Cell Origin and Differentiation in the Repair of Full-Thickness Defects of Articular Cartilage
Cell Origin and Differentiation in the Repair of Full-Thickness Defects of Articular Cartilage
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DOI：
10.1007/978-1-4471-5451-8_95
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发表时间：
2014
影响因子：
4.1
通讯作者：
C. Charalambous
中科院分区：
文献类型：
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作者：
C. Charalambous
用组织学方法研究了新西兰大白兔关节软骨3毫米直径、圆柱形、全层钻孔缺损修复过程中细胞的来源和分化情况。手术后，这些动物被允许自由活动。来自122只动物的364个个体缺陷在术后48周内被检查。在最初几天，纤维质拱廊在缺陷上建立，从表面边缘到表面边缘，这有助于引导间充质细胞沿长轴向内生长。第一个软骨细胞外基质合成的证据，由红花素- o染色确定，出现在第10天。两周后，几乎所有标本的胶原组织表面下都出现了软骨，胶原组织富含扁平的纤维软骨细胞。三周后，几乎所有的缺损部位都有一层清晰的软骨层，其中含有软骨细胞。缺损在6周、8周、10周和12周基本完全再生，细胞逐渐分化为成软骨细胞、软骨细胞和成骨细胞，软骨和骨基质在适当位置合成。24周时，潮水标记和紧密板层软骨下骨板均已重建。最初在缺损深处形成的松质编织骨被板层、粗松质骨所取代。用3h -胸腺嘧啶和3h -胞苷标记后的放射自显像显示来自邻近残余关节软骨的软骨细胞没有参与缺损的再生。修复完全由骨髓间充质细胞的增殖和分化介导。术后7天关节内注射3h -胸腺嘧啶清晰地标记了这个间充质细胞池。该标记最初由未分化的间充质细胞使用，逐渐出现在成纤维细胞、成骨细胞、关节成软骨细胞和软骨细胞中，表明它们起源于骨髓的原始间充质细胞。软骨基质退行性变的早期痕迹在许多缺陷中出现在12至20周，在24、36和48周时，退行性变的发生率和强度增加。偏振光显微镜显示新合成的修复基质不能附着在紧邻钻孔的软骨上并与之结合，即使光镜显示组织明显的连续性。在许多情况下，在修复软骨和残余软骨之间可以看到明显的间隙。（摘要删节为400字）
The origin and differentiation of cells in the repair of three-millimeter-diameter, cylindrical, full-thickness drilled defects of articular cartilage were studied histologically in New Zealand White rabbits. The animals were allowed to move freely after the operation. Three hundred and sixty-four individual defects from 122 animals were examined as long as forty-eight weeks postoperatively. In the first few days, fibrinous arcades were established across the defect, from surface edge to surface edge, and this served to orient mesenchymal cell ingrowth along the long axes. The first evidence of synthesis of a cartilage extracellular matrix, as defined by safranin-O staining, appeared at ten days. At two weeks, cartilage was present immediately beneath the surface of collagenous tissue that was rich in flattened fibrocartilaginous cells in virtually all specimens. At three weeks, the sites of almost all of the defects had a well demarcated layer of cartilage containing chondrocytes. An essentially complete repopulation of the defects occurred at six, eight, ten, and twelve weeks, with progressive differentiation of cells to chondroblasts, chondrocytes, and osteoblasts and synthesis of cartilage and bone matrices in their appropriate locations. At twenty-four weeks, both the tidemark and the compact lamellar subchondral bone plate had been re-established. The cancellous woven bone that had formed initially in the depths of the defect was replaced by lamellar, coarse cancellous bone. Autoradiography after labeling with 3H-thymidine and 3H-cytidine demonstrated that chondrocytes from the residual adjacent articular cartilage did not participate in the repopulation of the defect. The repair was mediated wholly by the proliferation and differentiation of mesenchymal cells of the marrow. Intra-articular injections of 3H-thymidine seven days after the operation clearly labeled this mesenchymal cell pool. The label, initially taken up by undifferentiated mesenchymal cells, progressively appeared in fibroblasts, osteoblasts, articular chondroblasts, and chondrocytes, indicating their origin from the primitive mesenchymal cells of the marrow. Early traces of degeneration of the cartilage matrix were seen in many defects at twelve to twenty weeks, with the prevalence and intensity of the degeneration increasing at twenty-four, thirty-six, and forty-eight weeks. Polarized light microscopy demonstrated failure of the newly synthesized repair matrix to become adherent to, and integrated with, the cartilage immediately adjacent to the drill-hole, even when light microscopy had shown apparent continuity of the tissue. In many instances, a clear gap was seen between repair and residual cartilage.(ABSTRACT TRUNCATED AT 400 WORDS)