Fan Zijing, Huang Liujing, Zheng Minghao, Lin Ziyin, Li Ze, Liu Yifan, Liu Bingdong, Xiao Lanlin, Chen Yixin, Mai Xudong, Xu Yinlan, Xie Liwei
School of Public Health, Xinxiang Medical University, Xinxiang 453003, China.
State Key Laboratory of Applied Microbiology Southern China, Guangdong Provincial Key Laboratory of Microbial Culture Collection and Application, Guangdong Open Laboratory of Applied Microbiology, Institute of Microbiology, Guangdong Academy of Sciences, Guangzhou 510070, China.
FEMS Microbiol Lett. 2025 Jan 10;372. doi: 10.1093/femsle/fnaf081.
Osteoporosis is characterized by low bone mineral density and deteriorated bone microarchitecture. The gut microbiota has emerged as a potential regulator of bone metabolism through the gut-bone axis. This study investigates the role of gut microbiota dysbiosis in osteoporosis. Fecal microbiota transplantation (FMT) was employed to assess the transferability of osteoporosis-associated gut microbiota dysbiosis to healthy mice and to explore whether restoration of gut microbial composition could reverse bone loss in OVX mice. It was demonstrated that gut microbiota from OVX mice induced osteoporosis in healthy recipient mice, establishing a causal link between gut microbiota dysbiosis and bone health. Short-term FMT from healthy donors restored microbial diversity; however, a significant improvement in trabecular bone density was not observed in OVX mice. This suggest that longer colonization periods or additional interventions may be required. Correlation analysis revealed significant associations between specific bacterial taxa and bone health parameters. These findings highlight the complexity of the gut-bone axis and underscore the need for further research investigating targeted microbial interventions for the management of osteoporosis. Future therapeutic strategies should be considered for modulation of the gut microbiota, enhancement of gut barrier integrity, and mitigation of systemic inflammation as novel approaches to osteoporosis treatment.
骨质疏松症的特征是骨矿物质密度低和骨微结构恶化。肠道微生物群已成为通过肠-骨轴调节骨代谢的潜在因素。本研究调查肠道微生物群失调在骨质疏松症中的作用。采用粪便微生物群移植(FMT)来评估与骨质疏松症相关的肠道微生物群失调向健康小鼠的转移性,并探讨恢复肠道微生物组成是否可以逆转去势(OVX)小鼠的骨质流失。结果表明,来自OVX小鼠的肠道微生物群在健康受体小鼠中诱发了骨质疏松症,从而在肠道微生物群失调与骨骼健康之间建立了因果联系。来自健康供体的短期FMT恢复了微生物多样性;然而,在OVX小鼠中未观察到小梁骨密度有显著改善。这表明可能需要更长的定植期或额外的干预措施。相关性分析揭示了特定细菌类群与骨骼健康参数之间的显著关联。这些发现凸显了肠-骨轴的复杂性,并强调需要进一步研究针对微生物的干预措施来管理骨质疏松症。未来的治疗策略应考虑调节肠道微生物群、增强肠道屏障完整性以及减轻全身炎症,作为治疗骨质疏松症的新方法。