*Department of Neurological Surgery, Weill Cornell Brain and Spine Institute, Weill Cornell Medical College, New York, NY; †Department of Biomedical Engineering, Cornell University, Ithaca, NY; and ‡Sibley School of Mechanical and Aerospace Engineering, Cornell University, Ithaca, NY.
Spine (Phila Pa 1976). 2014 Feb 1;39(3):198-206. doi: 10.1097/BRS.0000000000000103.
Animal in vivo study.
To test the capability of high-density collagen gel to repair annular defects.
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.
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.
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.
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.
N/A.
动物体内研究。
测试高密度胶原凝胶修复环形缺损的能力。
环形缺损与自发性椎间盘突出和椎间盘退变有关，可导致明显的发病率。手术后持续的环形缺损可增加再突出率。已经开发了几种合成和生物材料用于环形修复。这是第一个体内测试可注射生物材料的研究。
我们使用 18 号针在 42 只无胸腺大鼠的尾椎间盘中穿刺，以创建环形缺损。将高密度胶原（HDC）单独或用核黄素（RF）交联后注入缺损处。有 4 个单独的研究组：HDC、用 0.25mM RF 或 0.50mM RF 交联的 HDC，以及未处理的阴性对照。动物被随访 5 周；X 线片用于评估椎间盘高度，磁共振成像用于评估退行性变化。我们根据 T2 弛豫时间测量值开发了一种算法，以评估髓核的大小。收集尾巴进行组织学分析，以评估椎间盘退变并测量髓核的横截面积。
5 周后，对照组和未交联 HDC 组均显示出进行性退行性变化的迹象，椎间盘间隙中残留的髓核组织很少或没有。交联显著提高了 HDC 凝胶修复环形缺损的能力。与健康椎间盘相比，0.50mM RF 交联组的核组织仅略有减少，没有椎间盘（IVD）退变的迹象。纤维帽部分修复了纤维环，桥接了缺损。宿主成纤维细胞浸润并重塑了注射的胶原蛋白。
HDC 能够修复由针刺引起的环形缺损。HDC 的刚度可以通过核黄素交联来调节，并且似乎对修复机制有积极影响。这些结果需要在更大的动物模型中复制。
无。
