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PATHOPHYSIOLOGY AND CURRENT MANAGEMENT OF SPACE FLIGHT OSTEOPENIA: A REVIEW OF LITERATURE

机译：空间飞行性骨减少症的病理生理学和当前管理：文献综述

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There is evidence that astronauts go through many significant physiological changes during space flight. However, there isn't enough documentation around multiple diseases that result from these physiological changes, such as "Space Flight Osteopenia" which is considered to be a variant of osteoporosis. Bone remodeling is carried by osteoclasts (cells that produce bone resorption) an osteoblasts (cells that rebuild bone matrix). In the case of "common" osteoporosis found in women, the lack of estrogen (hormone that induces osteoclast apoptosis) post menopause results in the increasing activity of osteoclasts making osteoblasts unable to catch up with the bone resorption process and thus bones arc drastically debilitated. But in spaceflight osteopenia the pathogenesis is different. Bone remodels in response to a stimulus, areas with higher stress will have major bone density and areas with minor stimulus will have less density. Since gravity is minor in spaceflight than on earth, the entire skeleton of astronauts is under minor stress leading to loss of bone density. The purpose of this paper is to present a review of the pathophysiological process of space flight osteopenia, its current management and posible solutions for this problem.
机译：有证据表明，宇航员在太空飞行期间会经历许多重大的生理变化。但是，由于这些生理变化而引起的多种疾病的文献不足，例如“ Space Flight Osteopenia”被认为是骨质疏松症的一种变体。骨重塑由破骨细胞（产生骨吸收的细胞）和成骨细胞（重建骨基质的细胞）进行。在女性发现“常见”骨质疏松症的情况下，绝经后缺乏雌激素（诱导破骨细胞凋亡的激素）会导致破骨细胞活性增加，从而使成骨细胞无法跟上骨吸收过程，从而使骨骼严重衰弱。但是在航天性骨质减少的发病机理是不同的。骨骼因刺激而重塑，应力较高的区域将具有较大的骨密度，刺激较小的区域将具有较小的密度。由于在太空飞行中重力比在地球上轻，因此宇航员的整个骨骼承受的应力较小，从而导致骨密度降低。本文的目的是介绍太空飞行骨质减少的病理生理过程，其目前的管理方法和针对该问题的可能解决方案。

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