It is shown that the absence of the centrosome protein ninein provokes premature ossification during mouse development, due to a defect in the fusion of precursor cells into syncytial osteoclasts.

Senescent cells accumulate in the fracture callus and a reduction in the number of these cells accelerates fracture healing in mice.

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

Membrane potential adjustment required for growth plate chondrocytic signal conversion from cGMP to Ca²⁺ influx toward long bone outgrowth.

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.

Proline is essential for osteoblast differentiation and bone formation by facilitating the production of proline-enriched osteoblast proteins.

Analysis of 3D reconstructions of chondrocrania of the Fgfrc^C342Y/+ Crouzon syndrome mouse show the direct effects of this Fgfr2 mutation on embryonic cranial cartilage formation and the indirect effects of chondrocranial morphology on cranial dermal bone development.

Discoidin domain receptor 2 controls craniofacial morphology by acting in skeletal progenitor cells and chondrocytes to control collagen matrix organization, chondrocyte polarity, and growth.

Osteoblasts utilize an elegant mechanism by which they obtain and subsequently synthesize the requisite amino acids to support osteoblast differentiation and bone formation.

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.