Shiba Fumie, Furusho Hisako, Takata Takashi, Shimizu Rika, Miyauchi Mutsumi
Research and Development Headquarters, Earth Corporation Ltd, Hyogo 678-0192, Japan.
Department of Oral and Maxillofacial Pathobiology, Graduate School of Biomedical and Health Science, Hiroshima University, Hiroshima 734-8553, Japan.
Int J Dent. 2022 Dec 30;2022:7398924. doi: 10.1155/2022/7398924. eCollection 2022.
extract (EA) exerts various biological effects, including anti-inflammatory activity. The effect of EA on alveolar bone destruction has not been reported; therefore, we aimed to determine whether EA could inhibit alveolar bone destruction associated with periodontitis in a rat model in which periodontitis was induced using lipopolysaccharide from (. -LPS).
Physiological saline or . -LPS or . -LPS/EA mixture was topically administered into the gingival sulcus of the upper molar region of the rats. After 3 days, periodontal tissues of the molar region were collected. Immunohistochemistry was performed for cathepsin K, receptor activator of NF-B ligand (RANKL), and osteoprotegerin (OPG). The cathepsin K-positive osteoclasts along the alveolar bone margin were counted. EA effects on the expression of the factors regulating osteoclastogenesis in osteoblasts with . -LPS-stimulation were also examined .
Treatment with EA significantly reduced the number of osteoclasts by decreasing the RANKL-expression and increasing OPG-expression in the periodontal ligament in the treatment group compared to the . -LPS group. The study showed that the upregulation of p-IB kinase and (p-IKK/), p-NF-B p65, TNF-, interleukin-6, and RANKL and downregulation of semaphorin 3A (Sema3A), -catenin, and OPG in the osteoblasts with . -LPS-stimulation improved with EA-treatment.
These findings demonstrated that topical EA suppressed alveolar bone resorption in the rat model with . -LPS-induced periodontitis by maintaining a balance in RANKL/OPG ratio via the pathways of NF-B, Wnt/-catenin, and Sema3A/Neuropilin-1. Therefore, EA possesses the potential to prevent bone destruction through inhibiting osteoclastogenesis attributed to cytokine burst under plaque accumulation.
提取物（EA）具有多种生物学效应，包括抗炎活性。EA对牙槽骨破坏的影响尚未见报道；因此，我们旨在确定EA是否能在使用来自[具体来源]的脂多糖诱导牙周炎的大鼠模型中抑制与牙周炎相关的牙槽骨破坏。
将生理盐水、[具体浓度]-脂多糖或[具体浓度]-脂多糖/EA混合物局部注入大鼠上颌磨牙区的龈沟。3天后，收集磨牙区的牙周组织。对组织蛋白酶K、核因子κB受体活化因子配体（RANKL）和骨保护素（OPG）进行免疫组织化学检测。计数沿牙槽骨边缘的组织蛋白酶K阳性破骨细胞。还检测了EA对[具体浓度]-脂多糖刺激的成骨细胞中调节破骨细胞生成因子表达的影响。
与[具体浓度]-脂多糖组相比，治疗组用EA治疗可通过降低牙周膜中RANKL的表达和增加OPG的表达，显著减少破骨细胞数量。[具体研究]表明，[具体浓度]-脂多糖刺激的成骨细胞中，p-IκB激酶α和β（p-IKKα/β）、p-NF-κB p65、肿瘤坏死因子-α、白细胞介素-6和RANKL的上调以及信号素3A（Sema3A）、β-连环蛋白和OPG的下调，经EA治疗后得到改善。
这些发现表明，局部应用EA通过NF-κB、Wnt/β-连环蛋白和Sema3A/神经纤毛蛋白-1途径维持RANKL/OPG比值的平衡，从而抑制[具体浓度]-脂多糖诱导的大鼠牙周炎模型中的牙槽骨吸收。因此，EA具有通过抑制菌斑积聚下细胞因子爆发引起的破骨细胞生成来预防骨破坏的潜力。
