To test hypothsis that chemokine CCR7 would play crucial roles in physeal cartilage regeneration, we investigated the role of CCR7 in the repair process after physeal injury in mice.
Growth plate (GP) injury was made in the left proximal tibial GP in 3-week-old C57BL/6 mice (WT) and CCR7 knockout mice (KO) . Proximal tibial GP was entirely pierced with a 25-G needle. Right tibial GPs were sham operated with skin incision only. 3 and 5 weeks postoperatively, length of tibiae was measured macroscopically and height of proximal tibial GP were measured by micro-CT. The tibia shortening ratio (drop-ratio) was defined as percentage that the tibial length difference between sham operated and operated tibia divided by the length of sham operated tibia. Growth plate height ratio was defined as the growth plate length of the operated tibia divided by that of the sham operated tibia. Bone volume of the physeal bridge at the injury site and bone mineral density (BMD) of the subchondral area were measured using micro-CT. All results were statistically compared using unpaired t-tests to evaluate differences between pairs of groups. Significance was accepted with a p value < 0.05.
3 and 5 weeks postoperatively, drop ratio of tibial length and bone volume of physeal bridge in KO mice was significantly lower than those in WT mice (Fig. 1, 2). Growth plate height ratio in KO mice was significantly higher than those in WT mice at both 3 and 5 weeks (Fig. 2). In contrast, BMD of subchondral area were almost same between KO and WT mice, and between sham and operated tibia at either 3 or 5 weeks.
Depletion of CCR7 in mice inhibited physeal bridge formation and ameliorated growth imbalance after physeal injury. These results suggested that CCR7 might have important roles in physeal bridge formation.