Epigenetic and inflammatory events in experimental periodontitis following systemic microbial challenge

• Published in: Journal of clinical periodontology Vol. 46; no. 8; pp. 819 - 829
• Main Authors: Palioto, Daniela B., Finoti, Livia S., Kinane, Denis F., Benakanakere, Manjunatha
• Format: Journal Article
• Language: English
• Published: United States Blackwell Publishing Ltd 01.08.2019
• Subjects: Alveolar bone; Alveolar Bone Loss; Animals; BLyS protein; Bone loss; BTLA protein; chronic periodontal disease; Disease Models, Animal; Disseminated infection; Dysbacteriosis; Epigenesis, Genetic; Epigenetics; experimental models of periodontitis; Gum disease; Inflammation; Lymphocytes B; Lymphocytes T; Maxilla; Methylation; Mice; Mice, Inbred C57BL; Periodontitis; Porphyromonas gingivalis; RANTES; systemic disease; Systemic diseases; TRANCE protein; Vascular endothelial growth factor; chronic periodontal disease; systemic disease; inflammation; experimental models of periodontitis; epigenetics
• ISSN: 0303-6979; 1600-051X; 1600-051X
• DOI: 10.1111/jcpe.13151

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.