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Mediators of Inflammation
Volume 2014, Article ID 816320, 10 pages
Research Article

HMGB1 Localization during Experimental Periodontitis

1Department of Diagnosis and Surgery, School of Dentistry at Araraquara, Universidade Estadual Paulista (UNESP), Rua Humaitá, 1680, 2° Andar, Centro, 14801-903 Araraquara, SP, Brazil
2Department of Periodontics and Oral Medicine, School of Dentistry, University of Michigan, 1011 N. University Avenue, Ann Arbor, MI 48109-1078, USA

Received 10 September 2013; Revised 29 December 2013; Accepted 7 January 2014; Published 20 February 2014

Academic Editor: Stefanie B. Flohé

Copyright © 2014 Andressa Vilas Boas Nogueira et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Aim. This study sought to investigate the in vitro expression profile of high mobility group box 1 (HMGB1) in murine periodontal ligament fibroblasts (mPDL) stimulated with LPS or IL-1β and in vivo during ligature- or LPS-induced periodontitis in rats. Material and Methods. For the in vivo study, 36 rats were divided into experimental and control groups, and biopsies were harvested at 7–30 d following disease induction. Bone loss and inflammation were evaluated. HMGB1 expression was assessed by immunohistochemistry, qPCR, and Western blot. Results. Significant increases in mPDL HMGB1 mRNA occurred at 4, 8, and 12 h with protein expression elevated by 24 h. HMGB1 mRNA expression in gingival tissues was significantly increased at 15 d in the LPS-PD model and at 7 and 15 d in the ligature model. Immunohistochemical staining revealed a significant increase in the number of HMGB1-positive cells during the experimental periods. Conclusion. The results show that PDL cells produce HMGB1, which is increased and secreted extracellularly after inflammatory stimuli. In conclusion, this study demonstrates that HMGB1 may be associated with the onset and progression of periodontitis, suggesting that further studies should investigate the potential role of HMGB1 on periodontal tissue destruction.