Periostin is essential for periodontal tissue integrity and homeostasis and also associated with periodontitis and periodontitis healing. This study aims to investigate the temporal and spatial expression of Periostin and Wnt5a/CaMKII in periodontitis and how the Wnt5a regulates Periostin through CaMKII signaling pathway in PDLCs in inflammatory environment. The experimental periodontitis mice were adopted to clarify the temporal and spatial expression of Wnt5a, CaMKII and Periostin during early periodontitis. And the Wnt5a, CaMKII and Periostin expression pattern and regulation mechanism in PDLCs were clarified in Porphyromonas gingivalis Lipopolysaccharide (P.g. LPS) induced inflammatory condition. Along with the periodontitis development, Wnt5a, CaMKII and Periostin significantly increased in periodontal ligament and partially increased in gingiva during 0 to 6 day (P < 0.05). They were involved in early periodontitis homeostasis especially in periodontal ligament tissue. Meanwhile, Wnt5a, CaMKII and Periostin were significantly decreased at 12 h (P < 0.05) and increased at 48 h (P < 0.05) in PDLCs after induced by P.g. LPS. Besides, Wnt5a significantly enhanced total CaMKII protein (P < 0.05), pCaMKII (P < 0.001) and Periostin (P < 0.001), and this could be blocked by CaMKII inhibitor KN93 (P < 0.05). In conclusions, in early periodontitis, Wnt5a/CaMKII and Periostin should be involved in maintaining periodontal homeostasis and Wnt5a could up-regulate Periostin via CaMKII pathway in inflammation, which would provide new clues for us to understand the pathogenesis of periodontitis and develop better therapeutic strategies.

骨膜素对于牙周组织的完整性和稳态至关重要，也与牙周炎和牙周炎愈合有关。本研究旨在探讨炎症环境下PDLCs中Periostin和Wnt5a/CaMKII在牙周炎中的时空表达，以及Wnt5a如何通过CaMKII信号通路调节Periostin。采用实验性牙周炎小鼠来阐明早期牙周炎过程中Wnt5a、CaMKII和Periostin的时空表达。阐明了牙龈卟啉单胞菌脂多糖（ Pg LPS）诱导的炎症条件下PDLCs中Wnt5a、CaMKII和Periostin的表达模式和调控机制。随着牙周炎的发展，第0～6天，牙周膜中Wnt5a、CaMKII和Periostin显着增加，牙龈中部分增加(P<<0.05)。它们参与早期牙周炎的稳态，尤其是牙周膜组织的稳态。同时， Pg LPS诱导后的PDLCs中Wnt5a、CaMKII和Periostin在12小时显着降低（P< 0.05），在48小时显着增加（P< 0.05）。此外，Wnt5a 显着增强总 CaMKII 蛋白 (P < 0.05)、pCaMKII (P < 0.001) 和 Periostin (P < 0.001)，并且可以被 CaMKII 抑制剂 KN93 (P < 0.05) 阻断。综上所述，在早期牙周炎中，Wnt5a/CaMKII和Periostin应该参与维持牙周稳态，并且Wnt5a在炎症过程中可以通过CaMKII通路上调Periostin，这将为我们了解牙周炎的发病机制和制定更好的治疗策略提供新的线索。 。