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二氢睾酮、17-β-雌激素、染料木黄酮和雌马酚对骨质疏松雄性大鼠骨愈合过程中骨重塑和形态的影响

Effect of dihydrotestosterone, 17-β-estrogen, genistein and equol on remodeling and morphology of bone in osteoporotic male rats during bone healing.

作者信息

Kauffmann Philipp, Rau Anna, Seidlová-Wuttke Dana, Jarry Hubertus, Schminke Boris, Matthes Swantje, Wiese Karl Günter

机构信息

Department of Oral and Maxillofacial Surgery, University Medical Center Goettingen, Georg-August-University Goettingen, Robert-Koch-Str. 40, D-37099 Goettingen, Germany.

Department of Department of Anesthesiology, University Medical Center Goettingen, Georg-August-University Goettingen, Robert-Koch-Str. 40, D-37099 Goettingen, Germany.

出版信息

Bone Rep. 2020 Jul 28;13:100300. doi: 10.1016/j.bonr.2020.100300. eCollection 2020 Dec.

DOI:10.1016/j.bonr.2020.100300
PMID:32802919
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7419585/
Abstract

INTRODUCTION

The aim of this study was to investigate the effect of dihydrotestosterone (DHT), 17-β-estrogen (E2), genistein (GEN) and equol (EQ) on bone remodeling and bone morphology during healing of osteoporotic male rat tibiae.

MATERIALS AND METHODS

180 Sprague-Dawley male rats were divided in 5 groups of 36 animals. After orchidectomy (ORX) and development of osteoporosis, trepanation of the tibia was performed. Until the time of trepanation all groups received soya free food (SF), then food change occurred and treatment started. At day 95, 102 and 151, samples were taken and histomorphometry was performed to analyze changes in bone structure under treatment. At day 33 and 70 all animals received calcein respective alizarin for polychrome bone labeling.

RESULTS

The cortical bone was particularly affected. Treatment with DHT and E2 led to a significant long-term expansion of the thickness of the diaphyseal cortical bone, while the phytoestrogens EQ and GEN only had a positive short-term effect in this area. Only E2 preserved the trabecular bone for a limited time. In all groups, periosteal and endosteal bone areas showed the highest bone formation activity. The osteoporotic male injured bone shows a shift in mineral apposition rate (MAR) from periosteal to endosteal bone in the SF, DHT and E2 groups but not in the GEN and EQ phytohormones groups. An MAR decrease in trabecular bone formation was observed at day 70 in all groups except the E2 group.

CONCLUSION

We conclude from our results that healing of cortical bone defects in a rat model of male osteoporosis are mainly influenced by the estrogen pathway. Nevertheless, effects via purely androgenic mechanisms can also be demonstrated. The role of a phytohormone therapy is only marginal and if only useful for a short-term supportive approach. The role of the periosteal to endosteal shift during male osteoporotic bone healing needs to be further examined.

摘要

引言

本研究旨在探讨二氢睾酮(DHT)、17-β-雌二醇(E2)、染料木黄酮(GEN)和雌马酚(EQ)对雄性骨质疏松大鼠胫骨愈合过程中骨重塑和骨形态的影响。

材料与方法

将180只Sprague-Dawley雄性大鼠分为5组,每组36只。进行去势手术(ORX)并诱发骨质疏松后,对胫骨进行环钻术。在进行环钻术之前,所有组均给予无大豆食物(SF),然后更换食物并开始治疗。在第95、102和151天,采集样本并进行组织形态计量学分析,以分析治疗过程中骨结构的变化。在第33天和第70天,所有动物分别接受钙黄绿素和茜素进行多色骨标记。

结果

皮质骨受到的影响尤为明显。DHT和E2治疗导致骨干皮质骨厚度长期显著增加,而植物雌激素EQ和GEN仅在该区域有短期积极作用。只有E2在有限时间内保留了小梁骨。在所有组中,骨膜和骨内膜骨区域的骨形成活性最高。在SF、DHT和E2组中,骨质疏松雄性损伤骨的矿物质沉积率(MAR)从骨膜向骨内膜骨发生了转变,但在GEN和EQ植物激素组中未发生这种转变。除E2组外,所有组在第70天均观察到小梁骨形成的MAR降低。

结论

我们从结果中得出结论,雄性骨质疏松大鼠模型中皮质骨缺损的愈合主要受雌激素途径影响。然而,也可以证明存在通过纯雄激素机制产生的作用。植物激素疗法的作用仅处于边缘地位,且仅对短期支持性治疗有用。雄性骨质疏松性骨愈合过程中骨膜向骨内膜转变的作用需要进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/905f/7419585/04e5d25fb8fb/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/905f/7419585/eb5c124f43ca/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/905f/7419585/01089b132e24/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/905f/7419585/2126fabfbd21/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/905f/7419585/83700afa9007/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/905f/7419585/04e5d25fb8fb/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/905f/7419585/eb5c124f43ca/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/905f/7419585/01089b132e24/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/905f/7419585/2126fabfbd21/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/905f/7419585/83700afa9007/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/905f/7419585/04e5d25fb8fb/gr5.jpg

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