Division of Microbiology and Infectious Diseases, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan; Division of Periodontology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Division of Microbiology and Infectious Diseases, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan; Research Center for Advanced Oral Science, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Arch Oral Biol. 2020 Apr;112:104679. doi: 10.1016/j.archoralbio.2020.104679. Epub 2020 Feb 7.
The overall objective of this study was to investigate the effects of hinokitiol on periodontal bone loss in a murine model of experimental periodontitis and evaluate the anti-inflammatory activity of hinokitiol in vitro.
Periodontitis was induced by tying a silk ligature around the maxillary second molar of mice for 8 days. Hinokitiol was injected once a day for 7 days into the palatal gingiva of the ligated molar. Periodontal bone loss was then assessed morphometrically in the maxillary second molar, and the number of tartrate-resistant acid phosphatase positive multinucleated giant cells around the molar was quantified. The bacterial load of the silk ligature was calculated by counting the number of colony-forming units, while the transcription levels of proinflammatory cytokine-related genes in the palatal gingiva were evaluated by real-time qPCR. The activity of hinokitiol against LPS-induced transcription of proinflammatory genes in RAW 264.7 macrophages was also examined.
Local treatment with hinokitiol significantly inhibited the alveolar bone loss and osteoclast differentiation induced by tooth ligation. In addition, hinokitiol treatment decreased the oral bacterial load of the silk ligature and downregulated the mRNA levels of inflammatory cytokine-related genes, both in vitro and in vivo.
The results indicated that hinokitiol exhibits antibacterial and anti-inflammatory activity and exerts a protective effect against periodontitis.
本研究的总体目的是探讨桧醇在实验性牙周炎小鼠模型中对牙周骨丧失的影响，并评估桧醇的体外抗炎活性。
通过在小鼠上颌第二磨牙周围系上丝线结扎 8 天来诱导牙周炎。桧醇每天一次注射到结扎磨牙的腭牙龈中，共 7 天。然后通过形态计量学评估上颌第二磨牙的牙周骨丧失情况，并定量测定磨牙周围耐酒石酸酸性磷酸酶阳性多核巨细胞的数量。通过计算菌落形成单位的数量来计算丝线结扎的细菌负荷，同时通过实时 qPCR 评估腭牙龈中促炎细胞因子相关基因的转录水平。还检查了桧醇对 LPS 诱导 RAW 264.7 巨噬细胞中促炎基因转录的活性。
局部应用桧醇可显著抑制牙结扎诱导的牙槽骨丧失和破骨细胞分化。此外，桧醇治疗可降低丝线结扎的口腔细菌负荷，并下调体内外炎症细胞因子相关基因的 mRNA 水平。
结果表明桧醇具有抗菌和抗炎活性，对牙周炎具有保护作用。
