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: Verdugo, Fernando, Castillo, Ana, Castillo, Francisca, Uribarri, Agurne
Médium: Journal Article
Jazyk:angličtina
Vydáno: Berlin/Heidelberg Springer Berlin Heidelberg 01.03.2015
Springer Nature B.V
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ISSN:1432-6981, 1436-3771, 1436-3771
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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
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  givenname: Fernando
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  fullname: Verdugo, Fernando
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  organization: Department of Periodontics, VA Hospital, Greater Los Angeles, Healthcare System, Private practice
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  givenname: Ana
  surname: Castillo
  fullname: Castillo, Ana
  organization: Department of Microbiology, School of Medicine, University of Granada
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  surname: Castillo
  fullname: Castillo, Francisca
  organization: Department of Microbiology, School of Dentistry, University of Granada
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  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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1436-3771
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Tue Nov 25 13:22:38 EST 2025
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Fri Feb 21 02:33:12 EST 2025
IsPeerReviewed true
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Issue 2
Keywords Polymerase chain reaction
Peri-implantitis
Microbiology
Epstein–Barr virus infections
Saliva
Human herpesvirus 4
Language English
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PublicationTitle Clinical oral investigations
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Publisher Springer Berlin Heidelberg
Springer Nature B.V
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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...
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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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