Genetics of osteoporosis: perspectives for personalized medicine

Author:

Li Wen-Feng1,Hou Shu-Xun1,Yu Bin2,Jin Dan2,Férec Claude345,Chen Jian-Min

Affiliation:

1. Department of Orthopaedics, The First Affiliated Hospital, General Hospital of the People’s Liberation Army, Beijing, China

2. Department of Orthopaedic Trauma, Nanfang Hospital, Southern Medical University, Guangzhou, China

3. Institut National de la Santé et de la Recherche Médicale (INSERM), U613, Brest, France; INSERM, U613 and EFS – Bretagne, 46 rue Félix Le Dantec, 29218 Brest, France

4. Etablissement Français du Sang (EFS) – Bretagne, Brest, France

5. Faculté de Médecine et des Sciences de la Santé, Université de Bretagne Occidentale (UBO), Brest, France

Abstract

Osteoporosis is the most common metabolic bone disorder worldwide. At least 15 genes (e.g., ESR1, LRP5, SOST, OPG, RANK and RANKL) have been confirmed as osteoporosis susceptibility genes, and another 30 have been highlighted as promising susceptibility genes. Notably, these genes are clustered in three biological pathways: the estrogen endocrine pathway, the Wnt/β-catenin signaling pathway and the RANK/RANKL/osteoprotegerin (OPG) pathway. In this article, using data pertaining to these three biological pathways as examples, we illustrate possible principles of personalized therapy for osteoporosis. In particular, we propose to use inhibitors (e.g., denosumab) of the RANK/RANKL/OPG signaling pathway to circumvent resistance to estrogen-replacement therapy: a novel idea resulting from the consideration of a mechanistic link between the estrogen endocrine pathway and the RANK/RANKL/OPG signaling pathway. In addition, we call for more attention to be focused on rare variants of major effects in future studies.

Publisher

Future Medicine Ltd

Subject

Pharmacology,Molecular Medicine,General Medicine

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