Oshitani Masayuki, Takaoka Kazuki, Ueta Miho, Tomimoto Kohei, Hattori Hirokazu, Yoneda Naomichi, Yamanegi Koji, Noguchi Kazuma, Kishimoto Hiromitsu
Department of Oral and Maxillofacial Surgery, Hyogo Medical University, Nishinomiya, Hyogo 663-8501, Japan.
Department of Pathology, School of Medicine, Hyogo Medical University, Nishinomiya, Hyogo 663-8501, Japan.
Exp Ther Med. 2023 Jan 20;25(3):104. doi: 10.3892/etm.2023.11803. eCollection 2023 Mar.
Granulocyte colony-stimulating factor (G-CSF) regulates the survival, proliferation and differentiation of all cells in the neutrophil lineage, and is consequently used for neutropenic conditions. Upon G-CSF administration, osteoblasts and osteocytes are suppressed, and the support system allowing hematopoietic stem cells to remain in the microenvironment is diminished. The present study focused on and investigated G-CSF as a regulatory factor of bone remodeling. The aim of the present study was to investigate the effect of G-CSF administration on the bone healing of tooth extraction sockets. Significant differences in the bone volume fraction, and trabecular separation of the proximal femurs and alveolar septa were observed between the G-CSF and control (saline-treated) groups. The trabecular bone of the femur and alveolar septa was reduced in the G-CSF group compared with that in the control group. In addition, serum procollagen type 1 N-terminal propeptide levels, a marker of bone formation, were lower in the G-CSF group compared with in the control group. Fibrous connective tissues and immature bone were observed in the extraction socket, and bone healing was delayed in the G-CSF group compared with that in the control group. The bone area in the extraction socket 6 days after tooth extraction was significantly smaller in the G-CSF group (23.6%) than that in the control group (45.1%). Furthermore, G-CSF administration reduced the number of canaliculi per osteocyte and inhibited the connection of osteocyte networks. Consequently, osteoblast activation was inhibited and bone remodeling changed to a state of low bone turnover in the G-CSG group. Analysis of bone formation parameters revealed that the G-CSF group exhibited a lower mineral apposition rate compared with in the control group. In conclusion, these findings indicated that G-CSF may delay bone healing of the socket after tooth extraction.
粒细胞集落刺激因子（G-CSF）调节中性粒细胞谱系中所有细胞的存活、增殖和分化，因此用于治疗中性粒细胞减少症。给予G-CSF后，成骨细胞和骨细胞受到抑制，使造血干细胞得以保留的微环境支持系统减少。本研究聚焦并探讨了G-CSF作为骨重塑调节因子的作用。本研究的目的是调查给予G-CSF对拔牙创骨愈合的影响。在G-CSF组和对照组（生理盐水处理组）之间，观察到股骨近端和牙槽间隔的骨体积分数及小梁间距存在显著差异。与对照组相比，G-CSF组股骨和牙槽间隔的小梁骨减少。此外，作为骨形成标志物的血清1型前胶原N端前肽水平，G-CSF组低于对照组。在拔牙创中观察到纤维结缔组织和未成熟骨，与对照组相比，G-CSF组的骨愈合延迟。拔牙后6天，G-CSF组拔牙创的骨面积（23.6%）显著小于对照组（45.1%）。此外，给予G-CSF减少了每个骨细胞的小管数量，并抑制了骨细胞网络的连接。因此，在G-CSG组中，成骨细胞活化受到抑制，骨重塑转变为低骨转换状态。骨形成参数分析显示，与对照组相比，G-CSF组的矿物质沉积率较低。总之，这些发现表明G-CSF可能会延迟拔牙后牙槽窝的骨愈合。
