Ⅱ型糖尿病合并牙周炎患者龈下菌斑微生物群落分析

目的：本研究旨在比较Ⅱ型糖尿病合并慢性牙周炎患者与无糖尿病的牙周炎患者龈下菌斑微生物构成。方法：12名患者分为糖尿病合并慢性牙周炎组（T2DM＋CP组）与慢性牙周炎组（CP组）2组,各6人。记录所有患者基本信息及牙周临床参数,包括年龄、性别、探诊深度和附着丧失。根据探诊深度和附着丧失取患病位点的菌斑样本。PCR检测7种牙周可疑致病菌。采用DGGE分离扩增的16SrDNA片段。结果：两组结果显示两组牙周参数无显著差异。两组7种细菌检出率相似。所有对象中均检出牙龈卟啉单胞菌、福塞坦氏菌、齿垢密螺旋体和中间普氏菌,而具核梭杆菌在两组中均有一个样本未检出。变黑普氏菌在T2DM＋CP组的2个样本中检出,而CP组有4个样本检出。伴放线共聚菌在所有样本中均未检测到。DGGE分析结果示两组间条带数量及树状聚类分析均无显著差异。结论：Ⅱ型糖尿病合并牙周炎患者龈下菌斑的牙周可疑致病菌的检出情况以及DGGE分析与无糖尿病患者相似。     

棋盘式DNA-DNA杂交法检测中国人的龈下细菌

目的检测牙周健康者和快速进展性牙周炎（ｒａｐｉｄｌｙｐｒｏｇｒｅｓｓｉｖｅｐｅｒｉｏｄｏｎｔｉｔｉｓ，ＲＰＰ）患者的龈下细菌，旨在寻找ＲＰＰ的主要致病菌。方法采用棋盘式ＤＮＡＤＮＡ杂交技术，将５名牙周健康者和６例ＲＰＰ患者的８４个龈下菌斑ＤＮＡ样本与３７种龈下细菌的ＤＮＡ探针杂交。结果埃氏腐蚀菌等６种细菌的检出率高于９０％。牙周可疑致病菌，如伴放线放线杆菌血清ｂ型、牙密螺旋体、具核梭杆菌具核梭亚种、佛赛类杆菌、变黑普菌、产琥珀酸沃廉菌、直弯曲菌、微小消化链球菌、中间链球菌和牙龈卟啉菌，在ＲＰＰ组的检出率和细菌数均显著高于牙周健康组。结论牙周致病菌具备一定数量才能引起牙周组织的破坏，ＲＰＰ是由多种致病菌所致     

慢性牙周炎EBV-1和HHV-6感染及危险因素分析

目的探讨慢性牙周炎龈沟液中EB病毒1型（EBV-1）、人疱疹病毒6型（HHV-6）感染率及其感染发生的相关危险因素。方法采用巢式PCR检测并比较59例慢性牙周炎（CP）患者、56例牙周健康者龈下样本中的EBV-1和HHV-6阳性率。用病例-对照研究策略,EBV-1和HHV-6阳性者为病例组,EBV-1和HHV-6阴性者为对照组,应用logistic多因素回归分析EBV-1和HHV-6在牙周组织的感染与性别、年龄、是否吸烟、牙周袋深度、慢性牙周炎、糖尿病、冠心病、慢性胃炎等是否相关。结果慢性牙周炎（CP）样本中EBV-1的阳性感染率是71.2%,显著高于牙周健康者的EBV-1阳性感染率17.9%（P〈0.01）。CP样本中HHV-6的阳性感染率是47.5%,显著高于牙周健康者的HHV-6阳性感染率10.7%（P〈0.01）。EBV-1感染与年龄、牙周袋深度、CP有相关性（均P〈0.05,OR值分别为11.374,7.695,4.498,95%可信区间均不包含1）,HHV-6感染与年龄、CP有相关性（均P〈0.05,OR值分别为6.909,5.193,95%可信区间不包含1）。结论慢性牙周炎患者牙周组织具有EBV-1和HHV-6的高感染率,且EBV-1的感染危险因素可能与年龄、牙周袋深度和慢性牙周炎有关;HHV-6的感染危险因素可能与年龄、慢性牙周炎有关。     

侵袭性牙周炎病原微生物的检测

目的检测侵袭性牙周炎（AgP）患者和牙周健康者龈下菌斑中的7种病原微生物,旨在寻找AgP的主要致病微生物.方法应用以16S rRNA为基础的聚合酶链反应（PCR）技术,检测55例AgP患者和17名健康对照者龈下菌斑中的7种牙周病原微生物：伴放线放线杆菌（Aa）,牙龈卟啉单胞菌（Pg）,福赛坦氏菌（Tf）,牙密螺旋体（Td）,直肠弯曲杆菌（Cr）,中间普氏菌（Pi）,变黑普氏菌（Pn）.结果55例AgP患者中仅有1例检测出Aa,而在健康对照者中未检出该菌.Pg、Tf、Td和Cr在AgP组的检出率分别为81.8%、83.6%、80.0%和81.8%,显著高于健康对照者（17.6%、11.8%、5.9%、29.4%）,差异有统计学意义（P＜0.01）.结论Pd、Tf、Td和Cr 4种微生物在AgP患者中有较高的检出率,提示它们的共同定植可能在AgP中起重要作用.     

慢性牙周炎合并糖尿病患者唾液及龈下菌斑中牙周致病菌检测临床研究

目的    探讨慢性牙周炎（CP）合并2型糖尿病（T2DM）患者与单纯CP患者唾液及龈下菌斑中牙周致病菌的差异性。方法    选择河南大学第一附属医院口腔科2012年8月至2015年9月伴T2DM的CP患者40例为CP+T2DM组,同时选取背景相似的慢性CP患者65例为CP组,并选取健康体检者35名作为对照组,采用聚合酶链反应（PCR）检测各组受试者唾液及龈下菌斑中牙龈卟啉单胞菌（Pg）、放线共生放线杆菌（Aa）、具核梭杆菌（Fn）、福塞坦菌（Tf）、中间型普里沃菌（Pi）、齿垢密螺旋体（Td）等可疑致病菌种类和相对含量。结果    3组受试者唾液及龈下菌斑中Pg、Aa和Tf检出率比较差异有统计学意义（P＜0.05）,而Fn、Pi和Td检出率差异无统计学意义（P＞0.05）,3组受试者唾液及龈下菌斑中Fn检出率均最高,CP+T2DM组唾液及龈下菌斑中Pg、Aa、Tf检出率均显著高于对照组和CP组（P＜0.05）,而CP组仅Pg检出率显著高于对照组（P＜0.05）,CP+T2DM组和CP组唾液及龈下菌斑中Pg、Aa和Tf相对含量均显著高于对照组（P＜0.05）,且CP+T2DM组唾液及龈下菌斑中Aa和Tf相对含量显著高于CP组,差异有统计学意义（P＜0.05）。结论    CP患者和伴糖尿病的CP患者牙周可疑致病菌的种类和数量存在明显差异,CP+T2DM组患者Pg、Aa和Tf检出率更高,可能与糖尿病关系更为密切。     

老年卧床肺感染病人牙周袋需氧致病菌的分离和研究

目的：了解重症老年卧床肺感染伴牙周病病人龈下菌斑中需氧致病菌的定植情况及其与肺感染致病菌的关系。方法：选我院重症卧床老年肺感染伴牙周病病人50名，记录其牙周状况、全身状况、痰培养结果，并选牙周炎症最重的1～2个观测牙进行龈下菌斑需氧菌培养和细菌分类计数，观察其龈下菌斑中需氧致病菌的定植情况及其与呼吸道致病菌的一致性，并分析其危险因素。结果：实验组龈下菌斑需氧致病菌检出率达23．96％，显著高于对照组（检出率7．45％，P=0．001），导致致病菌定植的危险因素主要包括：性别因素、住院天数、抗生素使用时间、体温、社区牙周指数（CPI）记分。实验组老年病人龈下菌斑与肺感染致病菌一致率为24％，其危险因素包括：性别因素、住院天数、抗生素的使用时间、体温、中性粒细胞分类、CPI记分、龈下菌斑中杆菌的百分比。结论：重症卧床老年病人的龈下菌斑较普通老年人更易定植需氧致病菌，且易被吸入导致呼吸道感染。这种细菌的定植和口腔肺脏细菌一致性与牙周炎症程度相关，也与性别、卧床时间、抗生素的使用、全身炎症程度相关。     

正畸治疗中牙龈增生的致病因素分析

目的 探讨正畸治疗中牙龈增生的相关致病因素.方法 12例因接受固定正畸治疗而出现牙龈增生的患者纳入牙龈增生组,对照组为12例牙龈健康者.分别于基线时采集两组研究对象的牙周检查指标、龈下菌斑标本和龈沟液标本,采用实时PCR技术对龈下菌斑内的牙龈卟啉单孢菌（Pg）、伴放线放线杆菌（Aa）、中间普氏菌（Pi）、齿密螺旋体（Td）和福赛氏类杆菌（Tf）进行定量检测,使用ELISA法测量龈沟液中白介素-1β的含量,比较牙龈增生组和对照组各项指标间的差异.对牙龈增生组患者实施牙周基础治疗,并于4周后重新采样比较牙周治疗前后上述指标间的差异.结果 基线时,牙龈增生组中龈下菌斑内五种牙周可疑微生物的检出率均显著高于对照组（P＜0.05）,龈沟液内白介素-1β的含量显著高于对照组（P＜0.05）.牙周基础治疗后4周时,牙龈增生患者的各项牙周检查指标均明显下降,同时Pg、Aa和Td的检出率、细菌数量以及龈沟液内白介素-1β的含量均显著减少（P＜0.05）.结论 Pg、Aa和Td等牙周病原菌和白介素-1β与正畸治疗中牙龈增生的发生和发展密切相关.     

不同牙周状况龈下菌斑中福赛斯坦纳菌分布

目的：分析牙周健康者和慢性牙周炎病人龈下菌斑中福赛斯坦纳菌的分布情况,探讨该菌与不同牙周状况的关系。方法：收集111例牙周健康者、108例慢性牙周炎病人,病变位点和健康位点共327个龈下菌斑,采用16S rRNA PCR方法检测福赛斯坦纳菌的分布。结果：牙周炎病人病变位点福赛斯坦纳菌检出率为56.5%,显著高于牙周健康者（10.8%,P〈0.001）。慢性牙周炎病人健康位点福赛斯坦纳菌检出率为3.7%,显著低于病变位点（P〈0.001）,牙周健康者该菌的检出率比牙周炎健康位点高（P〈0.05）。结论：龈下菌斑中福赛斯坦纳菌的存在与牙周炎症的发生有密切关系。     

实时荧光定量PCR检测牙周炎患者龈下菌斑的分布

目的 应用实时荧光定量PCR技术探索侵袭性牙周炎（aggressive periodontitis,AgP）、慢性牙周炎（chronic periodontitis,CP）患者龈下菌斑中伴放线聚集杆菌(A. actinomycetemcomitans,Aa)、牙龈卟啉单胞菌（P. gingivalis,Pg）的分布规律。方法 采集32例AgP、33例CP、32例牙周健康者的龈下菌斑,构建含有2种待测细菌基因片段的重组质粒,建立定量标准,采用TaqManMGB探针实时荧光定量PCR方法检测样本中细菌数量。结果 本实验构建的引物及TaqManMGB探针特异性及敏感性较好。AgP组龈下菌斑Aa的检出率高于CP组（P＜0.01）,但2种细菌数量在组间无显著差异,两组内Pg的检出率及数量都明显高于Aa（P＜0.001）,另外AgP组Aa的数量、CP组Pg数量与牙周探诊深度密切相关（P＜0.01及P＜0.001）。结论 龈下菌斑Aa的检出率可能与牙周炎类型存在一定关联,Aa可能并不是中国人群样本AgP患者龈下菌斑的优势菌,实时荧光定量PCR对牙周病学研究有广泛应用前景。     

心脏移植患者3种牙周可疑致病菌的检测

目的：应用聚合酶链反应法对心脏移植患者龈上菌斑中牙龈卟啉单胞菌、福赛坦氏菌和齿垢密螺旋体进行检测,分析其存在状况与牙周临床指标的关系。方法：55例心脏移植患者为实验组,36例正常成人为对照组。以16、26为受检牙位,分别采集龈上菌斑,应用PCR技术检测菌斑中的Pg,Tf,Td。同时记录受检牙位的菌斑指数、龈沟出血指数,龈沟探诊深度及附着丧失。结果：心脏移植组PLI、SBI、PD均高于对照组（P〈0.05）,心脏移植组龈上菌斑中Pg、Tf、Td检出率分别为为81.8%、69.1%、76.4%,对照组中3种细菌检出率分别为58.3%、41.7%、41.7%。检出率均高于对照组（P〈0.05）。心脏移植组3种致病菌同时检测出率为53.6%（59/110）,对照组3种致病菌同时检出率为29.2%（21/72）,两组差异有统计学意义（P〈0.05）。心脏移植组中3种致病菌均为阳性患者的PLI、SBI、PD均高于对照组（P〈0.05）。结论：心脏移植患者口腔卫生状况较差,为防止牙周疾病的发生,应及早进行口腔卫生干预治疗。     

Herpesviruses and periodontopathic bacteria in Trisomy 21 periodontitis

BACKGROUND: Little is known about the etiology and pathogenesis of periodontal disease in Trisomy 21 patients. This study determined the occurrence of herpesviruses and putative periodontopathic bacteria in Trisomy 21 periodontitis. METHODS: Nineteen Trisomy 21 patients (17 to 37 years of age) contributed subgingival samples from molar and bicuspid teeth presenting interproximal periodontitis lesions (probing depths, 5 to 8 mm) and from shallow periodontal sites (probing depths, 1 to 3 mm). Samples were obtained at baseline, and at 1 and 4 weeks after subgingival debridement by means of hand instruments and ultrasonic scalers. Epstein-Barr virus type 1 and 2 (EBV-1 and EBV-2), human cytomegalovirus (HCMV), and herpes simplex virus (HSV) were identified by sensitive and specific nested polymerase chain reaction. Putative periodontopathic bacteria were identified by means of non-selective and selective culture. RESULTS: Of 19 Trisomy 21 periodontitis lesions, 6 (32%) were positive for EBV-1, 5 (26%) were positive for HCMV, 3 (16%) were positive for HSV, and 2 (11%) showed viral co-infection. Of 19 shallow periodontal sites, only one revealed HCMV. Prevotella intermedia, Bacteroides forsythus, and Capnocytophaga species were detected in higher proportions in deep than in shallow periodontal pockets (P = 0.02). Subgingival debridement did not reduce genomic herpesvirus presence but caused a decrease in proportions of Porphyromonas gingivalis and Capnocytophaga species. CONCLUSIONS: Periodontal herpesvirus-bacteria coinfections may play important roles in the pathogenesis of destructive periodontal disease in Trisomy 21 patients. Herpesviruses may reduce the periodontal defense and promote growth of subgingival bacteria capable of causing periodontal breakdown.     

Herpes viruses and periodontopathic bacteria in early-onset periodontitis

OBJECTIVES: This study examined the occurrence of human herpes viruses and suspected periodontopathic bacteria in early-onset periodontitis patients who experienced progressive disease in at least 2 periodontal sites during the maintenance phase of therapy. MATERIAL AND METHODS: In each of 16 individuals (9 male and 7 female; mean age 33.1+/-2.6 years), subgingival plaque samples were collected from 2 deteriorating and 2 stable periodontitis sites. A nested polymerase chain reaction method determined the presence of human cytomegalovirus (HCMV), Epstein-Barr virus type 1 (EBV-1) and herpes simplex virus (HSV). A 16s rRNA polymerase chain reaction method identified Porphyromonas gingivalis, Dialister pneumosintes, Bacteroides forsythus and Actinobacillus actinomycetemcomitans. RESULTS: HCMV was detected in 59.4% of active and in 12.5% of stable sites (p<0.001), EBV-1 in 43.8% of active and in 12.5 % of stable sites (p=0.01), HSV in 34.5% of active and in 9.4% of stable sites (p=0.03), and co-infection with any of the 3 test herpesviruses in 43.8% of active and in 3.1% of stable sites (p<0.001). P. gingivalis was detected in 71.9% of active and in 37.5% of stable sites (p=0.01), D. pneumosintes in 62.5% of active and in 18.8% of stable sites (p=0.04), co-infection with P. gingivalis and D. pneumosintes in 50% of active and in 0% of stable sites (p<0.001), and co-infection with any 3 or 4 of the test bacteria in 40.6% of active and in 0% of stable sites (p=0.001). All periodontitis sites showing herpesvirus co-infection and all but one site showing P. gingivalis and D. pneumosintes co-infection revealed bleeding upon probing. CONCLUSIONS: HCMV, EBV-1, HSV and herpesvirus co-infection, as well as P. gingivalis, D. pneumosintes and P. gingivalis-D. pneumosintes co-infection were statistically associated with active periodontitis. Herpesviruses are immunosuppressive and may set the stage for overgrowth of subgingival P. gingivalis, D. pneumosintes and other periodontopathic bacteria. Understanding the significance of herpesviruses in human periodontitis may allow for improved diagnosis, more specific therapy and, ultimately, disease prevention.     

The herpesvirus-Porphyromonas gingivalis-periodontitis axis

OBJECTIVES AND BACKGROUND: Members of the herpesvirus family have accumulated considerable support for a role in severe types of periodontitis. This study aimed to examine whether human cytomegalovirus (HCMV), Epstein-Barr virus type 1 (EBV-1) or herpes simplex virus (HSV) together with the major periodontopathic bacterium Porphyromonas gingivalis might interact in the pathogenesis of periodontal breakdown. METHODS: Sixteen subjects each contributed paper point samples from two progressing and two stable periodontitis lesions, as determined by ongoing loss of probing attachment. Polymerase chain reaction methodology was used to identify subgingival herpesviruses, P. gingivalis and other bacterial pathogens. Chi-squared tests and multivariate logistic regression were employed to identify statistical associations between herpesviruses, periodontopathic bacteria and clinical variables. RESULTS: HCMV and HSV were both significant predictors of the presence of subgingival P. gingivalis. In turn, P. gingivalis was positively associated with periodontitis active disease, probing attachment level, probing pocket depth, gingival bleeding upon probing and patient age. EBV-1 was not linked to P. gingivalis, although the virus was predictive of periodontitis active disease. The periodontitis disease risk associated with herpesvirus-P. gingivalis combinations depended on both site-specific and subject-specific factors. CONCLUSION: The present data of aggressive periodontitis implicate HCMV, HSV and P. gingivalis as either cofactors in its etiology or triggers of relapses. Further studies are needed to determine the spectrum of periodontopathogenicity of herpesviruses and effective management of these viruses in periodontal sites.     

Herpesviruses in human periodontal disease

Recent studies have identified various herpesviruses in human periodontal disease. Epstein–Barr virus type 1 (EBV‐1) infects periodontal B‐lymphocytes and human cytomegalovirus (HCMV) infects periodontal monocytes/macrophages and T‐lymphocytes. EBV‐1, HCMV and other herpesviruses are present more frequently in periodontitis lesions and acute necrotizing ulcerative gingivitis‐lesions than in gingivitis or periodontally healthy sites. Reactivation of HCMV in periodontitis lesions tends to be associated with progressing periodontal disease. Herpesvirus‐associated periodontitis lesions harbor elevated levels of periodontopathic bacteria, including Acrinobacillus actinomycetemcomitans , Porphyromonas gingivalis , Bacteriodes forsythus , Prevotella intermedia , Prevotella nigrescens and Treponema denticola . It may be that active periodontal herpesvirus infection impairs periodontal defenses, thereby permitting subgingival overgrowth of periodontopathic bacteria. Alteration between latent and active herpesvirus infection in the periodontium might lead to transient local immunosuppression and explain in part the episodic progressive nature of human periodontitis. Tissue tropism of herpesvirus infections might help explain the localized pattern of tissue destruction in periodontitis. Absence of herpesvirus infection or viral reactivation might explain why some individuals carry periodontopathic bacteria while still maintaining periodontal health. Further studies are warranted to delineate whether the proposed herpesvirus‐periodontopathic bacteria model might account for some of the pathogenic features of human periodontal disease.     

Detection of Epstein-Barr virus and human cytomegalovirus in blood and oral samples: comparison of three sampling methods

The purpose of this study was to identify and compare the presence of HCMV and EBV-1 in subgingival plaque, unstimulated saliva and peripheral blood of patients with chronic periodontitis. Forty patients diagnosed with chronic periodontitis (mean age, 41.7 years) were recruited. Unstimulated saliva, subgingival plaque and peripheral blood were collected from each patient and the DNA of each sample was isolated. The viruses were detected using the nested PCR technique. The detection frequency of EBV-1 in subgingival plaque, saliva and peripheral blood was 45%, 37.5% and 25%, respectively. HCMV was detected in 82.5% of subgingival plaque samples and peripheral blood and in 75% of salivary samples. The sensitivity for detecting EBV-1 in saliva and peripheral blood when EBV-1 was detected in subgingival plaque samples was low (22% and 27.7%, respectively) and the sensitivity for detecting HCMV in saliva and peripheral blood when compared to subgingival plaque was high (81.8% and 87.8%, respectively). There is a high agreement among the three sampling methods in detection of HCMV, but the detection of EBV-1 would require a combination of saliva and subgingival plaque sampling to avoid false negative results.     

Prevalence of human herpesviruses in patients with aggressive periodontitis

BACKGROUND: Recent studies have demonstrated that various human viruses, especially cytomegalovirus (HCMV) and Epstein-Barr virus type-1 (EBV-1), seem to play a part in the pathogenesis of human periodontitis. The aim of this investigation was to evaluate the subgingival presence of HCMV and EBV in patients with aggressive periodontitis (AgP) and healthy subjects and to examine the effect of treatment on the incidence of these viruses 3 months following surgery. METHODS: A polymerase chain reaction (PCR) method determined the presence of HCMV and EBV-1. Subgingival plaque samples from 17 consecutive AgP patients and 16 healthy controls were collected. The following indices were measured: plaque index (PI), gingival index (GI), probing depths (PD), and clinical attachment loss (CAL). Clinical parameters were assessed pretherapy and at 3 months following surgical and antimicrobial therapy. RESULTS: HCMV was detected in 64.7% of AgP patients but not detected in healthy subjects (P < 0.001) and EBV-1 in 70.6% of AgP patients and 6.3% of the healthy controls (P < 0.001). HCMV and EBV-1 coinfection was detected in 41.7% of AgP patients. A statistically significant decrease was found in all clinical parameters 3 months after treatment. There was a statistically significant decrease in HCMV and EBV-1 following therapy (P < 0.001; no HCMV; 1 patient with EBV-1). CONCLUSIONS: These findings indicate that subgingival presence of EBV-1 HCMV is strongly associated with aggressive periodontitis, and coinfection with HCMV and EBV-1 appears to be particularly deleterious to periodontal health.     

Human cytomegalovirus and Epstein-Barr virus type 1 in periodontal abscesses

OBJECTIVES: Recent studies have linked herpesviruses to severe types of periodontal disease, but no information exists on their relationship to periodontal abscesses. The present study determined the presence of human cytomegalovirus (HCMV) and Epstein-Barr virus type 1 (EBV-1) in periodontal abscesses and the effect of treatment on the subgingival occurrence of these viruses. MATERIAL AND METHODS: Eighteen adults with periodontal abscesses participated in the study. Subgingival samples were collected from each patient with sterile curettes from an abscess-affected site and a healthy control site. HCMV and EBV-1 were identified by polymerase chain reaction at the time of the abscess and at 4 months after surgical and systemic doxycycline therapy. RESULTS: HCMV was detected in 66.7% of periodontal abscess sites and in 5.6% of healthy sites (P=0.002). EBV-1 occurred in 72.2% of abscess sites but not in any healthy site (P<0.001). HCMV and EBV-1 co-infection was identified in 55.6% of the abscess sites. Posttreatment, HCMV and EBV-1 were not found in any study site. CONCLUSIONS: HCMV and EBV-1 genomes are commonly found in periodontal abscesses. These data favor a model in which a herpesvirus infection of the periodontium impairs the host defense and serves as a platform for the entrance of bacterial pathogens into gingival tissue with subsequent risk of abscess development.     

Relationship between herpesviruses and adult periodontitis and periodontopathic bacteria.

BACKGROUND: Various mammalian viruses and specific bacteria seem to play important roles in the pathogenesis of human periodontitis. This study examined the relationship between subgingival herpesviruses and periodontal disease and potential periodontopathic bacteria in 140 adults exhibiting either periodontitis or gingivitis. METHODS: A nested-polymerase chain reaction (PCR) method determined the presence of Epstein-Barr virus type 1 and type 2 (EBV-1, EBV-2), human cytomegalovirus (HCMV), and herpes simplex virus (HSV) and a 16S rRNA PCR detection method identified Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Bacteroides forsythus, Prevotella intermedia, Prevotella nigrescens, and Treponema denticola. RESULTS: Using a logistic analysis, EBV-1 showed significant positive association with P. gingivalis (odds ratio [OR] 3.37), and with coinfections of P. gingivalis and P. intermedia (OR 4.03); P. gingivalis and B. forsythus (OR 3.84); P. gingivalis and T. denticola (OR 4.17); P. gingivalis, B. forsythus, and T. denticola (OR 4.06); and P. gingivalis, P. nigrescens, and T. denticola (OR 3.29). EBV-1 also showed positive association with severe periodontitis (OR 5.09), with increasing age (OR 1.03), and with periodontal probing depth at the sample sites (OR 1.77). HCMV was positively associated with coinfections of P. gingivalis and P. nigrescens (OR 3.23); P. gingivalis, B. forsythus, and P. nigrescens (OR 3.23); and P. gingivalis, P. nigrescens, and T. denticola (OR 2.59); with severe periodontitis (OR 4.65); and with age (OR 1.03). Patients with mixed viral infections revealed significant associations with P. gingivalis (OR 2.27), and with coinfections of P. gingivalis and B. forsythus (OR 2.06); P. gingivalis and P. nigrescens (OR 2.91); P. gingivalis, B. forsythus, and P. nigrescens (OR 2.91); and P. gingivalis, P. nigrescens, and T. denticola (OR 2.70) with the clinical diagnosis of slight (OR 3.73), moderate (OR 3.82), or severe periodontitis (OR 4.36), and with probing depth at the sample sites (OR 1.39). HSV and EBV-2 showed no significant associations with any of the variables tested. CONCLUSIONS: The results indicate that subgingival EBV-1, HCMV, and viral coinfections are associated with the subgingival presence of some periodontal pathogens and periodontitis. Herpesviruses may exert periodontopathic potential by decreasing the host resistance against subgingival colonization and multiplication of periodontal pathogens.     

Herpesviruses in periodontal pocket and gingival tissue specimens

Human cytomegalovirus (HCMV) and Epstein-Barr virus type 1 (EBV-1) are frequently detected in crevicular fluid of deep periodontal pockets, but little or no information is available on occurrence of herpesviruses in gingival tissue. This investigation studied the presence of herpesviruses in periodontal pockets and the corresponding gingival tissues from 11 periodontally healthy and 14 periodontitis sites. A nested-polymerase chain reaction was employed to identify the presence of HCMV, EBV-1, EBV-2, herpes simplex virus, human herpesvirus (HHV)-6, HHV-7 and HHV-8 in each test sample. In healthy periodontal sites, HCMV was detected in 1 (9%) and EBV-1 in 2 (18%) pocket samples, and HCMV was detected in 2 (18%) and EBV-1 in 3 (27%) gingival tissue samples. In periodontitis lesions, HCMV was detected in 9 (64%) pocket samples and in 12 (86%) gingival tissue samples, and EBV-1 was detected in 6 (43%) pocket samples and in 11 (79%) gingival tissue samples. HHV-6 and HHV-8 were detected exclusively in gingival tissue samples. The present findings confirm the frequent presence of HCMV and EBV-1 in periodontitis lesions and suggest using gingival tissue specimens for detecting periodontal HHV-6, HHV-7 and HHV-8.