Premium
Epigenetic and inflammatory events in experimental periodontitis following systemic microbial challenge
Author(s) -
Palioto Daniela B.,
Finoti Livia S.,
Kinane Denis F.,
Benakanakere Manjunatha
Publication year - 2019
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/jcpe.13151
Subject(s) - btla , periodontitis , dnmt3b , immunology , medicine , systemic inflammation , systemic administration , inflammation , gut flora , dental alveolus , porphyromonas gingivalis , rankl , biology , methylation , dentistry , immune system , methyltransferase , biochemistry , microbiology and biotechnology , receptor , t lymphocyte , activator (genetics) , in vivo , gene
Abstract Aim The purpose of this study was to determine inflammatory and epigenetic features following induction of oral and gut dysbiosis in experimental periodontitis in order to examine the interplay between oral and systemic infection. Materials and Methods Periodontitis was induced in 6‐ to 8‐week‐old C57BL/6 mice by (a) Ligature placement (Lig group) (oral challenge); (b) P. gingivalis gavage ( Pg group) (systemic challenge); and (c) the combination of the two models oral and systemic challenge ( Pg + Lig). The duration of the experiment was 60 days, and the animals were then sacrificed for analyses. Alveolar bone loss was assessed, and a multiplex immunoassay was performed. Maxillae and gut tissues were immunostained for DNMT3b (de novo methylation marker), B and T lymphocyte attenuator (BTLA) and IL‐18R1 (inflammation markers). Results Pg and Pg + Lig groups exhibited higher bone loss when compared to Sham. BAFF, VEGF, RANKL, RANTES and IP‐10 were significantly higher with Pg gavage. Likewise, DNMT3b was overexpressed in both gut and maxilla after the Pg administration. The same pattern was observed for BTLA and IL‐18R1 in gut tissues. Conclusions The systemic microbial challenge either alone or in combination with local challenge leads to distinct patterns of inflammatory and epigenetic features when compared to simply locally induced experimental periodontitis.