Kava-241 reduced periodontal destruction in a collagen antibody primed Porphyromonas gingivalis model of periodontitis.
Kava-241 reduced periodontal destruction in a collagen antibody primed Porphyromonas gingivalis model of periodontitis.
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DOI：
10.1111/jcpe.12784
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发表时间：
2017-11
影响因子：
6.7
通讯作者：
Amar S
中科院分区：
文献类型：
--
作者：
Alshammari A;Patel J;Al-Hashemi J;Cai B;Panek J;Huck O;Amar S
本研究旨在评价优化后的卡瓦胡椒化合物Kava-241在胶原抗体诱导的牙周炎灌胃模型中对牙周破坏的影响。采用牙龈卟啉单胞菌(P.gingivalis) + ii型胶原抗体（AB）灌胃15 d，诱导小鼠实验性牙周炎。小鼠在灌胃牙龈单胞菌时或灌胃前给予Kava-241，并与未给药小鼠进行比较。进行了全面的组织形态学分析。牙龈假单胞菌灌胃可引起轻度上皮细胞生长下降和牙槽骨丢失，而加AB灌胃比单独灌胃对组织的破坏更大（p<0.05）。卡瓦-241治疗显著（p<0.05）降低了龈裂牙+AB组上皮细胞生长下降（72%）和牙槽骨丢失（36%）。这种Kava-241效应与软组织内炎症细胞计数减少和成纤维细胞增加有关（p<0.05）。ii型胶原抗体灌胃是一种快速、可重复的牙周破坏模型，足以评估新的治疗方法。Kava-241在预防和治疗与牙周炎相关的炎症和牙槽骨丢失方面显示出良好的效果。需要进一步的实验来确定这种治疗剂靶向的分子途径。
The aim of this study was to evaluate the effect of Kava-241, an optimized Piper methysticum Kava compound, on periodontal destruction in a collagen antibody primed oral gavage model of periodontitis. Experimental periodontitis was induced by oral gavage of Porphyromonas gingivalis (P.gingivalis) + type-II collagen antibody (AB) in mice during 15 days. Mice were treated with Kava-241 concomitantly or prior to P.gingivalis gavage and compared to untreated mice. Comprehensive histomorphometric analyses were performed. Oral gavage with P.gingivalis induced mild epithelial downgrowth and alveolar bone loss while oral gavage with additional AB priming had greater tissular destruction in comparison to gavage alone (p<0.05). Kava-241 treatment significantly (p<0.05) reduced epithelial downgrowth (72%) and alveolar bone loss (36%) in P.gingivalis+AB group. This Kava-241 effect was associated to a reduction of inflammatory cells counts within soft tissues and an increase of fibroblasts (p<0.05). Priming with type-II collagen antibody with oral gavage is a fast and reproducible model of periodontal destruction adequate for the evaluation of novel therapeutics. The effect of Kava-241 shows promise in the prevention and treatment of inflammation and alveolar bone loss associated with periodontitis. Further experiments are required to determine molecular pathways targeted by this therapeutic agent.
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