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Journal of Dental Research
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BIOLOGICAL

Diclofenac Sodium Inhibits NF{kappa}B Transcription in Osteoclasts

A. Karakawa1,*, Y. Fukawa2, M. Okazaki1, K. Takahashi3, T. Sano4, H. Amano1, M. Yamamoto2 and S. Yamada1

1 Department of Pharmacology and
4 Department of Oral Anatomy, Showa University School of Dentistry, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan;
2 Department of Periodontology, Showa University School of Dentistry, 2-1-1 Kitasenzoku, Ohta-ku, Tokyo 145-8515, Japan;
3 Physiological Chemistry Research Laboratory, Hoshi University, Institute of Medicinal Chemistry, 2-4-41 Ebara, Shinagawa-ku, Tokyo 142-8501, Japan

Correspondence: * a-karakawa{at}dent.showa-u.ac.jp

A non-steroidal anti-inflammatory drug, diclofenac, acts efficiently against inflammation; however, down-regulation of diclofenac on bone remodeling has raised concerns. The inhibitory mechanisms of diclofenac are poorly understood. We hypothesized that diclofenac down-regulates osteoclast differentiation and activation via inhibition of the translocation of phosphorylated nuclear factor kappa B (NF{kappa}B). When osteoclasts prepared from mouse hematopoietic stem cells were treated with diclofenac, tartrateresistant acid phosphatase-positive multinucleated cells decreased in a concentration-dependent manner. Pit formation assay revealed the abolition of osteoclastic bone resorption; levels of cathepsin K transcripts, an osteoclastic resorption marker, were down-regulated time-dependently. Diclofenac induced the accumulation of the inhibitor of kappa B in cytosol, which led to suppression of the nuclear translocation of NF{kappa}B and phosphorylated NF{kappa}B. These results suggest that the novel mechanism of diclofenac for bone remodeling is associated with phosphorylated NF{kappa}B reduction, which regulates osteoclast differentiation and activation.

Key Words: diclofenac sodium • NSAIDs • osteoclast • NF{kappa}B • bone remodeling

Journal of Dental Research, Vol. 88, No. 11, 1042-1047 (2009)
DOI: 10.1177/0022034509346147
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