This work evaluated biomechanical deterioration and the related risk of ASD after OLIF fixed by PFS with different insertional screw positions (Fig. 2). An intact lumbosacral model and corresponding OLIF models were constructed, and biomechanical indicators closely related to ASD were computed and evaluated. The importance of the biomechanical environment for achieving positive postoperative clinical outcomes has been repeatedly demonstrated [2, 17, 48]. Thus, investigations on the biomechanical changes caused by different insertional screw positions and adjacent segments moment arms are of great significance for optimal operative strategy.
OLIF, rather than other LIF operations, has been selected for the following reasons. The percutaneous pedicle screw insertion was accomplished under C-arm fluoroscopy in OLIF, and the adjustment of insertion positions is feasible in this operation. By contrast, the selection of screw insertion positions in other lumbar fusion operations (e.g., transforaminal and posterior lumbar interbody fusion) was based on identifying anatomic structures [13, 14]. Considering the prevalence of anatomic variations and the hypertrophy of the articular process during the pathological process of spinal stenosis [50, 51], it’s difficult to accurately judge and adjust the exact insertional screw position under the freehand pedicle insertion process. Furthermore, for the same reason, the promotion of the optimized insertional screw positions elucidated by this study may also be limited in LIF fixed by percutaneous pedicle screw.
The deterioration of the biomechanical environment caused by inappropriate surgery may be continuously amplified and lead to a devastating prognosis [20, 22, 52]. Therefore, the optimization of a surgical technique based on a biomechanical in-silico study are of great significance. There are three common pathological changes of ASD, including disc degeneration, ZJ degenerative osteoarthritis and spinal stenosis, and segmental instability [20, 21]. Herein, mechanical indicators related to these pathological changes have been computed. In the disc degeneration process, the endplate calcification and the annulus tears are two common phenotypes in the lumbar spine [53, 54]. IVD is an avascular structure. Therefore, trans-cartilage endplate diffusion is the primary nutrition and metabolism pathway of IVD [53, 55, 56]. Aberrant increase of average strain energy density is a compensatory reaction to endplate stress concentration, and this change was proved to be a predictor of the calcium deposition and osteogenesis process [57, 58]. The resulting occlusion of IVD metabolism could accelerate disc degeneration [55, 56].
The annulus-driven phenotype is the most common reason for disc degeneration in the lower lumbar spine [54, 55]. Different kinds of stress concentration on the annulus, especially on the post and post-lateral parts of the annulus, were proved to be related to different types of annulus tears [37, 59]. Meanwhile, the aberrant increase of IDP could also increase the risk of annulus failure [31, 60]; therefore, annulus stress distribution and IDP are critical indicators in related mechanical studies [31, 59]. Simultaneously annulus tears and increased intradiscal pressure would promote disc herniation, a common type of ASD. The in-growth of blood vessels along annulus tears will promote locally the inflammatory response, leading to extracellular matrix catabolism and further disc degeneration [56, 61]. The in-growth of pain-sensing nerve fibers is also the primary reason for postoperative pain recurrence in ASD [61, 62].
It is worth noting that the pathological change in ASD was not limited to IVD. The degenerative osteoarthritis, hypertrophy of the articular process, and resulting spinal canal stenosis were also essential triggers for the recompression of nerve structures, symptoms recurrence, and revision surgery [47, 63]. In other words, ZJ degeneration should also be taken into consideration in studies related to ASD, and which can be well reflected by evaluating the change of FCF [2, 22, 31]. Additionally, as mentioned above, postoperative pathological motility compensation and resulting spinal instability is also a basic form of ASD [20, 47], which could be reflected by the variation of ROM and its proportion [6, 22, 52]. Therefore, ROM can be used as an indicator not only for model calibration and validation but also for assessing ASD’s risk. Moreover, close interactions were observed amongst different biomechanical indicators, and the interaction between segmental instability and spinal canal stenosis was also clearly elucidated. Reactive hyperplasia of the articular process and ligamentum structures caused by segmental instability was the main reason for spinal stenosis over a long period [50, 64]. In a word, by computing these biomechanical indicators, the risk of ASD could be investigated systematically.
Based on the current computational results, slight changes in stress concentration on the disc can be observed in cranial and caudal IVDs. Therefore, we can deduce that the tendency of disc degeneration acceleration may not be changed obviously with the change of moment arms (Fig. 6). By contrast, the fixation stiffness in the surgical segment and motility compensation in adjacent segments could be distinctly affected by the change of fixation length. It is worth noting that pronounced motility compensation can be recorded when the absolute value of the fixation length increased, and when the moment arm decreased is caused by the PFS shifts towards the measured side (Fig. 4). Meanwhile, although the range of variations is higher in the cranial than the caudal segment, the overall variation tendency of FCF is still consistent with which of the motility compensation (Fig. 5). Considering above mentioned interaction between segmental instability and spinal canal stenosis [50, 64], the optimization of insertional screw positions (i.e., reduce the fixation length) could optimize the biomechanical environment and reduce the risk of adjacent segmental instability in the short term and spinal stenosis in the long term.