Magnesium degradation-induced variable fixation plates promote the vascularization of femoral fracture in rabbits.

BACKGROUND

Magnesium degradation-induced variable fixation plate (MVFP) has been shown to promote femoral fracture healing in rabbits. However, its potential to enhance angiogenesis at the fracture site and the underlying mechanisms require further investigation.

METHODS

A transverse fracture model was created in the right femur of adult male rabbits. The fracture was stabilized with a locking plate (LP), axial micromovement locking plate (AMLP), or MVFP. Angiogenesis around the fracture was assessed using arterial perfusion angiography, and osteoblasts and type H vessels were labeled with fluorescent double staining. RT-PCR and Western blotting were used to measure the expression of HIF1A, VEGFA, and ANG in the callus. Transcriptome analysis was performed to identify differentially expressed genes and their functional enrichment in each group.

RESULTS

Arterial perfusion angiography revealed the MVFP group had the highest arterial volume and volume fraction around the fracture site, though the mean arterial diameter was similar across all groups. Compared to the LP group, both the MVFP and AMLP groups exhibited more H-type vessels with osteoblasts clustered around them. RT-PCR and Western blotting showed that the MVFP group had the highest expression of HIF1A, VEGFA, and ANG. Transcriptome analysis identified significant differences between the MVFP and LP groups, with differentially expressed genes primarily enriched in the JAK-STAT and PI3K-Akt signaling pathways, both of which were upregulated in the MVFP group.

CONCLUSION

MVFP's variable fixation, which initially provides stability and then transitions to micro-motion, more effectively promotes angiogenesis at the fracture site compared to the rigid LP and AMLP fixation methods, facilitating fracture healing. MVFP may enhance angiogenesis through the JAK-STAT, VEGF, and PI3K-Akt signaling pathways.