Gli1+ Periodontal Mesenchymal Stem Cells in Periodontitis.

Journal of dental research Pub Date : 2024-03-01 Epub Date: 2024-01-29 DOI:10.1177/00220345231220915
Y Deng, Q Li, K K H Svoboda, L A Opperman, L B Ruest, X Liu
{"title":"Gli1<sup>+</sup> Periodontal Mesenchymal Stem Cells in Periodontitis.","authors":"Y Deng, Q Li, K K H Svoboda, L A Opperman, L B Ruest, X Liu","doi":"10.1177/00220345231220915","DOIUrl":null,"url":null,"abstract":"<p><p>Periodontal mesenchymal stem cells (MSCs) play a crucial role in maintaining periodontium homeostasis and in tissue repair. However, little is known about how periodontal MSCs in vivo respond under periodontal disease conditions, posing a challenge for periodontium tissue regeneration. In this study, Gli1 was used as a periodontal MSC marker and combined with a Gli1-cre ERT2 mouse model for lineage tracing to investigate periodontal MSC fate in an induced periodontitis model. Our findings show significant changes in the number and contribution of Gli1<sup>+</sup> MSCs within the inflamed periodontium. The number of Gli1<sup>+</sup> MSCs that contributed to periodontal ligament homeostasis decreased in the periodontitis-induced teeth. While the proliferation of Gli1<sup>+</sup> MSCs had no significant difference between the periodontitis and the control groups, more Gli1<sup>+</sup> MSCs underwent apoptosis in diseased teeth. In addition, the number of Gli1<sup>+</sup> MSCs for osteogenic differentiation decreased during the progression of periodontitis. Following tooth extraction, the contribution of Gli1<sup>+</sup> MSCs to the tooth socket repair was significantly reduced in the periodontitis-induced teeth. Collectively, these findings indicate that the function of Gli1<sup>+</sup> MSCs in periodontitis was compromised, including reduced contribution to periodontium homeostasis and impaired injury response.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":" ","pages":"279-288"},"PeriodicalIF":0.0000,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of dental research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1177/00220345231220915","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/29 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Periodontal mesenchymal stem cells (MSCs) play a crucial role in maintaining periodontium homeostasis and in tissue repair. However, little is known about how periodontal MSCs in vivo respond under periodontal disease conditions, posing a challenge for periodontium tissue regeneration. In this study, Gli1 was used as a periodontal MSC marker and combined with a Gli1-cre ERT2 mouse model for lineage tracing to investigate periodontal MSC fate in an induced periodontitis model. Our findings show significant changes in the number and contribution of Gli1+ MSCs within the inflamed periodontium. The number of Gli1+ MSCs that contributed to periodontal ligament homeostasis decreased in the periodontitis-induced teeth. While the proliferation of Gli1+ MSCs had no significant difference between the periodontitis and the control groups, more Gli1+ MSCs underwent apoptosis in diseased teeth. In addition, the number of Gli1+ MSCs for osteogenic differentiation decreased during the progression of periodontitis. Following tooth extraction, the contribution of Gli1+ MSCs to the tooth socket repair was significantly reduced in the periodontitis-induced teeth. Collectively, these findings indicate that the function of Gli1+ MSCs in periodontitis was compromised, including reduced contribution to periodontium homeostasis and impaired injury response.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
牙周炎中的 Gli1+ 牙周间充质干细胞
牙周间充质干细胞(MSCs)在维持牙周稳态和组织修复方面发挥着至关重要的作用。然而,人们对牙周间充质干细胞在牙周疾病条件下的体内反应知之甚少,这给牙周组织再生带来了挑战。在这项研究中,Gli1被用作牙周间充质干细胞的标记物,并结合Gli1-cre ERT2小鼠模型进行系谱追踪,以研究诱导性牙周炎模型中牙周间充质干细胞的命运。我们的研究结果表明,在发炎的牙周中,Gli1+间充质干细胞的数量和贡献率发生了重大变化。在牙周炎诱导的牙齿中,促进牙周韧带平衡的 Gli1+ 间充质干细胞数量减少。虽然 Gli1+ 间充质干细胞的增殖在牙周炎组和对照组之间没有显著差异,但在病变牙中有更多的 Gli1+ 间充质干细胞发生凋亡。此外,随着牙周炎的发展,用于成骨分化的 Gli1+ 间充质干细胞数量减少。拔牙后,Gli1+间充质干细胞对牙周炎引起的牙槽骨修复的贡献明显减少。总之,这些研究结果表明,Gli1+间充质干细胞在牙周炎中的功能受到损害,包括对牙周稳态的贡献减少和损伤反应受损。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
KDM6B-Mediated HADHA Demethylation/Lactylation Regulates Cementogenesis. System Dynamics Modeling of Caries Severity States in Long-Term Care. Terahertz Imaging Detects Oral Cariogenic Microbial Domains Characteristics. Explainable Deep Learning Approaches for Risk Screening of Periodontitis. Geo-Net: Geometry-Guided Pretraining for Tooth Point Cloud Segmentation.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1