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正畸力作用下牙周膜内的细胞反应。

Cellular response within the periodontal ligament on application of orthodontic forces.

作者信息

Meeran Nazeer Ahmed

机构信息

Department of Orthodontics and Dentofacial Orthopedics, Priyadarshini Dental College and Hospital, Thiruvallur Taluk, Pandur, Tamilnadu, India.

出版信息

J Indian Soc Periodontol. 2013 Jan;17(1):16-20. doi: 10.4103/0972-124X.107468.

DOI:10.4103/0972-124X.107468
PMID:23633766
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3636936/
Abstract

During application of controlled orthodontic force on teeth, remodeling of the periodontal ligament (PDL) and the alveolar bone takes place. Orthodontic forces induce a multifaceted bone remodeling response. Osteoclasts responsible for bone resorption are mainly derived from the macrophages and osteoblasts are produced by proliferations of the cells of the periodontal ligament. Orthodontic force produces local alterations in vascularity, as well as cellular and extracellular matrix reorganization, leading to the synthesis and release of various neurotransmitters, cytokines, growth factors, colony-stimulating factors, and metabolites of arachidonic acid. Although many studies have been reported in the orthodontic and related scientific literature, research is constantly being done in this field resulting in numerous current updates in the biology of tooth movement, in response to orthodontic force. Therefore, the aim of this review is to describe the mechanical and biological processes taking place at the cellular level during orthodontic tooth movement.

摘要

在对牙齿施加控制性正畸力的过程中,牙周韧带(PDL)和牙槽骨会发生重塑。正畸力会引发多方面的骨重塑反应。负责骨吸收的破骨细胞主要来源于巨噬细胞,而成骨细胞则由牙周韧带细胞增殖产生。正畸力会引起局部血管变化以及细胞和细胞外基质的重组,导致各种神经递质、细胞因子、生长因子、集落刺激因子和花生四烯酸代谢产物的合成与释放。尽管正畸及相关科学文献中已有许多研究报道,但该领域仍在不断开展研究,从而在牙齿移动生物学方面产生了众多最新进展,以应对正畸力。因此,本综述的目的是描述正畸牙齿移动过程中细胞水平上发生的机械和生物学过程。

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本文引用的文献

1
Role of CCR2 in orthodontic tooth movement.CCR2 在正畸牙齿移动中的作用。
Am J Orthod Dentofacial Orthop. 2012 Feb;141(2):153-60. doi: 10.1016/j.ajodo.2011.07.019.
2
Myeloperoxidase activity is increased in gingival crevicular fluid and whole saliva after fixed orthodontic appliance activation.固定正畸矫治器激活后,龈沟液和全唾液中的髓过氧化物酶活性增加。
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Expression of Msx-1 is suppressed in bisphosphonate associated osteonecrosis related jaw tissue-etiopathology considerations respecting jaw developmental biology-related unique features.表达受双膦酸盐相关的颌骨坏死相关组织抑制-考虑颌骨发育生物学相关独特特征的发病机制。
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CCR5 down-regulates osteoclast function in orthodontic tooth movement.CCR5在正畸牙齿移动中下调破骨细胞功能。
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On a path to unfolding the biological mechanisms of orthodontic tooth movement.在探索正畸牙齿移动生物学机制的道路上。
J Dent Res. 2009 Jul;88(7):597-608. doi: 10.1177/0022034509338914.
6
Orthodontic force stimulates eNOS and iNOS in rat osteocytes.正畸力刺激大鼠骨细胞中的内皮型一氧化氮合酶和诱导型一氧化氮合酶。
J Dent Res. 2009 Mar;88(3):255-60. doi: 10.1177/0022034508330861.
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Leptin as a modulator of osteogenesis.瘦素作为骨生成的调节因子。
Ortop Traumatol Rehabil. 2009 Jan-Feb;11(1):1-6.
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Cystatins and cathepsin B during orthodontic tooth movement.
Am J Orthod Dentofacial Orthop. 2009 Jan;135(1):99-105. doi: 10.1016/j.ajodo.2006.10.029.
9
Role of Msx2 as a promoting factor for Runx2 at the periodontal tension sides elicited by mechanical stress.Msx2作为机械应力引起的牙周张力侧Runx2促进因子的作用。
Eur J Med Res. 2008 Sep 22;13(9):425-31.
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The endothelin system mediates bone modeling in the late stage of orthodontic tooth movement in rats.内皮素系统介导大鼠正畸牙齿移动后期的骨改建。
Bone. 2008 Oct;43(4):740-7. doi: 10.1016/j.bone.2008.06.012. Epub 2008 Jul 4.