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成骨细胞机械转导在正畸牙齿移动中的作用。

Osteocyte Mechanotransduction in Orthodontic Tooth Movement.

机构信息

Department of Oral Cell Biology, Academic Centre for Dentistry Amsterdam (ACTA), Amsterdam Movement Sciences, University of Amsterdam and Vrije Universiteit Amsterdam, Gustav Mahlerlaan 3004, 1081 LA, Amsterdam, The Netherlands.

出版信息

Curr Osteoporos Rep. 2023 Dec;21(6):731-742. doi: 10.1007/s11914-023-00826-2. Epub 2023 Oct 4.


DOI:10.1007/s11914-023-00826-2
PMID:37792246
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10724326/
Abstract

PURPOSE OF REVIEW: Orthodontic tooth movement is characterized by periodontal tissue responses to mechanical loading, leading to clinically relevant functional adaptation of jaw bone. Since osteocytes are significant in mechanotransduction and orchestrate osteoclast and osteoblast activity, they likely play a central role in orthodontic tooth movement. In this review, we attempt to shed light on the impact and role of osteocyte mechanotransduction during orthodontic tooth movement. RECENT FINDINGS: Mechanically loaded osteocytes produce signaling molecules, e.g., bone morphogenetic proteins, Wnts, prostaglandins, osteopontin, nitric oxide, sclerostin, and RANKL, which modulate the recruitment, differentiation, and activity of osteoblasts and osteoclasts. The major signaling pathways activated by mechanical loading in osteocytes are the wingless-related integration site (Wnt)/β-catenin and RANKL pathways, which are key regulators of bone metabolism. Moreover, osteocytes are capable of orchestrating bone adaptation during orthodontic tooth movement. A better understanding of the role of osteocyte mechanotransduction is crucial to advance orthodontic treatment. The optimal force level on the periodontal tissues for orthodontic tooth movement producing an adequate biological response, is debated. This review emphasizes that both mechanoresponses and inflammation are essential for achieving tooth movement clinically. To fully comprehend the role of osteocyte mechanotransduction in orthodontic tooth movement, more knowledge is needed of the biological pathways involved. This will contribute to optimization of orthodontic treatment and enhance patient outcomes.

摘要

目的综述:正畸牙齿移动的特征是牙周组织对机械加载的反应,导致颌骨的临床相关功能适应。由于骨细胞在机械转导中具有重要作用,并协调破骨细胞和成骨细胞的活性,因此它们可能在正畸牙齿移动中发挥核心作用。在这篇综述中,我们试图阐明骨细胞机械转导在正畸牙齿移动中的作用和影响。

最近的发现:机械加载的骨细胞产生信号分子,例如骨形态发生蛋白、Wnt、前列腺素、骨桥蛋白、一氧化氮、硬骨素和 RANKL,这些信号分子调节破骨细胞和成骨细胞的募集、分化和活性。骨细胞中机械加载激活的主要信号通路是 Wnt/β-连环蛋白和 RANKL 通路,它们是骨代谢的关键调节剂。此外,骨细胞能够协调正畸牙齿移动过程中的骨适应。更好地理解骨细胞机械转导的作用对于推进正畸治疗至关重要。对于产生足够生物学反应的正畸牙齿移动,牙周组织的最佳力水平存在争议。这篇综述强调,机械反应和炎症对于实现临床牙齿移动都是必不可少的。为了充分理解骨细胞机械转导在正畸牙齿移动中的作用,需要更多地了解所涉及的生物学途径。这将有助于优化正畸治疗并提高患者的治疗效果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2546/10724326/5ebe85fc8bac/11914_2023_826_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2546/10724326/5ebe85fc8bac/11914_2023_826_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2546/10724326/5ebe85fc8bac/11914_2023_826_Fig1_HTML.jpg

相似文献

[1]
Osteocyte Mechanotransduction in Orthodontic Tooth Movement.

Curr Osteoporos Rep. 2023-12

[2]
Osteocyte-Mediated Translation of Mechanical Stimuli to Cellular Signaling and Its Role in Bone and Non-bone-Related Clinical Complications.

Curr Osteoporos Rep. 2020-2

[3]
The role of osteocytes during experimental orthodontic tooth movement: A review.

Arch Oral Biol. 2017-1

[4]
Osteocyte control of bone remodeling: is sclerostin a key molecular coordinator of the balanced bone resorption-formation cycles?

Osteoporos Int. 2014-12

[5]
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Front Endocrinol (Lausanne). 2020

[6]
Osteoclastogenesis and Osteogenesis during Tooth Movement.

Front Oral Biol. 2016

[7]
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Prog Orthod. 2021-7-26

[8]
Role of Osteocyte-PDL Crosstalk in Tooth Movement via SOST/Sclerostin.

J Dent Res. 2018-6-4

[9]
IL-6 alters osteocyte signaling toward osteoblasts but not osteoclasts.

J Dent Res. 2014-2-3

[10]
Role of nitric oxide in orthodontic tooth movement (Review).

Int J Mol Med. 2021-9

引用本文的文献

[1]
Invisible appliance promotes bone reconstruction via modulating the periodontal immune microenvironment.

Eur J Med Res. 2025-5-12

[2]
Tensile force promotes osteogenic differentiation via ephrinB2-EphB4 signaling pathway in orthodontic tooth movement.

BMC Oral Health. 2025-1-22

[3]
IGF-1 c.258 A > G synonymous mutation ameliorates senile osteoporosis.

Commun Biol. 2024-12-19

[4]
Catalpol Enhances Osteogenic Differentiation of Human Periodontal Stem Cells and Modulates Periodontal Tissue Remodeling in an Orthodontic Tooth Movement Rat Model.

Drug Des Devel Ther. 2024

[5]
Emerging role of liver-bone axis in osteoporosis.

J Orthop Translat. 2024-9-4

本文引用的文献

[1]
The osteocyte and its osteoclastogenic potential.

Front Endocrinol (Lausanne). 2023

[2]
Oscillating Fluid Flow Activated Osteocyte Lysate-Based Hydrogel for Regulating Osteoblast/Osteoclast Homeostasis to Enhance Bone Repair.

Adv Sci (Weinh). 2023-5

[3]
Functional Roles of Connexins and Gap Junctions in Osteo-Chondral Cellular Components.

Int J Mol Sci. 2023-2-19

[4]
Orthodontic treatment in periodontally compromised patients: a systematic review.

Clin Oral Investig. 2023-1

[5]
Protein Kinase G2 Is Essential for Skeletal Homeostasis and Adaptation to Mechanical Loading in Male but Not Female Mice.

J Bone Miner Res. 2023-1

[6]
The Effect of IFT80 Deficiency in Osteocytes on Orthodontic Loading-Induced and Physiologic Bone Remodeling: In Vivo Study.

Life (Basel). 2022-7-29

[7]
Iron overload induced osteocytes apoptosis and led to bone loss in Hepcidin mice through increasing sclerostin and RANKL/OPG.

Bone. 2022-11

[8]
Mechanical Compression by Simulating Orthodontic Tooth Movement in an In Vitro Model Modulates Phosphorylation of AKT and MAPKs via TLR4 in Human Periodontal Ligament Cells.

Int J Mol Sci. 2022-7-22

[9]
Bone remodeling: an operational process ensuring survival and bone mechanical competence.

Bone Res. 2022-7-18

[10]
Effects of anti-mouse RANKL antibody on orthodontic tooth movement in mice.

J Dent Sci. 2022-7

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