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在Legg-Calvé-Perthes病大型动物模型中，使用水凝胶载体局部给药骨形态发生蛋白-2以实现强劲的骨再生

Local Administration of Bone Morphogenetic Protein-2 Using a Hydrogel Carrier for Robust Bone Regeneration in a Large Animal Model of Legg-Calvé-Perthes disease.

作者信息

Kim Harry, Ma Chi, Park Minsung, Monte Felipe, Gokani Vishal, Aruwajoye Olumide, Ren Yinshi, Liu Xiaohua

机构信息

Scottish Rite for Children.

Texas A&M School of Dentistry.

出版信息

Res Sq. 2023 Jan 17:rs.3.rs-2465423. doi: 10.21203/rs.3.rs-2465423/v1.

DOI:10.21203/rs.3.rs-2465423/v1
PMID:36711714
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9882687/
Abstract

Legg-Calvé-Perthes disease is juvenile idiopathic osteonecrosis of the femoral head (ONFH) that has no effective clinical resolutions. Previously, local injection of bone morphogenetic protein-2 (BMP2) for ONFH treatment showed a heterogeneous bone repair and a high incidence of heterotopic ossification (HO) due to the BMP2 leakage. Here, we developed a BMP2-hydrogel treatment via a transphyseal bone wash and subsequential injection of BMP2-loaded hydrogel. In vivo studies showed that a hydrogel of gelatin-heparin-tyramine retained the BMP2 for four weeks. The injection of the hydrogel can efficiently prevent leakage. With the bone wash, the injected hydrogel had a broad distribution in the head. In vivo studies on pigs revealed that the BMP2-hydrogel treatment produced a homogeneous bone regeneration without HO. It preserved the subchondral contour and restored the subchondral endochondral ossification, although it increased growth plate fusions. In summary, the study demonstrated a promising BMP2-hydrogel treatment for ONFH treatment, especially for teenagers.

摘要

Legg-Calvé-Perthes病是一种股骨头的青少年特发性骨坏死（ONFH），目前尚无有效的临床治疗方法。此前，局部注射骨形态发生蛋白-2（BMP2）治疗ONFH时，由于BMP2渗漏，骨修复情况不一，异位骨化（HO）发生率较高。在此，我们通过经骨骺骨冲洗及随后注射负载BMP2的水凝胶开发了一种BMP2-水凝胶治疗方法。体内研究表明，明胶-肝素-酪胺水凝胶可将BMP2保留四周。水凝胶注射可有效防止渗漏。经骨冲洗后，注射的水凝胶在股骨头内分布广泛。对猪的体内研究表明，BMP2-水凝胶治疗可产生均匀的骨再生且无HO。尽管它增加了生长板融合，但保留了软骨下轮廓并恢复了软骨下软骨内成骨。总之，该研究证明了一种有前景的BMP2-水凝胶治疗ONFH的方法，尤其适用于青少年。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/150e/9882687/7a52d5441480/nihpp-rs2465423v1-f0008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/150e/9882687/d579789e8910/nihpp-rs2465423v1-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/150e/9882687/aaca5c34ee7d/nihpp-rs2465423v1-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/150e/9882687/37ca0d0edb4e/nihpp-rs2465423v1-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/150e/9882687/fae7e150f826/nihpp-rs2465423v1-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/150e/9882687/6df748dc57d5/nihpp-rs2465423v1-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/150e/9882687/23f6a313fcf5/nihpp-rs2465423v1-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/150e/9882687/7a52d5441480/nihpp-rs2465423v1-f0008.jpg

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本文引用的文献

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J Bone Joint Surg Am. 2021 Jul 7;103(13):1193-1202. doi: 10.2106/JBJS.20.00578.
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Osteocyte necrosis triggers osteoclast-mediated bone loss through macrophage-inducible C-type lectin.破骨细胞介导体细胞坏死触发的骨丢失通过巨噬细胞诱导的 C 型凝集素。
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成人股骨头坏死临床诊疗指南（2019年版）
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