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. 2016 Jul 12;18:161. doi: 10.1186/s13075-016-1056-4

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© The Author(s). 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 1 — Establishment of periodontal disease in B10.RIII mice. a Schematic diagram of the experimental design. b (i), (ii) Polybacterial-infected mice IgG, IgM systemic immune response against P. gingivalis (Pg), T. denticola (Td), and T. forsythia (Tf), respectively; (iii), (iv) polybacterial-infected + collagen type II (CII)-immunized mice IgG, IgM systemic immune response against Pg, Td, and Tf, respectively. c (i) Representative images of horizontal alveolar bone resorption area in mandibular surfaces of B10.RIII mice; (ii) total alveolar bone resorption in B10.RIII mice. Each bar indicates the mean alveolar bone resorption for three molars in each quadrant. Three bacteria were used in oral infection for 24 weeks. N = 10 in each group. *P < 0.05, ***P < 0.001. Cont control