This 1999 study by Ferguson et al. uses in situ hybridization in a murine closed tibial fracture model to ask whether adult fracture repair reactivates the same molecular program as fetal endochondral ossification — examining expression of cbfa1, ihh, gli1, osteocalcin, VEGF, and MMP13 across embryonic development (e12–e18) and fracture healing (days 3–14).
When you see a hypertrophic non-union (abundant callus, excess motion), think arrest of MMP13/VEGF-mediated cartilage remodeling — stabilization restores the angiogenic signal needed to convert cartilage to bone.
When you see an atrophic non-union (no callus, poor vascularity at the tibial diaphysis), the problem is upstream: inadequate mesenchymal progenitor recruitment or frank ischemia, not just mechanical instability.
This 1999 study by Ferguson et al. uses in situ hybridization in a murine closed tibial fracture model to ask whether adult fracture repair reactivates the same molecular program as fetal endochondral ossification — examining expression of cbfa1, ihh, gli1, osteocalcin, VEGF, and MMP13 across embryonic development (e12–e18) and fracture healing (days 3–14).
When you see a hypertrophic non-union (abundant callus, excess motion), think arrest of MMP13/VEGF-mediated cartilage remodeling — stabilization restores the angiogenic signal needed to convert cartilage to bone.
When you see an atrophic non-union (no callus, poor vascularity at the tibial diaphysis), the problem is upstream: inadequate mesenchymal progenitor recruitment or frank ischemia, not just mechanical instability.