Helicobacter pylori in dental plaque and stomach of patients from Northern Brazil

AIM: To establish whether virulence factor genes vacA and cagA are present in Helicobacter pylori (H. pylori) retrieved from gastric mucosa and dental plaque in pa-tients with dyspepsia. METHODS: Cumulative dental plaque specimens and gastric biopsies were submitted to histological exami-nation, rapid urease test and polymerase chain reac-tion (PCR) assays to detect the presence of cagA and vacA polymorphisms.RESULTS: Detection of H. pylori from dental plaque and gastric biopsy samples was greater by PCR com-pared to histological examination and the rapid ure-ase test. DNA from H. pylori was detected in 96% of gastric mucosa samples and in 72% of dental plaque samples. Sixty-three (89%) of 71 dental plaque sam-ples that were H. pylori-positive also exhibited identical vacA and cagA genotypes in gastric mucosa. The most common genotype was vacAs1bm1 and cagA positive, either in dental plaque or gastric mucosa. These viru-lent H. pylori isolates were involved in the severity of clinical outcome.CONCLUSION: These pathogenic strains were found simultaneously in dental plaque and gastric mucosa, which suggests that gastric infection is correlated with the presence of H. pylori in the mouth.

Role of dental plaque,saliva and periodontal disease in Helicobacter pylori infection

Helicobacter pylori(H.pylori)infection is one of the most common bacterial infections in humans.Although H.pylori may be detected in the stomach of approximately half of the world’s population,the mechanisms of transmission of the microorganism from individual to individual are not yet clear.Transmission of H.pylori could occur through iatrogenic,fecal-oral,and oral-oral routes,and through food and water.The microorganism may be transmitted orally and has been detected in dental plaque and saliva.However,the role of the oral cavity in the transmission and recurrence of H.pylori infection has been the subject of debate.A large number of studies investigating the role of oral hygiene and periodontal disease in H.pylori infection have varied significantly in terms of their methodology and sample population,resulting in a wide variation in the reported results.Nevertheless,recent studies have not only shown that the microorganism can be detected fairly consistently from the oral cavity but also demonstrated that the chances of recurrence of H.pylori infection is more likely among patients who harbor the organism in the oral cavity.Furthermore,initial results from clinical trials have shown that H.pylori-positive dyspeptic patients may benefit from periodontal therapy.This paper attempts to review the current body of evidence regarding the role of dental plaque,saliva,and periodontal disease in H.pylori infection.

Study of Helicobacter pylori genotype status in saliva,dental plaques,stool and gastric biopsy samples

AIM:To compare genotype of Helicobacter pylori(H.pylori) isolated from saliva,dental plaques,gastric biopsy,and stool of each patient in order to evaluate the mode of transmission of H.pylori infection.METHODS:This cross-sectional descriptive study was performed on 300 antral gastric biopsy,saliva,dental plaque and stool samples which were obtained from patients undergoing upper gastrointestinal tract endoscopy referred to endoscopy centre of Hajar hospital of Shahrekord,Iran from March 2010 to February 2011.Initially,H.pylori strains were identified by rapid urease test(RUT) and polymerase chain reaction(PCR) were applied to determine the presence of H.pylori(ureC) and for genotyping of voculating cytotoxin gene A(vacA) and cytotoxin associated gene A(cagA) genesin each specimen.Finally the data were analyzed by using statistical formulas such as Chi-square and Fisher's exact tests to find any significant relationship between these genes and patient's diseases.P < 0.05 was considered statistically significant,RESULTS:Of 300 gastric biopsy samples,77.66% were confirmed to be H.pylori positive by PCR assay while this bacterium were detected in 10.72% of saliva,71.67% of stool samples.We were not able to find it in dental plaque specimens.The prevalence of H.pylori was 90.47% among patients with peptic ulcer disease(PUD),80% among patients with gastric cancer,and 74.13% among patients with none ulcer dyspepsia(NUD) by PCR assay.The evaluation of vacA and cagA genes showed 6 differences between gastric biopsy and saliva specimens and 11 differences between gastric and stool specimens.94.42% of H.pylori positive specimens were cagA positive and all samples had amplified band both for vacA s and m regions.There was significant relationship between vacA s1a/m1a and PUD diseases(P = 0.04),s2/m2 genotype and NUD diseases(P = 0.05).No statically significant relationship was found between cagA status with clinical outcomes and vacA genotypes(P = 0.65).The evaluation of vacA and cagA genes showed 6 differences between gastric biopsy and saliva specimens and 11 differences between gastric and stool specimens,CONCLUSION:Regard to high similarity in genotype of H.pylori isolates from saliva,stomach and stool,this study support the idea which fecal-oral is the main route of H.pylori transmission and oral cavity may serve as a reservoir for H.pylori,however,remarkable genotype diversity among stomach,saliva and stool samples showed that more than one H.pylori genotype may exist in a same patient.

Can eradication rate of gastric Helicobacter pylori be improved by killing oral Helicobacter pylori ?

AIM:To evaluate the influence of oral Helicobacter pylori(H.pylori)on the success of eradication therapy against gastric H.pylori.METHODS:A total of 391 patients with dyspepsia were examined for H.pylori using the saliva H.pylori antigen test(HPS),13C-urea breath test(UBT),gastroscopy,and gastric mucosal histopathological detection.Another 40 volunteers without discomfort were subjected to HPS and13C-UBT,and served as the control group.The 233 patients who were13C-UBT+were enrolled in this study and divided into 4 groups.Patients who were HPS-and13C-UBT+(n=53)received triple therapy alone.Those who were both HPS+and13CUBT+(n=180)were randomly divided into 3 groups:(1)the O+G+t group which received triple therapy alone(n=53);(2)the O+G+tm group which received both triple therapy and mouthrinse treatment(n=65);and(3)the O+G+tmp group which received triple therapy,mouthrinse,and periodontal treatment(n=62).The HPS and13C-UBT were continued for 4 wk after completion of treatment,and the eradication rate of gastric H.pylori and the prevalence of oral H.pylori in the 4 groups were then compared.RESULTS:The eradication rates of gastric H.pylori in the O-G+t group,the O+G+tm group,and the O+G+tmp group were 93.3%,90.0%,and 94.7%respectively;all of these rates were higher than that of the O+G+t group(78.4%)[O-G+t group vs O+G+t group(P=0.039);O+G+tm group vs O+G+t group(P=0.092);O+G+tmp group vs O+G+t group(P=0.012);O+G+tm group vs O-G+t group(P=0.546);O+G+tmp group vs O-G+t group(P=0.765);O+G+tm group vs O+G+tmp group(P=0.924)].The eradication of gastric H.pylori was significantly improved using the combination of triple therapy,mouthrinse,and periodontal treatment.The eradication rates of gastric H.pylori in the peptic ulcer group,chronic atrophic gastritis group and control group were higher than in the duodenitis group and the superficial gastritis group.The prevalence rates of oral H.pylori in the O-G+t group,O+G+t group,O+G+tm group and O+G+tmp group following treatment were 0%,76.5%,53.3%,and 50.9%,respectively[O-G+t group vs O+G+t group(P<0.0001);O+G+tm group vs O+G+t group(P=0.011);O+G+tmp group vs O+G+t group(P=0.006);O+G+tm group vs O-G+t group(P<0.0001);O+G+tmp group vs O-G+t group(P<0.0001);O+G+tm group vs the O+G+tmp group(P=0.790)].Both mouthrinse and periodontal treatment significantly reduced the prevalence of oral H.pylori.CONCLUSION:Mouthrinse treatment alone or combined with periodontal treatment can,to some extent,reduce the prevalence of oral H.pylori and improve the eradication rate of gastric H.pylori.

Pyrosequencing检测口腔与胃中的幽门螺杆菌16SrDNAV1区基因序列

目的通过Pyrosequencing检测口腔与胃幽门螺杆菌16SrDNAV1区序列基因片段分析,以进一步验证口—口传播的的假设。方法选择18例患有慢性中度牙周炎且胃镜活检Hp感染阳性患者及其中10例患者的家属。提取患者胃、牙菌斑和含漱液共74例样本中的DNA,PCR扩增阳性后pyrosequecing检测16SrDNAV1区序列基因片段。结果患者胃和口腔Hp及其家属口腔Hp的序列相比较,有0～1个碱基不同。结论口腔中的Hp与胃内Hp16SrDNAV1区基因型比较95.8%～100%的同源性,口腔可能为Hp的聚集地。口腔Hp可能与胃Hp感染的复发或再感染有关。

幽门螺杆菌在口腔中的特征性分布

目的 :研究幽门螺杆菌 (Helicobacterpylori,Hp)在慢性胃炎患者口腔中的分布。 方法 :依据Hp尿素酶C基因和细胞毒素相关基因 (cagA)设计引物建立PCR方法 ,从 32例慢性胃炎患者口腔内多部位采集标本 ,检测和鉴定牙菌斑 (每人采集 6个牙的龈上和龈下菌斑 )、含漱液、舌背黏膜、颊黏膜及腭黏膜表面中的Hp。 结果 :32例患者中有 2 9例 (90 6 % )从口腔内牙菌斑、含漱液、舌背黏膜、颊黏膜及腭黏膜至少一处检测出Hp ,其中 2 8例 (87 5 % )从胃和口腔内同时检出Hp ,口腔内各部位标本中Hp检出率依次为牙菌斑 84 4 % ,口腔含漱液 5 6 2 % ,舌背黏膜 4 3 8% ,颊黏膜 2 8 1% ,腭黏膜 9 4 % ;在 384份牙菌斑中 ,磨牙的牙菌斑Hp的检出率高于前牙 (33 2 %vs 2 1 9% ,P <0 0 1) ;而上下牙的牙菌斑Hp的阳性率差异无显著性 (2 9 7%vs 2 9 2 % ,P >0 0 5 ) ;在PD >4mm的牙周袋 ,菌斑Hp检出率显著高于PD <4mm的袋 (P <0 0 5 ) ,龈下菌班Hp的阳性率显著高于龈上菌斑 (P <0 0 1)。 结论 :口腔多部位存在Hp ,牙菌斑中居多 ,并呈一定的分布规律 ;口腔Hp可能是胃Hp感染的重要来源。

牙周基础治疗对胃内幽门螺杆菌根除率的影响

目的 :分析牙周炎与胃内幽门螺杆菌 (Helicobacterpylori ,Hp)的关系以及牙周基础治疗对胃内幽门螺杆菌根除率的影响。方法 :选择有慢性牙周炎且胃镜活检尿素酶阳性、病理诊断为慢性胃炎、胃或十二指肠溃疡患者91人进行三联药物治疗 ,其中 3 3人还同时进行了牙周基础治疗。三联药物治疗后分析胃内幽门螺杆菌根除率与患者牙周临床指数的关系 ,以及牙周基础治疗对胃内Hp根除率的影响。 结果 :4个位点平均牙周袋深 <4mm组的患者三联药物治疗 4周后及 1年后的Hp根除率明显高于平均袋深≥ 4mm组的患者 (80 %vs5 2 .2 % ,62 .9%vs 3 4.5 % ,P <0 .0 5 )。经过牙周基础治疗的患者 1年后的Hp根除率显著高于未做牙周基础治疗的患者 (63 .6%vs 3 4.5 % ,P <0 .0 5 )。结论 :药物治疗Hp的根除率与患者的牙周状况和口腔卫生状况有关。口腔Hp可能是胃Hp再感染的病原因素 ,因此对胃内Hp感染同时伴有牙周炎的患者在进行三联药物治疗的同时应配合牙周基础治疗。

牙周基础治疗对口腔幽门螺杆菌的影响及其基因型关系的研究

目的 :明确牙周基础治疗与口腔幽门螺杆菌 (Helicobacterpylori ,Hp)存在的关系。分析胃Hp与口腔Hp的基因型 ,以明确胃与口腔的Hp是否具有同源性。 方法 :选择 5 6例有慢性中度牙周炎且胃镜活检Hp感染阳性患者分为 2组。提取所有口腔样本中的DNA ,PCR扩增 ,比较药物治疗组与药物治疗加牙周基础治疗组治疗前后 2组口腔Hp检出率的差别。对比分析其中 5位患者和 1位家属胃和口腔PCR产物的序列。结果 :2组患者不同的治疗后口腔Hp检出率有显著性差别 ( 3 .0 %vs 2 6.1% ,P <0 .0 5 )。胃和口腔Hp的序列相比较 ,相同者 1例 ,可能相同者 1例 ,有 1～ 4个碱基不同者 2例。 1例患者及其家属口腔中均检出Hp ,两者的序列有 3个不同。 结论 :牙周基础治疗有助于口腔Hp的根除。口腔中有可能同时存在多个Hp菌株 。

胃病患者口腔中的幽门螺杆菌

目的 通过多聚酶链反应(PCR) 检测胃病患者口腔中的幽门螺杆菌( Hp) 。方法 从13 例有上消化道症状经内镜检查证实的胃病患者采集胃粘膜、口腔含漱液和6 个牙位的龈上及龈下菌斑,应用PCR 检测标本中的Hp 。同时用酶联免疫法(ELISA) 检测静脉血、唾液、龈沟液中抗Hp 特异性IgG 抗体。结果 PCR 检测胃粘膜均为Hp 阳性。6 例患者(46 .2 % ) 的含漱液和11 例患者(84 .6 % ) 的至少一份菌斑样本中检测出Hp 。龈下菌斑中Hp 的检出率(38 .5 % ) 显著高于龈上菌斑(19 .2 % )(P< 0 .01) 。此外, 从患者静脉血、唾液、龈沟液中均可检测到抗Hp 特异性IgG 抗体。结论 本研究结果表明龈沟或牙周袋可能是口腔Hp

幽门螺杆菌在牙菌斑中的分布研究

目的：为探讨幽门螺杆菌（ＨＰ）在口腔内的分布及感染方式，本实验对不同程度牙周炎患者４６例，对照组２０例进行了龈上及龈下菌斑研究。方法：采用ＰＣＲ技术，提取ＨＰ的染色体ＤＮＡ，对其特异性片段进行诊断。结果：牙周炎组ＨＰ阳性率平均３９．１％，健康对照组１５％，重症牙周炎组阳性率５２．３％，显示了ＨＰ在口腔分布与年龄、牙位、牙周炎的程度密切相关。结论：牙菌斑是ＨＰ孳生地，口腔环境可能是ＨＰ一条传播通道，有关ＨＰ对牙周组织损害的研究尚待深入。

牙斑幽门螺杆菌与慢性胃炎之间的关系

目的研究牙斑幽门螺杆菌与慢性胃炎之间的关系。方法对胃炎组、胃炎治疗组分别进行牙斑和胃黏膜幽门螺杆菌培养和比较。结果牙斑细菌培养:胃炎组阳性14例,阳性率为12.8%;治疗组阳性11例,阳性率为10.1%。胃黏膜细菌培养:胃炎组阳性47例,阳性率为43.1%;治疗组阳性19例,阳性率为17.4%。治疗前后比较牙斑标本差异无显著性(P>0.05),胃黏膜标本差异有非常显著性(P<0.001)。结论牙斑中确实存在着幽门螺杆菌,而且是胃内反复感染的源泉,以致慢性胃病反复发作,难以治愈。

基因克隆和扩增口腔幽门螺杆菌

近年来发现幽门螺杆菌可以驻存于口腔,但检测阳性率不一,来源不确定。采用p Bluescript SK+ 载体,与幽门螺杆菌基因片段重组并克隆成质粒p Bluescript SK- Hp。经比较比常规用的幽门螺杆菌标准菌株更适合用作分子生物学检测技术的阳性标准。应用它为阳性对照,基因扩增胃病组和非胃病组患者龈袋幽门螺杆菌的特异基因片段,结果表明胃病组阳性检出率(45.95% )显著大于非胃病组(23.53% ),p< 0.05。

控制牙菌斑对胃粘膜幽门螺旋杆菌检出率的影响

目的通过检测胃粘膜幽门螺旋杆菌(HP),观察控制牙菌斑对胃粘膜HP检出率的影响,探讨口腔和胃内HP的相关性。方法将根除胃内HP的患者108例分为试验组(n=56)和对照组(n=52)。试验组行彻底的牙菌斑控制,对照组未行牙菌斑控制或控制失败。半年后均行胃镜复查,并行病理检查和快速尿素酶试验检测胃内HP,确定其检出率。结果试验组56例患者中胃HP阳性者11例,检出率为19.6%;对照组52例患者中胃HP阳性者42例,检出率为80.8%,试验组胃粘膜中HP的检出率明显低于对照组(P<0.05)。结论口腔与胃HP感染之间具有明显相关性。提示治疗HP相关性胃病时,应注意口腔卫生,控制牙菌斑。

牙菌斑中幽门螺杆菌与胃病的关系

目的 :分离培养口腔牙菌斑中的幽门螺杆菌 (Helicobackerpylori,Hp)并探讨它与Hp相关性慢性胃病之间的相互关系。方法 :采用细菌培养的方法检测 40例体检者的龈下牙菌斑和胃黏膜中的Hp。 结果 :10例 ( 2 7.0 3 % )慢性胃病患者的胃黏膜Hp培养阳性 ,其中 5例 ( 13 .5 1% )牙菌斑Hp培养阳性。 3例胃黏膜Hp培养阴性的非慢性胃病患者中有 1例牙菌斑Hp培养阳性。 结论 :牙菌斑是Hp的另一个重要储存库 ,口腔Hp的存在可能与慢性胃病有一定的相关性。

3种方法检测口腔中幽门螺杆菌的效果

目的比较快速尿素酶、多聚酶链反应(PCR)及细菌培养法检测胃炎或消化性溃疡患者口腔中的幽门螺杆菌(Hp)的效果。方法选取经胃镜证实为慢性胃炎或消化性溃疡的患者50例,在磨牙区刮取3份龈下菌斑,分别采用快速尿素酶、PCR、细菌培养法测定Hp。结果快速尿素酶、PCR、细菌培养法的Hp阳性率分别为80%、64%、26%,3种方法比较差异有统计学意义(P<0.05)。结论快速尿素酶、PCR、细菌培养法检测口腔中Hp有明显差异性,其中PCR法不仅特异敏感,而且速度较快、准确率高,是县及县以上医院较好的检测口腔中Hp的方法。

口腔卫生状况对慢性胃炎发病的影响

目的 探讨口腔卫生状况对慢性胃炎发病有无影响。方法 对 2 945名中老年人的口腔卫生状况进行检查并抽样 (口腔卫生较好和较差各 2 40名组成A、B两组 )测定牙菌斑指数、牙石指数 ,通过聚合酶链反应(PCR)检测菌斑中幽门螺杆菌 (Hp) ,通过胃镜检查慢性胃炎发病情况。结果 A、B两组间菌斑、牙石指数检测结果差别显著 ,刷牙效果亦有非常明显的差异 ;菌斑Hp检测两组阳性率分别为76 .3%和 78.3% ,差别无统计学意义 ;胃炎发病率分别为 5 .83%和 5 0 .83% ,具有高度显著性差异 ;另外 ,胃炎患者与非胃炎受检者菌斑Hp阳性率亦有差别。

PCR和PCR—SSCP检测分析口腔和胃的幽门螺杆菌

目的研究胃炎患者口腔中的幽门螺杆菌(Hp)并分析其和胃内Hp的基因型异同.方法依据Hp特异的尿素酶C和cagA基因设计引物建立PCR方法.检测和鉴定32例慢性胃炎患者不同牙齿的龈上和龈下菌斑(12份菌斑/6牙/人)中的Hp,并用单链构象多态性(SSCP)分析菌斑和胃内Hp的基因型异同.结果有27例患者至少一份牙菌斑中检出Hp,共计384份菌斑有113份(29.4％)检测出Hp,龈下菌斑中Hp检出率(37％)显著高于龈上菌斑(21.9％)(P<0.01).同一家庭4例患者中有3例菌斑与胃内Hp的SSCP带型相同,4例患者菌斑中至少有一种相同SSCP带型的Hp.结论口腔Hp可能是胃Hp感染的重要来源.

唾液、牙斑与胃黏膜幽门螺杆菌感染关系的研究

幽门螺杆菌(H.pylori)在人群中感染率高,但其传播途径仍不清楚。目前有关口腔中H.pylori感染与胃黏膜H.pylori感染关系的研究不多。目的:了解口腔中的H.pylori感染状况及其与胃黏膜H.pylori感染的关系。方法:应用聚合酶链反应(PCR)技术同时检测60例非萎缩性胃炎患者唾液、牙斑和胃黏膜中的H.pylori。结果:47例胃黏膜H.pylori阳性的胃炎患者中有31例(66.0％)唾液中检出H.pylori,17例(36.2％)牙斑中检出H.Pylori;而13例胃黏膜H.pylori阴性的胃炎患者中仍有1例(7.7％)唾液中检出H.pylori,2例(15.4％)牙斑中检出H.pylori。胃黏膜H.pylori阳性与阴性胃炎患者唾液和牙斑中的H.pylori检出率有显著差异(P<0.01)。结论:口腔中的H.pylori与胃黏膜中的H.pylori之间可能存在一定的病因学联系。

幽门螺杆菌与口腔扁平苔藓关系的探讨

目的探讨HP与OLP之间的关系方法对50例口腔扁平苔藓OLP分组作幽门螺杆菌检测一组采用快速尿素酶试验12例HP检出率83.33%二组14C一尿素呼吸试验21例HP检出率61.90%三组HP抗体金标快速检测17例HP检出率76.47%结果50例OLP中HP阳性为36例其中伴有粘膜充血、糜烂或牙龈上皮剥脱。

高压氧对口腔牙菌斑幽门螺杆菌的作用

目的 :寻找一种较为理想的根除口腔幽门螺杆菌 (Hp)的方法。方法 :将 12 0例口腔牙菌斑Hp -PCR检测阳性的Ⅱ度牙周炎患者分为A、B、C、D 4组 ,治疗 1、3、6月后分别对所有患者牙周参数和龈下菌斑进行Hp -PCR检测并比较检测结果。结果 :4组Hp阳性率分别为 96 .7%、80 .0 %、73.3%和 0 ,有显著性差异(P <0 .0 5 ) ,其中以D组最低 (P <0 .0 1) ;临床牙周参数变化亦有显著差别 (P <0 .0 5 )。结论 :高压氧对口腔Hp有明显抑制或杀灭作用 ,高压氧配合治疗 ,有助于口腔Hp的根除和与Hp有关的疾病的治疗。