔鳞状细胞癌组织标本进行超氧化物歧化酶（ＳＯＤ）免疫组化研究（ＡＢＣ法）。结果发现，鳞癌组织中ＳＯＤ标记阳性率和阳性程度均显著高于癌旁和正常上皮组织（Ｐ＜０．００１）；癌组织分化程度越差，其ＳＯＤ标记阳性率和阳性程度亦越高（Ｐ＜０．０５）；高分化舌癌的ＳＯＤ阳性率和阳性程度较高分化唇癌为高（Ｐ＜０．０５）。结果表明：①本研究方法具有定位及半定量特点，特异性及灵敏度高，组织对比性好，检测误差少，结果判断可靠等优点。②口腔鳞癌组织的生物学特性，分化程度及预后与ＳＯＤ含量增高有关。     

地鼠颊粘膜癌变过程中增殖细胞核抗原及核仁组成区表达变化实验研究

目的：探讨癌变过程中增殖细胞核抗原（ＰＣＮＡ）、核仁组成区（ＮＯＲ）的表达变化。方法：利用地鼠颊粘膜癌模型采用免疫组化ＬＳＡＢ法检测ＰＣＮＡ,阳性对照为人类炎性增生淋巴结标本,阴性对照为ＰＢＳ代替单抗。采用硝酸银染色法检测ＮＯＲ。结果：①正常粘膜ＡｇＮＯＲ颗粒主要见于基底层细胞,以单一型为主。重度异常增生以聚集型为主。浸润癌以混合型为主。②随恶变进展,ＰＣＮＡ表达逐渐增强,重度异常增生阳性细胞见于上皮全层。结论：ＰＣＮＡ与ＡｇＮＯＲ表达有相关性（ｒ＝０．６３５,Ｐ〈０．００１）,但ＰＣＮＡ更为直观、清晰,实用价值更大。     

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。