title: Significance of human cytomegalovirus and Epstein-Barr virus in inducing cytokine expression in periapical lesions.
abstract: BACKGROUND
  Because herpesviruses might be etiologically involved in periapical pathosis of endodontic origin, this study aimed to determine the occurrence of human cytomegalovirus (HCMV), Epstein-Barr virus (EBV), and the expression of mRNA transcripts of tumor necrosis factor (TNF)-α, γ-interferon (IFN), interleukin (IL)-1β, IL-6, IL-12, and IL-10 in periapical granulomatous lesions collected in conjunction with apicoectomy.
  
  
  METHODS
  A total of 9 symptomatic and 6 asymptomatic teeth with periapical lesions were studied. Periapical samples were collected in conjunction with apicoectomy, which was being performed because of radiographic evidence of incomplete periapical healing after conventional root canal therapy. By using established polymerase chain reaction primers and procedures, polymerase chain reaction assays were used to identify herpesvirus and cytokine gene expression.
  
  
  RESULTS
  The difference in occurrence of HCMV, EBV, and cytokines between symptomatic and asymptomatic periapical lesions was statistically significant: HCMV (P = .048), EBV (P = .002), IFN (P = .001), IL-1 (P = .012), IL-6 (P = .026), IL-10 (P = .026), IL-12 (P = .012), and TNF (P < .001) (Mann-Whitney U test). There was a significant correlation between EBV, HCMV, and TNF, γ-IFN, IL-1, and IL-12 in symptomatic periapical lesions (Spearman test).
  
  
  CONCLUSIONS
  The present findings provide evidence of a putative role of HCMV and EBV in the pathogenesis of symptomatic periapical pathosis. The release of tissue-destructive cytokines might be of pathogenetic significance.
authors.affiliation: Department of Endodontics, University of Southern California, School of Dentistry, Los Angeles, California, USA. sabeti2001@yahoo.com
authors.forename: Mohammad
authors.initials: M
authors.lastname: Sabeti
authors.forename: Vali
authors.initials: V
authors.lastname: Kermani
authors.forename: Sara
authors.initials: S
authors.lastname: Sabeti
authors.forename: James H
authors.initials: JH
authors.lastname: Simon
mesh_terms: D000328:Adult; D001047:Apicoectomy; D058070:Asymptomatic Diseases; D060085:Coinfection; D003587:Cytomegalovirus / Q000276:immunology*; D003586:Cytomegalovirus Infections / Q000276:immunology*; D020031:Epstein-Barr Virus Infections / Q000276:immunology*; D004854:Herpesvirus 4, Human / Q000276:immunology*; D006801:Humans; D007371:Interferon-gamma / Q000032:analysis*; D016753:Interleukin-10 / Q000032:analysis; D018664:Interleukin-12 / Q000032:analysis; D053583:Interleukin-1beta / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D007378:Interleukins / Q000032:analysis*; D008875:Middle Aged; D010483:Periapical Diseases / Q000276:immunology / Q000821:virology*; D010484:Periapical Granuloma / Q000276:immunology / Q000821:virology; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012390:Root Canal Therapy; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis*; D055815:Young Adult
chemical_list: D053583:Interleukin-1beta; D015850:Interleukin-6; D007378:Interleukins; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D018664:Interleukin-12; D007371:Interferon-gamma