The WNT1G177C mutation specifically affects skeletal integrity in a mouse model of osteogenesis imperfecta type ⅩⅤ

• 作者: Nele Vollersen Wenbo Zhao Tim Rolvien Fabiola Lange Felix Nikolai Schmidt Stephan Sonntag Doron Shmerling Simon von Kroge Kilian Elia Stockhausen Ahmed Sharaf Michaela Schweizer Meliha Karsak Björn Busse Ernesto Bockamp Oliver Semler Michael Amling Ralf Oheim Thorsten Schinke Timur Alexander Yorgan
• 来源期刊: 骨研究（英文版）
• 年，卷（期）: 2021,（4）
• 所属期刊栏目: ORIGINAL ARTICLES
• 页码范围: 593-605
• 页数: 13页
• 语种: 英文

摘要

INTRODUCTION Osteoporosis, the most prevalent skeletal remodeling disorder, is primarily treated by antiresorptive drugs inhibiting the differentia-tion and/or activity of osteoclasts.1 Although osteoanabolic treatment options, stimulating osteoblast-mediated bone forma-tion, are available, they are not commonly used to treat osteoporotic patients.2 In the case of teriparatide, a fragment of parathyroid hormone (PTH), this is mostly explained by the relatively high costs and the mode of application (daily injection). In the case of romosozumab, an antibody blocking the action of the bone formation inhibitor sclerostin, there is still no long-lasting clinical experience, as this type of treatment was approved only recently.3 This explains why it is of highest clinical relevance to uncover additional molecular mechanisms regulating bone formation and skeletal integrity to optimize the treatment of not only osteoporosis but also various other skeletal disorders.