Pharmacological manipulation of early zebrafish skeletal development shows an important role for Smad9 in control of skeletal progenitor populations

Osteoporosis and other conditions associated with low bone density or quality are highly prevalent, increasing as the population ages increased glucocorticoid use to treat elevated inflammation. There is an unmet need for therapeutics which can target skeletal precursors induce osteoblast differentiation osteogenesis. Genes high mass represent interesting targets manipulation, they could offer ways increase density. A damaging mutation in SMAD9 has recently been mass. Here we show that Smad9 labels groups of osteochondral precursor cells, not labelled by Regulatory Smads: Smad1 Smad5. We Smad9+ cells proliferative, pocket expands following ablation induced regeneration. further treatment retinoic acid, prednisolone, dorsomorphin all alter expression, consistent effects these drugs on system. Taken together results demonstrate undifferentiated population, be manipulated commonly used drugs. conclude represents a future osteoanabolic therapies.