Objective   To investigate whether exogenous parathyroid hormone (PTH) can stimulate bone fracture healing.    Methods   Closed proximal tibia fracture was created and stabilized with an intramedullary pin in 60 2-month-old mice. The 50 surviving mice were randomly and equally divided into PTH treatment group and control group. Mice of different groups received a daily injection of PTH1-34 (80 μg/kg) or saline for 1 to 28 d post-fracture

and the concentration of serum calcium and phosphorus were measured and callus tissue properties was analyzed at 1

2 and 3 weeks post-fracture by radiography and histology. Total RNA was extracted from callus tissues

and the expression levels of bone formation-related genes were evaluated by real-time PCR.    Results   The serum calcium and phosphorus levels were not significant different between 2 groups. In 7 d post-fracture

cartilaginous callus areas were increased in PTH-treated mice compared with that of control mice. In contrast

in 14 d post-fracture

the remnant cartilaginous callus areas were smaller in PTH-treated mice than that in control mice. The remnant fibrous bone areas in marrow cavity were also reduced in PTH-treated mice compared to control mice in 21 d after fracture. In the early stages of fracture (3 to 7 d)

compared with the control group

the PCNA and IGF-1 mRNA expressions were obviously increased in PTH treatment group. In the middle and late (7  to 28 d) stages of fracture

compared with the control group

the Cbfa-1

Col-1

OCN

ALP mRNA expressions were significant increased in PTH treatment group.    Conclusion   These results indicate that exogenous PTH enhances bone fracture healing in terms of increasing callus areas

endochondral bone formation and osteoblastic bone formation

possibly through upregulating PCNA

IGF-1

Cbfa-1

Col-1

OCN

and ALP at different stage of the healing process.