Objective Autogenic bone grafts have shown successful fusion rates in the treatment of degenerative lumbar disorders, but taking too many autogenic bones may result in donor site ischemia or infection. This study aimed to evaluate the outcomes of single‐level oblique lumbar interbody fusion (OLIF) using pure allograft combined with posterior pedicle screw instrumentation through the Wiltse approach. Methods A retrospective case analysis was performed on a series of consecutive patients who received a single‐level OLIF procedure combined with posterior pedicle screw instrumentation through the Wiltse approach between July 1, 2017, and December 31, 2019, in which pure allogenic bone graft was used and filled in the large window of the cage. The patients were followed up as scheduled at 1 day and 3, 6, 12, 24 months after operation. Clinical outcome was assessed by multiple questionnaires, including Oswestry disability index (ODI), Japanese Orthopaedic Association (JOA) score rating system, short form‐36 health survey (SF‐36), and visual analog scale (VAS) for low back pain. Radiographic outcome was evaluated by measuring the parameters such as disc height, lumbar lordosis, and segmental angle on the standard standing lateral radiographs, and the space angle of the fusion level on the dynamic views of the lateral radiographs. Subsidence of the cage and intervertebral fusion status were evaluated on both the radiographic and CT scan images. Results A total of 34 patients were finally included in this study. At 2‐year follow‐up, the VAS for low back pain, ODI, JOA, and SF‐36 scores all had significant improvement (p < 0.001). Substantial increase of anterior and posterior disc heights was observed (p < 0.001). Both lumbar lordosis and segmental angle became larger (p < 0.05). No visible change of the space angle of the fusion level was found on the dynamic views. The 1‐year fusion rate of 73.5% on CT scans proceeded to 82.4% at 2‐year follow‐up. The fusion rate was as high as 91.2% according to Bridwell interbody fusion grading system on radiographic images. The clinical outcomes in patients with incomplete fusion were just as good as those with complete fusion. The six patients with cage subsidence had higher ODI (p < 0.001) and lower JOA (p < 0.001) and SF‐36 PCS (p = 0.011) scores than those without cage subsidence. Conclusion The use of pure allograft in single‐level OLIF resulted in an acceptable fusion rate and satisfactory clinical effect at 2‐year follow‐up. Supplementation of posterior pedicle screw through the minimally invasive Wiltse approach ensured the favorable outcomes both clinically and radiographically.

Background. Abnormal Smad7 expression can lead to apoptosis in different cell types. Previously, we found high expression of Smad7 in rat degenerative discs. However, the exact role of Smad7 in the apoptosis of disc cells and the possible underlying mechanism remain unclear. Methods. Degenerative and nondegenerative human lumbar intervertebral discs were collected from patients during operation. The expressions of SMAD7 mRNA and protein in the different components of these discs were measured with real-time PCR and Western blotting, respectively. Annulus fibrosus (AF) cells were isolated and cultivated from the discs of young healthy rats. Smad7 in the AF cells was overexpressed with adenovirus and knocked down with siRNA. IL-1β was used to induce apoptosis in the AF cells. Loss-and-gain cell function experiments were performed to show the effect of Smad7 on the apoptosis of AF cells. The function recovery experiments were performed to verify whether Smad7 regulates the apoptosis of AF cells through the mitochondria-mediated pathway. Results. Both the mRNA and protein expressions of Smad7 were significantly higher in the different components of human degenerative discs than in those of the nondegenerative discs. IL-1β stimulated apoptosis while upregulating the Smad7 expression in the AF cells in vitro. Overexpression of Smad7 in AF cells exaggerated the IL-1β-induced apoptosis in the cells while knockdown of Smad7 expression suppressed this apoptosis. With the exaggerated apoptosis in the AF cells with Smad7 overexpression, both active cleaved caspase-3 and cleaved caspase-9, the ratio of Bax/Bcl-2, and Cyt-c increased significantly. However, the inhibitor of caspase-9, Z-LEHD-FMK, significantly diminished the apoptosis in these cells. Conclusion. Smad7 is highly expressed in human degenerative discs and participates in IL-1β-induced apoptosis of rat AF cells via the mitochondria pathway. Smad7 may be a potential target for the prevention and treatment of degenerative disc disease.

There have been an increasing number of patients with degenerative disc diseases due to the aging population. In light of this, studies on the pathogenesis of intervertebral disc degeneration have become a hot topic, and gene knockout mice have become a valuable tool in this field of research. With the development of science and technology, constitutive gene knockout mice can be constructed using homologous recombination, zinc finger nuclease, transcription activator‐like effector nuclease technology and clustered regularly interspaced short palindromic repeats/Cas9 (CRISPR/Cas9) system, and conditional gene knockout mice can be constructed using the Cre/LoxP system. The gene‐edited mice using these techniques have been widely used in the studies on disc degeneration. This paper reviews the development process and principles of these technologies, functions of the edited genes in disc degeneration, advantages, and disadvantages of different methods and possible targets of the specific Cre recombinase in intervertebral discs. Recommendations for the choice of suitable gene‐edited model mice are presented. At the same time, possible technological improvements in the future are also discussed.