Recently published work from the Killian Lab describes the role of Scleraxis in the formation of a symmetric callus following long bone fracture. The paper, titled: “Loss of scleraxis in mice leads to geometric and structural changes in cortical bone, as well as asymmetry in fracture healing,” was accepted for publication in The FASEB Journal. Authors on this work are Jennifer A. McKenzie, PhD; Evan Buettmann; Adam C. Abraham, PhD; Michael J. Gardner, MD; Matthew J. Silva, PhD’ and Megan L. Killian, PhD. The work was performed in collaboration with the Musculoskeletal Research Center at Washington University School of Medicine in Saint Louis.
In this paper, we explored the role of Scleraxis (Scx), which is a known regulator of tendon development, in the development and healing of long bones. Scx-mutant long bones had structural and mechanical defects compared to wildtype bones, and the scx gene expression was elevated at 24hr following fracture. ScxGFP+ cells were localized throughout the healing callus after fracture. Scx-mutants demonstrated disrupted callus healing and asymmetry. We also showed that asymmetry of the callus was not due to asymmetric muscle unloading. 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 Scx may play a role in the periosteal response during fracture healing.