Murine periosteum is highly enriched for osteoprogenitors, many of which express αSMA, but fracture callus chondrocytes are partially derived from other sources.

A single-nucleus atlas of bone repair uncovers the trajectories of periosteal skeletal stem/progenitor cells in response to fracture and identifies injury-induced fibrogenic cells as intermediate osteochondroprogenitors and key paracrine regulators.

A periosteal Bmp2 signaling center couples bone length to bone width during development and must be reactivated by clinical bone anabolic therapies to reduce fracture risk and accelerate fracture repair.

Large-scale skeletal regeneration requires Hh signaling in Sox9+ lineage cells to coordinate callus formation and bone repair.

Activation of Activin A-expressing progenitor cells emerges as a pivotal mechanism in bone fracture healing, shedding light on a potential therapeutic avenue to augment bone repair processes.

Sequential live imaging of abnormal skull bone fusion in zebrafish reveals a deeply conserved role of two transcription factors, Twist1 and Tcf12, in regulating stem cell activity during growth of the skull.

Hypertrophic chondrocytes of the growth plate undergo a process of dedifferentiation to generate marrow associated skeletal stem and progenitor cells (SSPCs), which ultimately re-differentiate into cells of the osteoblast or adipocyte lineages during skeletal development.

Cartilage cells transition through a proliferative intermediate to give rise to bone and marrow fat cells in long bones.

Short-term interventions, including intermittent fasting, boosting cellular energy, and promoting beneficial gut bacteria, rejuvenate osteoprogenitors in aged animals and, when combined with localized Wnt, restore youthful bone healing.