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Achondroplasia(ACH) is the most common form of dwarfism caused by activated mutations of FGFR3 gene.Gain-of-function mutation of FGFR3 in mice (FGFR3G369C/+ mice, ACH mice) resulted in delayed fracture healing by inhibiting chondrocyte differentiation and bone resorption.The expression of PTHrP in callus is lower in ACH.Researches have demonstrated that PTH1-34 preferentially enhanced chondrocyte recruitment the rate of chondrocyte maturation to stimulate endochondral ossification.In this study, we explored the effect of PTH1-34 on the delayed fracture healing resulting from ACH.