Herpesvirus infection of inflammatory cells in human periodontitis

Human cytomegalovirus (HCMV) and Epstein-Barr virus type 1 (EBV-1) are frequently detected in human periodontitis lesions. However, no information is available on the types of gingival cells infected by herpesviruses. The present study determined the presence of herpesviruses in polymorphonuclear neutrophils, monocytes, macrophages and T and B lymphocytes in biopsies of periodontitis lesions from 20 adults. A nested polymerase chain reaction method was employed to detect HCMV, EBV-1, EBV-2, human herpes virus-6 and herpes simplex virus (HSV) in periodontal tissue biopsy and in gingival cell fractions separated by immunomagnetic cell sorting. Tissue specimens from 18 (90%) and cell fractions from 14 (70%) patients demonstrated herpesviruses. Periodontitis-derived monocytes and macrophages revealed HCMV in cell fractions from 11 (55%) patients and HSV in cells from 1 (5%) patient. T lymphocytes harbored HCMV in cell fractions from 4 (20%) patients and HSV in cell fractions from 4 (20%) patients. B lymphocytes showed EBV-1 in cell fractions from 9 (45%) patients. Periodontal polymorphonuclear neutrophils demonstrated no herpesviruses. This study suggests that HCMV mainly infects periodontal monocytes, macrophages and less frequently T lymphocytes and that EBV-1 infects periodontal B lymphocytes. The possible etio-pathologic significance of periodontal herpesvirus infection is discussed.     

Herpesviruses in HIV-periodontitis

BACKGROUND/AIMS: Human herpesvirus-associated diseases exhibit elevated morbidity and mortality in patients infected with human immunodeficiency virus (HIV).This study aimed to investigate the occurrence of herpesviruses in HIV-periodontitis. METHOD: Gingival biopsies from periodontitis lesions of 21 HIV-patients and 14 non HIV-patients were studied. Nested-polymerase chain reaction methods were employed to detect human cytomegalovirus, Epstein-Barr virus type 1 and 2 (EBV-1, EBV-2), herpes simplex virus, human herpes virus (HHV)-6, HHV-7 and HHV-8. RESULTS: Gingival biopsies from HIV-periodontitis lesions showed on average 4.0 herpesvirus species and gingival biopsies from HIV periodontitis lesions of non-HIV patients revealed an average of 1.9 herpesvirus species (p<0.001). Occurrence of 4 to 6 different herpesviruses was more common in HIV- than in non HIV-gingival biopsies (71% vs. 7%) (p<0.001). EVB-2 was detected in 12 (57%) biopsies from HIV-periodontitis but was absent in non HIV-periodontitis biopsies (p= 0.002). HHV-6 also occurred in significantly higher frequency in HIV-periodontitis (71%) than in non HIV-periodontitis (21%) (p=0.01). HHV-8 was detected only in biopsies from HIV-periodontitis lesions.. CONCLUSION: HIV-periodontitis seems to be associated with elevated occurrence of EBV-2, HHV-6 and herpesvirus co-infections compared to periodontitis in non-HIV-patients. The periodontopathic significance of herpesviruses in HIV-periodontitis constitutes a research topic of considerable interest.     

Real-time polymerase chain reaction quantification of human cytomegalovirus and Epstein-Barr virus in periodontal pockets and the adjacent gingiva of periodontitis lesions

BACKGROUND: Genomic sequences of human cytomegalovirus (HCMV) and Epstein-Barr virus (EBV), two herpesviruses, can frequently be detected in periodontal pockets of progressive periodontitis lesions, but the prevalence and load of the two viruses in gingival tissue are unknown. This study determined levels of HCMV and EBV DNA in the periodontal pocket and in the adjacent gingiva of periodontitis lesions using a real-time polymerase chain reaction (PCR) assay. MATERIAL AND METHODS: A total of 20 systemically healthy periodontitis patients participated in the study. Nine patients below 35 years of age were tentatively diagnosed as having aggressive (early onset) periodontitis, and 11 patients 36-56 years of age as having chronic (adult) periodontitis. Clinical parameters were evaluated using established methods. Using periodontal curettes, specimens were harvested from 6-10 mm periodontal pockets and from the adjacent inflamed periodontal pocket wall. A 5'-nuclease (TaqMan) real-time PCR assay was used to identify and quantify genomic copies of periodontal HCMV and EBV. RESULTS: HCMV DNA was detected in 78% of subgingival and 33% of gingival tissue samples from aggressive periodontitis lesions, but only in 46% of subgingival and 9% of gingival tissue samples from chronic periodontitis lesions. In aggressive periodontitis, HCMV subgingival and gingival tissue counts were positively correlated with periodontal pocket depth and probing attachment loss at sample sites (p6 mm, but none of 14 patients having mean pocket depth at sample teeth相似文献   

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。     

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.     

Human Herpesviridae in acute necrotizing ulcerative gingivitis in children in Nigeria

Herpesviruses have been implicated in the pathogenesis of human periodontitis. The present study investigated whether herpeasviruses are present in the lesions of acute necrotizing ulcerative gingivitis. Sixty-two Nigerian children, aged 3–14 years, were studied. Twenty-two children had acute necrotizing ulcerative gingivitis and were also malnourished, 20 exhibited no acute necrotizing ulcerative gingivitis but were malnourished, and 20 were free of acute necrotizing ulcerative gingivitis and in a good nutritional state. Polymerase chain reaction methods were used to determine the presence of human cytomegalovirus (HCMV), Epstein-Barr virus type 1 and type 2 (EBV-1, EBV-2), herpes simplex virus (HSV), human herpes virus 6 (HHV-6), human papilloma virus and human immunodeficiency virus type 1 in crevicular fluid specimens collected by paper points. Of the 22 acute necrotizing ulcerative gingivitis patients, 15 (68%) revealed viral infection and 8 (36%) viral coinfection. Thirteen (59%) acute necrotizing ulcerative gingivitis patients demonstrated HCMV, 6 (27%) EBV-1, 5 (23%) HSV and 1 (5%) HHV-6. Only 2 (10%) subjects from each group not affected by acute necrotizing ulcerative gingivitis showed viral presence, and no control subject revealed viral coinfection. These findings suggest that HCMV and possibly other herpesviruses contribute to the onset and/or progression of acute necrotizing ulcerative gingivitis in malnourished Nigerian children.     

Mammalian viruses in human periodontitis

A prior investigation has demonstrated a higher prevalence of human cytomegalovirus (HCMV) and Epstein-Barr virus (EBV) in subgingival specimens from periodontitis patients than from gingivitis patients. This study aimed to determine the frequency of HCMV, EBV-1, EBV-2, herpes simplex virus (HSV) and human immunodeficiency virus (HIV) in subgingival samples from 27 adults who each contributed both a periodontitis and a gingivitis site. Viral detection was performed using a nested-polymerase chain reaction method. Twenty-four subjects (89%) yielded at least one of the five test viruses from deep periodontal pockets, wheras only 15 (56%) showed viruses from shallow periodontal sites ( P =0.015; chi-square test). Viral co-infection occurred more frequently in deep than in shallow periodontal sites ( P =0.015). HCMV was detected with higher frequency in deep than in shallow periodontal sites ( P =0.023). The possible periodontopathogenic mechanisms of mammalian viruses in human periodontitis are discussed. The role and importance of HCMV and other mammalian viruses in the initiation and progression of destructive periodontal disease merits further investigation.     

HHV-6, HHV-7, HHV-8 in gingival biopsies from chronic adult periodontitis patients. A case-control study

BACKGROUND: Recent reports have suggested that various herpesviruses may be involved in the occurrence and progression of different forms of periodontal disease. OBJECTIVE: The objective of the present study was to investigate the presence of the novel herpesviruses HHV-6, HHV-7 and HHV-8 in gingival biopsies from patients affected by chronic adult periodontitis. As control, gingival biopsies from periodontally healthy subjects were analysed. MATERIALS AND METHODS: Gingival biopsies were harvested from 23 volunteers: 13 patients affected by chronic adult periodontitis (CAP) and 10 periodontally healthy subjects. Each CAP patient contributed two biopsies involving the epithelium and connective tissue facing the sulcus/periodontal pockets: one biopsy from a site having a probing pocket depth (PPD) > or =5 mm and presenting with bleeding upon probing (affected site) at the time of biopsy collection, and the other biopsy from a site with PPD< or =3 mm and without bleeding on probing (nonaffected site). After DNA extraction, nested PCR was used in herpesvirus identification. RESULTS: HHV-6 DNA sequences were detected in one non-affected site (8%) and no affected sites (0%) of CAP patients. One biopsy (10%) in healthy subjects revealed HHV-6 positivity. Tissue specimens in 10/13 CAP patients (77%) and 7/10 healthy subjects (70%) contained HHV-7 DNA. HHV-7 prevalence in affected and nonaffected sites of CAP patients was 77% and 54%, respectively. HHV-8 was detected in 7.7% of CAP patients and 0% of healthy subjects. CONCLUSIONS: Gingival tissue may act as a reservoir for HHV-7. A high prevalence of HHV-7 was detected in both periodontally diseased and healthy individuals. The prevalence of HHV-6 and -8 was similarly low in both groups. Our data do not support an association of investigated herpesvirus species with destructive periodontal disease.     

Herpesviral-bacterial interrelationships in aggressive periodontitis

BACKGROUND: Recent findings have begun to provide a basis for a causal link between herpesviruses and aggressive periodontitis. One theory is that herpesviruses cooperate with specific bacteria in the etiopathogenesis of the disease. This study examined whether the presence of herpesviruses [human cytomegalovirus (HCMV), Epstein-Barr virus (EBV) type 1, herpes simplex virus (HSV) type 1 and 2] is associated with the presence of putative pathogenic bacteria (Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia, Campylobacter rectus, Actinobacillus actinomycetemcomitans) in aggressive periodontitis lesions. METHODS: The study included 18 young adults with advanced periodontitis and 16 periodontally healthy subjects from Ankara, Turkey. Subgingival specimens pooled from two sites in each subject were collected by a periodontal curette. Qualitative polymerase chain reaction methodology was used to identify herpesviruses and bacteria. Chi-square tests were employed to determine statistical associations among herpesviruses, bacteria and periodontal disease. RESULTS: HCMV, EBV-1 and HSV-1 were each detected in 72-78% of the aggressive periodontitis patients. HSV-2 occurred in 17% of the periodontitis patients. EBV-1 was detected in one periodontally healthy subject. The study bacteria occurred in 78-83% (P. gingivalis, T. forsythia, C. rectus) and in 44% (P. intermedia, A. actinomycetemcomitans) of the periodontitis samples, and in 0-19% of the samples from healthy periodontal sites. HCMV, EBV-1 and HSV-1 were positively associated with P. gingivalis, P. intermedia, T. forsythia and C. rectus, but not with A. actinomycetemcomitans. HSV-2 was not associated with any test bacteria. CONCLUSIONS: These results support the notion that the clinical outcome of some types of severe periodontal infection depends on the presence of specific herpesviruses and bacterial pathogens. Our findings open the door to testing a variety of hypotheses regarding the deleterious aspects of combined herpesviral-bacterial infections in periodontal sites.     

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.     

EBV-1 and HCMV in aggressive periodontitis in Brazilian patients

The purpose of the present investigation was to compare the presence of Epstein-Barr virus type 1 (EBV-1) and of Human Cytomegalovirus (HCMV) in crevicular fluid samples from deep and shallow periodontal pocket sites of Brazilian patients with aggressive periodontitis. A total of 30 systemically healthy patients with aggressive periodontitis participated in the study. Paper points were inserted into 2 gingivitis sites (<3 mm) and into 2 periodontitis sites (>5 mm) in each patient. PCR assay was used to identify genomic copies of HCMV and EBV-1. Twenty-three patients (77%) were positive for EBV-1, while only 2 patients (6%) were positive for HCMV. The McNemar test revealed a positive association between EBV-1 and periodontal lesions (p=0.043). Thirty-four (57%) out of 60 periodontitis sites were positive for EBV-1, whereas 18 (30%) gingivitis sites were positive (p=0.01). Only two sites (6.7%) were positive for HCMV. No positive association was found between HCMV and periodontitis or gingivitis (p=0.479). The elevated occurrence of EBV-1 DNA in periodontal pockets of patients with aggressive periodontitis supports a possible periodontopathic role of this virus.     

Herpesviruses 6, 7 and 8 in HIV- and non-HIV-associated periodontitis

Human herpesviruses, especially cytomegalovirus and Epstein Barr virus type-1, occur with higher frequency in subgingival specimens from periodontitis lesions than from healthy/gingivitis sites. Little or no information is available on the relationship between herpesvirus 6 (HHV-6), herpesvirus 7 (HHV-7) and herpesvirus 8 (HHV-8) and periodontal disease. This study determined the periodontal occurrence of HHV-6, HHV-7 and HHV-8 in 21 HIV-seropositive and 14 HIV-negative adults affected by periodontitis. Gingival biopsy specimens and paper-point samples of subgingival plaque were collected from sites showing 5 mm or more in probing depth. Nested polymerase chain reaction methodology was employed in herpesvirus identification. In the HIV-seropositive periodontitis group, 90% of gingival biopsies and 62% of subgingival plaque samples revealed at least one of the test viruses. HHV-6 occurred in 71%, HHV-7 in 67% and HHV-8 in 24% of gingival biopsies. In the HIV-negative adult periodontitis group, 43% of gingival biopsies showed at least 1 of the test viruses, with HHV-6 present in 21% and H HV-7 in 29% of gingival biopsies and with no detection of HHV-8. The combined occurrence of the 3 test herpesviruses was significantly higher in HIV-seropositive than in HIV-negative adult periodontitis patients (p = 0.008). The human periodontium might constitute a site of infection or reservoir for HHV-6, -7, -8.     

Cytomegalovirus periodontal presence is associated with subgingival Dialister pneumosintes and alveolar bone loss

Destructive periodontal disease is associated with human cytomegalovirus (HCMV), Epstein-Barr type 1 virus (EBV-1) and other members of the Herpesviridae family as well as with various gram-negative anaerobic bacteria, including the Dialister pneumosintes species. This study aimed to determine possible interrelationships between periodontal HCMV, EBV-1, herpes simplex virus and D. pneumosintes, and relate the microbiological findings to periodontitis clinical status. 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 the study herpesviruses and D. pneumosintes. Chi-squared tests, Fisher exact tests and multivariate logistic regression were employed to identify statistical associations among herpesviruses, bacteria and clinical variables. HCMV, and no other virus or combination of viruses, was positively associated with the presence of D. pneumosintes, and the relationship was specific for individual periodontitis sites with no detectable subject effect. D. pneumosintes was in turn positively associated with periodontal pocket depth and disease-active periodontitis. When the average percentage of alveolar bone loss in all teeth was treated as a response, HCMV remained significant even after D. pneumosintes was included in the model, suggesting that both HCMV and D. pneumosintes affected bone loss or, alternatively, HCMV affected factors not studied that themselves can induce bone loss. We hypothesize that periodontal HCMV sets the stage for subgingival proliferation of D. pneumosintes and subsequent periodontal disease progression. Studies on herpesviral-bacterial interactions may hold great promise for delineating important etio-pathogenic aspects of destructive periodontal disease.     

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.     

Viruses in periodontal disease - a review

The purpose of this review was to evaluate the evidence supporting the hypothesis that viral infection plays a role in the development of periodontitis. An involvement in periodontal diseases has been suspected specifically for human immunodeficiency virus (HIV) and herpes viruses. An association has been demonstrated between HIV infection and some distinct forms of periodontal infection, i.e. necrotizing lesions. Furthermore, reports of increased prevalence and severity of chronic periodontitis in HIV-positive subjects suggests that HIV infection predispose to chronic periodontitis. Several studies, most of them from the same research group, have demonstrated an association of herpesviruses with periodontal disease. Viral DNA have been detected in gingival tissue, gingival cervicular fluid (GCF) and subgingival plaque from periodontaly diseased sites. In addition markers of herpesviral activation have been demonstrated in the GCF from periodontal lesions. Active human cytomegalovirus (HCMV) replication in periodontal sites may suggest that HCMV re-activation triggers periodontal disease activity. Concerns regarding sampling, methods and interpretation cast doubts on the role of viruses as causes of periodontal disease.     

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.     

Typing of herpes simplex virus from human periodontium

Herpes simplex virus (HSV) is frequently detected in gingival crevicular fluid and in gingival biopsies of periodontal lesions; however, the relative occurrence of HSV type 1 and 2 in periodontal specimens has not been established. This investigation used type-specific polymerase chain reaction (PCR) to detect the presence of HSV-1 and HSV-2 in periodontal pocket samples from 26 patients who had previously been revealed to have periodontal HSV by PCR amplification of a gene shared by HSV-1 and HSV-2. HSV-1 was detected in all 26 periodontal pocket specimens and HSV-2 was not detected. Apparently, HSV-2 is a rare inhabitant of periodontal sites.     

Detection of human viruses in patients with chronic periodontitis and the relationship between viruses and clinical parameters

BACKGROUND: Recent studies have demonstrated that various human viruses, especially cytomegalovirus (HCMV), Epstein-Barr virus type-1 (EBV-1), and herpes simplex virus (HSV), seem to play a part in the pathogenesis of human periodontitis. Little information is available on the relationship between these viruses and clinical periodontal parameters in patients with chronic periodontitis. This study examined the occurrence of HCMV, EBV-1, and HSV in patients with chronic periodontitis and the relationship between these viruses and clinical parameters. METHODS: A nested polymerase chain reaction (PCR) method determined the presence of HCMV, EBV-1, and HSV. Subgingival plaque samples from 30 patients with chronic periodontitis and 21 randomly selected healthy controls were collected by paper points, and clinical measurements were recorded from both sampling sites and entire dentition. The following indices were measured: plaque index (PI), gingival index (GI), probing depth (PD), and clinical attachment loss (CAL). Results: HCMV was detected in 44.3% of chronic periodontitis patients and 14.3% of healthy persons (P < 0.05); EBV-1 in 16.7% of chronic periodontitis patients and 14.3% of healthy persons (P = 1.00); and HSV in 6.7% of chronic periodontitis patients and in no healthy persons. HCMV and EBV-1 detected and undetected sites in patients with periodontitis showed statistically significant differences in sampling clinical depth (SPD) and sampling clinical attachment loss (SCAL). Differences in the measurements of PI of entire dentition and GI of entire dentition between HSV detected and undetected sites were statistically significant. CONCLUSIONS: Findings of the present study confirm the frequent presence of HCMV in crevicular samples of chronic periodontitis lesions, and suggest a strong relationship between the presence of HCMV and EBV-1 in subgingival areas and the measurements of probing depth and probing attachment loss.     

Periodontitis lesions are a source of salivary cytomegalovirus and Epstein-Barr virus

AIM: Several herpesvirus species can be detected in periodontal pockets and saliva. This study compared human cytomegalovirus (HCMV) and Epstein-Barr virus (EBV) DNA copy counts in periodontitis sites and in whole saliva, and evaluated the potential of periodontal therapy to reduce the salivary level of the two viruses. MATERIAL AND METHODS: A total of 20 systemically healthy periodontitis patients, 21-56 years of age, participated in the study. All 20 patients were examined at baseline, and seven patients also at 3 months after periodontal therapy. Treatment included oral hygiene instruction, scaling and root planing, and surgery. Clinical parameters were evaluated using established methods. In each patient, virological samples were collected from one periodontal pocket of 6-10 mm probing depth, from the adjacent inflamed periodontal pocket wall, and from unstimulated whole saliva. Relationships between subgingival, gingival tissue and salivary herpesvirus counts were evaluated using Spearman's and Kendall's rank correlation coefficient tests. The 5'-nuclease (TaqMan) real-time polymerase chain reaction (PCR) assay was employed to quantify genomic copies of periodontal HCMV and EBV. RESULTS: At baseline, the 20 periodontitis patients showed significant positive correlations between gingival tissue and salivary counts of HCMV DNA (p=0.003) and EBV DNA (p=0.045). Periodontal pocket depth was positively correlated with salivary EBV DNA counts (p=0.002). Periodontal therapy reduced average full-mouth periodontal pocket depth from 4.6 mm to 1.4 mm, plaque index from 2.1 to 0.9, and gingival index from 2.1 to 0.4. Following treatment, HCMV DNA counts decreased 37.5 fold in subgingival sites and 64.6 fold in saliva, and EBV DNA counts decreased 5.7 fold in subgingival sites and 12.9 fold in saliva. CONCLUSIONS: The present study provides compelling evidence of a periodontitis source for salivary HCMV and EBV. The potential of periodontal therapy to decrease herpesvirus salivary counts may help diminish herpesvirus transmission from person to person and herpesvirus-related diseases in exposed individuals. Further research is warranted to determine the relationship between periodontal herpesvirus counts and the risk of viral transmission to close acquaintances.