罕见低骨量病对骨质疏松症遗传学的价值。

BoneKEy reports Pub Date : 2016-01-06 eCollection Date: 2016-01-01 DOI:10.1038/bonekey.2015.143
Alice Costantini, Outi Mäkitie
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引用次数: 11

摘要

骨质疏松症表现为骨质流失和骨骼微结构受损导致骨折易感性增加。骨质疏松症主要影响老年人,但越来越多的人认识到,骨量低和骨折增加导致的骨骼健康受损可能早在儿童时期就开始了。在这种情况下,遗传因素可能比生活方式因素对疾病发病的影响更大。在过去的十年中,通过家族研究、候选基因研究和全基因组关联研究(GWASs),我们对骨质疏松症遗传决定因素的了解显著增加。GWASs已经鉴定出几个与骨质疏松症相关的基因位点。通过对儿童期罕见骨病(如成骨不全症、骨质疏松-假性胶质瘤综合征和各种其他骨量减少的骨骼发育不良)家庭的研究,对该研究领域做出了有价值的贡献。一些与罕见的低骨量疾病相关的基因,如LRP5和WNT1,参与了Wnt/β-catenin通路,它们的发现强调了该通路对正常骨骼健康的重要性。对各种低骨量表型的基因缺陷的不断发现有助于我们对正常骨代谢的理解,并使骨质疏松症的新疗法得以发展。
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Value of rare low bone mass diseases for osteoporosis genetics.

Osteoporosis presents as increased susceptibility to fractures due to bone loss and compromised bone microstructure. Osteoporosis mainly affects the elderly population, but it is increasingly recognized that compromised bone health with low bone mass and increased fractures may have its onset already in childhood. In such cases, genetic component is likely to contribute more than lifestyle factors to disease onset. During the last decade, our understanding of the genetic determinants of osteoporosis has significantly increased through family studies, candidate gene studies and genome-wide association studies (GWASs). GWASs have led to identification of several genetic loci associated with osteoporosis. A valuable contribution to the research field has been made through studies involving families with childhood-onset rare bone diseases such as osteogenesis imperfecta, osteoporosis-pseudoglioma syndrome and various other skeletal dysplasias with reduced bone mass. Some genes involved in rare low bone mass diseases, such as LRP5 and WNT1, participate in the Wnt/β-catenin pathway, and their discovery has underscored the importance of this pathway for normal skeletal health. The still continuing discovery of gene defects underlying various low bone mass phenotypes contributes to our understanding of normal bone metabolism and enables development of new therapies for osteoporosis.

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