p53 is known to advance the cell arrest and cell senescence in human tumors. In this study, we displayed that osteogenic ability of p53-knockout (p53^−/−) mice was significantly increased in the tooth extraction socket compared with wild-type (WT) counterparts. Bone marrow mesenchymal stem cells (BM-MSCs) from mandibular were collected and exhibited with elevated proliferation potential and colony-forming units compared with the control, as well as stronger mineral deposits and osteogenic markers. Besides, the bone mass and bone parameter in p53^−/− mice were markedly enhanced compared with the counterpart after extractions by micro-CT. Masson’s trichrome staining and immunohistochemistry also revealed that new bone filling and osterix/osteocalcin (Osx/OCN)-immunopositive staining in p53^−/− mice were remarkably increased at each time point. Furthermore, consistent with the enhanced osteogenic markers, the angiogenic marker of blood vessels (alpha smooth muscle actin, α-SMA) was significantly elevated in p53^−/− mice in contrast to WT mice. Importantly, we found that the osteoclast numbers exhibited an increased trend in p53^−/− mice compared with WT mice during socket healing. Collectively, our result suggest that p53 deficiency could promote the osteogenesis and angiogenesis in the tooth extraction socket and might lend possibility for p53-based therapeutic approaches in acceleration of extraction bone healing.

中文翻译：

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p53缺乏在拔牙后牙槽窝愈合中的作用。

已知p53可促进人肿瘤中的细胞停滞和细胞衰老。在这项研究中，我们显示与野生型（WT）相比，拔牙窝中p53基因敲除（p53 ^-/-）小鼠的成骨能力显着提高。收集来自下颌骨的骨髓间充质干细胞（BM-MSC），与对照组相比，它们具有更高的增殖潜能和集落形成单位，以及更强的矿物质沉积和成骨标记。此外，p53中的骨骼质量和骨骼参数^-/-与通过微型CT提取后的小鼠相比，小鼠明显增强。Masson的三色染色和免疫组织化学还显示，在每个时间点，p53 ^-/-小鼠的新骨填充和osterix / osteocalcin（Osx / OCN）免疫阳性染色均显着增加。此外，与增强的成骨标记物一致，与WT小鼠相比，p53 ^-/-小鼠中血管的血管生成标记物（α平滑肌肌动蛋白，α-SMA）显着升高。重要的是，我们发现破骨细胞数量在p53 ^-/-上呈现增加的趋势小鼠在窝愈合期间与野生型小鼠相比。总的来说，我们的结果表明，p53缺乏症可以促进拔牙窝中的成骨和血管生成，并可能为基于p53的治疗方法加速拔牙的愈合提供可能性。