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牙龈卟啉单胞菌经口感染诱导小鼠种植体周围炎:骨丧失和局部炎症反应的评估。

Oral infection with Porphyromonas gingivalis induces peri-implantitis in a murine model: Evaluation of bone loss and the local inflammatory response.

机构信息

Department of Periodontology, Faculty of Dental Medicine, The Hebrew University-Hadassah Medical Center, Jerusalem, Israel.

The Institute of Dental Sciences, Faculty of Dental Medicine, The Hebrew University-Hadassah Medical Center, Jerusalem, Israel.

出版信息

J Clin Periodontol. 2017 Jul;44(7):739-748. doi: 10.1111/jcpe.12735. Epub 2017 Jun 23.

DOI:10.1111/jcpe.12735
PMID:28453225
Abstract

AIM

Peri-implantitis is a major health concern, with unclear pathogenesis, and with no accessible animal models. Our aim was to establish a mouse model for peri-implantitis and to investigate mediators of inflammation.

MATERIALS AND METHODS

Mice were divided into implanted versus non-implanted groups. Implants were inserted immediately following the extraction of the upper first molar. Four weeks following implantation, implanted and non-implanted mice were challenged with either Porphyromonas gingivalis or vehicle (eight mice in each subgroup, 32 mice in total). Alveolar bone loss and expression of inflammatory mediators in the soft tissue were assessed 42 days following infection.

RESULTS

Porphyromonas gingivalis infection induced greater bone loss around implants than around teeth. In non-infected animals, the presence of the implant correlated with elevated expression of Il-10, Foxp3 and Rankl/Opg ratio, while Tnf-α levels were decreased relative to tissue around teeth. Six weeks following infection, Tnf-α increased significantly while the expression of Foxp3 decreased in the tissue around the implants. No significant differences in anti- or pro-inflammatory mediators were found around teeth of infected, relative to non-infected mice.

CONCLUSIONS

Oral infection with P. gingivalis of mice with implants induced bone loss and a shift in gingival cytokine expression. This mouse model enables exploration of the pathogenesis of peri-implantitis and testing of novel treatments.

摘要

目的

种植体周围炎是一个主要的健康关注点,其发病机制尚不清楚,也没有可用于研究的动物模型。本研究旨在建立一种用于研究种植体周围炎的小鼠模型,并探讨炎症反应的介质。

材料和方法

将小鼠分为植入组和非植入组。在上颌第一磨牙拔除后立即植入种植体。植入 4 周后,将植入组和非植入组小鼠分别用牙龈卟啉单胞菌或载体进行攻毒(每组 8 只小鼠,共 32 只小鼠)。感染 42 天后,评估牙槽骨丧失和软组织中炎症介质的表达情况。

结果

牙龈卟啉单胞菌感染导致种植体周围的骨丧失大于牙齿周围。在未感染的动物中,种植体的存在与 Il-10、Foxp3 和 Rankl/Opg 比值的升高相关,而 Tnf-α水平则低于牙齿周围组织。感染 6 周后,Tnf-α水平显著升高,而 Foxp3 的表达在种植体周围组织中降低。与非感染的小鼠相比,感染的小鼠牙齿周围的抗炎或促炎介质没有显著差异。

结论

牙龈卟啉单胞菌感染植入小鼠可诱导骨丧失和牙龈细胞因子表达的改变。这种小鼠模型可用于研究种植体周围炎的发病机制,并测试新的治疗方法。

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