Fracture healing is a complex process that involves several cell types; as a previous report suggested an increase in osteoblast (OB) precursors in peripheral blood during this process, this paper examines the role of circulating bone cell precursors in this process in the light of a prior suggestion that OB precursors are increased. Nine healthy men less than 60 years old with traumatic fractures were enrolled. The parameters circulating OB precursors (osteocalcin+/alkaline phosphatase+/CD15- cells) and osteoclast precursors (CD14+/CD11b+/vitronectin receptor + cells) were measured by flow cytometry; bone formation markers and TGFbeta1, by ELISA; and PTH, by RIA in serum on arrival at the emergency department (baseline) and 15 days after fracture. Bone cell precursors behaved differently during healing. TGFbeta1 was inversely correlated with OB number, but increased their degree of maturation at baseline. Bone formation markers and TGFbeta1 were increased after fracture, whereas PTH was decreased. The TGFbeta1 increase was directly correlated with age, whereas age was not correlated with the precursors. In conclusion, we confirm the role of TGFbeta1 in fracture healing; and its possible role in the control of pre-OB homeostasis. There was no variation in circulating precursor cells during healing, though the increase in TGFbeta1 may suggest increased pre-OB maturation and homing to the injured site.