Beyond Achondroplasia

Growing together with Clara

Increased bone turnover and possible accelerated fracture healing in a murine model with an increased circulating C-type natriuretic peptide – Nakao 2015

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Bone turnover – total volume of bone that is resorbed and formed over a period of time, usually expressed as percent/year. It can be estimated by measuring relevant bone biomarkers [1].

Bone remodelling – It’s a dynamic physiological event and active process throughout the skeleton, essential for calcium homeostasis and preserving the integrity of the skeleton, through the coupled activity of osteoclasts and osteoblasts [2]. In adults, bone turnover occurs mainly through bone remodelling [3].

[1] Parfitt AM. Bone. 2004; 35(1):1-3.
[2] Fazzalari NL. Semin Cell Dev Biol. 2008; 19(5):467-72

[3] Parfitt AM et al. J Bone Miner Res. 1996; 11(2):150-9

In this article, published at Endocrinology. 2015 Apr 10:en20141801, from Nakao´s team, they show a link between CNP and bone turnover:

Abstract

Recent studies have revealed that C-type natriuretic peptide (CNP) is a potent stimulator of endochondral bone growth. Nevertheless, the effect of CNP on bone turnover has not yet been well studied. In order to elucidate this issue, we investigated the bone phenotype of a mouse model with elevated plasma CNP concentrations (SAP-CNP-Tg mice) in the present study. Micro-CT analysis revealed less bone in femurs, but not in lumber vertebrae, of young adult SAP-CNP-Tg mice than that of wild-type mice. Bone histomorphometry of the tibiae from 8-week-old SAP-CNP-Tg mice showed enhanced osteoblastic and osteoclastic activities, in accordance with elevated serum levels of osteocalcin and TRAP5b, respectively. Next we performed an open and stabilized femoral fracture using 8-week-old SAP-CNP-Tg mice and compared the healing process with age-matched wild-type mice. Immunohistochemical study revealed that CNP and its receptors, natriuretic peptide receptor-B (NPR-B) and natriuretic peptide clearance receptor are expressed in hard calluses of wild-type mice, suggesting possible role of CNP/NPR-B signaling in fracture repair, especially in bone remodeling stage. On micro-CT analysis, rapid decrease in callus volume was observed in SAP-CNP-Tg mice, followed by generation of significantly higher new bone volume with a tendency of increased bone strength. In addition, micro-CT analysis also showed that bone remodeling was accelerated in SAP-CNP-Tg mice, which was also evident from increased serum osteocalcin and TRAP5b levels in SAP-CNP-Tg mice at remodeling stage of fracture repair. These results indicate that CNP activates bone turnover and remodeling in vivo and possibly accelerates fracture healing in our mouse model.”

This article raises expectations about the possible effect of BMN-111.

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