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雌激素受体β介导雌性小鼠咬合负荷降低诱导的软骨细胞成熟抑制。

Oestrogen receptor beta mediates decreased occlusal loading induced inhibition of chondrocyte maturation in female mice.

作者信息

Polur Ilona, Kamiya Yosuke, Xu Manshan, Cabri Bianca S, Alshabeeb Marwa, Wadhwa Sunil, Chen Jing

机构信息

Division of Orthodontics, Columbia University College of Dental Medicine, New York, NY 10032, USA.

Columbia University College of Dental Medicine, New York, NY 10032, USA.

出版信息

Arch Oral Biol. 2015 Jun;60(6):818-24. doi: 10.1016/j.archoralbio.2015.02.007. Epub 2015 Feb 20.

Abstract

OBJECTIVE

Temporomandibular joint (TMJ) disorders predominantly afflict women, suggesting that estrogen may play a role in the disease process. Defects in mechanical loading-induced TMJ remodelling are believed to be a major etiological factor in TMJ degenerative disease. Previously, we found that, decreased occlusal loading caused a significant decrease in early chondrocyte maturation markers (Sox9 and Col 2) in female, but not male, C57BL/6 wild type mice (1). The goal of this study was to examine the role of Estrogen Receptor (ER) beta in mediating these effects.

DESIGN

21-day-old male (n = 24) and female (n = 25) ER beta KO mice were exposed to decreased occlusal loading (soft diet administration and incisor trimming) for 4 weeks. At 49 days of age the mice were sacrificed. Proliferation, gene expression, Col 2 immunohistochemistry and micro-CT analysis were performed on the mandibular condyles.

RESULTS

Decreased occlusal loading triggered similar effects in male and female ER beta KO mice; specifically, significant decreases in Col 10 expression, subchondral total volume, bone volume, and trabecular number.

CONCLUSION

Decreased occlusal loading induced inhibition of chondrocyte maturation markers (Sox9 and Col 2) did not occur in female ER beta deficient mice.

摘要

目的

颞下颌关节(TMJ)疾病主要影响女性,提示雌激素可能在疾病进程中起作用。机械负荷诱导的颞下颌关节重塑缺陷被认为是颞下颌关节退行性疾病的主要病因。此前,我们发现,在雌性而非雄性C57BL/6野生型小鼠中,咬合负荷降低导致早期软骨细胞成熟标志物(Sox9和Col 2)显著减少(1)。本研究的目的是探讨雌激素受体(ER)β在介导这些效应中的作用。

设计

将21日龄的雄性(n = 24)和雌性(n = 25)ERβ基因敲除小鼠暴露于降低的咬合负荷(给予软食并修剪门牙)4周。在49日龄时处死小鼠。对下颌髁突进行增殖、基因表达、Col 2免疫组织化学和微型计算机断层扫描(micro-CT)分析。

结果

咬合负荷降低在雄性和雌性ERβ基因敲除小鼠中引发了类似的效应;具体而言,Col 10表达、软骨下总体积、骨体积和小梁数量显著减少。

结论

在雌性ERβ缺陷小鼠中未出现咬合负荷降低诱导的软骨细胞成熟标志物(Sox9和Col 2)抑制现象。

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