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大鼠损伤模型中膝关节韧带对注射疗法的反应

Response of knee ligaments to prolotherapy in a rat injury model.

作者信息

Jensen Kristina T, Rabago David P, Best Thomas M, Patterson Jeffrey J, Vanderby Ray

机构信息

Department of Biomedical Engineering, University of Wisconsin, Madison, Wisconsin, USA.

出版信息

Am J Sports Med. 2008 Jul;36(7):1347-57. doi: 10.1177/0363546508314431. Epub 2008 Feb 29.

DOI:10.1177/0363546508314431
PMID:18310313
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3164307/
Abstract

BACKGROUND

Prolotherapy is an alternative therapy for chronic musculoskeletal injury including joint laxity. The commonly used injectant, D-glucose (dextrose), is hypothesized to improve ligament mechanics and decrease pain through an inflammatory mechanism. No study has investigated the mechanical effects of prolotherapy on stretch-injured ligaments.

HYPOTHESES

Dextrose injections will enlarge cross-sectional area, decrease laxity, strengthen, and stiffen stretch-injured medial collateral ligaments (MCLs) compared with controls. Dextrose prolotherapy will increase collagen fibril diameter and density of stretch-injured MCLs.

STUDY DESIGN

Controlled laboratory study.

METHODS

Twenty-four rats were bilaterally MCL stretch-injured, and the induced laxity was measured. After 2 weeks, 32 MCLs were injected twice, 1 week apart, with either dextrose or saline control; 16 MCLs received no injection. Seven uninjured rats (14 MCLs) were additional controls. Two weeks after the second injection, ligament laxity, mechanical properties (n = 8), and collagen fibril diameter and density (n = 3) were assessed.

RESULTS

The injury model created consistent ligament laxity (P < .05) that was not altered by dextrose injections. Cross-sectional area of dextrose-injected MCLs was increased 30% and 90% compared with saline and uninjured controls, respectively (P < .05). Collagen fibril diameter and density were decreased in injured ligaments compared with uninjured controls (P < .05), but collagen fibril characteristics were not different between injured groups.

CONCLUSION

Dextrose injections increased the cross-sectional area of MCLs compared with saline-injected and uninjured controls. Dextrose injections did not alter other measured properties in this model.

CLINICAL RELEVANCE

Our results suggest that clinical improvement from prolotherapy may not result from direct effects on ligament biomechanics.

摘要

背景

注射疗法是一种针对包括关节松弛在内的慢性肌肉骨骼损伤的替代疗法。常用的注射剂D - 葡萄糖(右旋糖)被假定通过炎症机制改善韧带力学性能并减轻疼痛。尚无研究调查注射疗法对拉伸损伤韧带的力学影响。

假设

与对照组相比,葡萄糖注射将增大拉伸损伤的内侧副韧带(MCL)的横截面积,降低松弛度,增强并使其变硬。葡萄糖注射疗法将增加拉伸损伤的MCL的胶原纤维直径和密度。

研究设计

对照实验室研究。

方法

对24只大鼠双侧MCL进行拉伸损伤,并测量诱导的松弛度。2周后,32条MCL分别注射葡萄糖或生理盐水对照,间隔1周注射两次;16条MCL未接受注射。另外7只未受伤的大鼠(14条MCL)作为对照。第二次注射后2周,评估韧带松弛度、力学性能(n = 8)以及胶原纤维直径和密度(n = 3)。

结果

损伤模型产生了一致的韧带松弛(P < .05),葡萄糖注射并未改变这一情况。与生理盐水和未受伤对照组相比,注射葡萄糖的MCL的横截面积分别增加了30%和90%(P < .05)。与未受伤对照组相比,损伤韧带中的胶原纤维直径和密度降低(P < .05),但损伤组之间的胶原纤维特征并无差异。

结论

与注射生理盐水和未受伤对照组相比,葡萄糖注射增加了MCL的横截面积。在该模型中,葡萄糖注射并未改变其他测量属性。

临床意义

我们的结果表明,注射疗法带来的临床改善可能并非源于对韧带生物力学的直接影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ceb/3164307/5f0621f6b9e1/nihms318786f10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ceb/3164307/6d5ce3f2d346/nihms318786f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ceb/3164307/4673a51c7e97/nihms318786f7.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ceb/3164307/f5bf534e1586/nihms318786f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ceb/3164307/5f0621f6b9e1/nihms318786f10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ceb/3164307/6d5ce3f2d346/nihms318786f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ceb/3164307/1daa1bc32b51/nihms318786f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ceb/3164307/ca74e626396c/nihms318786f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ceb/3164307/4da8a533daca/nihms318786f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ceb/3164307/c94e51630cac/nihms318786f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ceb/3164307/1092590159c1/nihms318786f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ceb/3164307/4673a51c7e97/nihms318786f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ceb/3164307/4587b0d13219/nihms318786f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ceb/3164307/f5bf534e1586/nihms318786f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ceb/3164307/5f0621f6b9e1/nihms318786f10.jpg

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