Department of Periodontology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Section of Periodontology, Department of Odontology, Fukuoka Dental College, Fukuoka, Japan.
J Periodontal Res. 2018 Jun;53(3):422-429. doi: 10.1111/jre.12529. Epub 2018 Feb 15.
Attachment loss of the junctional epithelium and alveolar bone destruction are signs of periodontitis, which is mainly caused by an inflammatory response to dental plaque. Glycyrrhetinic acid (GA), a component of the licorice herb, has been shown to have important anti-inflammatory activities; however, there are no previous reports on the ability of its inhibitory effects to prevent periodontal diseases. Hence, in this study, using our experimental periodontitis model, we attempted to evaluate whether GA had an effect on the prevention of attachment loss and alveolar bone loss.
Rats were intraperitoneally immunized with Escherichia coli lipopolysaccharide (LPS). The LPS group (n = 5) received 3 topical applications of 50 μg/μL of LPS followed by one application of the vehicle (propylene glycol:ethyl alcohol:phosphate-buffered saline [PBS] = 8:1:1) into the gingival sulcus. This protocol was repeated twice per day for 10 days. The low (n = 5) and high (n = 5) groups received topical application of LPS and 0.03% or 0.3% GA, respectively. The control group received topical application of PBS and vehicle. The rats were killed on the 10th day. Attachment loss, alveolar bone level and inflammatory cell infiltration were investigated histometrically. The formation of immune complexes and infiltration of LPS were evaluated immunohistologically.
Attachment loss, formation of immune complexes and infiltration of inflammatory cells were increased in the LPS group compared with the control group, and were completely inhibited in the low and high groups compared with the LPS group. The LPS group showed greater alveolar bone destruction compared with the control group and GA-treated groups. In addition, invasion of LPS was detected in the LPS group, was absent in the control group and was weaker in the GA-treated groups than in the LPS group.
In the present study, we showed that GA inhibits periodontal destruction in the rat experimental periodontitis model.
结合上皮丧失和牙槽骨破坏是牙周炎的标志，其主要由对牙菌斑的炎症反应引起。甘草酸（GA）是甘草植物的一种成分，具有重要的抗炎活性；然而，目前尚无关于其抑制作用预防牙周病能力的报道。因此，在这项研究中，我们使用实验性牙周炎模型，试图评估 GA 是否对预防附着丧失和牙槽骨丧失有作用。
大鼠经腹腔内注射大肠杆菌脂多糖（LPS）免疫。LPS 组（n=5）接受 3 次 50μg/μL LPS 的局部应用，随后龈沟内单次应用载体（丙二醇：乙醇：磷酸盐缓冲液[PBS] = 8:1:1）。该方案每天重复 2 次，共 10 天。低浓度（n=5）和高浓度（n=5）组分别接受 LPS 和 0.03%或 0.3%GA 的局部应用。对照组接受 PBS 和载体的局部应用。第 10 天处死大鼠。组织学研究附着丧失、牙槽骨水平和炎症细胞浸润。免疫组织化学评价免疫复合物的形成和 LPS 的浸润。
与对照组相比，LPS 组的附着丧失、免疫复合物形成和炎症细胞浸润增加，与 LPS 组相比，低浓度和高浓度组完全抑制。与对照组和 GA 处理组相比，LPS 组的牙槽骨破坏更严重。此外，在 LPS 组检测到 LPS 的入侵，在对照组中不存在，在 GA 处理组中比 LPS 组弱。
在本研究中，我们表明 GA 抑制大鼠实验性牙周炎模型中的牙周破坏。
