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Background: Multiple animal models have previously been utilized to investigate anterior fusion techniques, but a mouse model has yet to be developed. The purpose of this study was to develop murine anterior interbody and posterolateral fusion techniques., Methods: Mice underwent either anterior interbody or posterolateral spinal fusion. A protocol was developed for both procedures, including a description of the relevant anatomy. Samples were subjected to micro-computed tomography to assess fusion success and underwent biomechanical testing with use of 4-point bending. Lastly, samples were fixed and embedded for histologic evaluation., Results: Surgical techniques for anterior interbody and posterolateral fusion were developed. The fusion rate was 83.3% in the anterior interbody model and 100% in the posterolateral model. Compared with a control, the posterolateral model exhibited a greater elastic modulus. Histologic analysis demonstrated endochondral ossification between bridging segments, further confirming the fusion efficacy in both models., Conclusions: The murine anterior interbody and posterolateral fusion models are efficacious and provide an ideal platform for studying the molecular and cellular mechanisms mediating spinal fusion., Clinical Relevance: Given the extensive genetic tools available in murine disease models, use of fusion models such as ours can enable determination of the underlying genetic pathways involved in spinal fusion., Competing Interests: Disclosure: This study was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health (NIH) under award number T32-AR078751 (K.W.M.) and by NIH awards DP5OD021351 and R01AR075585 (M.B.G.). This study is also based on research supported by Pershing Square Sohn Cancer Research Alliance and Pershing Square Foundation MIND Prize awards to M.B.G. M.B.G. holds a Career Award for Medical Scientists from the Burroughs Welcome Fund. S.I. is supported by the Kellen Scholar Award. J.S. is supported by a Children’s Tumor Foundation Young Investigator Award (CTF-2023-01-005; https://doi.org/10.48105/CTF.CTF-2023-01-005.pc.gr.172007 ). A.R.Y. is supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health under award number T32-AR071302-07. S.B. is supported by a National Research Foundation of Korea award funded by the Ministry of Education (NRF-2021R1A6A3A14038667), the Arthritis Grant Program from the Arthritis National Research Foundation (1065843), and Weill Cornell Medicine JumpStart Awards (Year 2022). S.D. is supported by an NIH K99 grant (DE031819-01), a Department of Defense grant (W81XWH-22-PRMRP-DA), and Weill Cornell Medicine JumpStart Awards (Year 2019). The Disclosure of Potential Conflicts of Interest forms are provided with the online version of the article ( http://links.lww.com/JBJS/H833 )., (Copyright © 2024 by The Journal of Bone and Joint Surgery, Incorporated.)

Background: Identifying genetic risk factors for spinal disorders may lead to knowledge regarding underlying molecular mechanisms and the development of new treatments., Methods: Cases of lumbar spondylolisthesis, spinal stenosis, degenerative disc disease, and pseudarthrosis after spinal fusion were identified from the UK Biobank. Controls were patients without the diagnosis. Whole-genome regressions were used to test for genetic variants potentially implicated in the occurrence of each phenotype. External validation was performed in FinnGen., Results: A total of 389,413 participants were identified from the UK Biobank. A locus on chromosome 2 spanning GFPT1, NFU1, AAK1, and LOC124906020 was implicated in lumbar spondylolisthesis. Two loci on chromosomes 2 and 12 spanning genes GFPT1, NFU1, and PDE3A were implicated in spinal stenosis. Three loci on chromosomes 6, 10, and 15 spanning genes CHST3, LOC102723493, and SMAD3 were implicated in degenerative disc disease. Finally, 2 novel loci on chromosomes 5 and 9, with the latter corresponding to the LOC105376270 gene, were implicated in pseudarthrosis. Some of these variants associated with spinal stenosis and degenerative disc disease were also replicated in FinnGen., Conclusions: This study revealed nucleotide variations in select genetic loci that were potentially implicated in 4 different spinal pathologies, providing potential insights into the pathological mechanisms., Level of Evidence: Prognostic Level III. See Instructions for Authors for a complete description of levels of evidence., Competing Interests: Disclosure: The Disclosure of Potential Conflicts of Interest forms are provided with the online version of the article (http://links.lww.com/JBJS/H454)., (Copyright © 2023 by The Journal of Bone and Joint Surgery, Incorporated.)