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结扎诱导牙周炎在小鼠模型中用于探索牙周病的分子机制。

Application of Ligature-Induced Periodontitis in Mice to Explore the Molecular Mechanism of Periodontal Disease.

机构信息

Department of Periodontology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo 113-8549, Japan.

Department of Lifetime Oral Health Care Sciences, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo 113-8549, Japan.

出版信息

Int J Mol Sci. 2021 Aug 18;22(16):8900. doi: 10.3390/ijms22168900.

Abstract

Periodontitis is an inflammatory disease characterized by the destruction of the periodontium. In the last decade, a new murine model of periodontitis has been widely used to simulate alveolar bone resorption and periodontal soft tissue destruction by ligation. Typically, 3-0 to 9-0 silks are selected for ligation around the molars in mice, and significant bone loss and inflammatory infiltration are observed within a week. The ligature-maintained period can vary according to specific aims. We reviewed the findings on the interaction of systemic diseases with periodontitis, periodontal tissue destruction, the immunological and bacteriological responses, and new treatments. In these studies, the activation of osteoclasts, upregulation of pro-inflammatory factors, and excessive immune response have been considered as major factors in periodontal disruption. Multiple genes identified in periodontal tissues partly reflect the complexity of the pathogenesis of periodontitis. The effects of novel treatment methods on periodontitis have also been evaluated in a ligature-induced periodontitis model in mice. This model cannot completely represent all aspects of periodontitis in humans but is considered an effective method for the exploration of its mechanisms. Through this review, we aimed to provide evidence and enlightenment for future studies planning to use this model.

摘要

牙周炎是一种炎症性疾病,其特征为牙周组织的破坏。在过去十年中,一种新的牙周炎小鼠模型已被广泛用于模拟通过结扎导致的牙槽骨吸收和牙周软组织破坏。通常,在小鼠的磨牙周围选择 3-0 至 9-0 的丝线进行结扎,并且在一周内观察到明显的骨丢失和炎症浸润。结扎维持的时间可根据具体目的而变化。我们综述了系统性疾病与牙周炎、牙周组织破坏、免疫和细菌学反应以及新治疗方法之间相互作用的研究结果。在这些研究中,破骨细胞的激活、促炎因子的上调和过度的免疫反应被认为是牙周破坏的主要因素。牙周组织中鉴定的多个基因部分反映了牙周炎发病机制的复杂性。新型治疗方法对结扎诱导的牙周炎模型小鼠的疗效也进行了评估。该模型不能完全代表人类牙周炎的所有方面,但被认为是探索其机制的有效方法。通过本次综述,我们旨在为未来计划使用该模型的研究提供证据和启示。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/412c/8396362/89a5732e1ce6/ijms-22-08900-g001.jpg

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