Journal of Cellular Biochemistry

Sodium hydrogen sulfide inhibits nicotine and lipopolysaccharide-induced osteoclastic differentiation and reversed osteoblastic differentiation in human periodontal ligament cells

Authors

  • Sun-Kyung Lee,

    1. Department of Maxillofacial Tissue Regeneration, School of Dentistry and Institute of Oral Biology, Kyung Hee University, Seoul, Republic of Korea
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  • Jong-Hyuk Chung,

    1. Department of Periodontology, School of Dentistry and Institute of Oral Biology, Kyung Hee University, Seoul, Republic of Korea
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  • Sung-Chul Choi,

    1. Department of Pediatrc Dentistry, School of Dentistry and Institute of Oral Biology, Kyung Hee University, Seoul, Republic of Korea
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  • Q-Schick Auh,

    1. Department of Oral Medicine, School of Dentistry and Institute of Oral Biology, Kyung Hee University, Seoul, Republic of Korea
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  • Young-Man Lee,

    1. Department of Maxillofacial Tissue Regeneration, School of Dentistry and Institute of Oral Biology, Kyung Hee University, Seoul, Republic of Korea
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  • Sang-Im Lee,

    1. Department of Maxillofacial Tissue Regeneration, School of Dentistry and Institute of Oral Biology, Kyung Hee University, Seoul, Republic of Korea
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  • Eun-Cheol Kim

    Corresponding author
    1. Department of Maxillofacial Tissue Regeneration, School of Dentistry and Institute of Oral Biology, Kyung Hee University, Seoul, Republic of Korea
    • Department of Maxillofacial Tissue Regeneration, School of Dentistry, Kyung Hee University, 1 Heogi-dong, Dongdaemun-gu, Seoul 130-701, Republic of Korea.
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  • Sun-Kyung Lee and Jong-Hyuk Chung contributed equally to this work.

Abstract

Although previous studies have demonstrated that hydrogen sulfide (H2S) stimulated or inhibited osteoclastic differentiation, little is known about the effects of H2S on the differentiation of osteoblasts and osteoclasts. To determine the possible bioactivities of H2S on bone metabolism, we investigated the in vitro effects of H2S on cytotoxicity, osteoblastic, and osteoclastic differentiation as well as the underlying mechanism in lipopolysaccharide (LPS) and nicotine-stimulated human periodontal ligament cells (hPDLCs). The H2S donor, NaHS, protected hPDLCs from nicotine and LPS-induced cytotoxicity and recovered nicotine- and LPS-downregulated osteoblastic differentiation, such as alkaline phosphatase (ALP) activity, mRNA expression of osteoblasts, including ALP, osteopontin (OPN), and osteocalcin (OCN), and mineralized nodule formation. Concomitantly, NaHS inhibited the differentiation of tartrate-resistant acid phosphatase (TRAP)-positive osteoclasts in mouse bone marrow cells and blocked nicotine- and LPS-induced osteoclastogenesis regulatory molecules, such as RANKL, OPG, M-CSF, MMP-9, TRAP, and cathepsin K mRNA. NaHS blocked nicotine and LPS-induced activation of p38, ERK, MKP-1, PI3K, PKC, and PKC isoenzymes, and NF-κB. The effects of H2S on nicotine- and LPS-induced osteoblastic and osteoclastic differentiation were remarkably reversed by MKP-1 enzyme inhibitor (vanadate) and expression inhibitor (triptolide). Taken together, we report for the first time that H2S inhibited cytotoxicity and osteoclastic differentiation and recovered osteoblastic differentiation in a nicotine- and periodontopathogen-stimulated hPDLCs model, which has potential therapeutic value for treatment of periodontal and inflammatory bone diseases. J. Cell. Biochem. 114: 1183–1193, 2013. © 2012 Wiley Periodicals, Inc.

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