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首页> 外文期刊>Journal of orthopaedic research >Macrophages accumulate in the early phase of tendon-bone healing.
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Macrophages accumulate in the early phase of tendon-bone healing.

机译：巨噬细胞在腱骨愈合的早期阶段积累。

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A scar tissue interface forms rather than a normal ligament insertion site following attachment of a tendon graft to bone. The specific cell types that initiate the process of tendon-to-bone healing are unknown. We hypothesized that inflammatory cell accumulation following tendon-to-bone repair results in this scar interface. We used a rodent model to examine the temporal and spatial pattern of accumulation of hematopoietic lineage cells in the early phase of tendon-to-bone healing. Thirty-six Lewis rats underwent anterior cruciate ligament (ACL) reconstruction in the left knee using a flexor digitorum longus tendon graft. Six animals were sacrificed at 4, 7, 11, 14, 21, and 28 days after surgery. Serial sections were analyzed for proliferating cells (PCNA), recruited macrophages (ED1), resident macrophages (ED2), neutrophils, T-lymphocytes (CD3), mast cells, immature progenitor cells/pericytes (expressing the NG2 cell-surface chondroitin sulfate proteoglycan), and newly-formed blood vessels (Factor VIII). Neutrophils, ED1(+) and ED2(+) macrophages accumulated sequentially in the healing tendon graft, with progressive cell ingrowth from the interface towards the inner tendon. Neutrophils and ED1(+) cells were seen in the tendon-bone interface at 4 days after surgery, while ED2(+) macrophages were not identified until 11 days. These cells progressively repopulated the tendon graft. NG2-positive progenitor cells were found along the edge of the bone tunnel in the interface, but these cells did not invade the tendon. Occasional T-lymphocytes and mast cells were seen in the tendon-bone interface. There was no proliferation of intrinsic tendon cells, indicating that the tendon does not directly contribute to healing. We hypothesize that cytokines produced by infiltrating macrophages are likely to contribute to the formation of a fibrous scar tissue interface rather than a normal insertion site.
机译：在将肌腱移植物附着到骨上之后，瘢痕组织界面形成而不是正常的韧带插入部位。启动肌腱到骨愈合过程的特定细胞类型是未知的。我们假设腱-骨修复后炎症细胞的积累导致了这种疤痕界面。我们使用了一种啮齿动物模型来检查肌腱-骨愈合早期阶段造血谱系细胞积累的时空格局。三十六只Lewis大鼠使用趾长屈肌腱移植物进行左膝前交叉韧带（ACL）重建。在手术后第4、7、11、14、21和28天处死6只动物。分析了连续切片的增殖细胞（PCNA），募集的巨噬细胞（ED1），常驻巨噬细胞（ED2），嗜中性粒细胞，T淋巴细胞（CD3），肥大细胞，未成熟祖细胞/周细胞（表达NG2细胞表面硫酸软骨素蛋白多糖） ）和新形成的血管（因子VIII）。中性粒细胞，ED1（+）和ED2（+）巨噬细胞在愈合的肌腱移植物中顺序积累，细胞从界面向内肌腱逐渐向内生长。术后4天在肌腱-骨界面中可见嗜中性粒细胞和ED1（+）细胞，而直到11天才鉴定出ED2（+）巨噬细胞。这些细胞逐渐重新填充肌腱移植物。在界面的骨隧道边缘发现了NG2阳性祖细胞，但这些细胞并未侵入肌腱。在腱-骨界面中观察到偶尔的T淋巴细胞和肥大细胞。内在的肌腱细胞没有增殖，表明肌腱不直接促进愈合。我们假设渗透巨噬细胞产生的细胞因子可能有助于形成纤维性瘢痕组织界面，而不是正常的插入位点。

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