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Reducing macrophage numbers alleviates temporomandibular joint ankylosis

机译：减少巨噬细胞数量减轻了颞下颌关节触角

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摘要

Temporomandibular joint (TMJ) ankylosis is a severe joint disease mainly caused by trauma that leads to a series of oral and maxillofacial function disorders and psychological problems. Our series of studies indicate that TMJ ankylosis development is similar to fracture healing and that severe trauma results in bony ankylosis instead of fibrous ankylosis. Macrophages are early infiltrating inflammatory cells in fracture and play a critical role in initiating fracture repair. We hypothesize that the large numbers of macrophages in the early phase of TMJ ankylosis trigger ankylosed bone mass formation and that the depletion of these macrophages in the early phase could inhibit the development of TMJ ankylosis. By analysing human TMJ ankylosis specimens, we found large numbers of infiltrated macrophages in the less-than-1-year ankylosis samples. A rabbit model of TMJ bony ankylosis was established and large numbers of infiltrated macrophages were found at 4 days post-operation. Local clodronate liposome (CLD-lip) injection, which depleted macrophages, alleviated the severity of ankylosis compared with local phosphate-buffered saline (PBS)-loaded liposome (PBS-lip) injection (macrophage number, PBS-lips vs. CLD-lips: 626.03 +/- 164.53 vs. 341.4 +/- 108.88 n/mm(2); ankylosis calcification score, PBS-lips vs. CLD-lips: 2.11 +/- 0.78 vs. 0.78 +/- 0.66). Histological results showed that the cartilage area was reduced in the CLD-lip-treated side (PBS-lips vs. CLD-lips: 6.82 +/- 4.42% vs. 2.71 +/- 2.78%) and that the Wnt signalling regulating cartilage formation was disrupted (Wnt5a expression decreased 60% and Wnt4 expression decreased 73%). Thus, our study showed that large numbers of macrophages infiltrated during the early phase of ankylosis and that reducing macrophage numbers alleviated ankylosis development by reducing cartilage formation.
机译：颞下颌关节（TMJ）强直性疾病是一种严重的联合疾病，主要由创伤引起，导致一系列口腔和颌面功能障碍和心理问题。我们的一系列研究表明，TMJ触角发育类似于骨折愈合，并且严重的创伤导致骨骨骨病而不是纤维状吻不衰。巨噬细胞早期浸润骨折炎性细胞，并在启动断裂修复方面发挥关键作用。我们假设TMJ触发炎症早期癌症的大量巨噬细胞引发了致叉骨髓形成，并且在早期阶段的这些巨噬细胞的消耗可以抑制TMJ强直的发育。通过分析人类TMJ强直处标本，我们发现在少于1年的强触发病例中发现了大量渗透巨噬细胞。建立了TMJ骨骨的兔模型，并在操作后4天内发现了大量渗透巨噬细胞。含有巨噬细胞的本地克莱膦酸盐脂质体（CLD-唇）注射，减轻了与局部磷酸盐缓冲盐水（PBS）加载的脂质体（PBS-LIP）注射（PBS-LIP）注射（PBS-LIP）的严重程度（PBS-LIP）注射（PBS-LIPS与CLD-LIPS）相比：626.03 +/- 164.53与341.4 +/- 108.88 n / mm（2）; ankylosis钙化得分，pbs-lips与cld-lips：2.11 +/- 0.78与0.78 +/- 0.66）。组织学结果表明，CLD唇处理侧的软骨面积降低（PBS-嘴唇与CLD-嘴唇：6.82 +/- 4.42％vs.271 +/- 2.78％），并且WNT信号传导调节软骨形成被破坏（WNT5a表达减少60％，WNT4表达减少73％）。因此，我们的研究表明，通过减少软骨形成，减少巨噬细胞数量减少了巨噬细胞数量的大量巨噬细胞渗透。

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  • 来源
    《Cell and Tissue Research》 |2020年第3期|共16页
  • 作者

    Zhao Lu; Xiao E.; He Linhai; Duan Denghui; He Yang; Chen Shuo; Zhang Yi; Gan Yehua;

  • 作者单位

    Peking Univ Sch Hosp Stomatol Dept Oral Maxillofacial Surg #22 Zhongguancun S Ave Haidian Dist;

    Peking Univ Sch Hosp Stomatol Dept Oral Maxillofacial Surg #22 Zhongguancun S Ave Haidian Dist;

    Peking Univ Sch Hosp Stomatol Dept Oral Maxillofacial Surg #22 Zhongguancun S Ave Haidian Dist;

    Peking Univ Sch Hosp Stomatol Dept Oral Maxillofacial Surg #22 Zhongguancun S Ave Haidian Dist;

    Peking Univ Sch Hosp Stomatol Dept Oral Maxillofacial Surg #22 Zhongguancun S Ave Haidian Dist;

    Peking Univ Sch Hosp Stomatol Dept Oral Maxillofacial Surg #22 Zhongguancun S Ave Haidian Dist;

    Peking Univ Sch Hosp Stomatol Dept Oral Maxillofacial Surg #22 Zhongguancun S Ave Haidian Dist;

    Peking Univ Sch Hosp Stomatol Dept Oral Maxillofacial Surg #22 Zhongguancun S Ave Haidian Dist;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
  • 关键词

    Macrophage; Temporomandibular joint; Fracture healing; Cartilage; Inflammation;

    机译：巨噬细胞;颞下颌关节;骨折愈合;软骨;炎症;

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