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对幼猪股骨远端软骨管进行非线性光学显微镜检查可能揭示关节骨软骨病的病因。

Non-linear optical microscopy of cartilage canals in the distal femur of young pigs may reveal the cause of articular osteochondrosis.

作者信息

Finnøy Andreas, Olstad Kristin, Lilledahl Magnus B

机构信息

Department of Physics, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.

Faculty of Veterinary Medicine and Biosciences, Equine Section, Norwegian University of Life Sciences, P.O. Box 8146, Oslo, Norway.

出版信息

BMC Vet Res. 2017 Aug 22;13(1):270. doi: 10.1186/s12917-017-1197-y.

DOI:10.1186/s12917-017-1197-y
PMID:28830435
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5568222/
Abstract

BACKGROUND

Articular osteochondrosis is a common cause of leg weakness in pigs and is defined as a focal delay in the endochondral ossification of the epiphysis. The first demonstrated steps in the pathogenesis consist of loss of blood supply and subsequent chondronecrosis in the epiphyseal growth cartilage. Blood vessels in cartilage are located in cartilage canals and become incorporated into the secondary ossification centre during growth. It has been hypothesized that vascular failure occurs during this incorporation process, but it is not known what predisposes a canal to fail. To obtain new information that may reveal the cause of vascular failure, the distal femur of 4 pigs aged 82-140 days was sampled and examined by non-linear optical microscopy. This novel technique was used for its ability to reveal information about collagen by second harmonic generation and cellular morphology by two-photon-excited fluorescence in thick sections without staining. The aims were to identify morphological variations between cartilage canal segments and to examine if failed cartilage canals could be followed back to the location where the blood supply ceased.

RESULTS

The cartilage canals were shown to vary in their content of collagen fibres (112/412 segments), and the second harmonic and fluorescence signals indicated a variation in the bundling of collagen fibrils (245/412 segments) and in the calcification (30/412 segments) of the adjacent cartilage matrix. Failed cartilage canals associated with chondronecrosis were shown to enter the epiphyseal growth cartilage from not only the secondary ossification centre, but also the attachment site of the caudal cruciate ligament.

CONCLUSION

The variations between cartilage canal segments could potentially explain why the blood supply fails at the osteochondral junction in only a subset of the canals. Proteins linked to these variations should be examined in future genomic studies. Although incorporation can still be a major cause, it could not account for all cases of vascular failure. The role of the caudal cruciate ligament in the cause of osteochondrosis should therefore be investigated further.

摘要

背景

关节骨软骨病是猪腿部无力的常见原因,被定义为骨骺软骨内成骨的局灶性延迟。发病机制中首先显示的步骤包括骨骺生长软骨的血供丧失和随后的软骨坏死。软骨中的血管位于软骨管内,并在生长过程中融入次级骨化中心。据推测,血管衰竭发生在这个融合过程中,但尚不清楚是什么因素导致软骨管发生衰竭。为了获得可能揭示血管衰竭原因的新信息,对4头年龄在82 - 140天的猪的股骨远端进行采样,并通过非线性光学显微镜检查。这项新技术被用于其在厚切片中无需染色就能通过二次谐波产生揭示胶原蛋白信息以及通过双光子激发荧光揭示细胞形态的能力。目的是识别软骨管段之间的形态学差异,并检查是否可以追踪到衰竭的软骨管的血供停止位置。

结果

软骨管在胶原纤维含量(112/412段)上存在差异,二次谐波和荧光信号表明相邻软骨基质中胶原原纤维的束状排列(245/412段)和钙化(30/412段)存在变化。与软骨坏死相关的衰竭软骨管不仅从次级骨化中心进入骨骺生长软骨,还从后交叉韧带的附着部位进入。

结论

软骨管段之间的差异可能解释为什么只有一部分软骨管在骨软骨交界处血供会衰竭。与这些差异相关的蛋白质应在未来的基因组研究中进行检查。虽然融合仍然可能是主要原因,但它不能解释所有血管衰竭的情况。因此,应进一步研究后交叉韧带在骨软骨病病因中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4342/5568222/bde653d29a93/12917_2017_1197_Fig9_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4342/5568222/5d0b475026ca/12917_2017_1197_Fig2_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4342/5568222/2070cf752dc4/12917_2017_1197_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4342/5568222/62178de30ef9/12917_2017_1197_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4342/5568222/b95d5a7f8177/12917_2017_1197_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4342/5568222/12ee647a4c3e/12917_2017_1197_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4342/5568222/db1e6d831e9a/12917_2017_1197_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4342/5568222/bde653d29a93/12917_2017_1197_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4342/5568222/beccb567c416/12917_2017_1197_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4342/5568222/5d0b475026ca/12917_2017_1197_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4342/5568222/ce0b1d09c10a/12917_2017_1197_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4342/5568222/2070cf752dc4/12917_2017_1197_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4342/5568222/62178de30ef9/12917_2017_1197_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4342/5568222/b95d5a7f8177/12917_2017_1197_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4342/5568222/12ee647a4c3e/12917_2017_1197_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4342/5568222/db1e6d831e9a/12917_2017_1197_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4342/5568222/bde653d29a93/12917_2017_1197_Fig9_HTML.jpg

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