Annular repair using high-density collagen gel: a rat-tail in vivo model.
Annular repair using high-density collagen gel: a rat-tail in vivo model.
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DOI：
10.1097/brs.0000000000000103
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发表时间：
2014-02-01
期刊：
影响因子：
3
通讯作者：
Härtl R
中科院分区：
文献类型：
--
作者：
Grunert P;Borde BH;Hudson KD;Macielak MR;Bonassar LJ;Härtl R
研究设计：动物体内研究目的：测试高密度胶原蛋白凝胶修复纤维环缺损的能力。背景资料概要：纤维环缺损与自发性椎间盘突出和椎间盘退变有关，可导致严重的发病率。椎间盘切除术后持续性的纤维环缺损会增加再突出率。已经开发了几种合成和生物材料用于瓣环修复。这是第一个在活体内测试可注射生物材料的研究。方法：我们用18号针头穿刺42只无胸腺大鼠的尾侧椎间盘，造成环状缺损。将单独或与核黄素（RF）交联的高密度胶原蛋白（HDC）注射到缺损处。有4个单独的研究组：HDC、与0.25 mM RF或0.50 mM RF交联的HDC，以及穿刺且未处理的阴性对照。对动物随访5周;使用X线片评估椎间盘高度，使用磁共振成像评估退行性变化。我们开发了一种算法的基础上T2弛豫时间测量，以评估髓核的大小。收集尾部进行组织学分析，以评估椎间盘退变，并测量髓核的横截面积。Results.After 5 weeks，对照组和未交联的HDC组都表现出进行性退行性变化的迹象，椎间盘间隙中有少量或没有残留的髓核组织。交联显著提高了HDC凝胶修复瓣环缺损的能力。与健康椎间盘相比，0.50 mM RF交联组的核组织仅轻微减少，无椎间盘（IVD）退变迹象。纤维环被桥接缺损的纤维帽部分修复。结论：人成纤维细胞具有修复纤维环缺损的能力。HDC的刚度可以通过核黄素交联进行修改，并且似乎对修复机制产生积极影响。这些结果需要在更大的动物模型中进行复制。证据等级：N/A环形缺损与椎间盘退行性改变相关。这是第一项在体内测试用于瓣环修复的可注射生物材料的研究。高密度胶原蛋白能够在针刺大鼠尾部模型中修复环状缺损。核黄素纤维交联增强了修复机制。
Study Design.Animal in vivo study.Objective.To test the capability of high-density collagen gel to repair annular defects.Summary of Background Data.Annular defects are associated with spontaneous disc herniations and disc degeneration, which can lead to significant morbidity. Persistent annular defects after surgical discectomies can increase reherniation rates. Several synthetic and biological materials have been developed for annular repair. This is the first study to test an injectable biomaterial in vivo.Methods.We punctured caudal intervertebral discs in 42 athymic rats, using an 18-gauge needle to create an annular defect. High-density collagen (HDC), either alone or cross-linked with riboflavin (RF), was injected into the defect. There were 4 separate study groups: HDC, HDC cross-linked with either 0.25 mM RF or 0.50 mM RF, and a negative control that was punctured and not treated. The animals were followed for 5 weeks; radiographs were used to assess disc heights and magnetic resonance images were used to evaluate degenerative changes. We developed an algorithm on the basis of T2-relaxation time measurements to assess the size of the nucleus pulposus. Tails were collected for histological analysis to evaluate disc degeneration and measure the cross-sectional area of the nucleus pulposus.Results.After 5 weeks, the control and the uncross-linked HDC groups both showed signs of progressive degenerative changes with minimal or no residual nucleus pulposus tissue in the disc space. Cross-linking significantly improved the ability of HDC gels to repair annular defects. The 0.50 mM RF cross-linked group showed only a slight decrease in nuclear tissue when compared with healthy discs, with no signs of intervertebral disc (IVD) degeneration. The annulus fibrosus was partially repaired by a fibrous cap that bridged the defect. Host fibroblasts infiltrated and remodeled the injected collagen.Conclusion.HDC is capable of repairing annular defects induced by needle puncture. The stiffness of HDC can be modified by riboflavin cross-linking and seems to positively affect the repair mechanism. These results need to be replicated in a larger animal model.Level of Evidence: N/AAnnular defects are associated with degenerative changes of intervertebral discs. This is the first study to test an injectable biomaterial for annular repair in vivo. High-density collagen was capable of repairing annular defects in a needle puncture rat-tail model. Riboflavin fiber cross-linking enhanced the repair mechanism.