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Letter to the Editor

机译:给编辑的信

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We read with great interest the review by Saxon and Turner entitled, "Estrogen receptor beta: the antimechanostat?" . In it, they propose that signaling through ER(J retards periosteal bone formation and suppresses gains in bone size and bone strength, and for these reasons they postulate that ER(beta) behaves as an "antimechanostaf . Based on animal and human data, there is considerable evidence, as indicated by the authors, that estrogen suppresses periosteal bone formation but stimulates endo-cortical bone formation. The real issue is whether this is due, as suggested by Saxon and Turner, to ER(beta) action on the periosteal surface vs. ERa action on the endocortical surface, or due to differential effects of estrogen acting via ERa on the periosteal vs. endocortical surfaces. We believe the latter possibility is much more likely and as such, have to disagree with the fundamental hypothesis of the review for several reasons.
机译:我们非常感兴趣地阅读了Saxon和Turner的题为“雌激素受体β:antimechanostat?”的评论。 。在其中,他们提出通过ER(J进行信号传导可延缓骨膜的骨形成并抑制骨大小和骨强度的增加,并且由于这些原因,他们推测ER(β)的作用类似于“ anchanchanostaf。基于动物和人类的数据,正如作者所指出的,大量证据表明雌激素抑制了骨膜的骨形成,但刺激了皮质内骨的形成,真正的问题是,这是否如Saxon和Turner所暗示的,是由于对骨膜表面的ERβ作用所致。与ERa在皮质内表面上的作用,或由于雌激素通过ERa在骨膜与皮质内表面上的差异作用,我们认为后者的可能性更大,因此,必须与本综述的基本假设相抵触有几个原因。

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