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作 者:王天琦 廖成成 刘建国 陈鹿鹿 赵飘 肖琳琳 管晓燕 Wang Tianqi;Liao Chengcheng;Liu Jianguo;Chen Lulu;Zhao Piao;Xiao Linlin;Guan Xiaoyan(Affiliated Stomatological Hospital of Zunyi Medical University,Zunyi 563000,Guizhou Province,China;Guizhou Provincial Key Laboratory of Oral Disease Research in Colleges and Universities,Zunyi 563000,Guizhou Province,China;West China School of Stomatology,Sichuan University,Chengdu 610000,Sichuan Province,China)
机构地区:[1]遵义医科大学附属口腔医院,贵州省遵义市563000 [2]贵州省普通高等学校口腔疾病研究特色重点实验室,贵州省遵义市563000 [3]四川大学华西口腔医学院,四川省成都市610000
出 处:《中国组织工程研究》2024年第34期5558-5564,共7页Chinese Journal of Tissue Engineering Research
基 金:贵州省教育厅高等学校科学研究项目[黔教技(2022)238号],项目负责人:肖琳琳;遵义市科技计划项目[遵市科合HZ字(2022)423号],项目负责人:管晓燕。
摘 要:背景:正畸力通过多种信号通路激活牙周组织自噬,进一步增强或减弱相关细胞(牙周膜细胞、骨细胞、破骨细胞和成骨细胞等)的活性来促进牙周重塑。目的:综述目前正畸力介导牙周组织自噬的研究进展和其对正畸牙齿移动的影响。方法:在PubMed、Web of Science、中国生物医学文献数据库和中国知网数据库进行文献检索,设置检索时限为2010-2023年,总结了2010年以来正畸与自噬相关研究进展,最终纳入76篇文献进行分析讨论。结果与结论:(1)正畸力可通过牙周机械感受器和其造成的无菌性炎症引发一系列生物化学信号的转变,进而引起牙周组织自噬。(2)自噬通过级联放大的信号通路如磷脂酰肌醇-3-激酶/蛋白激酶B通路、河马通路及丝裂原活化蛋白激酶通路等,产生相应反馈从而促进牙周组织改建,最终实现牙齿的移动与稳定。正畸力诱导的自噬可差异性调节牙齿压力侧骨吸收和张力侧骨形成,相关靶点在正畸临床治疗的应用中具有良好前景。(3)然而,正畸力与自噬的机制较为复杂,现有研究仅停留在探究自噬对正畸牙齿移动的作用,自噬与正畸牙齿移动过程中的相互调节作用、涉及相关通路上游机械受体及信号通路间的交互作用均需要进一步的探究。BACKGROUND:The application of orthodontic force triggers autophagy in the periodontal tissue via diverse signaling pathways,augmenting or attenuating the activity of relevant cell types such as periodontal ligament cells,osteocytes,osteoclasts,and osteoblasts,thus facilitating the process of periodontal remodeling.OBJECTIVE:To review the research progress in orthodontic force mediated autophagy in periodontal tissue and its impact on orthodontic tooth movement.METHODS:The PubMed,Web of Science,China Biology Medicine disc and CNKI were searched for literature published from 2010 to 2023 to summarize the progress in orthodontics-related autophagy.And 76 papers were finally included in the analysis and discussion.RESULTS AND CONCLUSION:Orthodontic force can trigger a series of biochemical signal changes through periodontal mechanical receptors and aseptic inflammation they cause,leading to autophagy in periodontal tissue.Subsequently,autophagy generates corresponding feedback through cascaded amplified signaling pathways such as Phosphoinositide 3-kinase/protein kinase B,Hippo,and mitogen-activated protein kinase pathways,promoting periodontal tissue remodeling and ultimately achieving tooth movement and stability.Orthodontic force-induced autophagy can differentially regulate bone resorption on the tooth pressure side and bone formation on the tension side.Related targets have good prospects in the clinical application of orthodontic treatment.Orthodontics and autophagy have complex mechanisms.However,existing research has only focused on exploring the role of autophagy in orthodontic tooth movement.Further exploration is needed to investigate the mutual regulatory effects between autophagy and orthodontic tooth movement,as well as the interactions between upstream mechanical receptors and signaling pathways involved in related pathways.
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