儿童口腔尖锐湿疣的临床表现及HPV检测

目的:探讨儿童口腔粘膜尖锐湿疣的病毒类型、传播途径、临床病理特点及预后等。方法:回顾6 例被确诊为口腔粘膜尖锐湿疣患儿的临床特点及HE 切片,并对其中5 例采用免疫组化染色及原位杂交检测人乳头状瘤病毒(HPV)DNA。结果:儿童口腔尖锐湿疣多发生在2 岁左右,发病部位多位于腭部,并且多数有家族感染史,镜下见棘层上部或角化层常出现灶性凹空细胞,免疫组化检测结果显示5 例HPV 共同抗原全部阳性,5 例中有4 例HPV16P18- E6 阳性;原位杂交结果显示仅1 例HPV6 和HPV11 同时阳性,另1 例初发时HPV6 阳性而复发后呈阴性。结论:儿童口腔尖锐湿疣的病毒类型、传播途径可能与成人不同。     

口腔黏膜良性淋巴组织增生病的免疫组化研究

目的　研究口腔黏膜良性淋巴组织增生病与口腔癌的细胞增殖能力、血管密度和细胞凋亡的变化。方法　采用免疫组化SP法检测 15例黏膜良性淋巴组织增生病、9例黏膜良性淋巴组织增生病伴上皮异常增生、15例口腔癌及 10例正常黏膜组织中Ki 6 7的表达、细胞凋亡及微血管密度。结果　口腔黏膜良性淋巴组织增生病伴异常增生及鳞状细胞癌中Ki 6 7的表达明显高于不伴异常增生的口腔黏膜良性淋巴组织增生病及正常黏膜 (P <0 0 5 ) ,在所有的口腔黏膜良性淋巴组织增生病及鳞状细胞癌中微血管密度均明显高于正常组 (P <0 0 5 )。口腔黏膜良性淋巴组织增生病中细胞凋亡明显高于正常黏膜及口腔癌 (P <0 0 5 )。结论　在伴有上皮异常增生的口腔黏膜良性淋巴组织增生病中Ki 6 7表达及微血管密度均介于正常组织和口腔癌之间 ,凋亡细胞数也明显多于正常组织。研究结果提示 :口腔黏膜良性淋巴组织增生病是一种具有癌变潜能的疾患     

口腔黏膜人乳头瘤病毒感染的研究现状

人乳头瘤病毒(HPV)在人类广泛传播,与许多人类常见病有关,已证实HPV感染是导致宫颈癌的主要病因。随着分子生物学技术的发展,已在多种口腔黏膜病损中检测出不同型别的HPV感染,越来越多研究表明HPV可能是引起多种口腔病损的致病因素。HPV在口腔黏膜的感染情况及其引起的口腔黏膜病损日益受到关注。本文对HPV的生物学特性、口腔黏膜HPV感染的途径、检测方法、HPV相关口腔黏膜损害及其可能的致病机制等进行综述。     

湖北地区HIV阳性人群口腔内HPV感染状况研究

目的：对HIV感染者口腔黏膜乳头状瘤病毒（HPV）感染进行研究,并对比其中女性宫颈的感染状况,了解湖北地区HIV感染者口腔内HPV感染的流行和分布,证实HPV与HIV之间及相关疾病的相互关系。方法：收集40例自愿接受检查的HIV感染者的一般情况,检测其CD4＋T细胞计数,并对受检者中的女性进行宫颈检测,使用PCR方法检测口腔及宫颈处HPV亚型,采用SPSS 17．0软件进行统计分析。结果：有1例（2．5％）患者检测出口腔HPV52型,10例女性患者（38．5％）在宫颈黏膜样本中检测出HPV感染,且有2例同时检测出2种以上HPV基因型。结论：HIV感染者口腔内HPV感染率远低于宫颈黏膜HPV感染率,两区域间HPV感染状况没有明显联系。     

人类免疫缺陷病毒(HIV)感染的口腔表现及其处理——Ⅱ.较少见的病变

感染咽炎伴发热可见于HIV感染的早期。各种形状的口腔粘膜良性上皮疣样增生如寻常疣、尖锐湿疣和病灶性上皮增生可见于某些HIV阳性者,它们与人乳头状瘤病毒(HPV)的7,13,18,32型和新型有关。然而,口腔乳头状瘤很少见于HIV感染者。可用冷冻、激光或手术治疗。与巨细胞病毒感染有关的慢性口腔溃疡偶见于艾滋病。组织学上类似于卡波济肉瘤(KS)并与猫抓病有关的口腔血管病变可见于HIV疾病。虽然结核常见于HIV疾病,但少发生在口腔。不能消除的牙源性感染或发展成颌下蜂窝织炎,拔牙创口感染或延迟愈合、放线菌病等均有报告。     

EMS1基因扩增与口腔黏膜癌变的相关研究

目的 了解EMS1基因扩增是否参与口腔黏膜癌变。方法采用显微解剖技术分别获取正常口腔黏膜上皮，口腔白斑患者的单纯增生，轻、中、重度异常增生上皮和原发性口腔鳞癌组织标本78例，应用差示PCR反应检测EMS1基因扩增。结果①分别有20．0％的口腔白斑组织，57．6％的口腔鳞癌组织观察到EMS1扩增；②在口腔黏膜癌变进程中，EMS1扩增开始于中度异常增生黏膜，在伴有淋巴结转移的口腔鳞癌组织中其扩增率有显著增高(P=0．015)。结论EMS1基因扩增与口腔黏膜癌变的演进相平行，似是口腔黏膜癌变的早期分子事件。     

乳头状瘤病毒与口腔粘膜病损关系研究现状

早在50年前,有关口腔乳头状瘤与病毒的关系首先在动物体内得到了证实。目前,对乳头状瘤病毒(papillomaviruses,PVs)在人体口腔粘膜病损方面所起的作用尤为关注。最近发现该病毒与各种疣状损害、癌前病变和恶性上皮瘤的病因学相关,本文就乳头状瘤病毒的基本特性及其在口腔粘膜良性病变、癌前病损和一些口腔癌的发生发展中可能起到的作用作一综述。一、基本特性 1、性质和种类: 乳头状瘤病毒属乳头状瘤多型空泡形病毒A亚群。本病毒是一些最小的DNA病毒(直径为50—55nm),无包膜,含有蛋白及超螺旋单环双股DNA;其二十面体微粒含72质粒。PVs与大多数     

艾滋病毒感染患者口腔黏膜疣状肿块人类乳头状瘤病毒感染的分型研究

目的探讨艾滋病毒感染患者口腔戮膜疵状肿块人类乳头状瘤病毒(1-IPV)感染及感染类型。方法应用 HPV Ll区通用引物Gp5十//G p6+和1-IPV特型引物(HPV6/II,16,18,31,33),通过聚合酶链反应(PCR),对34例艾滋病毒感染患者口腔豁膜沈状肿块人类乳头状瘤病毒(HPV) DNA进行检测。结果艾滋病毒感染患者口腔豁膜优状肿块中,HPV感染率为88.2%;亚型HPV6/II感染率为47.06%, HPV16感染率为II.76%, 1U〕V 18感染率为 2.94 % , HPV31感染率为5.88%。结论艾滋病毒感染患者口腔庆状肿块和H PV感染关系密切,而且大多数和低危型HPV6/II感染有关,少数病例和高危型HPV16,18,31感染有关;同一病例可以感染两种以上HPV亚型。     

COX-2在口腔扁平苔藓、口腔乳头状瘤及口腔鳞状细胞癌中的表达

目的:研究COX-2在口腔扁平苔藓(OLP)、口腔乳头状瘤(SCP)及口腔鳞状细胞癌(SCC)中的表达情况,探讨其在口腔黏膜炎症、增生及癌发生过程中的意义。方法:用免疫组化方法检测COX-2在20例口腔黏膜扁平苔藓(单纯增生10例,伴糜烂10例)、20例口腔乳头状瘤(单纯增生10例,伴糜烂10例)、20例口腔鳞状细胞癌及5例正常口腔黏膜中的表达情况。采用Fromowitz法计数阳性细胞。应用统计学方法分析COX-2在不同病变中的表达。结果:在舌背斑块型扁平苔藓中为阴性或弱阳性表达;在糜烂型扁平苔藓中50%为中度阳性表达,40%为强阳性表达。在口腔乳头状瘤中,同样发现单纯增生的乳头状瘤组织中COX-2的表达为阴性或弱阳性,合并炎症的乳头状瘤组织中均有COX-2的高表达。本实验结果显示,糜烂型扁平苔藓组及乳头状瘤组与鳞癌组相比较,COX-2的强阳性表达无率明显差异。但COX-2在口腔鳞癌中的表达细胞与糜烂型扁平苔藓组及乳头状瘤组有明显差异。结论:扁平苔藓组和乳头瘤组炎症程度与COX-2的高表达有一定的相关性。即随着炎症加重,COX-2的表达加强。口腔鳞癌中炎症程度与COX-2的高表达无一定的相关性。     

EB病毒感染与涎腺良性淋巴上皮病损恶变的关系

目的 了解Epstein-Barr病毒(EBV)感染与涎腺良性淋巴上皮病损恶变的关系。方法 采用针对EB病毒编码的小分子RNA(EBER-1)的寡核苷酸探针对2例涎腺良性淋巴上皮病损灶性恶变、14例恶性淋巴上皮病损(MLEL)、4例良性淋巴上皮病损(BLEL)、4例非特异性慢性涎腺炎石蜡包埋组织进行原位杂交检测;采用聚合酶链反应(PCR)进行EBV BamHI-W片段检测。结果 2例良性淋巴上皮病损灶性恶变形态学上良性区域或恶性区域,EBER-1及EBV BamHI-W片段均为阳性,14例MLEL的癌细胞核均可见EBER-1强阳性信号,其中12例EBV BamHI-W片段阳性,4例BLEL及4例非特异性慢性涎腺炎均为阴性。结论 少数恶性淋巴上皮病损可能在BLEL基础上发生,EB病毒感染与涎腺良性淋巴上皮病损癌变发生可能有密切关系,EBV感染可发生在BLEL癌变形态学改变之前。     

口腔鳞状细胞乳头状瘤组织中HPV DNA的原位杂交研究

目的 探讨人乳头瘤病毒（ｈｕｍａｎ ｐａｐｉｌｌｏｍａｖｉｒｕｓ，ＨＰＶ）感染与口腔鳞状细胞乳头状瘤（ｓｑｕａｍｏｕｓ ｃｅｌｌ ｐａｐｉｌｌｏｍａ，ＳＣＰ）的发生之间的关系。方法 应用地高辛标记的ＨＰＶ６／１１和ＨＰＶ１６／１８核酸探针分别在３０例口腔ＳＣＰ组织上进行原位杂交，检测口腔ＳＣＰ组织中ＨＰＶ ＤＮＡ的特征。结果 ＨＰＶ６／１１ ＤＮＡ阳性１６例（５３％），ＨＰＶ１６／１８ＤＮＡ未检出，ＨＰＶ６／１１ＤＮＡ阳性细胞多数分布在鳞状上皮的表层、中层和基底层。结论 原位杂交方法可以检测口腔ＳＣＰ组织中ＨＰＶ ＤＮＡ的存在并能准确组织定位，进一步支持ＨＰＶ６／１感染与口腔ＳＣＰ的发生密切相关。     

Condyloma acuminatum and human papilloma virus infection in the oral mucosa of children

PURPOSE: The purpose of this study was to investigate the clinicopathological features of oral condylomas in children and condylomatous lesions of their mothers. Moreover, the authors sought to determine the mode of transmission of this disease and to find the genotype of human papilloma virus (HPV) in the children's oral condyloma. METHODS: Nine instances of oral condyloma acuminatum in children and lesions in their mothers were reviewed. Their HPV genotypes were evaluated by in situ hybridization (ISH). RESULTS: This study revealed that the lesions appeared during 3 years of age and the most common location was the hard and soft palate. Seven of the 9 mothers had experienced vulva and/or oral cavity condylomata during pregnancy. Social evaluation confirmed sexual abuse in 1 girl, and probable sexual abuse in another girl. The results of ISH demonstrated HPV 16/18 DNA being positive in 5 of the 9 cases, and HPV 6 and HPV 11, HPV 6 and HPV 16/18, HPV 6, and HPV 11 DNA being positive, respectively, in 1 case. HPV DNA types in mother-child pairs were not concordant. CONCLUSIONS: Oral condyloma acuminatum in children is probably induced by HPV 16/18. The mode of transmission by sexual abuse is the most likely route. Prenatal transmission of HPV to children is rare. This study provides further confirmation of possible different genotype and transmission in oral CA of children and adults.     

Human papillomavirus infection in cyclosporin-induced gingival overgrowth in renal allograft recipients.

BACKGROUND: Host immunity plays an important role in the development of human papillomavirus (HPV)-associated disease. The HPV infection in oral cyclosporin-induced gingival overgrowth in renal transplant recipients has not been investigated previously. The aim of this study was to establish the HPV infection of cyclosporin-induced gingival hyperplasia in renal transplant recipients through morphological changes and use of the in situ hybridization technique. METHODS: We examined 13 renal transplant recipient biopsies with gingival overgrowth lesions and 4 healthy mucosa samples of these patients. The histopathological diagnoses were established on the basis of widely accepted criteria, and the pathologist was not aware of the HPV result. An in situ molecular hybridization was carried out under low stringent conditions to detect HPV species with mixed biotin-labeled probes of HPV 6 and HPV 11, and under high stringent conditions with HPV 6, HPV 11, HPV 16, and HPV 18 probes for HPV typing. RESULTS: The HPV prevalence among the 13 samples studied was 92.31% (12/13), of which 4 tested positive for HPV 6-11 and 1 for HPV 16. The 4 biopsies of normal mucosa from gingival overgrowth patients were also reactive for HPV DNA. In 11/12 (91.7%) HPV-positive cases, koilocytotic atypia was found. CONCLUSIONS: The suppression of T-cell function by cyclosporin therapy can result in an increase of HPV infection, adding to the proliferative activity of cyclosporin in the oral mucosa.     

Biopsy vs. superficial scraping: detection of human papillomavirus 6, 11, 16, and 18 in potentially malignant and malignant oral lesions

BACKGROUND: Several epidemiologic studies have shown a broad variation in the prevalence of human papillomavirus (HPV) in oral precancerous tissues and oral carcinomas. METHODS: Biopsies and superficial scrapes of lesions, clinically suspected of HPV infection, were taken from patients with potentially malignant and malignant oral lesions, and subject to HPV DNA detection by PCR-Southern blot analysis. RESULTS: From 22 patients with potentially malignant and malignant lesions analyzed, 41% of the biopsies were HPV DNA positive, whereas 95-100% of the superficial scrapes were positive (McNemar, P < 0.0001). Clinical presumption of HPV infection detected 67% (P < 0.0001) of the HPV DNA positive cases compared with 48% (P < 0.0001) determined by cytology and histopathology. The prevalence of HPV 6, 11, 16 and 18 in the oral mucosa was studied in 59 individuals. While 9% of normal controls were HPV DNA positive, 100% of the patients with potentially malignant and malignant lesions were HPV DNA positive, and the prevailing genotype was HPV 16 followed by HPV 18. CONCLUSIONS: The higher HPV DNA detection rate in superficial oral scrapes than in biopsies suggests that accurate epidemiological information on oral HPV infection/oral carcinogenesis depends not only on the DNA detection technique, but also on the tissue/cell sampling procedure.     

口腔鳞状细胞癌中人乳头瘤病毒感染的检测

目的检测人乳头瘤病毒(HPV)在口腔鳞状细胞癌中感染及其与口腔癌发生的相关性.方法采用PCR方法,检测30例口腔鳞状细胞癌及5例正常口腔黏膜中HPV 16和18感染.结果 7/30例标本中检测出HPV 16(23.3%);10/30例标本中检测出HPV 18(33.3%).3/30例标本中存在HPV 16和18共感染(10%).5例正常口腔黏膜中未发现HPV 16和HPV 18感染.在检测HPV 16时发现一条新片断(186 nt),经测序此序列与人5号染色体的核酸序列65-175存在99%同源.结论 HPV 16和18可能与口腔鳞状细胞癌的发生密切相关.     

Detection of human papillomavirus DNA in benign oral squamous epithelial lesions in Venezuela

The polymerase chain reaction (PCR) was applied to the detection of human papillomavirus (HPV) infection in biopsies taken from clinically normal oral mucosa of 20 subjects and clinical lesions of 40 patients. PCR for HPV-DNA amplification was performed using consensus primers MYO9/MYO11 and subsequent typing for HPV of high and low oncogenic risk HPV types were identified by restriction enzyme analysis (restriction fragment length polymorphism, RFLP). The HPV viral genome was present in 55% (22/40) of the oral benign lesions (OBL) and in 10% (2/20) of the control samples. In the PCR+ OBL, we observed 90.9% of low oncogenic risk types (HPV-6 -13 and -32) and 9.1% of the samples had a mixed infection with low and high oncogenic types (HPV-6 and -16). In the control samples, we observed one patient with HPV-6 and another with HPV-6 and -16 in the same sample. All of the eight focal epithelial hyperplasia cases were positive for low risk HPV types (88% HPV-13 and 12.5% HPV-32). In conclusion, this study demonstrates a high incidence of HPV in oral benign lesions from Venezuelan patients.     

The prevalence and distribution of human papillomavirus genotypes in oral epithelial hyperplasia: proposal of a concept

Background:  Evidence is accumulating for the aetiological role of human papillomavirus (HPV) in the pathogenesis of potentially malignant oral mucosal lesions and squamous cell carcinomas.
Methods:  Paraffin tissue sections from 49 patients with 'white patches' of the oral mucosa were investigated histologically, by broad-spectrum PCR followed by genotyping and chromogenic in situ hybridisation (CISH).
Results:  Histologically, 33 flat hyperplasias and 16 papillary hyperplasias were diagnosed. Twenty-two of 28 samples studied (78.6%) were positive for HPV DNA by PCR and six were negative. The following HPV types were detected in decreasing order of prevalence: HPV 35, HPV 6, HPV16, HPV 53, HPV 18, HPV 51 and HPV 55. Seventeen samples (60.7%) contained high-risk HPV DNA. Using CISH, ≥ 1 HPV signals were detected at least in a few epithelial cells in 95% of cases studied. All but one case were positive with the high-risk HPV probe and all HPV infections contained low viral load. Concordant positive results both by PCR and CISH were detected in 14 of 19 cases (73.7%) analysed.
Conclusions:  The high prevalence of HPV infection in hyperplastic 'white patches' of the oral mucosa supports the putative role of HPV at an early stage of oral carcinogenesis. These results further indicate that the majority of white oral mucosal lesions – flat, exophytic, wart-like or papillary proliferations – could be considered as the clinical manifestations of oral HPV infection. This finding has clinical relevance regarding therapy and patient management and may help in elucidating the role of HPV infection in oral carcinogenesis.