Periostin Deficiency Increases Bone Damage and Impairs Injury Response to Fatigue Loading in Adult Mice

Nicolas Bonnet, Evelyne Gineyts, Patrick Ammann, Simon Conway, Patrick Garnero, Serge Ferrari

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

Bone damage removal and callus formation in response to fatigue loading are essential to prevent fractures. Periostin (Postn) is a matricellular protein that mediates adaptive response of cortical bone to loading. Whether and how periostin influences damage and the injury response to fatigue remains unknown. We investigated the skeletal response of Postn-/- and Postn+/+ mice after fatigue stimulus by axial compression of their tibia. In Postn+/+ mice, cracks number and surface (CsNb, CsS) increased 1h after fatigue, with a decrease in strength compared to non-fatigued tibia. At 15 days, CsNb had started to decline, while CtTV and CtBV increased in fatigued vs non-fatigued tibia, reflecting a woven bone response that was present in 75% of the fatigued bones. Cortical porosity and remodelling also prominently increased in the fatigued tibia of Postn+/+ mice. At 30 days, paralleling a continuous removal of cortical damage, strength of the fatigued tibia was similar to the non-fatigue tibia. In Postn-/- mice, cracks were detectable even in the absence of fatigue, while the amount of collagen crosslinks and tissue hardness was decreased compared to Postn+/+. Fatigue significantly increased CsNb and CsS in Postn-/-, but was not associated with changes in CtTV and CtBV, as only 16% of the fatigued bones formed some woven bone. Cortical porosity and remodelling did not increase either after fatigue in Postn-/-, and the level of damage remained high even after 30 days. As a result, strength remained compromised in Postn-/- mice. Contrary to Postn+/+, which osteocytic lacunae showed a change in the degree of anisotropy (DA) after fatigue, Postn-/- showed no DA change. Hence periostin appears to influence bone materials properties, damage accumulation and repair, including local modeling/remodeling processes in response to fatigue. These observations suggest that the level of periostin expression could influence the propensity to fatigue fractures.

Original languageEnglish
Article numbere78347
JournalPLoS One
Volume8
Issue number10
DOIs
StatePublished - Oct 22 2013

Fingerprint

Fatigue
tibia
Bone
bones
Fatigue of materials
Tibia
Bone and Bones
mice
Wounds and Injuries
porosity
Porosity
Anisotropy
stress fractures
bone formation
Stress Fractures
Cracks
hardness
collagen
Hardness
Bony Callus

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)

Cite this

Periostin Deficiency Increases Bone Damage and Impairs Injury Response to Fatigue Loading in Adult Mice. / Bonnet, Nicolas; Gineyts, Evelyne; Ammann, Patrick; Conway, Simon; Garnero, Patrick; Ferrari, Serge.

In: PLoS One, Vol. 8, No. 10, e78347, 22.10.2013.

Research output: Contribution to journalArticle

Bonnet, Nicolas ; Gineyts, Evelyne ; Ammann, Patrick ; Conway, Simon ; Garnero, Patrick ; Ferrari, Serge. / Periostin Deficiency Increases Bone Damage and Impairs Injury Response to Fatigue Loading in Adult Mice. In: PLoS One. 2013 ; Vol. 8, No. 10.
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abstract = "Bone damage removal and callus formation in response to fatigue loading are essential to prevent fractures. Periostin (Postn) is a matricellular protein that mediates adaptive response of cortical bone to loading. Whether and how periostin influences damage and the injury response to fatigue remains unknown. We investigated the skeletal response of Postn-/- and Postn+/+ mice after fatigue stimulus by axial compression of their tibia. In Postn+/+ mice, cracks number and surface (CsNb, CsS) increased 1h after fatigue, with a decrease in strength compared to non-fatigued tibia. At 15 days, CsNb had started to decline, while CtTV and CtBV increased in fatigued vs non-fatigued tibia, reflecting a woven bone response that was present in 75{\%} of the fatigued bones. Cortical porosity and remodelling also prominently increased in the fatigued tibia of Postn+/+ mice. At 30 days, paralleling a continuous removal of cortical damage, strength of the fatigued tibia was similar to the non-fatigue tibia. In Postn-/- mice, cracks were detectable even in the absence of fatigue, while the amount of collagen crosslinks and tissue hardness was decreased compared to Postn+/+. Fatigue significantly increased CsNb and CsS in Postn-/-, but was not associated with changes in CtTV and CtBV, as only 16{\%} of the fatigued bones formed some woven bone. Cortical porosity and remodelling did not increase either after fatigue in Postn-/-, and the level of damage remained high even after 30 days. As a result, strength remained compromised in Postn-/- mice. Contrary to Postn+/+, which osteocytic lacunae showed a change in the degree of anisotropy (DA) after fatigue, Postn-/- showed no DA change. Hence periostin appears to influence bone materials properties, damage accumulation and repair, including local modeling/remodeling processes in response to fatigue. These observations suggest that the level of periostin expression could influence the propensity to fatigue fractures.",
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