Relationship between fluoride exposure and osteoclast markers during RANKL-induced osteoclast differentiation

Relationship between fluoride exposure and osteoclast markers during RANKL-induced osteoclast differentiation
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DOI:
10.1016/j.etap.2016.08.001
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发表时间:
2016-09-01
影响因子:
4.3
通讯作者:
Sun Dianjun
Sun Dianjun
中科院分区:
环境科学与生态学3区
文献类型:
--
作者:
Pei Junrui;Li Bingyun;Sun Dianjun

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Skeletal fluorosis is a metabolic bone disease caused by excessive accumulation of fluoride. Although the cause of this disease is known, the mechanism by which fluoride accumulates on the bone has not been clearly defined, thus there are no markers that can be used for screening skeletal fluorosis in epidemiology. In this study, osteoclasts were formed from bone marrow cells of C57BL/6 mice-treated with macrophage colony stimulating factor and receptor activator of nuclear factor kappa-B ligand: The mRNA expression of tartrate-resistant acid phosphatase 5b (TRAP5b), osteoclast-associated receptor (OSCAR), calcitonin receptor (CTR), matrix metalloproteinase 9 (MMP9) and cathepsin K (CK) were detected using real-time PCR (RT-PCR). Results showed that fluoride between 0.5 and 8 mg/l had no effect on osteoclast formation. However fluoride at 0.5 mg/l level significantly decreased the activity of osteoclast bone resorption. Fluoride concentration was negatively correlated with the activity of osteoclast bone resorption. On day 5 of osteoclast differentiation maturity, MMP9 and CK mRNA expression were not only negatively correlated with fluoride concentration, but directly correlated with the activity of osteoclast bone resorption. TRAP5b, CTR and OSCAR mRNA expression were positively correlated with the number of osteoclast and they had no correlation with the activity of osteoclast bone resorption. Thus, it can be seen that MMP9 and CK may reflect the change of activity of bone resorption as well the degree of fluoride exposure. TRAP5b, CTR and OSCAR can represent the change of number of osteoclast formed. (C) 2016 Elsevier B.V. All rights reserved.