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骨质疏松症的发病机制。

Pathogenesis of osteoporosis.

作者信息

Väänänen H K

机构信息

Department of Anatomy, University of Oulu, Finland.

出版信息

Calcif Tissue Int. 1991;49 Suppl:S11-4. doi: 10.1007/BF02555080.

Abstract

The final clinical outcome of the osteoporotic process is a fracture, which can occur as a result of minimal trauma or even spontaneously. At present low bone mass is regarded as the main contributor to bone fragility, but possible qualitative changes in the bone matrix must also be considered. Two factors which determine the level of bone mass at any age are the obtained peak bone mass and duration and rate of bone loss. Peak bone mass is achieved during the first three decades of life. Genetic and nutritional factors as well as mechanical stress on the skeleton obviously play crucial roles in determining peak bone mass. Two phases of bone loss--age-related and menopause-related--dictate the final bone mass at old age. Postmenopausal osteoporosis is a particular example of unbalanced bone resorption leading to net bone loss. An increasing number of systemic and local factors have been found to participate in the regulation of bone remodeling.

摘要

骨质疏松过程的最终临床结果是骨折,骨折可能因轻微创伤甚至自发发生。目前,低骨量被认为是导致骨脆性的主要因素,但骨基质可能的质的变化也必须予以考虑。决定任何年龄骨量水平的两个因素是获得的峰值骨量以及骨质流失的持续时间和速率。峰值骨量在生命的头三十年达到。遗传和营养因素以及骨骼上的机械应力显然在决定峰值骨量方面起着关键作用。骨质流失的两个阶段——与年龄相关的和与绝经相关的——决定了老年时的最终骨量。绝经后骨质疏松症是骨吸收失衡导致净骨量减少的一个特殊例子。已发现越来越多的全身和局部因素参与骨重塑的调节。

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