Loss of scleraxis in mice leads to geometric & structural changes in cortical bone, as well as asymmetry in fracture healing

Jennifer A. Mckenzie, Evan Buettmann, Adam C. Abraham, Michael J. Gardner, Matthew J. Silva, Megan L. Killian

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

Scleraxis (Scx) is aknownregulator of tendon development, and recentwork has identified the role of Scx in bone modeling.However, the role of Scx in fracture healing has not yet been explored. This study was conducted to identify the role of Scx in cortical bone development and fracture healing. Scx green fluorescent protein-labeled (ScxGFP) reporter and Scx-knockout (Scx-mutant) mice were used to assess bone morphometry and the effects of fracture healing on Scx localization and gene expression, aswell as callus healing response. Botulinumtoxin (BTX) was used to investigate muscle unloading effects on callus shape. Scx-mutant long bones had structural and mechanicaldefects. Scx gene expression was elevated and bmp4was decreased at 24 h after fracture. ScxGFP+ cellswere localized throughout the healing callus after fracture. Scx-mutant mice demonstrated disrupted callus healing and asymmetry. Asymmetry of Scx-mutant calluswas not due to muscle unloading.Wild-Type littermates (age matched) served as controls. This is the first study to explore the role of Scx in cortical bone mechanics and fracture healing. Deletion of Scx during development led to altered long bone properties and callus healing. This study also demonstrated that Scxmay play a role in the periosteal response during fracture healing.

Original languageEnglish
Pages (from-to)882-892
Number of pages11
JournalFASEB Journal
Volume31
Issue number3
DOIs
StatePublished - Mar 2017

Keywords

  • Callus
  • Development
  • Skeletal repair
  • Tendon
  • Transcription factors

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