Treatment with 50 μM Sodium Fluoride Suppresses Aging-Induced Alveolar Bone Resorption in Mice

Abstract

Ingestion of excess systemic fluoride results in physiological and pathological disturbances of bone homeostasis. We and others have established that treatment with 50 μM sodium fluoride (NaF) is safe and effective for bone remodeling in cellular and animal models. This study aimed to study the effects of treatment with 50 μM NaF on macrophage-driven osteoclastogenesis and to characterize the function of 50 μM NaF in alveolar bone resorption during aging. Murine RAW264.7 monocytic cells were treated with RANKL in the presence or absence of 50 μM NaF. The mRNA expression levels of Cathepsin K and nuclear factor-activated T-cell cytoplasmic 1 (NFATc1), which are involved in the mechanism of osteoclast induction, were measured using quantitative real time RT-PCR. An experimental 50 μM NaF-treated aging mouse model was used to confirm alveolar bone resorption. Micro-CT was used to assess bone loss and immunohistochemistry was performed to detect the protein expression levels of RANKL and Cathepsin K in periodontal tissues. Treatment of RAW264.7 cells with 50 μM NaF repressed osteoclastogenesis. Micro-CT results confirmed that treatment with 50 μM NaF alleviated alveolar bone resorption in aging. Immunohistochemical analysis revealed decreased expression levels of RANKL and cathepsin K in 50 μM NaF-treated mice during aging. Taken together, these results contribute fascinating experimental clues that 50 μM NaF has the potential to function as an anti-resorptive agent during alveolar bone aging.