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Mediators of Inflammation
Volume 2017, Article ID 4786170, 10 pages
Research Article

Role of Cathepsin S in Periodontal Inflammation and Infection

1Section of Experimental Dento-Maxillo-Facial Medicine, Center of Dento-Maxillo-Facial Medicine, University of Bonn, Bonn, Germany
2Department of Orthodontics, Center of Dento-Maxillo-Facial Medicine, University of Bonn, Bonn, Germany
3Department of Diagnosis and Surgery, School of Dentistry at Araraquara, Sao Paulo State University (UNESP), Araraquara, SP, Brazil
4Department of Periodontology, Laboratory for Oral Microbiology, School of Dental Medicine, University of Bern, Bern, Switzerland
5Discipline of Orthodontics, Faculty of Dentistry, University of Sydney, Sydney, NSW, Australia
6Institute of Reconstructive Neurobiology, Life & Brain Center, University of Bonn, Bonn, Germany
7Department of Periodontology, Operative and Preventive Dentistry, University of Bonn, Bonn, Germany
8Department of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, Athens, Greece
9Noel Martin Visiting Chair, Faculty of Dentistry, University of Sydney, Sydney, NSW, Australia

Correspondence should be addressed to S. Memmert; ed.nnob-inu.bku@tremmem.ajnevs

Received 10 July 2017; Accepted 29 October 2017; Published 6 December 2017

Academic Editor: Settimio Rossi

Copyright © 2017 S. Memmert 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.


Cathepsin S is a cysteine protease and regulator of autophagy with possible involvement in periodontitis. The objective of this study was to investigate whether cathepsin S is involved in the pathogenesis of periodontal diseases. Human periodontal fibroblasts were cultured under inflammatory and infectious conditions elicited by interleukin-1β and Fusobacterium nucleatum, respectively. An array-based approach was used to analyze differential expression of autophagy-associated genes. Cathepsin S was upregulated most strongly and thus further studied in vitro at gene and protein levels. In vivo, gingival tissue biopsies from rats with ligature-induced periodontitis and from periodontitis patients were also analyzed at transcriptional and protein levels. Multiple gene expression changes due to interleukin-1β and F. nucleatum were observed in vitro. Both stimulants caused a significant cathepsin S upregulation. A significantly elevated cathepsin S expression in gingival biopsies from rats with experimental periodontitis was found in vivo, as compared to that from control. Gingival biopsies from periodontitis patients showed a significantly higher cathepsin S expression than those from healthy gingiva. Our findings provide original evidence that cathepsin S is increased in periodontal cells and tissues under inflammatory and infectious conditions, suggesting a critical role of this autophagy-associated molecule in the pathogenesis of periodontitis.