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一种调节破骨细胞命运以促进骨髓炎骨修复的微环境响应性纳米颗粒。

A microenvironment responsive nanoparticle regulating osteoclast fate to promote bone repair in osteomyelitis.

作者信息

Zeng Huan, Li Dize, He Qingqing, Zheng Xinhui, Chen Xu, Jian Guangyu, Zhang Hongmei, Chen Tao

机构信息

Stomatological Hospital of Chongqing Medical University, Chongqing Key Laboratory of Oral Diseases and Biomedical Sciences, Chongqing Municipal Key Laboratory of Oral Biomedical Engineering of Higher Education, Chongqing, 401147, China.

Department of Pediatric Dentistry, The Affiliated Hospital of Stomatology of Chongqing Medical University, Chongqing, 401147, China.

出版信息

Mater Today Bio. 2025 Apr 17;32:101777. doi: 10.1016/j.mtbio.2025.101777. eCollection 2025 Jun.

DOI:10.1016/j.mtbio.2025.101777
PMID:40321696
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12049845/
Abstract

Osteomyelitis exhibits bone defects in an inflammatory and acid microenvironment. As a crucial factor in this inflammation responses, the macrophage-osteoclast axis is absolutely the core to regulate. The research explored a shell-core structured biomaterial, consisting of a gelatin nanoparticle (GNP) platform loaded with bone morphogenetic protein 9 (BMP9) and coated with a metal phenolic network (TA-Ce), which exhibited adaptive sensitivity to pH values. Extracellularly, it rapidly responded to lower pH, achieving specific release in an inflammatory microenvironment. Intracellularly, it impacted the formation, function, and differentiation of osteoclasts through the macrophage-osteoclast axis, thereby promoting bone defect repair. and studies showed GNPs-BMP9@TA-Ce regulated osteoclasts to optimize osteomyelitis treatment strategies, highlighting the potential of modified nanobiomaterials for clinical application.

摘要

骨髓炎在炎症和酸性微环境中表现出骨缺损。作为这种炎症反应的关键因素,巨噬细胞-破骨细胞轴绝对是调控的核心。该研究探索了一种核壳结构的生物材料,它由负载骨形态发生蛋白9(BMP9)的明胶纳米颗粒(GNP)平台和涂覆有金属酚醛网络(TA-Ce)组成,对pH值具有适应性敏感性。在细胞外,它对较低的pH值迅速做出反应,在炎症微环境中实现特异性释放。在细胞内,它通过巨噬细胞-破骨细胞轴影响破骨细胞的形成、功能和分化,从而促进骨缺损修复。 和 研究表明,GNPs-BMP9@TA-Ce调节破骨细胞以优化骨髓炎治疗策略,突出了改性纳米生物材料在临床应用中的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92eb/12049845/371cae292acd/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92eb/12049845/6170500c5a9c/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92eb/12049845/3f894b58bc0a/sc1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92eb/12049845/d9b3b89db0c7/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92eb/12049845/263fa696a6de/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92eb/12049845/6fe38e480468/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92eb/12049845/430b3d36833e/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92eb/12049845/3aaf778b12e1/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92eb/12049845/b372ca20fb98/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92eb/12049845/371cae292acd/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92eb/12049845/6170500c5a9c/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92eb/12049845/3f894b58bc0a/sc1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92eb/12049845/d9b3b89db0c7/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92eb/12049845/263fa696a6de/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92eb/12049845/6fe38e480468/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92eb/12049845/430b3d36833e/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92eb/12049845/3aaf778b12e1/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92eb/12049845/b372ca20fb98/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92eb/12049845/371cae292acd/gr7.jpg

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本文引用的文献

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The ability of to limit protease production plays a key role in the pathogenesis of osteomyelitis irrespective of the functional status of .无论[具体因素]的功能状态如何,[具体物质]限制蛋白酶产生的能力在骨髓炎发病机制中起关键作用。
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Association of Antibiotic Route and Outcomes in Children with Methicillin-Resistant Staphylococcus aureus Bacteremic Osteomyelitis.
耐甲氧西林金黄色葡萄球菌菌血症性骨髓炎患儿抗生素给药途径与治疗结果的相关性
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