Nagashima Hidekazu, Shinoda Masamichi, Honda Kuniya, Kamio Noriaki, Hasuike Akira, Sugano Naoyuki, Arai Yoshinori, Sato Shuichi, Iwata Koichi
Division of Applied Oral Sciences, Nihon University Graduate School of Dentistry.
Department of Physiology, Nihon University School of Dentistry.
J Oral Sci. 2017 Dec 27;59(4):571-577. doi: 10.2334/josnusd.16-0830. Epub 2017 Oct 31.
Periodontitis caused by bacterial infection gradually progresses accompanied by periodontal tissue destruction. As a result, teeth lose their supporting structures, and this leads to tooth exfoliation. CXC-chemokine receptor 4 (CXCR4) is known to be expressed in lymphocytes, fibroblasts and osteoclasts in periodontal tissues, suggesting that periodontal CXCR4 signaling contributes to alveolar bone resorption in the milieu of periodontitis. However, the role of CXCR4 signaling in the pathogenesis of periodontitis has remained unknown. We established a mouse model of periodontitis by inoculation of Porphyromonas gingivalis (P.g.) into a silk ligature placed around the maxillary molar. Although there was no significant difference in the mechanical sensitivity in the periodontal tissue between P.g. treatment and sham treatment during the experimental period, mechanical allodynia in the periodontal tissue was induced after gingival injection of complete Freund's adjuvant compared with that resulting from sham and P.g. treatment alone. Moreover, CXCR4 neutralization in the periodontal tissue following P.g. treatment enhanced periodontal inflammatory cell infiltration and depressed alveolar bone resorption. These findings suggest that periodontal CXCR4 signaling in several cell types in P.g.-induced periodontal inflammation depresses alveolar bone resorption in periodontitis. CXCR4 signaling might be a target for therapeutic intervention to prevent alveolar bone resorption in periodontitis.
由细菌感染引起的牙周炎会随着牙周组织破坏而逐渐发展。结果，牙齿失去其支持结构，进而导致牙齿脱落。已知CXC趋化因子受体4（CXCR4）在牙周组织的淋巴细胞、成纤维细胞和破骨细胞中表达，这表明牙周CXCR4信号通路在牙周炎环境中促进牙槽骨吸收。然而，CXCR4信号通路在牙周炎发病机制中的作用尚不清楚。我们通过将牙龈卟啉单胞菌（P.g.）接种到上颌磨牙周围放置的丝线结扎处建立了牙周炎小鼠模型。尽管在实验期间，P.g.处理组和假处理组的牙周组织机械敏感性没有显著差异，但与假处理组和单独P.g.处理组相比，在牙龈注射完全弗氏佐剂后，牙周组织诱导出机械性异常性疼痛。此外，P.g.处理后牙周组织中的CXCR4中和增强了牙周炎症细胞浸润并抑制了牙槽骨吸收。这些发现表明，在P.g.诱导的牙周炎症中，几种细胞类型中的牙周CXCR4信号通路抑制了牙周炎中的牙槽骨吸收。CXCR4信号通路可能是预防牙周炎中牙槽骨吸收的治疗干预靶点。
