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本文引用的文献

1
Activation of β-catenin signalling leads to temporomandibular joint defects.β-连环蛋白信号通路的激活会导致颞下颌关节缺陷。
Eur Cell Mater. 2014 Oct 23;28:223-35. doi: 10.22203/ecm.v028a15.
2
BMPRIA mediated signaling is essential for temporomandibular joint development in mice.BMPRIA介导的信号传导对于小鼠颞下颌关节的发育至关重要。
PLoS One. 2014 Aug 5;9(8):e101000. doi: 10.1371/journal.pone.0101000. eCollection 2014.
3
Overexpression of Shox2 leads to congenital dysplasia of the temporomandibular joint in mice.Shox2的过表达导致小鼠颞下颌关节先天性发育异常。
Int J Mol Sci. 2014 Jul 24;15(8):13135-50. doi: 10.3390/ijms150813135.
4
Genes that regulate morphogenesis and growth of the temporomandibular joint: a review.调节颞下颌关节形态发生和生长的基因:综述
Dev Dyn. 2014 Jul;243(7):864-74. doi: 10.1002/dvdy.24130. Epub 2014 Apr 16.
5
Cartilage-specific deletion of Mig-6 results in osteoarthritis-like disorder with excessive articular chondrocyte proliferation.软骨特异性敲除 Mig-6 导致类似骨关节炎的疾病,伴有关节软骨细胞过度增殖。
Proc Natl Acad Sci U S A. 2014 Feb 18;111(7):2590-5. doi: 10.1073/pnas.1400744111. Epub 2014 Feb 3.
6
TMJ degeneration in SAMP8 mice is accompanied by deranged Ihh signaling.SAMP8 小鼠的 TMJ 退变伴随着 Ihh 信号的紊乱。
J Dent Res. 2014 Mar;93(3):281-7. doi: 10.1177/0022034513519649. Epub 2014 Jan 22.
7
Overexpressed TGF-β in subchondral bone leads to mandibular condyle degradation.软骨下骨中过度表达的 TGF-β导致下颌骨髁突降解。
J Dent Res. 2014 Feb;93(2):140-7. doi: 10.1177/0022034513513034. Epub 2013 Dec 5.
8
Replacing Shox2 with human SHOX leads to congenital disc degeneration of the temporomandibular joint in mice.用人类 SHOX 替换 Shox2 会导致小鼠颞下颌关节先天性椎间盘退变。
Cell Tissue Res. 2014 Feb;355(2):345-54. doi: 10.1007/s00441-013-1743-2. Epub 2013 Nov 19.
9
A discoidin domain receptor 1 knock-out mouse as a novel model for osteoarthritis of the temporomandibular joint.Discoidin domain receptor 1 敲除小鼠作为颞下颌关节骨关节炎的新型模型。
Cell Mol Life Sci. 2014 Mar;71(6):1081-96. doi: 10.1007/s00018-013-1436-8. Epub 2013 Aug 4.
10
1,25(OH)2D deficiency induces temporomandibular joint osteoarthritis via secretion of senescence-associated inflammatory cytokines.1,25(OH)2D 缺乏通过分泌衰老相关的炎症细胞因子诱导颞下颌关节骨关节炎。
Bone. 2013 Aug;55(2):400-9. doi: 10.1016/j.bone.2013.04.015. Epub 2013 Apr 25.

用于颞下颌关节发育和疾病的小鼠遗传模型。

Mouse genetic models for temporomandibular joint development and disorders.

作者信息

Suzuki A, Iwata J

机构信息

Department of Diagnostic & Biomedical Sciences, School of Dentistry, The University of Texas Health Science Center at Houston (UTHealth), Houston, TX, USA.

Center for Craniofacial Research, UTHealth, Houston, TX, USA.

出版信息

Oral Dis. 2016 Jan;22(1):33-8. doi: 10.1111/odi.12353. Epub 2015 Jul 2.

DOI:10.1111/odi.12353
PMID:26096083
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4863704/
Abstract

The temporomandibular joint (TMJ) is a synovial joint essential for hinge and sliding movements of the mammalian jaw. Temporomandibular joint disorders (TMD) are dysregulations of the muscles or the TMJ in structure, function, and physiology, and result in pain, limited mandibular mobility, and TMJ noise and clicking. Although approximately 40-70% adults in the USA have at least one sign of TMD, the etiology of TMD remains largely unknown. Here, we highlight recent advances in our understanding of TMD in mouse models.

摘要

颞下颌关节(TMJ)是一种滑膜关节,对哺乳动物颌骨的铰链和滑动运动至关重要。颞下颌关节紊乱病(TMD)是指肌肉或颞下颌关节在结构、功能和生理方面的失调,会导致疼痛、下颌活动受限以及颞下颌关节出现杂音和弹响。尽管美国约40%-70%的成年人至少有一项颞下颌关节紊乱病的症状,但其病因在很大程度上仍不清楚。在此,我们重点介绍在小鼠模型中对颞下颌关节紊乱病的最新认识进展。