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International Journal of Endocrinology
Volume 2014, Article ID 180304, 13 pages
Research Article

Leptin Effects on the Regenerative Capacity of Human Periodontal Cells

1Experimental Dento-Maxillo-Facial Medicine, University of Bonn, 53111 Bonn, Germany
2Clinical Research Unit 208, University of Bonn, 53111 Bonn, Germany
3Department of Diagnosis and Surgery, School of Dentistry, UNESP, 14801-903 Araraquara, SP, Brazil
4Department of Orthodontics, University of Bonn, 53111 Bonn, Germany
5Department of Periodontology, Operative and Preventive Dentistry, University of Bonn, 53111 Bonn, Germany
6Oral Technology, Center of Dento-Maxillo-Facial Medicine, University of Bonn, 53111 Bonn, Germany
7Department of Periodontology, Laboratory of Oral Microbiology, University of Bern, 3010 Bern, Switzerland

Received 24 February 2014; Revised 26 June 2014; Accepted 4 July 2014; Published 22 July 2014

Academic Editor: Daniela Jezova

Copyright © 2014 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.


Obesity is increasing throughout the globe and characterized by excess adipose tissue, which represents a complex endocrine organ. Adipose tissue secrets bioactive molecules called adipokines, which act at endocrine, paracrine, and autocrine levels. Obesity has recently been shown to be associated with periodontitis, a disease characterized by the irreversible destruction of the tooth-supporting tissues, that is, periodontium, and also with compromised periodontal healing. Although the underlying mechanisms for these associations are not clear yet, increased levels of proinflammatory adipokines, such as leptin, as found in obese individuals, might be a critical pathomechanistic link. The objective of this study was to examine the impact of leptin on the regenerative capacity of human periodontal ligament (PDL) cells and also to study the local leptin production by these cells. Leptin caused a significant downregulation of growth (TGFβ1, and VEGFA) and transcription (RUNX2) factors as well as matrix molecules (collagen, and periostin) and inhibited SMAD signaling under regenerative conditions. Moreover, the local expression of leptin and its full-length receptor was significantly downregulated by inflammatory, microbial, and biomechanical signals. This study demonstrates that the hormone leptin negatively interferes with the regenerative capacity of PDL cells, suggesting leptin as a pathomechanistic link between obesity and compromised periodontal healing.