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首页> 外文期刊>Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research >Increased mandibular condylar growth in mice with estrogen receptor beta deficiency
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Increased mandibular condylar growth in mice with estrogen receptor beta deficiency

机译：雌激素受体β缺乏症小鼠下颌con突生长增加

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摘要

Temporomandibular joint (TMJ) disorders predominantly afflict women of childbearing age, suggesting a role for female hormones in the disease process. In long bones, estrogen acting via estrogen receptor beta (ERβ) inhibits axial skeletal growth in female mice. However, the role of ERβ in the mandibular condyle is largely unknown. We hypothesize that female ERβ-deficient mice will have increased mandibular condylar growth compared to wild-type (WT) female mice. This study examined female 7-day-old, 49-day-old, and 120-day-old WT and ERβ knockout (KO) mice. There was a significant increase in mandibular condylar cartilage thickness as a result of an increased number of cells, in the 49-day-old and 120-day-old female ERβ KO compared with WT controls. Analysis in 49-day-old female ERβ KO mice revealed a significant increase in collagen type X, parathyroid hormone-related protein (Pthrp), and osteoprotegerin gene expression and a significant decrease in receptor activator for nuclear factor κ B ligand (Rankl) and Indian hedgehog (Ihh) gene expression, compared with WT controls. Subchondral bone analysis revealed a significant increase in total condylar volume and a decrease in the number of osteoclasts in the 49-day-old ERβ KO compared with WT female mice. There was no difference in cell proliferation in condylar cartilage between the genotypes. However, there were differences in the expression of proteins that regulate the cell cycle; we found a decrease in the expression of Tieg1 and p57 in the mandibular condylar cartilage from ERβ KO mice compared with WT mice. Taken together, our results suggest that ERβ deficiency increases condylar growth in female mice by inhibiting the turnover of fibrocartilage.
机译：颞下颌关节（TMJ）疾病主要困扰育龄妇女，这提示女性荷尔蒙在疾病过程中起一定作用。在长骨中，通过雌激素受体β（ERβ）发挥作用的雌激素会抑制雌性小鼠的轴向骨骼生长。然而，ERβ在下颌con突中的作用尚不清楚。我们假设雌性ERβ缺陷型小鼠与野生型（WT）雌性小鼠相比，下颌con突生长会增加。这项研究检查了7日龄，49日龄和120日龄的WT和ERβ基因敲除（KO）小鼠的雌性。与WT对照相比，在49天和120天的雌性ERβKO中，由于细胞数量增加，下颌man突软骨厚度显着增加。对49天大的雌性ERβKO小鼠进行的分析显示，X型胶原蛋白，甲状旁腺激素相关蛋白（Pthrp）和骨保护素基因表达显着增加，而核因子κB配体（Rankl）和印度刺猬（Ihh）基因表达，与野生型对照相比。软骨下骨分析显示，与野生雌性小鼠相比，49天大的ERβKO中总con突体积显着增加，破骨细胞数量减少。基因型之间的con突软骨细胞增殖没有差异。但是，调节细胞周期的蛋白质表达存在差异。我们发现，与野生型小鼠相比，ERβKO小鼠下颌con突软骨中Tieg1和p57的表达减少。两者合计，我们的结果表明ERβ缺乏通过抑制纤维软骨的周转来增加雌性小鼠的con突生长。

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