OBJECTIVE Examination of intervertebral disc (IVD) regeneration in an ovine annular lesion model. HYPOTHESIS Sulfation motifs are important functional determinants in glycosaminoglycans (GAGs). Previous studies have correlated 3-B-3(-) and 7-D-4 chondroitin sulfate (CS) motifs in tissues undergoing morphogenetic transition in development. We hypothesize that these motifs may also be expressed in degenerate IVDs and may represent a reparative response. DESIGN Induction of disc degeneration by 5 mm or 6 × 20 mm lesions in the annulus fibrosus (AF) over 6 or 3 to 6 months postoperation (PO). Tissue sections were stained with toluidine blue-fast green, 3-B-3(-) and 7-D-4 CS-sulfation motifs were immunolocalized in 3-month PO 6 × 20 mm lesion IVDs. Sulfated glycosaminoglycan (GAG), 3-B-3(-), and 7-D-4 epitopes were quantitated by ELISIA (enzyme-linked immunosorbent inhibition assay) in extracts of AF (lesion site and contralateral half) and nucleus pulposus (NP) 0, 3, and 6 months PO. RESULTS Collagenous overgrowth of lesions occurred in the outer AF. Chondroid metaplasia in ~20% of the 6 × 20 mm affected discs resulted in integration of an outgrowth of NP tissue with the inner AF lamellae preventing propagation of the lesion. 3-B-3(-) and 7-D-4 CS sulfation motifs were immunolocalized in this chondroid tissue. ELISIA quantified CS sulfation motifs demonstrating an increase 3 to 6 months PO in the AF lesion and a reduction in sulfated GAG not evident in the contralateral AF. CONCLUSIONS (1) Outer annular lesions underwent spontaneous repair. (2) Chondroid metaplasia of the inner 6 × 20 mm defect prevented its propagation suggesting an apparent reparative response.

中文翻译：

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在绵羊椎间盘退变模型中3-B-3（-）和7-D-4软骨素的时空表达，组织重塑和尝试修复。

目的在绵羊环形病变模型中检查椎间盘（IVD）的再生。假设硫酸基序是糖胺聚糖（GAG）中重要的功能决定簇。先前的研究已将3-B-3（-）和7-D-4硫酸​​软骨素（CS）图案与发育中发生形态发生转变的组织相关联。我们假设这些基序也可能在简并的IVD中表达，并可能代表修复反应。设计术后6或3至6个月内，纤维环（AF）的5 mm或6×20 mm病变引起椎间盘退变。组织切片用甲苯胺蓝固绿染色，将3-B-3（-）和7-D-4 CS硫酸化基序免疫定位在3个月的PO 6×20 mm病变IVD中。硫酸糖胺聚糖（GAG），3-B-3（-），通过ELISIA（酶联免疫吸附抑制试验）对AF（病变部位和对侧一半）和髓核（NP）0、3和6个月PO提取物中的7和D-4表位进行定量。结果病变的胶原蛋白过度生长发生在外房颤。约20％的6×20 mm受累椎间盘中的软骨样化生导致NP组织的生长产物与内部AF薄片融合在一起，从而阻止了病变的扩散。3-B-3（-）和7-D-4 CS硫酸化基序被免疫定位在该软骨组织中。ELISIA量化了CS硫酸化基序，表明AF病变中PO增加3至6个月，而对侧AF中硫酸化GAG的降低则不明显。结论（1）环状外病变自发修复。