Abstract

Introduction Biological treatment options, such as disk-cell-therapy, have been proposed for only moderately degenerated disks. Therefore, surgical exposition of the disk is needed. However, the effect of surgery related soft-tissue damage on the maintenance of disk degeneration is poorly understood. Therefore, this study analyzes, if disk degeneration can be induced only by the surgical approach. Materials and Methods We used an established model with adult minipigs offering biomechanical properties similar to humans. Total 12 animals underwent surgery using an anterolateral retroperitoneal approach to the lumbar spine. At each animal, two disks were only exposed whereas two other disks were exposed and partially nucleotomized with a 16G-biopsy-needle. Animals received a second revision surgery after 12 weeks, using the same approach and all disks were exposed again. Total 13 or 24 weeks after first surgery, animals were sacrificed. Disk height was measured in the central part of the disk by micro-CT. Disk degeneration was evaluated by a semiquantitative histo-degeneration-score. Three untreated control animals served as controls. Results After the second surgery, increased scar tissue and less vascularization was found around the lumbar vertebral bodies on the side of the approach. Most degenerative changes were found after partial nucleotomy ( p < 0.05) and additional annular damage was detectable, with a trend to higher degeneration scores after 24 weeks; disk height was significantly reduced compared to all other groups ( p < 0.05; 3.2 and 3.3 mm). Disks that were only surgically exposed also revealed significant degenerative changes including increased osteophytes; disk height was also significantly reduced compared to healthy control disks from animals without surgery ( p < 0.05; 3.7 and 3.8 mm vs. 4.6 mm). Conclusion Surgical exposure of lumbar disks caused significant disk degeneration without further disk manipulations. Reduced nutrient supply to the disk caused by less vascularized scar tissue seems to be a reason, which will be analyzed by additional immunohistological stainings against CD31. I confirm having declared any potential conflict of interest for all authors listed on this abstract Yes Disclosure of Interest None declared

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