Real-time polymerase chain reaction to determine the prevalence and copy number of epstein-barr virus and cytomegalovirus DNA in subgingival plaque at individual healthy and periodontal disease sites.
ABSTRACT Detection of cytomegalovirus (CMV) and Epstein-Barr virus (EBV) in plaque from patients with periodontal disease provides support for the theory that these viruses play a role in the pathogenesis of periodontitis. This study sought to further define this relationship by determining the prevalence of these viruses at individual disease and healthy sites of patients with periodontal disease and to determine whether the presence and amount of viral DNA correlate with disease severity.
Subgingival plaque from three healthy and three disease sites of 65 patients who had chronic periodontitis were evaluated for the presence and amount of EBV, CMV, and Fusobacterium nucleatum DNA using real-time polymerase chain reaction. Patient serum was evaluated for antibodies against EBV and CMV using enzyme-linked immunosorbent assays.
EBV DNA was detected in 18.5% of subgingival plaque samples (72/390) and in at least one of the six plaque samples in 44.6% (29/65) of the patients. CMV DNA was detected in one plaque sample (0.3%). EBV was significantly more prevalent in disease sites (28.2%; 55/195) than in healthy sites (8.7%; 17/195; P = 0.002). However, neither EBV prevalence nor its amount correlated with increased probing depth >5 mm or attachment loss >2 mm, whereas the amount of F. nucleatum DNA did. Sites positive for EBV had a median copy number of eight. Antibodies against EBV and CMV were detected in 85.7% and 78.6% of persons evaluated, respectively.
EBV was infrequent and CMV was rarely present in individual subgingival sites affected by chronic periodontitis.
- SourceAvailable from: Charlene W J AfricaPeriodontal Diseases - A Clinician's Guide, 02/2012; , ISBN: 978-953-307-818-2
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ABSTRACT: In the past 50 years, conceptual changes in the field of periodontal diagnostics have paralleled those associated with a better scientific understanding of the full spectrum of processes that affect periodontal health and disease. Fifty years ago, concepts regarding the diagnosis of periodontal diseases followed the classical pathology paradigm. It was believed that the two basic forms of destructive periodontal disease were chronic inflammatory periodontitis and 'periodontosis'- a degenerative condition. In the subsequent 25 years it was shown that periodontosis was an infection. By 1987, major new concepts regarding the diagnosis and pathogenesis of periodontitis included: (i) all cases of untreated gingivitis do not inevitably progress to periodontitis; (ii) progression of untreated periodontitis is often episodic; (iii) some sites with untreated periodontitis do not progress; (iv) a rather small population of specific bacteria ('periodontal pathogens') appear to be the main etiologic agents of chronic inflammatory periodontitis; and (v) tissue damage in periodontitis is primarily caused by inflammatory and immunologic host responses to infecting agents. The concepts that were in place by 1987 are still largely intact in 2012. However, in the decades to come, it is likely that new information on the human microbiome will change our current concepts concerning the prevention, diagnosis and treatment of periodontal diseases.Periodontology 2000 06/2013; 62(1):20-36. · 4.01 Impact Factor
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ABSTRACT: The aim of this study was to determine the presence and quantity of human cytomegalovirus (CMV) and Epstein-Barr virus (EBV) DNA in the saliva of patients with periodontitis, and investigate the correlation between these factors. Presence and amounts of viral DNA in saliva and subgingival plaque samples, from healthy and disease sites, of 65 adults diagnosed with chronic periodontitis were determined using quantitative real-time polymerase chain reaction. Epstein-Barr virus DNA was detected in saliva of 81.5% (53/65) of patients at a median concentration of 4325 copies ml(-1). CMV DNA was detected in saliva of one individual (1.5%) at low copy number. Patients who had EBV in saliva were 10 times more likely to have EBV in subgingival plaque than patients lacking EBV in saliva (odds ratio = 10.1, 95% confidence interval = 2.6-39.5; P = 0.0009). EBV DNA burden in saliva positively correlated with the amounts detected in plaque and with amounts detected in increasing number of affected sites (P < 0.0001). EBV DNA presence and quantity in saliva did not correlate with increasing severity of disease as measured by periodontal indices. Epstein-Barr virus DNA presence and burden in saliva are associated with its presence and burden in subgingival plaque, but presence and burden in saliva does not correlate with periodontal disease severity.Oral Diseases 07/2009; 15(8):554-9. · 2.38 Impact Factor