Expression of bone matrix proteins during distraction osteogenesis of mouse tibia

objectives:To explore a mouse model for distraction osteogenesis and analyze the expression of bone matrix proteins and other related proteins during distraction osteogenesis.Methods:Thirty-six male CD-1mice,8weeks old,were used in the study.All animals received osteotomy and placement of the external fixa-tors on the left tibia.Distraction protocol included5days latency,12days distraction,and70days consolida-tion.Distraction rate was0.2mm/day.The animals were sacrificed at different time points postoperatively.The lengthened tibiae were harvested and distraction gaps were analyzed by histology,RT-PCR and in situ hy-bridization.Results:Histological analysis demonstrated that the healing process of osteotomic gap was similar to fracture repair in the latency.The distraction callus consisted of fibrous interzone,primary matrix front,and microcolumn formation during the distraction.In the early stage of consolidation the distraction gap was bridged by bony callus.The newly formed bone was remodeled and medullary canal formed by10weeks of the consolidation.mRNA analysis showed that endochondral ossification and intramembranous ossification oc-curred simultaneonsly in the early phase of distraction.The intramembranous ossification predominated the pro-cess of bone formation afterwards.Conclusion:By the analysis of bone matrix and other related proteins,it was suggested that distraction osteogenesis was different from fracture concrescence.Our data suggested that endochondral ossification and intramembranous ossification occurred simultaneously in the early stage of dis-traction osteogenesis.Under the mechanic stretching force,endochondral ossification has been inhibited and in-tramembranous ossification has become a predominant form of bone formation.Also,the study demonstrated that distraction osteogenesis of mouse tibia is similar to that of human and other animal models.It would be-come a useful model for studying bone regeneration and repair in vivo.