Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/78527
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Type: Journal article
Title: Azithromycin suppresses human osteoclast formation and activity in vitro
Author: Gannon, S.
Cantley, M.
Haynes, D.
Hirsch, R.
Bartold, P.
Citation: Journal of Cellular Physiology, 2013; 228(5):1098-1107
Publisher: Wiley-Liss
Issue Date: 2013
ISSN: 0021-9541
1097-4652
Statement of
Responsibility: 
Siobhan C. Gannon, Melissa D. Cantley, David R. Haynes, Robert Hirsch, and P. Mark Bartold
Abstract: Azithromycin is an antibiotic with anti-inflammatory properties used as an adjunct to treat periodontitis, a common inflammatory mediated condition featuring pathologic alveolar bone resorption. This study aimed to determine the effect of azithromycin on human osteoclast formation and resorptive activity in vitro. Osteoclasts were generated from peripheral blood mononuclear cells stimulated with macrophage colony stimulating factor (M-CSF) and receptor activator of nuclear factor kappa B (RANK) ligand. The effects of azithromycin at concentrations ranging from 0.5 to 40 µg/ml were tested. Osteoclast formation and activity, acidification, actin ring formation and expression of mRNA, and protein encoding for key osteoclast genes were assessed. The results demonstrated that azithromycin reduced osteoclast resorptive activity at all concentrations tested with osteoclast formation being significantly reduced at the higher concentrations (20 and 40 µg/ml). mRNA and protein expression of key osteoclast transcription factor Nuclear Factor of Activated T cells (NFATc1) was significantly reduced by azithromycin at later stages of osteoclast development (day 17). Azithromycin also reduced tumor necrosis factor receptor associated factor-6 (TRAF6) mRNA expression at day 14, and cathepsin K mRNA expression at days 14 and 17. Integrin β3 and MMP-9 mRNA expression was reduced by azithromycin at day 17 in osteoclasts cultured on dentine. The osteoclast proton pump did not appear to be affected by azithromycin, however formation of the actin ring cytoskeleton was inhibited. This study demonstrates that azithromycin inhibits human osteoclast function in vitro, which may account for at least some of the beneficial clinical effects observed with azithromycin treatment in periodontitis.
Keywords: Leukocytes, Mononuclear; Cytoskeleton; Osteoclasts; Humans; Periodontitis; Azithromycin; TNF Receptor-Associated Factor 6; Macrophage Colony-Stimulating Factor; Integrin beta3; Cell Survival; Gene Expression Regulation; NFATC Transcription Factors; Matrix Metalloproteinase 9; Receptor Activator of Nuclear Factor-kappa B; Cathepsin K; Blood Buffy Coat
Rights: Copyright © 2012 Wiley Periodicals, Inc.
RMID: 0020125646
DOI: 10.1002/jcp.24259
Appears in Collections:Dentistry publications

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