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雌激素缺乏加速腰椎小关节关节炎。

Estrogen deficiency accelerates lumbar facet joints arthritis.

机构信息

Department of Orthopaedics, The First Affiliated Hospital of Soochow University, No. 188 Shizi Street, Suzhou, Jiangsu, 215006, P.R. China.

Department of Orthopaedics, Affiliated Hospital of Nantong University, Xisi Road 20, Nantong, Jiangsu, 226001, P.R. China.

出版信息

Sci Rep. 2017 May 3;7(1):1379. doi: 10.1038/s41598-017-01427-7.

DOI:10.1038/s41598-017-01427-7
PMID:28469263
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5431109/
Abstract

Dramatic increase in the prevalence of lumbar facet joint (LFJ) arthritis in women around the age of menopause indicates a protective role for estrogen in LFJ arthritis. To date, there is no evidence for this indication and the mechanism of such an effect remains poorly understood. In this study, ovariectomized (OVX) mice were used to mimic the estrogen-deficient status of post-menopausal women. Micro-CT and immunohistochemistry was employed to assess the morphological and molecular changes in ovariectomy-induced LFJ arthritis. The results show that the LFJ subchondral bone mass was significantly decreased in OVX mice, with increased cavities on the interface of the subchondral bone. Severe cartilage degradation was observed in ovariectomy-induced LFJ arthritis. Increased blood vessels and innervations were also found in degenerated LFJ, particularly in the subchondral bone area. 17β-Estradiol treatment efficiently suppressed LFJ subchondral bone turnover, markedly inhibited cartilage degradation, and increased blood vessel and nerve ending growth in degenerated LFJ in OVX mice. Our study reveals that estrogen is a key factor in regulating LFJ metabolism. Severe LFJ degeneration occurs when estrogen is absent in vivo. Collapsed subchondral bone may be the initiation of this process, and estrogen replacement therapy can effectively prevent degeneration of LFJ under estrogen-deficient conditions.

摘要

绝经前后女性腰椎小关节(LFJ)关节炎患病率的急剧上升表明雌激素对 LFJ 关节炎具有保护作用。迄今为止,尚无此迹象的证据,其作用机制仍知之甚少。在这项研究中,使用去卵巢(OVX)小鼠来模拟绝经后女性的雌激素缺乏状态。采用微 CT 和免疫组织化学方法评估去卵巢诱导的 LFJ 关节炎的形态和分子变化。结果表明,OVX 小鼠的 LFJ 软骨下骨量明显减少,软骨下骨界面出现更多的腔隙。在去卵巢诱导的 LFJ 关节炎中观察到严重的软骨退化。退化的 LFJ 中还发现了更多的血管和神经末梢,尤其是在软骨下骨区域。17β-雌二醇治疗能有效抑制 LFJ 软骨下骨转换,显著抑制软骨降解,并促进 OVX 小鼠退化 LFJ 中的血管和神经末梢生长。我们的研究表明,雌激素是调节 LFJ 代谢的关键因素。体内缺乏雌激素时会发生严重的 LFJ 退化。塌陷的软骨下骨可能是该过程的启动因素,雌激素替代疗法可有效预防雌激素缺乏状态下 LFJ 的退化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16ab/5431109/399bd74146ab/41598_2017_1427_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16ab/5431109/c8106088e095/41598_2017_1427_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16ab/5431109/fdfe19ba0fe7/41598_2017_1427_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16ab/5431109/83d4c29e00d8/41598_2017_1427_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16ab/5431109/6a66b5920ad1/41598_2017_1427_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16ab/5431109/399bd74146ab/41598_2017_1427_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16ab/5431109/c8106088e095/41598_2017_1427_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16ab/5431109/fdfe19ba0fe7/41598_2017_1427_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16ab/5431109/83d4c29e00d8/41598_2017_1427_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16ab/5431109/6a66b5920ad1/41598_2017_1427_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16ab/5431109/399bd74146ab/41598_2017_1427_Fig5_HTML.jpg

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