Table of Contents Author Guidelines Submit a Manuscript
Mediators of Inflammation
Volume 2013, Article ID 437123, 12 pages
Research Article

Stimulation of MMP-1 and CCL2 by NAMPT in PDL Cells

1Experimental Dento-Maxillo-Facial Medicine, Center of Dento-Maxillo-Facial Medicine, University of Bonn, 53111 Bonn, Germany
2Clinical Research Unit 208, Center of Dento-Maxillo-Facial Medicine, University of Bonn, Welschnonnenstraße 17, 53111 Bonn, Germany
3Department of Periodontology, Laboratory of Oral Microbiology, University of Bern, 3010 Bern, Switzerland
4Department of Diagnosis and Surgery, School of Dentistry, SP, UNESP, 14801-903 Araraquara, Brazil
5Institute of Human Genetics, Biomedical Center, University of Bonn, 53127 Bonn, Germany
6Division of Medical Genetics, University Hospital Basel and Department of Biomedicine, University of Basel, 4058 Basel, Switzerland
7Bonn-Aachen International Center for IT, Algorithmic Bioinformatics, University of Bonn, 53113 Bonn, Germany
8Department of Periodontology, Operative and Preventive Dentistry, University of Bonn, 53111 Bonn, Germany
9Department of Orthodontics, University of Bonn, 53111 Bonn, Germany

Received 14 May 2013; Accepted 18 July 2013

Academic Editor: Timo Sorsa

Copyright © 2013 Marjan Nokhbehsaim 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.


Periodontitis is an inflammatory disease caused by pathogenic microorganisms and characterized by the destruction of the periodontium. Obese individuals have an increased risk of periodontitis, and elevated circulating levels of adipokines, such as nicotinamide phosphoribosyltransferase (NAMPT), may be a pathomechanistic link between both diseases. The aim of this in vitro study was to examine the regulation of periodontal ligament (PDL) cells by NAMPT and its production under inflammatory and infectious conditions. NAMPT caused a significant upregulation of 9 genes and downregulation of 3 genes, as analyzed by microarray analysis. Eight of these genes could be confirmed by real-time PCR: NAMPT induced a significant upregulation of EGR1, MMP-1, SYT7, ITPKA, CCL2, NTM, IGF2BP3, and NRP1. NAMPT also increased significantly the MMP-1 and CCL2 protein synthesis. NAMPT was significantly induced by interleukin-1β and the periodontal microorganism P. gingivalis. NAMPT may contribute to periodontitis through upregulation of MMP-1 and CCL2 in PDL cells. Increased NAMPT levels, as found in obesity, may therefore represent a mechanism whereby obesity could confer an increased risk of periodontitis. Furthermore, microbial and inflammatory signals may enhance the NAMPT synthesis in PDL cells and thereby contribute to the increased gingival and serum levels of this adipokine, as found in periodontitis.