Periostin expression contributes to cortical bone loss during unloading

Gerbaix, Maude; Vico, Laurence; Ferrari, Serge; Bonnet, Nicolas

doi:10.1016/j.bone.2014.10.011

Cited by 70 publications

(42 citation statements)

References 38 publications

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“…Osteoclast differentiation is tightly regulated by osteoblasts through several mechanisms. It has been reported that mechanical stimulation leads to expression of periostin in bone tissue (33,34). However, the influence of mechanical stimulation on semaphorin-3A expression, to our knowledge, has not been studied.…”

Section: Discussionmentioning

confidence: 91%

Influence of Mechanical Force on Bone Matrix Proteins in Ovariectomised Mice and Osteoblast-like MC3T3-E1 Cells

Zhang

Ishikawa

Tomoko

et al. 2017

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Section: Discussionmentioning

confidence: 91%

Influence of Mechanical Force on Bone Matrix Proteins in Ovariectomised Mice and Osteoblast-like MC3T3-E1 Cells

Zhang

Ishikawa

Tomoko

et al. 2017

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“…Another key molecule in this response and signaling activation is periostin (Postn), a matricellular protein of 90 kD secreted by osteocytes and osteoblasts . In mice, Postn is mainly localized to the cortical compartment and its expression is essential for the periosteal bone formation mediated by Wnt‐β‐catenin signaling in response to mechanical loading and parathyroid hormone (PTH) . Postn ‐/‐ mice are characterized by periodontitis and low BMD, altered microstructure, and reduced cortical bone strength .…”

Section: Introductionmentioning

confidence: 99%

Cathepsin K Controls Cortical Bone Formation by Degrading Periostin

Bonnet

Brun

Rousseau

et al. 2017

Journal of Bone and Mineral Research

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Although inhibitors of bone resorption concomitantly reduce bone formation because of the coupling between osteoclasts and osteoblasts, inhibition or deletion of cathepsin k (CatK) stimulates bone formation despite decreasing resorption. The molecular mechanisms responsible for this increase in bone formation, particularly at periosteal surfaces where osteoclasts are relatively poor, remain unclear. Here we show that CatK pharmacological inhibition or deletion (Ctsk mice) potentiates mechanotransduction signals mediating cortical bone formation. We identify periostin (Postn) as a direct molecular target for degradation by CatK and show that CatK deletion increases Postn and β-catenin expression in vivo, particularly at the periosteum. In turn, Postn deletion selectively abolishes cortical, but not trabecular, bone formation in CatK-deficient mice. Taken together, these data indicate that CatK not only plays a major role in bone remodeling but also modulates modeling-based cortical bone formation by degrading periostin and thereby moderating Wnt-β-catenin signaling. These findings provide novel insights into the role of CatK on bone homeostasis and the mechanisms of increased cortical bone volume with CatK mutations and pharmacological inhibitors. © 2017 American Society for Bone and Mineral Research.

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“…1 mCT has become standard practice in rodent studies examining bone structure because of its power to visualize and quantify the three-dimensional structure of trabecular and cortical bone compartments that were previously performed using two-dimensional histological techniques. This imaging technology has also become customary because of its increasing accessibility within the bone research community, allowing for the investigation of a wide range of interventions-drugs, 2,3 diet, 4,5 exercise, 6 mechanical loading 7,8 or unloading 9 -on bone structure and morphometry.…”

Section: Introductionmentioning

confidence: 99%

Repeated irradiation from micro-computed tomography scanning at 2, 4 and 6 months of age does not induce damage to tibial bone microstructure in male and female CD-1 mice

et al. 2017

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Long-term effects of repeated in vivo micro-computed tomography (lCT) scanning at key stages of growth and bone development (ages 2, 4 and 6 months) on trabecular and cortical bone structure, as well as developmental patterns, have not been studied. We determined the effect of repetitive lCT scanning at age 2, 4 and 6 months on tibia bone structure of male and female CD-1 mice and characterized developmental changes. At 2, 4 and 6 months of age, right tibias were scanned using in vivo lCT (Skyscan 1176) at one of three doses of radiation per scan: 222, 261 or 460 mGy. Left tibias of the same mice were scanned only at 6 months to serve as non-irradiated controls to determine whether recurrent radiation exposure alters trabecular and cortical bone structure at the proximal tibia. In males, eccentricity was lower (Po0.05) in irradiated compared with non-irradiated tibias (222 mGy group). Within each sex, all other structural outcomes were similar between irradiated and non-irradiated tibias regardless of dose. Trabecular bone loss occurred in all mice due to age while cortical development continued to age 6 months. In conclusion, repetitive lCT scans at various radiation doses did not damage trabecular or cortical bone structure of proximal tibia in male and female CD-1 mice. Moreover, scanning at 2, 4 and 6 months of age highlight the different developmental time course between trabecular and cortical bone. These scanning protocols can be used to investigate longitudinal responses of bone structures to an intervention.

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Periostin expression contributes to cortical bone loss during unloading

Cited by 70 publications

References 38 publications

Influence of Mechanical Force on Bone Matrix Proteins in Ovariectomised Mice and Osteoblast-like MC3T3-E1 Cells

Influence of Mechanical Force on Bone Matrix Proteins in Ovariectomised Mice and Osteoblast-like MC3T3-E1 Cells

Cathepsin K Controls Cortical Bone Formation by Degrading Periostin

Repeated irradiation from micro-computed tomography scanning at 2, 4 and 6 months of age does not induce damage to tibial bone microstructure in male and female CD-1 mice

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