Association of human T lymphotropic virus 1 amplification of periodontitis severity with altered cytokine expression in response to a standard periodontopathogen infection.
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.
Garlet
Gustavo Pompermaier
GP
Department of Biological Sciences, School of Dentistry of Bauru, São Paulo University, São Paulo, Brazil. garletgp@usp.br
Giozza
Silvana Pereira
SP
Silveira
Elcia Maria
EM
Claudino
Marcela
M
Santos
Silvane Braga
SB
Avila-Campos
Mario Julio
MJ
Martins
Walter
W
Cardoso
Cristina Ribeiro
CR
Trombone
Ana Paula Favaro
AP
Campanelli
Ana Paula
AP
Carvalho
Edgar Marcelino
EM
Silva
João Santana
JS
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
D016207:Cytokines