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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.

Bone formation in adult mice can be induced by a bone-binding, recombinant version of the Notch ligand Delta-like 4 without triggering adverse effects in other organs.

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

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

A novel secondary adipogenesis pathway is defined that is unique to the bone marrow and is activated with age and in states of metabolic stress.

In vitro and in vivo studies highlight the dual regulatory effects that 7,8-dihydroxyflavone exerts on bone formation and resorption.

Parathyroid hormone attenuates osteoarthritis pain and joint degeneration by modification of subchondral bone remodeling and could be a potential disease-modifying therapy for osteoarthritis.

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

CD107a expression divides osteogenic from adipogenic perivascular precursor cells within human white adipose tissue.

Osterix, a transcription factor regulating osteoblast differentiation and bone formation, is expressed in subsets of CAFs with osteogenic features and marks tumor infiltrating immune populations enriched in immune suppressive markers.