Abstract
BACKGROUND: Although recognition of avascular necrosis of the vertebral body in post-traumatic cases has increased, it remains underdiagnosed and is one of the most unpredictable and challenging complications in spinal trauma. Vertebral arterial supply may play a key role in fracture healing, yet this remains unproven and is not currently considered in treatment algorithms. Surgical decisions between preserving or replacing the vertebral body in burst fractures are difficult, mainly due to limited knowledge of the biological factors influencing bone repair. This study aims to demonstrate the impact of vertebral vascular disruption on vertebral body fracture healing. We developed an experimental model in Wistar rats to replicate an L1 vertebral body fracture and analyze the normal healing sequence. Additionally, we examined the effects of disrupting the anterolateral blood supply on bone regeneration. METHODS: Seventy female Wistar rats were divided into two groups. Group 1 (n=35) underwent an L1 burst fracture induced by ultrasonic tools. Group 2 (n=35) received the same fracture, followed by electrocauterization of the anterolateral vertebral surfaces and placement of a synthetic barrier to prevent revascularization. Vertebral specimens were collected weekly for 6 weeks. Healing was assessed macroscopically and histologically using an image-processing algorithm trained to identify inflammatory, fibroblastic/cartilaginous, and bone tissue. The predominant tissue type was used to determine the healing stage. RESULTS: At week 1, the vascular disruption group showed significantly more inflammatory tissue (56.34%) than controls (24.25%, P=0.03), while fibroblastic/cartilaginous tissue was more common in controls (58.82% vs. 19.18%, P=0.03). By week 6, this tissue remained more prevalent in the intervention group (37.4%), while bone tissue predominated in controls (66.71% vs. 45.54%, P=0.009). Among animals already in the bone phase, trabecular structures were significantly more developed in controls (80% vs. 20%, P=0.031). Notably, all control animals reached the soft callus stage by week 1, whereas intervention animals only transitioned out of the inflammatory phase after the first week. Across all phases, progression was consistently faster in the control group, with statistical significance in the soft callus stage (P=0.002). CONCLUSIONS: Disruption of the anterolateral vascular supply significantly delays healing in L1 vertebral body fractures in rats, evidenced by slower phase transitions and reduced bone maturation. These findings underscore the essential role of vascularization in successful vertebral repair and suggest it should be considered in future therapeutic strategies.