Fluoxetine inhibited RANKL-induced osteoclastic differentiation in vitro

Selective serotonin reuptake inhibitor correlates with decreased bone mineral density and impedes orthodontic tooth movement. The present study aimed to examine the effects of fluoxetine on osteoclast differentiation and function. Human peripheral blood mononuclear cells (hPBMCs) and murine RAW264.7...

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Main Authors: Zhang Jing-wen, Zhao Fang-bing, Ma Bing’er, Shen Xiao-qing, Geng Yuan-ming
Format: Article
Language:English
Published: De Gruyter 2024-12-01
Series:Open Medicine
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Online Access:https://doi.org/10.1515/med-2024-1094
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author Zhang Jing-wen
Zhao Fang-bing
Ma Bing’er
Shen Xiao-qing
Geng Yuan-ming
author_facet Zhang Jing-wen
Zhao Fang-bing
Ma Bing’er
Shen Xiao-qing
Geng Yuan-ming
author_sort Zhang Jing-wen
collection DOAJ
description Selective serotonin reuptake inhibitor correlates with decreased bone mineral density and impedes orthodontic tooth movement. The present study aimed to examine the effects of fluoxetine on osteoclast differentiation and function. Human peripheral blood mononuclear cells (hPBMCs) and murine RAW264.7 cells were cultured with RANKL to stimulate osteoclast differentiation. The resulting multinucleated cells displayed characteristics of mature osteoclasts. Fluoxetine at 0.01–1 μM did not impact cellular viability or oxidative stress. However, 10 μM fluoxetine significantly reduced clonal growth, cell viability, and increased cytotoxicity and lipid peroxidation in RAW 264.7 cells. Further, application of 0.1 μM fluoxetine potently suppressed osteoclast differentiation of both RAW264.7 and hPBMCs, with reduced osteoclast numbers and downregulation of osteoclastic genes matrix metalloproteinase-9, cathepsin K, and integrin β3 at mRNA and protein levels. Fluoxetine also disrupted F-actin ring formation essential for osteoclast resorptive function. Mechanistically, fluoxetine inhibited NF-kB signaling by reducing phosphorylation of pathway members IκBα and p65, preventing IκBα degradation and blocking p65 nuclear translocation. In conclusion, this study demonstrates fluoxetine suppressing osteoclast differentiation in association with disrupting NF-kB activation, providing insight into orthodontic treatment planning for patients taking fluoxetine.
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spelling doaj-art-c0bcd5517a41488daa160b78f7ac0f402025-08-20T02:42:59ZengDe GruyterOpen Medicine2391-54632024-12-011915738110.1515/med-2024-1094Fluoxetine inhibited RANKL-induced osteoclastic differentiation in vitroZhang Jing-wen0Zhao Fang-bing1Ma Bing’er2Shen Xiao-qing3Geng Yuan-ming4Department of Stomatology, Zhujiang Hospital, Southern Medical University, Guangzhou, ChinaDepartment of Stomatology, Zhujiang Hospital, Southern Medical University, Guangzhou, ChinaDepartment of Stomatology, Zhujiang Hospital, Southern Medical University, Guangzhou, ChinaDepartment of Stomatology, Zhujiang Hospital, Southern Medical University, Guangzhou, ChinaDepartment of Stomatology, Zhujiang Hospital, Southern Medical University, Guangzhou, ChinaSelective serotonin reuptake inhibitor correlates with decreased bone mineral density and impedes orthodontic tooth movement. The present study aimed to examine the effects of fluoxetine on osteoclast differentiation and function. Human peripheral blood mononuclear cells (hPBMCs) and murine RAW264.7 cells were cultured with RANKL to stimulate osteoclast differentiation. The resulting multinucleated cells displayed characteristics of mature osteoclasts. Fluoxetine at 0.01–1 μM did not impact cellular viability or oxidative stress. However, 10 μM fluoxetine significantly reduced clonal growth, cell viability, and increased cytotoxicity and lipid peroxidation in RAW 264.7 cells. Further, application of 0.1 μM fluoxetine potently suppressed osteoclast differentiation of both RAW264.7 and hPBMCs, with reduced osteoclast numbers and downregulation of osteoclastic genes matrix metalloproteinase-9, cathepsin K, and integrin β3 at mRNA and protein levels. Fluoxetine also disrupted F-actin ring formation essential for osteoclast resorptive function. Mechanistically, fluoxetine inhibited NF-kB signaling by reducing phosphorylation of pathway members IκBα and p65, preventing IκBα degradation and blocking p65 nuclear translocation. In conclusion, this study demonstrates fluoxetine suppressing osteoclast differentiation in association with disrupting NF-kB activation, providing insight into orthodontic treatment planning for patients taking fluoxetine.https://doi.org/10.1515/med-2024-1094osteoclastreceptor activator of nuclear factor kappa-b ligandselective serotonin reuptake inhibitorfluoxetineorthodontic tooth movement
spellingShingle Zhang Jing-wen
Zhao Fang-bing
Ma Bing’er
Shen Xiao-qing
Geng Yuan-ming
Fluoxetine inhibited RANKL-induced osteoclastic differentiation in vitro
Open Medicine
osteoclast
receptor activator of nuclear factor kappa-b ligand
selective serotonin reuptake inhibitor
fluoxetine
orthodontic tooth movement
title Fluoxetine inhibited RANKL-induced osteoclastic differentiation in vitro
title_full Fluoxetine inhibited RANKL-induced osteoclastic differentiation in vitro
title_fullStr Fluoxetine inhibited RANKL-induced osteoclastic differentiation in vitro
title_full_unstemmed Fluoxetine inhibited RANKL-induced osteoclastic differentiation in vitro
title_short Fluoxetine inhibited RANKL-induced osteoclastic differentiation in vitro
title_sort fluoxetine inhibited rankl induced osteoclastic differentiation in vitro
topic osteoclast
receptor activator of nuclear factor kappa-b ligand
selective serotonin reuptake inhibitor
fluoxetine
orthodontic tooth movement
url https://doi.org/10.1515/med-2024-1094
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AT zhaofangbing fluoxetineinhibitedranklinducedosteoclasticdifferentiationinvitro
AT mabinger fluoxetineinhibitedranklinducedosteoclasticdifferentiationinvitro
AT shenxiaoqing fluoxetineinhibitedranklinducedosteoclasticdifferentiationinvitro
AT gengyuanming fluoxetineinhibitedranklinducedosteoclasticdifferentiationinvitro