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用于研究年龄相关的尖周炎发生发展的小鼠模型

A Mouse Model for Studying the Development of Apical Periodontitis with Age.

机构信息

Faculty of Dental Medicine, Institute of Dental Sciences, The Hebrew University, Jerusalem 9112001, Israel.

Hadassah Medical Center, Department of Endodontics, Jerusalem 9112001, Israel.

出版信息

Cells. 2021 Mar 17;10(3):671. doi: 10.3390/cells10030671.

DOI:10.3390/cells10030671
PMID:33802950
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8002842/
Abstract

Older age is associated with reduced immune function. Our aim was to study how age affects the development of apical periodontitis (AP). AP was induced in two age groups of mice (young vs. adult). Histological samples were stained by Hematoxylin Eosin, Brown and Brenn, and Tartrate-Resistant Acid Phosphatase. In addition, the samples were scanned by Micro-Computerized-Tomography (micro-CT) to evaluate apical constriction and periapical lesion size. Cell density in the periapical region was computationally assessed. Moreover, lesion immune cell populations were characterized by flow cytometry and immunofluorescence. The young group presented more canals with necrotic radicular pulp compared to the adults. There was no difference in bacteria location in the canals between the groups. Apical constriction size was larger in the young mice compared to the adults. The periapical cell density was higher in the young group, while the dominant immune cells in the lesions were neutrophils, which also exhibited the highest young/adult ratio. Immunofluorescence demonstrated neutrophils in the lesion. More osteoclasts were present in the lesions of the young mice, in correlation to the higher volume of bone resorption in this group. Overall, we conclude that the immune reaction to AP stimuli was attenuated in the adult mice compared to the young.

摘要

年龄增长与免疫功能下降有关。我们的目的是研究年龄如何影响根尖周炎(AP)的发展。将两组年龄的小鼠(年轻组和成年组)用于诱导 AP。通过苏木精-伊红、布朗-布伦纳和耐酒石酸酸性磷酸酶染色对组织学样本进行染色。此外,通过微计算机断层扫描(micro-CT)对样本进行扫描,以评估根尖缩窄和根尖病变大小。通过计算评估根尖区域的细胞密度。此外,通过流式细胞术和免疫荧光术对病变免疫细胞群进行了表征。与成年人相比,年轻组的更多根管内有坏死的牙髓。两组之间根管内细菌位置无差异。与成年组相比,年轻组的根尖缩窄尺寸更大。年轻组的根尖细胞密度更高,而病变中的主要免疫细胞是中性粒细胞,其在年轻/成年的比例也最高。免疫荧光显示病变中有中性粒细胞。年轻组的病变中存在更多的破骨细胞,与该组中更高的骨吸收量相关。总的来说,我们得出结论,与年轻小鼠相比,成年小鼠对 AP 刺激的免疫反应减弱。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eefd/8002842/9eb7cb81b6eb/cells-10-00671-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eefd/8002842/36a4771c49e4/cells-10-00671-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eefd/8002842/def4e872935c/cells-10-00671-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eefd/8002842/ec9c89bb2fc9/cells-10-00671-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eefd/8002842/5ff6d52ddfa4/cells-10-00671-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eefd/8002842/9eb7cb81b6eb/cells-10-00671-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eefd/8002842/36a4771c49e4/cells-10-00671-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eefd/8002842/def4e872935c/cells-10-00671-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eefd/8002842/ec9c89bb2fc9/cells-10-00671-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eefd/8002842/5ff6d52ddfa4/cells-10-00671-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eefd/8002842/9eb7cb81b6eb/cells-10-00671-g005.jpg

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J Endod. 2020 Oct;46(10):1371-1386.e8. doi: 10.1016/j.joen.2020.07.007. Epub 2020 Jul 14.
3
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4
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