OBJECTIVE: To investigate the effect of nasal mucosal inflammation on bone remodeling and the inhibitory effect of macrolide antibiotics on bone remodeling through the inhibition of receptor activator of nuclear factor-kappaB ligand (RANKL) and macrophage colony-stimulating factor (M-CSF). STUDY DESIGN AND SETTING: Human nasal fibroblasts were primary-cultured from nasal polyp. After interleukin (IL)-1beta stimulation of fibroblasts with or without macrolide pretreatment, real-time polymerase chain reaction for RANKL messenger RNA (mRNA) and enzyme-linked immunosorbent assay for M-CSF were performed at various intervals. Peripheral blood mononuclear cells (PBMCs) were cultured for 10 days with M-CSF only, M-CSF plus RANKL, or macrolide antibiotic plus M-CSF and RANKL. RESULTS: IL-1beta stimulation of nasal polyp fibroblasts induced expression of RANKL mRNA and secretion of M-CSF. Macrolide antibiotics reduced RANKL mRNA and M-CSF expression by nasal polyp fibroblasts in a dose-dependent manner, and inhibited osteoclastogenesis from PBMCs. CONCLUSION: Nasal fibroblasts stimulated with IL-1beta may take on the role of osteoblasts in osteoclastogenesis, which may be inhibited by macrolide antibiotics.
OBJECTIVE: To investigate the effect of nasal mucosal inflammation on bone remodeling and the inhibitory effect of macrolide antibiotics on bone remodeling through the inhibition of receptor activator of nuclear factor-kappaB ligand (RANKL) and macrophage colony-stimulating factor (M-CSF). STUDY DESIGN AND SETTING:Human nasal fibroblasts were primary-cultured from nasal polyp. After interleukin (IL)-1beta stimulation of fibroblasts with or without macrolide pretreatment, real-time polymerase chain reaction for RANKL messenger RNA (mRNA) and enzyme-linked immunosorbent assay for M-CSF were performed at various intervals. Peripheral blood mononuclear cells (PBMCs) were cultured for 10 days with M-CSF only, M-CSF plus RANKL, or macrolide antibiotic plus M-CSF and RANKL. RESULTS:IL-1beta stimulation of nasal polyp fibroblasts induced expression of RANKL mRNA and secretion of M-CSF. Macrolide antibiotics reduced RANKL mRNA and M-CSF expression by nasal polyp fibroblasts in a dose-dependent manner, and inhibited osteoclastogenesis from PBMCs. CONCLUSION: Nasal fibroblasts stimulated with IL-1beta may take on the role of osteoblasts in osteoclastogenesis, which may be inhibited by macrolide antibiotics.