title: Association of human T lymphotropic virus 1 amplification of periodontitis severity with altered cytokine expression in response to a standard periodontopathogen infection.
abstract: BACKGROUND
  Periodontal diseases (PDs) are infectious diseases in which periodontopathogens trigger chronic inflammatory and immune responses that lead to tissue destruction. Recently, viruses have been implicated in the pathogenesis of PDs. Individuals infected with human T lymphotropic virus 1 (HTLV-1) present with abnormal oral health and a marked increased prevalence of periodontal disease.
  
  
  METHODS
  In this study, we investigated the patterns of periodontopathogen infection and local inflammatory immune markers in HTLV-1-seropositive individuals with chronic periodontitis (CP/HTLV-1 group) compared with HTLV-1-seronegative individuals with chronic periodontitis (CP group) and periodontally healthy, HTLV-1-seronegative individuals (control group).
  
  
  RESULTS
  Patients in the CP/HTLV-1 group had significantly higher values of bleeding on probing, mean probing depth, and attachment loss than patients in the CP group. The expression of tumor necrosis factor alpha and interleukin (IL) 4 was found to be similar in the CP and CP/HTLV-1 groups, whereas IL-12 and IL-17 levels trended toward a higher expression in the CP/HTLV-1 group. A significant increase was seen in the levels of IL-1beta and interferon gamma in the CP/HTLV-1 group compared with the CP group, whereas expression of the regulatory T cell marker FOXp3 and IL-10 was significantly decreased in the lesions from the CP/HTLV-1 group. Interestingly, similar frequency and/or load of periodontopathogens (Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, and Aggregatibacter actinomycetemcomitans) and frequency of viruses (herpes simplex virus 1, human cytomegalovirus, and Epstein-Barr virus) characteristically associated with PDs were found in the CP/HTLV and CP groups.
  
  
  CONCLUSIONS
  HTLV-1 may play a critical role in the pathogenesis of periodontal disease through the deregulation of the local cytokine network, resulting in an exacerbated response against a standard periodontopathogen infection.
authors.affiliation: Department of Biological Sciences, School of Dentistry of Bauru, São Paulo University, São Paulo, Brazil. garletgp@usp.br
authors.forename: Gustavo Pompermaier
authors.initials: GP
authors.lastname: Garlet
authors.forename: Silvana Pereira
authors.initials: SP
authors.lastname: Giozza
authors.forename: Elcia Maria
authors.initials: EM
authors.lastname: Silveira
authors.forename: Marcela
authors.initials: M
authors.lastname: Claudino
authors.forename: Silvane Braga
authors.initials: SB
authors.lastname: Santos
authors.forename: Mario Julio
authors.initials: MJ
authors.lastname: Avila-Campos
authors.forename: Walter
authors.initials: W
authors.lastname: Martins
authors.forename: Cristina Ribeiro
authors.initials: CR
authors.lastname: Cardoso
authors.forename: Ana Paula Favaro
authors.initials: AP
authors.lastname: Trombone
authors.forename: Ana Paula
authors.initials: AP
authors.lastname: Campanelli
authors.forename: Edgar Marcelino
authors.initials: EM
authors.lastname: Carvalho
authors.forename: João Santana
authors.initials: JS
authors.lastname: Silva
mesh_terms: D000328:Adult; D001421:Bacteria, Anaerobic / Q000302:isolation & purification*; D002908:Chronic Disease; D015169:Colony Count, Microbial; D016207:Cytokines / Q000096:biosynthesis*; D005260:Female; D005881:Gingiva / Q000473:pathology; D006090:Gram-Negative Bacteria / Q000302:isolation & purification*; D015490:HTLV-I Infections / Q000150:complications* / Q000276:immunology*; D006564:Herpesviridae / Q000302:isolation & purification; D015368:Human T-lymphotropic virus 1 / Q000302:isolation & purification*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010518:Periodontitis / Q000276:immunology / Q000382:microbiology* / Q000473:pathology / Q000821:virology
chemical_list: D016207:Cytokines