Epstein–Barr virus associated peri-implantitis: a split-mouth study
Objectives Herpesviral–bacterial synergism may play a potential role in periodontitis and peri-implantitis (PI) etiopathogenesis. PI lesions can worsen depending on specific microbial challenge and host susceptibility. This cross-sectional split-mouth study aimed to substantiate herpesviral–bacteria...
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| Vydáno v: | Clinical oral investigations Ročník 19; číslo 2; s. 535 - 543 |
|---|---|
| Hlavní autoři: | , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
Berlin/Heidelberg
Springer Berlin Heidelberg
01.03.2015
Springer Nature B.V |
| Témata: | |
| ISSN: | 1432-6981, 1436-3771, 1436-3771 |
| On-line přístup: | Získat plný text |
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| Abstract | Objectives
Herpesviral–bacterial synergism may play a potential role in periodontitis and peri-implantitis (PI) etiopathogenesis. PI lesions can worsen depending on specific microbial challenge and host susceptibility. This cross-sectional split-mouth study aimed to substantiate herpesviral–bacterial co-infection in PI patients and assess associations with periodontopathogen salivary contamination.
Methods
PCR-based identification was performed on 23 patients presenting PI and contralateral healthy implants, and compared to unstimulated whole saliva. Clinical evaluation included probing depths, bleeding on probing, and suppuration. Radiographs were assessed for the presence of lamina dura and bone loss. Three sample sites per patient were tested: PI lesions, healthy implant sulci, and saliva. Quantitative PCR evaluated Epstein–Barr virus (EBV) and cytomegalovirus (CMV) copy counts. Significance of group comparisons for binary-dependent variables, within-subjects designs, was determined by McNemar's chi-square test. Risk analysis was evaluated through odds ratios (OR).
Results
PI lesions were 14.2 (
P
= 0.001; 95 % confidence interval [CI], 1.6–124.1) and 3 times (
P
= 0.03; 95 % CI, 0.7–11.9) more likely to harbor EBV than healthy implants and saliva, respectively. EBV positive predictive value was 90 %. PI was associated with absence of lamina dura and higher periodontopathogen proportions. Saliva sampling showed high agreement with PI bacterial detection (89–100 % rate) but not with EBV (44.4 %). The OR of PI lesions harboring
Treponema denticola
or
Tannerella forsythia
was 6.79 (
P
= 0.007; 95 % CI, 1.8–25.0) and 3.3 (
P
< 0.0001; 95 % CI, 0.3–34.3) times higher than healthy implants, respectively. Saliva of patients with PI was 5.6 times more likely to be contaminated with
Prevotella nigrescens
than healthy peri-implant sulci (
P
= 0.002). PI lesions were 1.92 times more likely to harbor
Prevotella nigrescens
than healthy implants (
P
= 0.04).
Conclusions
EBV is a potential candidate in peri-implantitis etiopathogenesis. Saliva PCR analysis is useful in predicting peri-implantitis-specific bacterial infection but not EBV or CMV.
Clinical significance
Herpesviral–bacterial synergism may favor ongoing microbial challenge in peri-implant disease and exacerbate its progression. EBV infection may explain non-responsive to treatment PI. Peri-implantitis individuals may benefit from antiviral therapy. |
|---|---|
| AbstractList | Herpesviral-bacterial synergism may play a potential role in periodontitis and peri-implantitis (PI) etiopathogenesis. PI lesions can worsen depending on specific microbial challenge and host susceptibility. This cross-sectional split-mouth study aimed to substantiate herpesviral-bacterial co-infection in PI patients and assess associations with periodontopathogen salivary contamination. PCR-based identification was performed on 23 patients presenting PI and contralateral healthy implants, and compared to unstimulated whole saliva. Clinical evaluation included probing depths, bleeding on probing, and suppuration. Radiographs were assessed for the presence of lamina dura and bone loss. Three sample sites per patient were tested: PI lesions, healthy implant sulci, and saliva. Quantitative PCR evaluated Epstein-Barr virus (EBV) and cytomegalovirus (CMV) copy counts. Significance of group comparisons for binary-dependent variables, within-subjects designs, was determined by McNemar's chi-square test. Risk analysis was evaluated through odds ratios (OR). PI lesions were 14.2 (P=0.001; 95 % confidence interval [CI], 1.6-124.1) and 3 times (P=0.03; 95 % CI, 0.7-11.9) more likely to harbor EBV than healthy implants and saliva, respectively. EBV positive predictive value was 90 %. PI was associated with absence of lamina dura and higher periodontopathogen proportions. Saliva sampling showed high agreement with PI bacterial detection (89-100 % rate) but not with EBV (44.4 %). The OR of PI lesions harboring Treponema denticola or Tannerella forsythia was 6.79 (P=0.007; 95 % CI, 1.8-25.0) and 3.3 (P<0.0001; 95 % CI, 0.3-34.3) times higher than healthy implants, respectively. Saliva of patients with PI was 5.6 times more likely to be contaminated with Prevotella nigrescens than healthy peri-implant sulci (P=0.002). PI lesions were 1.92 times more likely to harbor Prevotella nigrescens than healthy implants (P=0.04). EBV is a potential candidate in peri-implantitis etiopathogenesis. Saliva PCR analysis is useful in predicting peri-implantitis-specific bacterial infection but not EBV or CMV. Herpesviral-bacterial synergism may favor ongoing microbial challenge in peri-implant disease and exacerbate its progression. EBV infection may explain non-responsive to treatment PI. Peri-implantitis individuals may benefit from antiviral therapy. Objectives: Herpesviral-bacterial synergism may play a potential role in periodontitis and peri-implantitis (PI) etiopathogenesis. PI lesions can worsen depending on specific microbial challenge and host susceptibility. This cross-sectional split-mouth study aimed to substantiate herpesviral-bacterial co-infection in PI patients and assess associations with periodontopathogen salivary contamination. Methods: PCR-based identification was performed on 23 patients presenting PI and contralateral healthy implants, and compared to unstimulated whole saliva. Clinical evaluation included probing depths, bleeding on probing, and suppuration. Radiographs were assessed for the presence of lamina dura and bone loss. Three sample sites per patient were tested: PI lesions, healthy implant sulci, and saliva. Quantitative PCR evaluated Epstein-Barr virus (EBV) and cytomegalovirus (CMV) copy counts. Significance of group comparisons for binary-dependent variables, within-subjects designs, was determined by McNemar's chi-square test. Risk analysis was evaluated through odds ratios (OR). Results: PI lesions were 14.2 (P=0.001; 95 % confidence interval [CI], 1.6-124.1) and 3 times (P=0.03; 95 % CI, 0.7-11.9) more likely to harbor EBV than healthy implants and saliva, respectively. EBV positive predictive value was 90 %. PI was associated with absence of lamina dura and higher periodontopathogen proportions. Saliva sampling showed high agreement with PI bacterial detection (89-100 % rate) but not with EBV (44.4 %). The OR of PI lesions harboring Treponema denticola or Tannerella forsythia was 6.79 (P=0.007; 95 % CI, 1.8-25.0) and 3.3 (P<0.0001; 95 % CI, 0.3-34.3) times higher than healthy implants, respectively. Saliva of patients with PI was 5.6 times more likely to be contaminated with Prevotella nigrescens than healthy peri-implant sulci (P=0.002). PI lesions were 1.92 times more likely to harbor Prevotella nigrescens than healthy implants (P=0.04). Conclusions: EBV is a potential candidate in peri-implantitis etiopathogenesis. Saliva PCR analysis is useful in predicting peri-implantitis-specific bacterial infection but not EBV or CMV. Clinical significance: Herpesviral-bacterial synergism may favor ongoing microbial challenge in peri-implant disease and exacerbate its progression. EBV infection may explain non-responsive to treatment PI. Peri-implantitis individuals may benefit from antiviral therapy. Herpesviral-bacterial synergism may play a potential role in periodontitis and peri-implantitis (PI) etiopathogenesis. PI lesions can worsen depending on specific microbial challenge and host susceptibility. This cross-sectional split-mouth study aimed to substantiate herpesviral-bacterial co-infection in PI patients and assess associations with periodontopathogen salivary contamination.OBJECTIVESHerpesviral-bacterial synergism may play a potential role in periodontitis and peri-implantitis (PI) etiopathogenesis. PI lesions can worsen depending on specific microbial challenge and host susceptibility. This cross-sectional split-mouth study aimed to substantiate herpesviral-bacterial co-infection in PI patients and assess associations with periodontopathogen salivary contamination.PCR-based identification was performed on 23 patients presenting PI and contralateral healthy implants, and compared to unstimulated whole saliva. Clinical evaluation included probing depths, bleeding on probing, and suppuration. Radiographs were assessed for the presence of lamina dura and bone loss. Three sample sites per patient were tested: PI lesions, healthy implant sulci, and saliva. Quantitative PCR evaluated Epstein-Barr virus (EBV) and cytomegalovirus (CMV) copy counts. Significance of group comparisons for binary-dependent variables, within-subjects designs, was determined by McNemar's chi-square test. Risk analysis was evaluated through odds ratios (OR).METHODSPCR-based identification was performed on 23 patients presenting PI and contralateral healthy implants, and compared to unstimulated whole saliva. Clinical evaluation included probing depths, bleeding on probing, and suppuration. Radiographs were assessed for the presence of lamina dura and bone loss. Three sample sites per patient were tested: PI lesions, healthy implant sulci, and saliva. Quantitative PCR evaluated Epstein-Barr virus (EBV) and cytomegalovirus (CMV) copy counts. Significance of group comparisons for binary-dependent variables, within-subjects designs, was determined by McNemar's chi-square test. Risk analysis was evaluated through odds ratios (OR).PI lesions were 14.2 (P = 0.001; 95 % confidence interval [CI], 1.6-124.1) and 3 times (P = 0.03; 95 % CI, 0.7-11.9) more likely to harbor EBV than healthy implants and saliva, respectively. EBV positive predictive value was 90 %. PI was associated with absence of lamina dura and higher periodontopathogen proportions. Saliva sampling showed high agreement with PI bacterial detection (89-100 % rate) but not with EBV (44.4 %). The OR of PI lesions harboring Treponema denticola or Tannerella forsythia was 6.79 (P = 0.007; 95 % CI, 1.8-25.0) and 3.3 (P < 0.0001; 95 % CI, 0.3-34.3) times higher than healthy implants, respectively. Saliva of patients with PI was 5.6 times more likely to be contaminated with Prevotella nigrescens than healthy peri-implant sulci (P = 0.002). PI lesions were 1.92 times more likely to harbor Prevotella nigrescens than healthy implants (P = 0.04).RESULTSPI lesions were 14.2 (P = 0.001; 95 % confidence interval [CI], 1.6-124.1) and 3 times (P = 0.03; 95 % CI, 0.7-11.9) more likely to harbor EBV than healthy implants and saliva, respectively. EBV positive predictive value was 90 %. PI was associated with absence of lamina dura and higher periodontopathogen proportions. Saliva sampling showed high agreement with PI bacterial detection (89-100 % rate) but not with EBV (44.4 %). The OR of PI lesions harboring Treponema denticola or Tannerella forsythia was 6.79 (P = 0.007; 95 % CI, 1.8-25.0) and 3.3 (P < 0.0001; 95 % CI, 0.3-34.3) times higher than healthy implants, respectively. Saliva of patients with PI was 5.6 times more likely to be contaminated with Prevotella nigrescens than healthy peri-implant sulci (P = 0.002). PI lesions were 1.92 times more likely to harbor Prevotella nigrescens than healthy implants (P = 0.04).EBV is a potential candidate in peri-implantitis etiopathogenesis. Saliva PCR analysis is useful in predicting peri-implantitis-specific bacterial infection but not EBV or CMV.CONCLUSIONSEBV is a potential candidate in peri-implantitis etiopathogenesis. Saliva PCR analysis is useful in predicting peri-implantitis-specific bacterial infection but not EBV or CMV.Herpesviral-bacterial synergism may favor ongoing microbial challenge in peri-implant disease and exacerbate its progression. EBV infection may explain non-responsive to treatment PI. Peri-implantitis individuals may benefit from antiviral therapy.CLINICAL SIGNIFICANCEHerpesviral-bacterial synergism may favor ongoing microbial challenge in peri-implant disease and exacerbate its progression. EBV infection may explain non-responsive to treatment PI. Peri-implantitis individuals may benefit from antiviral therapy. Objectives Herpesviral–bacterial synergism may play a potential role in periodontitis and peri-implantitis (PI) etiopathogenesis. PI lesions can worsen depending on specific microbial challenge and host susceptibility. This cross-sectional split-mouth study aimed to substantiate herpesviral–bacterial co-infection in PI patients and assess associations with periodontopathogen salivary contamination. Methods PCR-based identification was performed on 23 patients presenting PI and contralateral healthy implants, and compared to unstimulated whole saliva. Clinical evaluation included probing depths, bleeding on probing, and suppuration. Radiographs were assessed for the presence of lamina dura and bone loss. Three sample sites per patient were tested: PI lesions, healthy implant sulci, and saliva. Quantitative PCR evaluated Epstein–Barr virus (EBV) and cytomegalovirus (CMV) copy counts. Significance of group comparisons for binary-dependent variables, within-subjects designs, was determined by McNemar's chi-square test. Risk analysis was evaluated through odds ratios (OR). Results PI lesions were 14.2 ( P = 0.001; 95 % confidence interval [CI], 1.6–124.1) and 3 times ( P = 0.03; 95 % CI, 0.7–11.9) more likely to harbor EBV than healthy implants and saliva, respectively. EBV positive predictive value was 90 %. PI was associated with absence of lamina dura and higher periodontopathogen proportions. Saliva sampling showed high agreement with PI bacterial detection (89–100 % rate) but not with EBV (44.4 %). The OR of PI lesions harboring Treponema denticola or Tannerella forsythia was 6.79 ( P = 0.007; 95 % CI, 1.8–25.0) and 3.3 ( P < 0.0001; 95 % CI, 0.3–34.3) times higher than healthy implants, respectively. Saliva of patients with PI was 5.6 times more likely to be contaminated with Prevotella nigrescens than healthy peri-implant sulci ( P = 0.002). PI lesions were 1.92 times more likely to harbor Prevotella nigrescens than healthy implants ( P = 0.04). Conclusions EBV is a potential candidate in peri-implantitis etiopathogenesis. Saliva PCR analysis is useful in predicting peri-implantitis-specific bacterial infection but not EBV or CMV. Clinical significance Herpesviral–bacterial synergism may favor ongoing microbial challenge in peri-implant disease and exacerbate its progression. EBV infection may explain non-responsive to treatment PI. Peri-implantitis individuals may benefit from antiviral therapy. Herpesviral-bacterial synergism may play a potential role in periodontitis and peri-implantitis (PI) etiopathogenesis. PI lesions can worsen depending on specific microbial challenge and host susceptibility. This cross-sectional split-mouth study aimed to substantiate herpesviral-bacterial co-infection in PI patients and assess associations with periodontopathogen salivary contamination. PCR-based identification was performed on 23 patients presenting PI and contralateral healthy implants, and compared to unstimulated whole saliva. Clinical evaluation included probing depths, bleeding on probing, and suppuration. Radiographs were assessed for the presence of lamina dura and bone loss. Three sample sites per patient were tested: PI lesions, healthy implant sulci, and saliva. Quantitative PCR evaluated Epstein-Barr virus (EBV) and cytomegalovirus (CMV) copy counts. Significance of group comparisons for binary-dependent variables, within-subjects designs, was determined by McNemar's chi-square test. Risk analysis was evaluated through odds ratios (OR). PI lesions were 14.2 (P = 0.001; 95 % confidence interval [CI], 1.6-124.1) and 3 times (P = 0.03; 95 % CI, 0.7-11.9) more likely to harbor EBV than healthy implants and saliva, respectively. EBV positive predictive value was 90 %. PI was associated with absence of lamina dura and higher periodontopathogen proportions. Saliva sampling showed high agreement with PI bacterial detection (89-100 % rate) but not with EBV (44.4 %). The OR of PI lesions harboring Treponema denticola or Tannerella forsythia was 6.79 (P = 0.007; 95 % CI, 1.8-25.0) and 3.3 (P < 0.0001; 95 % CI, 0.3-34.3) times higher than healthy implants, respectively. Saliva of patients with PI was 5.6 times more likely to be contaminated with Prevotella nigrescens than healthy peri-implant sulci (P = 0.002). PI lesions were 1.92 times more likely to harbor Prevotella nigrescens than healthy implants (P = 0.04). EBV is a potential candidate in peri-implantitis etiopathogenesis. Saliva PCR analysis is useful in predicting peri-implantitis-specific bacterial infection but not EBV or CMV. Herpesviral-bacterial synergism may favor ongoing microbial challenge in peri-implant disease and exacerbate its progression. EBV infection may explain non-responsive to treatment PI. Peri-implantitis individuals may benefit from antiviral therapy. |
| Author | Verdugo, Fernando Castillo, Francisca Uribarri, Agurne Castillo, Ana |
| Author_xml | – sequence: 1 givenname: Fernando surname: Verdugo fullname: Verdugo, Fernando email: fverdugo@perio.org organization: Department of Periodontics, VA Hospital, Greater Los Angeles, Healthcare System, Private practice – sequence: 2 givenname: Ana surname: Castillo fullname: Castillo, Ana organization: Department of Microbiology, School of Medicine, University of Granada – sequence: 3 givenname: Francisca surname: Castillo fullname: Castillo, Francisca organization: Department of Microbiology, School of Dentistry, University of Granada – sequence: 4 givenname: Agurne surname: Uribarri fullname: Uribarri, Agurne organization: Department of Oral Medicine, School of Medicine and Odontology, University of Basque Country |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24802631$$D View this record in MEDLINE/PubMed |
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Aust Dent J. 2011 Dec;56(4):382-8 – reference: 11070030 - J Virol. 2000 Dec;74(23):11304-10 – reference: 21261620 - J Periodontal Res. 2011 Apr;46(2):235-9 – reference: 19126114 - Clin Oral Implants Res. 2009 Jan;20(1):99-108 – reference: 18304869 - J Clin Virol. 2008 Jun;42(2):176-8 – reference: 16398691 - Periodontol 2000. 2006;40:144-63 – reference: 20017799 - Periodontol 2000. 2010 Feb;52(1):117-40 – reference: 24367478 - PLoS One. 2013 Dec 19;8(12):e80336 – reference: 18384407 - Clin Implant Dent Relat Res. 2009 Mar;11(1):24-36 – reference: 21145210 - Int J Oral Maxillofac Surg. 2011 Mar;40(3):271-6 – reference: 23745964 - Clin Oral Implants Res. 2014 Aug;25(8):977-82 – reference: 23991022 - PLoS One. 2013 Aug 26;8(8):e71990 – reference: 22264211 - J Periodontol. 2012 Oct;83(10 ):1213-25 – reference: 22834392 - Eur J Oral Implantol. 2012;5 Suppl:S21-41 – reference: 18977445 - Semin Cancer Biol. 2008 Dec;18(6):397-408 – reference: 9624195 - N Engl J Med. 1998 Jun 11;338(24):1741-51 – reference: 19578433 - 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| Score | 2.2281845 |
| Snippet | Objectives
Herpesviral–bacterial synergism may play a potential role in periodontitis and peri-implantitis (PI) etiopathogenesis. PI lesions can worsen... Herpesviral-bacterial synergism may play a potential role in periodontitis and peri-implantitis (PI) etiopathogenesis. PI lesions can worsen depending on... Objectives: Herpesviral-bacterial synergism may play a potential role in periodontitis and peri-implantitis (PI) etiopathogenesis. PI lesions can worsen... |
| SourceID | proquest pubmed crossref springer |
| SourceType | Aggregation Database Index Database Enrichment Source Publisher |
| StartPage | 535 |
| SubjectTerms | Bacteroides forsythus Dentistry Electrophoresis, Agar Gel Epstein-Barr virus Herpesviridae Herpesvirus 4, Human - pathogenicity Humans Medicine Original Article Peri-Implantitis - virology Polymerase Chain Reaction Prevotella nigrescens Treponema denticola |
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| Title | Epstein–Barr virus associated peri-implantitis: a split-mouth study |
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