Role of p53 deficiency in socket healing after tooth extractions.

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.