Zhao Yuan, Zhang Yixuan, Liu Huijuan, Qiao Xing, Li Dongna, Zhu Yahui, Wu Zidan, Wang Wenqi, Ma Zhe, Liu Chunyan
Department of Orthodontics, School and Hospital of Stomatology, Hebei Key Laboratory of Stomatology & Hebei Technology Innovation Center of Oral Health, Hebei Medical University, East 383 Zhongshan Road, Shijiazhuang, Hebei Province, 050000, China.
The Key Laboratory of Stomatology, School and Hospital of Stomatology, Hebei Key Laboratory of Stomatology, Hebei Technology Innovation Center of Oral Health, Hebei Medical University, East 383 Zhongshan Road, Shijiazhuang, Hebei Province, 050017, China.
BMC Oral Health. 2025 May 24;25(1):788. doi: 10.1186/s12903-025-06101-3.
The cannabinoid receptor 2 (CB2) is implicated in bone metabolism and reconstruction of periodontal tissues. However, its role in bone formation during periodontitis remains to be elucidated. This study aims to explore the impact of CB2 on alveolar bone in periodontitis, as well as the associated signaling pathways.
Wild type (WT) and CB2 knockout (Cnr2) mice from the SPF C57BL/6J strain were utilized to establish periodontitis models via stainless steel wire ligation. Micro-CT, hematoxylin and eosin (HE) staining, and tartrate-resistant acid phosphatase (TRAP) staining were employed to assess morphological alterations in the periodontal tissues. Human primary periodontal ligament stem cells (PDLSCs) were obtained by tissue block culture method. Porphyromonas gingivalis lipopolysaccharide (P.g. LPS) was used to suppress PDLSCs. The study evaluated the influence of AM1241 on the osteogenic differentiation of PDLSCs under inflammatory conditions and the role of the ERK1/2 signaling pathway.
The absence of CB2 (Cnr2 knockout, Cnr2) exacerbated gingival inflammation and increased alveolar bone resorption by elevating osteoclast numbers. AM1241 was found to suppress inflammation in PDLSCs and to enhance their osteogenic differentiation under inflammatory conditions. Additionally, AM1241 could activate the ERK1/2 pathway.
The inhibition of CB2 facilitates osteoclast recruitment and exacerbates periodontitis. CB2 may promote the osteogenic differentiation of PDLSCs by activating ERK1/2 pathway.
大麻素受体2（CB2）与骨代谢及牙周组织的重建有关。然而，其在牙周炎期间骨形成中的作用仍有待阐明。本研究旨在探讨CB2对牙周炎中牙槽骨的影响以及相关信号通路。
利用来自无特定病原体（SPF）C57BL/6J品系的野生型（WT）和CB2基因敲除（Cnr2）小鼠，通过不锈钢丝结扎建立牙周炎模型。采用显微CT、苏木精-伊红（HE）染色和抗酒石酸酸性磷酸酶（TRAP）染色来评估牙周组织的形态学改变。通过组织块培养法获取人原代牙周膜干细胞（PDLSCs）。使用牙龈卟啉单胞菌脂多糖（P.g. LPS）抑制PDLSCs。本研究评估了AM1241在炎症条件下对PDLSCs成骨分化的影响以及细胞外信号调节激酶1/2（ERK1/2）信号通路的作用。
CB2缺失（Cnr2基因敲除，Cnr2）通过增加破骨细胞数量加剧了牙龈炎症并增加了牙槽骨吸收。发现AM1241可抑制PDLSCs中的炎症，并在炎症条件下增强其成骨分化。此外，AM1241可激活ERK1/2通路。
抑制CB2促进破骨细胞募集并加剧牙周炎。CB2可能通过激活ERK1/2通路促进PDLSCs的成骨分化。
