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Updated: Jun 21, 2025
Optical Sectioning and Visualization of the Intervertebral Disc from Embryonic Development to Degeneration
Published on: July 8, 2021
Intervertebral Disc Degeneration Induced by Vertebral Body Fracture Associated with Microcirculation Disruption of
Najah Elmounedi1, Olfa Jedli2, Walid Bahloul3
1Cell therapy and experimental surgery of musculoskeletal system LR18SP11 Lab, Faculty of Medicine, University of Sfax, Sfax, Tunisia.
Background:
Among the causes of the progression of intervertebral disc (IVD) degeneration (IDD) is the loss of nutrient intake to the IVD through the microcirculation disruption of the subendplate. Also, the vertebral body fracture intervenes in the degeneration the adjacent IVD. This research aimed to create an animal model of IDD using these 2 strategies.
Methods:
Thirty male Sprague-Dawley rats were split into 3 groups: a control group, a middle vertebral body injury (MI) associated with ethanol injection (MI + EtOH) group, and an MI associated with phosphate-buffered saline injection group. A vertebral body fracture with or without endplate injection of ethanol was generated by either drilling a hole in the center of a caudal rat vertebral body to form a fracture with an unabated endplate or drilling a hole in the center of a rat coccygeal vertebral body with endplate injection of ethanol to establish a vertebral body fracture with endplate damage. X-ray, macroscopic, histologic, and biochemical evaluations were utilized to assess IDD at weeks 3 and 6.
Results:
According to X-ray findings, the MI + EtOH group demonstrated a significant decrease in intervertebral space height over time in comparison to the 2 other groups. The water content also was significantly decreased. Macroscopic and histological analysis demonstrated progressive degenerative changes in the IVD of the MI + EtOH group.
Conclusions:
The caudal vertebra fracture with ethanol injection is more likely to induce degeneration of adjacent IVD. This model effectively reproduced IDD, which may serve as a theoretical basis for future clinical intervention for IDD.
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