作者: Keisuke Kimura , Hideki Kitaura , Masahiko Ishida , Zaki Hakami , Jafari Saeed
DOI: 10.1007/978-4-431-55192-8_22
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摘要: Lipopolysaccharide (LPS) is a major component of Gram-negative bacteria cell walls and well-known potent inducer inflammation pathogens inflammatory bone loss. Formation osteoclasts highly dependent on the presence macrophage colony-stimulating factor (M-CSF) receptor activator nuclear kappa-B ligand (RANKL). Recent reports indicate that biological preparations, including anti-RANKL antibody anti-tumor necrosis factor-α antibody, positively influence rheumatoid arthritis osteoporosis. In this study, we aimed to investigate whether M-CSF c-Fms would inhibit formation osteoclasts. C57BL6/J mice were injected with either LPS, LPS anti-c-Fms or PBS into supracalvariae. Animals sacrificed calvariae fixation demineralization performed. Histological sections stained for tartrate-resistant acid phosphatase (TRAP). administered both osteoclast numbers lower than those in alone. Moreover, levels TRACP-5b, resorption marker serum, These results suggest its are potential therapeutic targets LPS-induced osteoclastogenesis, might be useful inhibition inflammation-induced erosion. describe discuss effect has pathological osteoclastogenesis resorption.