World neurosurgery · 2023
Establishment of an Animal Model of Disk Degeneration by Intradiskal Injection of Monosodium Iodoacetate.
СтатьяНазвание и аннотация: Перевод в очереди
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Elmounedi Najah, Bahloul Walid, Guidara Ahmed Racem, Aoui Mourad, Trigui Moez, Keskes Hassib
Аннотация
BACKGROUND: Disk degeneration (DD) stands for the most common cause of low back pain. The establishment of an animal model plays an intrinsic role in the clarification of the physiopathology of DD. The purpose of this study is to select an optimal dose of monosodium iodoacetate (MIA) that may generate a reliable model of DD.
METHODS: Thirty-four rats were used in this study. The disks (Co7/8, Co8/9, and Co 9/10) received 1 shot of intradiskal injection of 0.02 mg, 0.1 mg, and 0.5 mg of MIA solution, respectively. Half of the rats were euthanized 3 weeks after MIA injection, and the other half 6 weeks after injection.
RESULTS: Magnetic resonance imaging evaluation showed that the mean T2-weighted signal intensity at 6 weeks decreased significantly in the 0.1 and 0.5 mg groups. The disk height of the control group was significantly higher than those of the 0.1 mg and 0.5 mg groups. Histologic and macroscopic results revealed time-and-dose-depending degeneration in the disks that received MIA. Additionally, MIA produced cell death in the nucleus pulposus cells with an elevated percentage. The injected disk with 0.1 mg MIA demonstrated a progressive degeneration, the disk injected with 0.5 mg MIA induced DD acutely 3 weeks post MIA injection, while the dose of 0.02 mg of MIA did not show much degeneration.
CONCLUSIONS: We concluded that 0.1 mg MIA is the most suitable dose to establish a model of DD, which enabled us to replicate the onset, progression, and outcome of diverse histopathologies of DD in the clinic.
METHODS: Thirty-four rats were used in this study. The disks (Co7/8, Co8/9, and Co 9/10) received 1 shot of intradiskal injection of 0.02 mg, 0.1 mg, and 0.5 mg of MIA solution, respectively. Half of the rats were euthanized 3 weeks after MIA injection, and the other half 6 weeks after injection.
RESULTS: Magnetic resonance imaging evaluation showed that the mean T2-weighted signal intensity at 6 weeks decreased significantly in the 0.1 and 0.5 mg groups. The disk height of the control group was significantly higher than those of the 0.1 mg and 0.5 mg groups. Histologic and macroscopic results revealed time-and-dose-depending degeneration in the disks that received MIA. Additionally, MIA produced cell death in the nucleus pulposus cells with an elevated percentage. The injected disk with 0.1 mg MIA demonstrated a progressive degeneration, the disk injected with 0.5 mg MIA induced DD acutely 3 weeks post MIA injection, while the dose of 0.02 mg of MIA did not show much degeneration.
CONCLUSIONS: We concluded that 0.1 mg MIA is the most suitable dose to establish a model of DD, which enabled us to replicate the onset, progression, and outcome of diverse histopathologies of DD in the clinic.