Gingival bleeding on probing: relationship to change in periodontal pocket depth and effect of sodium hypochlorite oral rinse.

BACKGROUND AND OBJECTIVE: This study evaluated the potential of gingival bleeding on probing to serve as a predictor of future periodontal breakdown. It also assessed the ability of 0.25% sodium hypochlorite twice-a-week oral rinse to convert periodontal pockets showing bleeding on probing to nonbleeding sites. MATERIAL AND METHODS: The study was performed as a randomized, single-blinded, clinical trial in parallel groups. Seven periodontitis patients rinsed twice-weekly for 3 mo with 15 mL of a fresh solution of 0.25% sodium hypochlorite, and five periodontitis patients rinsed with water. The 12 study patients received no subgingival or supragingival scaling. Clorox(®) Regular-Bleach was the source of sodium hypochlorite. At baseline and 3-mo visits, gingival bleeding was assessed within 30 s after probing to full pocket depth using an approximate force of 0.75 N. RESULTS: A total of 470 (38%) of 1230 periodontal pockets in the bleach-rinse group revealed bleeding on probing at the initial visit but not at the 3-mo visit; only 71 (9%) of 828 pockets in the control group became bleeding-negative during the study (p < 0.001). Bleeding on probing in 4- to 7-mm-deep pockets decreased by 53% in the bleach-rinse group but increased by 6% in the water-rinse group (p < 0.001). Ninety-seven pockets showed depth increases of ≥ 2 mm after 3 mo: 60 (62%) of those pockets exhibited bleeding on probing at both the initial and the 3-mo visits; 24 (25%) bled at only one of the two visits; and 13 (13%) never demonstrated gingival bleeding (p < 0.001). CONCLUSIONS: Persistent gingival bleeding on probing was associated with an increased risk for periodontal breakdown, and the absence of gingival bleeding seemed to be a useful, although not perfect, indicator of disease stability. Twice-weekly oral rinsing with dilute bleach (0.25% sodium hypochlorite) produced a significant reduction in bleeding on probing, even in deep unscaled pockets. Sodium hypochlorite constitutes a valuable antiseptic in periodontal self-care.

Periodontal effects of 0.25% sodium hypochlorite twice-weekly oral rinse. A pilot study.

BACKGROUND AND OBJECTIVE: The study aimed to evaluate the effect of 0.25% sodium hypochlorite twice-weekly oral rinse on plaque and gingivitis in patients with minimally treated periodontitis. MATERIAL AND METHODS: The study included 30 patients with periodontitis, it lasted 3 mo, and it was performed as a randomized, controlled, single-blinded, clinical trial in parallel groups. Fifteen patients rinsed for 30 s with 15 mL of a fresh solution of 0.25% sodium hypochlorite (test) and 15 patients rinsed with 15 mL of water (control). Clorox(®) regular bleach was the source of the sodium hypochlorite. At baseline and at 2 wk, the study patients received professional subgingival irrigation for 5 min with either 0.25% sodium hypochlorite or water, but no subgingival or supragingival scaling. The presence or absence of supragingival plaque on facial and lingual surfaces was determined by visual inspection; each tooth was dried with air and mouth mirror rotation was used to provide light reflection to identify plaque on smooth surfaces and at the tooth line angles. Gingival bleeding within 30 s after probing to full pocket depth was assessed in six sites of each tooth. Adverse events were evaluated by questionnaire and visual examination. RESULTS: All 30 patients in the study completed the baseline and the 2 wk parts of the study and a subset of 12 participants completed the 3 mo part of the study. The sodium hypochlorite rinse group and the water rinse group, respectively, showed increases from baseline to 3 mo of 94% and 29% (3.2-fold difference) in plaque-free facial surfaces, of 195% and 30% (6.5-fold difference) in plaque-free lingual surfaces, and of 421% and 29% (14.5-fold difference) in number of teeth with no bleeding on probing. The differences in clinical improvement between the sodium hypochlorite rinse group and the water rinse group were statistically significant. No adverse events were identified in any of the study patients, except for minor complaints about the taste of bleach. CONCLUSION: A twice-weekly oral rinse with 0.25% sodium hypochlorite produced marked decreases in dental plaque level and bleeding on probing and may constitute a promising new approach to the management of periodontal disease. Long-term controlled studies on the effectiveness of sodium hypochlorite oral rinse are needed and encouraged.

Salivary infectious agents and periodontal disease status.

BACKGROUND AND OBJECTIVES: The potential of salivary microorganisms to diagnose periodontal disease and to guide periodontal treatment is a research topic of current interest. This study aimed to determine whether the salivary counts of periodontopathic microbes correlated with the periodontal pocket counts of the same infectious agents, and whether the salivary counts of the test infectious agents could distinguish among individuals with periodontal health and various types of periodontal disease. MATERIAL AND METHODS: The study included 150 systemically healthy adults, of whom 37 were periodontally healthy, 31 had gingivitis, 46 had chronic periodontitis and 36 had aggressive periodontitis. Each study subject contributed microbial samples from the two deepest periodontal pockets of the dentition and from whole saliva. Aggregatibacter actinomycetemcomitans, Campylobacter rectus, Fusobacterium nucleatum, Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia and Epstein-Barr virus were identified using the TaqMan real-time PCR methodology. Statistical analysis was performed using the Mann-Whitney U-test and the receiver operating characteristic statistics. RESULTS: C. rectus, F. nucleatum, P. gingivalis, P. intermedia and T. forsythia occurred with significantly higher copy-counts in salivary samples from patients with gingivitis, chronic periodontitis and aggressive periodontitis than from periodontally healthy individuals. A. actinomycetemcomitans only showed higher salivary copy-counts in subjects with aggressive periodontitis compared with subjects with healthy periodontium, and the salivary copy-counts of Epstein-Barr virus did not reveal any significant difference among the four subject groups studied. The diagnostic sensitivity for periodontitis was 89.19 for P. gingivalis and for T. forsythia and 86.49 for P. intermedia, with specificities ranging from 83.78 to 94.59. The optimal copy-counts per mL saliva for identifying periodontitis were 40,000 for P. gingivalis, 700,000 for T. forsythia and 910,000 for P. intermedia. CONCLUSION: Salivary copy-counts of P. gingivalis, T. forsythia and P. intermedia appear to have the potential to identify the presence of periodontitis, whereas the salivary level of the other test infectious agents may possess little or no diagnostic utility. Longitudinal studies are warranted to determine the ability of salivary copy-counts of major periodontopathic bacteria to predict future periodontal breakdown.

Human cytomegalovirus in peripheral giant cell granuloma.

BACKGROUND: The peripheral giant cell granuloma is a relatively common non-neoplastic inflammatory lesion of gingiva, but the etiopathogeny remains unknown. This study aimed to evaluate the importance of human cytomegalovirus and Epstein-Barr virus in a peripheral giant cell granuloma of a 47-year-old female. METHODS: The lesion was studied clinically, histopathologically, immunologically and virologically using established procedures. RESULTS: The gingival growth was located at the mesial surface of the maxillary left canine having a vital pulp. The mass was 12 x 21 mm in size and exhibited a smooth surface with no evidence of fluctuation on palpation. An excisional biopsy revealed giant cells in a fibrohistiocytic stroma with areas of haemorrhage. Serum protein levels and lymphocyte subsets were within normal limits, except CD3(+) and CD4(+) cells were below normal ranges. Polymorphonuclear leukocytes expressed p150,95 (CD11c/CD18) and CXCR-2 receptors within normal ranges, but the CXCR1 receptor showed decreased density, and CD15 were below normal range. A virological sample of the tooth surface adjacent to the gingival swelling yielded 7.6 x 10(3) copy-counts of cytomegalovirus and 4.3 x 10(3) copy-counts of Epstein-Barr virus. CONCLUSIONS: The clinical and histological findings were consistent with the diagnosis of peripheral giant cell granuloma. Cytomegalovirus has the potential to induce multinucleated giant cells, and the possibility that the virus contribute to the development of peripheral giant cell granuloma merits further study.

Cytomegalovirus-infected inflammatory cells in dental periapical lesions.

INTRODUCTION: As cytomegalovirus may be etiologically involved in periapical pathosis of endodontic origin, this study aimed to determine the cellular source of periapical cytomegalovirus. METHODS: Periapical granulomatous tissue was collected from 15 extracted teeth with symptomatic periapical lesions. Multi-color flow cytometry was used to identify cytomegalovirus-infected cells. RESULTS: Cytomegalovirus infection was identified in 10 of the 15 (67%) study lesions, and in periapical monocytes/macrophages (40% of lesions) and T lymphocytes (54% of lesions), but not in periapical B lymphocytes. CONCLUSION: This study and previous polymerase chain reaction-based investigations show that cytomegalovirus is a frequent inhabitant of symptomatic periapical lesions.

Periodontitis lesions are the main source of salivary cytomegalovirus.

BACKGROUND: Herpesviruses play causal or cooperative roles in childhood infections, tumorigenesis, ulcerogenesis, and periodontitis. Saliva is a common vehicle of herpesvirus horizontal transmission, but the source of salivary herpesviruses remains obscure. To evaluate the significance of periodontal disease in shedding of oral herpesviruses, this study determined the genome-copy counts of human cytomegalovirus (HCMV) and Epstein-Barr virus (EBV) in whole saliva of subjects with periodontitis, gingivitis, or no natural teeth. METHODS: Whole saliva was collected from 14 periodontitis patients, 15 gingivitis patients and 13 complete denture wearers. The study subjects were systemically healthy and had not received periodontal treatment in the past 3 months. Real-time TaqMan polymerase chain reaction was used to determine the salivary load of HCMV and EBV. RESULTS: Salivary HCMV was detected in seven (50%) periodontitis patients, but not in any gingivitis or edentulous subjects (P < 0.001). Salivary EBV was detected in 11 (79%) periodontitis patients, in five (33%) gingivitis patients, and in seven (54%) edentulous subjects (P = 0.076). Salivary samples showed copy counts of HCMV in the range of 3.3 x 10(3)-4.2 x 10(4)/ml and of EBV in the range of 3.6 x 10(2)-1.6 x 10(9)/ml. CONCLUSIONS: HCMV and EBV are commonly present in the saliva of periodontitis patients. Periodontitis lesions of systemically healthy subjects seem to constitute the main origin of salivary HCMV, but do not comprise the sole source of salivary EBV.

Relationship between human cytomegalovirus transcription and symptomatic apical periodontitis in Iran.

BACKGROUND/AIMS: Apical periodontitis of endodontic origin may develop as a result of cooperative interactions among herpesviruses, specific pathogenic bacteria and tissue-destructive inflammatory mediators. This study sought to identify the presence of Epstein-Barr virus (EBV) and human cytomegalovirus (HCMV) transcripts in symptomatic and asymptomatic periapical lesions of individuals living in Iran. MATERIAL AND METHODS: Fifty endodontic patients (28 with symptomatic periapical lesions and 22 with asymptomatic periapical lesions) were included in the study. In each study subject, a microbiological periapical sample was collected using a curette in conjunction with periapical surgery. A reverse transcription-polymerase chain reaction assay was used to identify transcripts of EBV and HCMV. RESULTS: Human cytomegalovirus transcript was detected in 15 of the 28 (53.6%) symptomatic and in six of the 22 (27.3%) asymptomatic periapical study lesions (significant difference between symptomatic and asymptomatic lesions; P = 0.03, chi-square test). Epstein-Barr virus transcript was identified in one symptomatic and in two asymptomatic periapical lesions. CONCLUSION: This study establishes that HCMV transcription is common in apical periodontitis and is most frequent in symptomatic lesions. The high frequency of active herpesvirus infections in severe apical periodontitis changes the pathogenic paradigm of the disease and may also have preventive and therapeutic implications.

Quantitative analysis of association between herpesviruses and bacterial pathogens in periodontitis.

BACKGROUND AND OBJECTIVE: The development of human periodontitis may depend upon cooperative interactions among herpesviruses, specific pathogenic bacteria and tissue-destructive inflammatory mediators. This study sought to identify associations among human cytomegalovirus, Epstein-Barr virus and six putative periodontopathic bacteria in periodontitis lesions. MATERIAL AND METHODS: Fifteen periodontitis patients (nine with aggressive periodontitis and six with chronic periodontitis) and 15 periodontally normal subjects were included in the study. In each study subject, a microbiological sample was collected, using a curette, from the deepest periodontal probing depth of the dentition. A real-time TaqMan polymerase chain reaction assay was employed to determine the subgingival counts of human cytomegalovirus, Epstein-Barr virus, Porphyromonas gingivalis, Tannerella forsythia, Prevotella intermedia, Aggregatibacter actinomycetemcomitans, Fusobacterium nucleatum and Campylobacter rectus. Statistical analysis was performed using the Student's t-test, the Pearson correlation coefficient test and the single variable logistic regression test for odds ratio-based risk calculation. RESULTS: Human cytomegalovirus was detected in eight periodontitis lesions and in one normal periodontal site, Epstein-Barr virus was detected in nine periodontitis lesions and in two normal periodontal sites, and the study bacteria were detected in 6-15 periodontitis lesions and in 1-11 normal periodontal sites. Correlations were found between counts of human cytomegalovirus and Epstein-Barr virus, between counts of human cytomegalovirus and P. gingivalis, T. forsythia and C. rectus, and between counts of Epstein-Barr virus and P. gingivalis and T. forsythia. Human cytomegalovirus and Epstein-Barr virus counts were also positively associated with the level of periodontal attachment loss, probing pocket depth and gingival bleeding on probing. CONCLUSION: This study confirmed that periodontal human cytomegalovirus and Epstein-Barr virus are associated with major periodontopathic bacteria and with the severity of periodontal disease. The finding of abundant herpesviruses in periodontitis lesions redefines the pathogenic paradigm of the disease. Understanding the interplay between herpesviruses and specific bacterial species in the pathogenesis of periodontitis may form the basis for new approaches to preventing, reducing or delaying tissue breakdown from periodontal infections.

Epstein-Barr virus in oral diseases.

Epstein-Barr virus (EBV), a B-lymphotropic gamma-herpesvirus, causes infectious mononucleosis and oral hairy leukoplakia, and is associated with various types of lymphoid and epithelial malignancies. Saliva is the main vehicle for EBV transmission from individual to individual. Recent studies have also implicated EBV in the pathogenesis of advanced types of periodontal disease. EBV DNA is detected in 60-80% of aggressive periodontitis lesions and in 15-20% of gingivitis lesions or normal periodontal sites. The periodontal presence of EBV is associated with an elevated occurrence of periodontopathic anaerobic bacteria. Moreover, EBV active infection occurs in approximately 70% of symptomatic and large-size periapical lesions. EBV and cytomegalovirus often co-exist in marginal and apical periodontitis. Periodontal therapy can markedly suppress the EBV load in periodontal pockets as well as in saliva, which has the potential to reduce the risk of viral transmission between close individuals. EBV proteins up-regulate cytokines and growth factors, which seem to play a central role in the proliferative response of tongue epithelial cells in oral hairy leukoplakia and in the cell-transformation process of EBV-associated malignancies. Further research is needed to identify the full range of EBV-related diseases in the human oral cavity.

Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis subgingival presence, species-specific serum immunoglobulin G antibody levels, and periodontitis disease recurrence.

BACKGROUND AND OBJECTIVE: The biological and clinical effects of antibody against periodontal pathogenic bacteria are incompletely understood. This study evaluated the inter-relationships among periodontal levels of cultivable Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis, species-specific serum immunoglobulin G (IgG) antibody levels, and periodontitis disease activity. MATERIAL AND METHODS: Forty-three adults who had previously been treated for periodontitis and who also harbored cultivable A. actinomycetemcomitans or P. gingivalis were evaluated semiannually for clinical disease recurrence over a 36-month period. Each patient provided subgingival microbial samples, for the recovery of A. actinomycetemcomitans and P. gingivalis, from the two deepest pockets in each dentition sextant. A. actinomycetemcomitans and P. gingivalis serum IgG antibody levels were assessed using enzyme-linked immunosorbent assay (ELISA), together with whole-cell sonicate extracts from A. actinomycetemcomitans serotypes a-c and P. gingivalis ATCC 33277. Data were analyzed using the Mantel-Haenszel chi-square and Fisher exact two-tailed tests. RESULTS: Eighteen (60.0%) of 30 A. actinomycetemcomitans-positive subjects, and 10 (76.9%) of 13 P. gingivalis-positive subjects, exhibited recurrent periodontal breakdown within 36 months of periodontal therapy. Nineteen (67.9%) of the 28 patients with active periodontitis had A. actinomycetemcomitans or P. gingivalis serum antibody levels below designated threshold values. In comparison, 10 (66.7%) of 15 culture-positive clinically stable subjects showed A. actinomycetemcomitans or P. gingivalis serum antibody levels above threshold values. The difference between specific antibody levels in periodontitis-active and periodontitis-stable patients was statistically significant (p = 0.032). CONCLUSIONS: Serum levels of IgG antibodies against A. actinomycetemcomitans or P. gingivalis in periodontitis-stable patients were higher than those in patients with active periodontitis. The results suggest that elevated levels of IgG antibody against A. actinomycetemcomitans and P. gingivalis have a detectable protective effect against periodontal infections with these microorganisms.

Human cytomegalovirus, Epstein-Barr virus and bone resorption-inducing cytokines in periapical lesions of deciduous teeth.

BACKGROUND: A connection of herpesvirus periapical infection with symptomatic and large-size periapical lesions has been recognized in adult patients, but no data exist about a possible involvement of herpesviruses in severe periapical pathosis in children. Herpesviruses have the potential to elicit potent bone resorption-inducing cytokines in mammalian cells. AIM: This study aimed to determine the occurrence of human cytomegalovirus and Epstein-Barr virus DNA, and mRNA transcripts of receptor activator of nuclear kappa B ligand (RANKL), osteoprotegerin, core binding factor alpha-1, colony stimulating factor-1, transforming growth factor-beta, and monocyte chemoattractant protein-1 in periapical symptomatic pathosis of deciduous teeth. MATERIAL AND METHODS: Twelve deciduous molar teeth from patients aged 2-8 years were extracted due to severe periapical infection, and granulomatous tissue adherent to the root tip of the extracted teeth was collected using a surgical knife. Non-diseased pulpal tissue, obtained from 12 teeth extracted for orthodontic reasons, served as negative control. Polymerase chain reaction assays were employed to identify herpesvirus DNA and cytokine gene expression, using established polymerase chain reaction primers and procedures. RESULTS: Seven (58%) of the periapical lesions yielded human cytomegalovirus and eight (67%) Epstein-Barr virus. Only one (8%) periapical lesion showed neither human cytomegalovirus nor Epstein-Barr virus. In healthy pulpal tissue, one (8%) specimen demonstrated human cytomegalovirus and another (8%) specimen revealed Epstein-Barr virus. Of the cytokines examined, RANKL expression showed significantly higher occurrence in periapical pathosis than in healthy pulpal tissue (P < 0.040). No relationship was identified between the type of herpesvirus and cytokine expression in the periapical lesions studied. CONCLUSIONS: The present findings provide evidence of a putative role of human cytomegalovirus and Epstein-Barr virus in the pathogenesis of symptomatic periapical pathosis in deciduous teeth. Increased RANKL expression in periapical lesions may be of pathogenetic significance.

Severe periodontitis in a 5-year-old girl with hyperimmunoglobulin E syndrome.

The hyperimmunoglobulin E syndrome (HIES) is a multisystem disorder that affects the: (1) dentition; (2) skeleton; (3) connective tissues; and (4) immune system. Little is known about periodontal manifestations of the syndrome. The purpose of this report was to describe a 5-year-old girl with suspected autosomal-recessive HIES syndrome who revealed profusely bleeding and painful gingiva and generalized aggressive periodontitis. A polymerase chain reaction (PCR)-based microbiological examination detected Porphyromonas gingivalis, Tannerella forsythia, Prevotella nigrescens, Treponema denticola, Eikenella corrodens, and Campylobacter rectus in the deep periodontitis lesions. The extraction of all deciduous teeth due to a poor prognosis and risk of systemic infection led to resolution of the oral inflammation. Long-term follow-up is required to determine the periodontal prognosis of the erupting permanent teeth.

Initial antimicrobial effect of controlled-release doxycycline in subgingival sites.

OBJECTIVES: To determine the ability of a 10% doxycycline hyclate controlled-release polymer (Atridox) to suppress periodontopathic bacteria when placed subgingivally following scaling and root planing (Sc/Rp). METHODS: Eight males and seven females, mean age 48 years, with moderate to advanced periodontitis participated in the study. In each patient, bilateral periodontal pockets probing 6-7 mm were randomly assigned to treatment by Sc/Rp + doxycycline polymer or by Sc/Rp alone. Subgingival placement of doxycycline polymer was carried out according to the manufacturer's instructions. Sc/Rp was performed with hand instruments for at least 10 min in each study tooth. Subgingival samples were collected by paper-points at baseline, at 2 weeks and at 4 weeks post-treatment. Culture methodology was used to isolate and identify putative periodontal pathogens, including Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Dialister pneumosintes, Tannerella forsythia, Prevotella intermedia/Prevotella nigrescens, Campylobacter species, Eubacterium species, Fusobacterium species, Peptostreptococcus micros, Eikenella corrodens, Staphylococcus species, enteric gram-negative rods, beta-hemolytic streptococci and yeasts. The microbiologic examination was carried out blindly. Microbiological data were analyzed using a General Linear Model Analysis of Variance for within and between group effects. RESULTS: Sites receiving Sc/Rp + doxycycline polymer and sites receiving Sc/Rp alone exhibited similar levels of periodontal pathogens at baseline and did not differ significantly in total viable counts and proportional recovery of periodontopathic bacteria post-treatment. CONCLUSIONS: Controlled-release doxycycline placed in moderate to deep periodontal pockets caused no significant additional reduction in the subgingival pathogenic microbiota compared to thorough Sc/Rp alone. Since controlled-release doxycycline may not significantly suppress several subgingival pathogenic microorganisms and seems to possess no distinct advantage over broad-spectra, safe and inexpensive antiseptics, the rationale for its employment in periodontal therapy remains unclear.

Cytomegalovirus infection in symptomatic periapical pathosis.

AIM: To compare the presence of human cytomegalovirus (HCMV) and Epstein-Barr virus (EBV) infections in samples from 25 symptomatic and 19 asymptomatic periapical lesions. METHODOLOGY: Periapical samples were collected by sterile curettes in conjunction with apicectomy. cDNA-based HCMV and EBV identification was performed on total mRNAs extracted from peripapical tissues, using primers for genes transcribed during the productive phase of the herpesvirus infection. Statistical analysis was performed using chi-squared test. RESULTS: HCMV was detected in 100% of the symptomatic and in 37% of the asymptomatic study lesions. EBV was identified only in HCMV-infected periapical lesions. The difference in occurrence of HCMV and EBV between symptomatic and asymptomatic periapical lesions was statistically significant (P < 0.0001). CONCLUSIONS: The noteworthy finding of this study was the ubiquitous occurrence of HCMV active infection in symptomatic periapical pathosis. EBV may contribute to periapical pathogenesis in a subset of symptomatic lesions. HCMV and EBV infections may cause periapical pathosis by inducing cytokine and chemokine release from inflammatory or connective tissue cells, or by impairing local host defences resulting in heightened virulence of resident bacterial pathogens. Knowledge about the role of herpesviruses in periapical pathosis seems important to fully delineate the pathogenesis of endodontic infectious diseases. HCMV and probably EBV should be added to the list of putative pathogenic agents in symptomatic periapical disease.

Update on human cytomegalovirus in destructive periodontal disease.

AIM: Human cytomegalovirus (HCMV), a herpesvirus, is discussed in this review as it relates to destructive periodontal disease in humans. RESULTS: HCMV genomic sequences, detected by polymerase chain reaction identification, occur with elevated frequency in severe adult periodontitis, localized and generalized aggressive (juvenile) periodontitis, Papillon-Lefèvre syndrome periodontitis, acute necrotizing ulcerative gingivitis, and periodontal abscesses. DISCUSSION: Herpesviruses establish lifelong persistent infections. HCMV infection involves an asymptomatic latent phase interrupted by periods of recrudescence where viral replication and possibly clinical disease become manifest. HCMV reactivation is triggered by a number of immunosuppressive factors, some of which have been shown also to be risk factors/indicators of periodontitis. HCMV periodontal infection may cause release of tissue-destructive cytokines, overgrowth of pathogenic periodontal bacteria, and initiation of cytotoxic or immunopathologic events. CONCLUSIONS: A growing body of data supports the concept that HCMV contributes to severe types of periodontal disease. HCMV infection of the periodontium may alter the immune control of resident microorganisms and be important in a multistage pathogenesis of periodontitis involving viral activation, periodontopathic bacteria, and host immune responses. Understanding the significance of HCMV and other herpesviruses in the development of periodontal disease may have important therapeutic implications. Vaccines against HCMV, which are in various stages of development, need to be evaluated for their ability to decrease the incidence of destructive periodontal disease.

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.

Cytomegalovirus and Epstein-Barr virus are associated with symptomatic periapical pathosis.

BACKGROUND: Recent studies have identified human cytomegalovirus (HCMV) and Epstein-Barr virus (EBV) in symptomatic periapical lesions. Little information exists on HCMV and EBV in asymptomatic periapical lesions. AIM: To compare the presence of late transcripts of HCMV, EBV and herpes simplex virus (HSV) in symptomatic and asymptomatic periapical lesions. METHODS: Periapical samples were collected from seven symptomatic and seven asymptomatic periapical lesions at the time of apicoectomy. HCMV, EBV and HSV late mRNAs were identified by reverse transcription polymerase chain reaction. RESULTS: HCMV mRNA was detected in all seven symptomatic periapical lesions and in one asymptomatic lesion (Chi-squared test, Yates'P-value = 0.007). EBV mRNA was detected in six symptomatic lesions and in one asymptomatic lesion (P = 0.04). One asymptomatic lesion yielded HSV mRNA. CONCLUSIONS: HCMV and EBV active infections are associated with acute exacerbation of apical periodontitis. HSV seems to be unimportant in periapical pathosis.

Povidone-iodine as a periodontal pocket disinfectant.

OBJECTIVES AND BACKGROUND: Povidone-iodine [polyvinylpyrrolidone-iodine complex (PVP-iodine)] might constitute a valuable adjunct to current periodontal therapy because of its broad-spectrum antimicrobial activity, low potential for developing resistance and adverse reactions, wide availability, ease of use, and low financial cost. This investigation employed a randomized, split-mouth study design to determine the microbiological and clinical effects of 10% PVP-iodine subgingival irrigation in periodontitis lesions showing radiographic evidence of subgingival calculus. METHODS: Sixteen adults having at least one periodontal pocket of 6 mm or more in each quadrant of the dentition and harboring one or more periodontopathic bacteria participated in the study. In each subject, a study site in each quadrant was randomly chosen to receive either subgingival irrigation with 10% PVP-iodine together with scaling and root planing, scaling and root planing alone, subgingival irrigation with 10% PVP-iodine, or subgingival irrigation with sterile saline. Prior to therapy and at 5 weeks post-treatment, microbiological culture was carried out without knowledge of the clinical status or the type of treatment rendered. A blinded clinical examiner determined presence of dental plaque, probing pocket depth, and gingival bleeding on probing. Microbiological and clinical data were analyzed using a repeated measures analysis of variance and Kruskal-Wallis rank test with the Tukey and Mann-Whitney post hoc tests. RESULTS: At 5 weeks post-treatment, subgingival irrigation with PVP-iodine together with scaling and root planing caused a 95% or greater reduction in total pathogen counts in 44% of pockets having >/= 6 mm depth whereas scaling and root planing alone, povidone-iodine irrigation alone and water irrigation alone caused 95% reduction of total pathogens only in 6-13% of similar study sites (P = 0.02). Reduction in mean pocket depth was 1.8 mm for the PVP-iodine/scaling and root planing group, 1.6 mm for the scaling and root planing group, and 0.9 mm for the PVP-iodine and the saline monotherapy groups, with statistical significance reached for the scaling and root planing group vs. the PVP-iodine group (P = 0.04) and for the scaling and root planing group vs. the saline group (P = 0.02). Reduction in visible dental plaque, which ranged from 38% to 62%, showed no significant differences among treatment groups. CONCLUSIONS: The addition of subgingival PVP-iodine irrigation to conventional mechanical therapy may be a cost-effective means of reducing total counts of periodontal pathogens and helping control periodontal disease. However, subgingival irrigation with PVP-iodine without concomitant mechanical debridement might not improve microbiological and clinical variables in comparison with saline irrigation, at least not in sites with radiographic evidence of subgingival calculus.

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.

Cytomegalovirus and Epstein-Barr virus active infection in periapical lesions of teeth with intact crowns.

Herpesviruses seem to play an important role in the pathogenesis of aggressive periodontitis and may also contribute to periapical pathosis. This study determined the presence of human cytomegalovirus, Epstein-Barr virus, and herpes simplex virus productive infection in five symptomatic periapical lesions of teeth having intact crowns and calcified necrotic pulps. Periapical samples were collected in conjunction with periapical surgery and kept frozen until virological examination. Reverse transcription-polymerase chain reaction was used in herpesviral identification. RNA was isolated from periapical tissue by a guanidinium isothiocyanate-acid phenol procedure. cDNAs were generated from highly conserved regions of the test viruses using a preamplification kit. Sensitivity and validity of the PCR-primers were determined according to established methods. Amplification products were identified using gel electrophoresis. Human cytomegalovirus and Epstein-Barr virus dual transcription was detected in all five periapical lesions studied. Herpes simplex virus transcript was not identified in any lesion. The present data suggest that human cytomegalovirus or Epstein-Barr virus activation participate in the pathogenesis of symptomatic periapical lesions. We hypothesize that periapical active herpesvirus infection impairs local defenses, thereby inducing overgrowth of endodontopathic bacteria and the clinical flare-up of inflammation.