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Updated: Jun 18, 2026

A Rat Tibial Growth Plate Injury Model to Characterize Repair Mechanisms and Evaluate Growth Plate Regeneration Strategies
Published on: July 4, 2017
Prevention of growth arrest by fibrin interposition into physeal injury
Qiang Jie1, Yunyu Hu, Liu Yang
1Department of Orthopaedic Surgery, Xi-jing Hospital, Xi'an, China. jiqiang@fmmu.edu.cn
Abstract:
This study investigated the repair effects of fat and fibrin graft interposition through a proximal tibia transphyseal injury model and assessed the effectiveness of treatment to physeal injury with the fibrin. In this study, a unilateral growth plate injury was created in the right proximal tibia of 28 rats without any graft interposition; all left tibias were left untouched. In the other group of 28 rats, a bilateral physeal injury was made with the left tibia filled with autogenously adipose tissue and the right tibia filled with fibrin. To compare the malformed extents induced by different interventions, the length and the metaphyseal-diaphyseal angle of the tibia of three injured groups were examined. Further studies on bone density analysis and histological change were used to compare the bony bridge formation under different interventions. Results showed that the deformity angle and medial length of the tibia were significantly different between the grafted groups and nongrafted group at 4, 16, and 24 weeks postoperative (P<0.01). Results also showed no significant difference between fibrin-graft and fat-graft groups (P>0.05). Furthermore, the bone mineralization density of bony bridge induced by injury was significantly different between the grafted group and nongrafted group at 4, 16, and 24 weeks postoperative (P<0.01). Histological findings showed that bony repair after physeal injury was inhibited by both fibrin and fat interventions. We concluded that fibrin could be a substitute of adipose tissue in preventing the deformities induced by epiphyseal injury. Similar to autogenous fat, fibrin was found to alleviate limb shortness and prevent angular malformation by forming a scar instead of a bony bridge. The use of fibrin can help us to develop effective and compound intervention grafts to prevent skeletal deformity and regenerate normal cartilage tissue in the future.
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