• Tingkui Wu, Hong Wang, Kangkang Huang, Junbo He, Chunyi Yan, Chen Ding, Beiyu Wang, and Hao Liu.
• Department of Orthopedics, West China Hospital of Sichuan University, 37 Guoxue Alley, Wuhou District, Chengdu, 610041, Sichuan Province, China.
• Eur Spine J. 2024 Jul 20.

PurposeCervical disc arthroplasty (CDA) is widely employed for patients diagnosed with cervical degenerative disc disease (CDDD). Postoperative bone loss (BL) represents a radiological alteration that is a relatively novel consideration in the realm of CDA. This study endeavors to examine the risk factors associated with BL following CDA, aiming to elucidate the underlying mechanisms and the impact of BL on surgical outcomes.MethodsA retrospective study was undertaken, encompassing consecutive patients subjected to one-level CDA, two-level CDA, or two-level hybrid surgery (HS) for the treatment of CDDD at our institution. Patient demographic and perioperative data were systematically recorded. Radiological images obtained preoperatively, at 1-week post-operation, and during the last follow-up were collected and evaluated, following with statistical analyses.ResultsA total of 295 patients and 351 arthroplasty segments were involved in this study. Univariate logistic regressions indicated that age ≥ 45 years and two-level HS was associated with lower risk of BL; and a greater ΔDA (change of disc angle before and after surgery) was correlated with an increased risk of BL. Multivariate logistic regression determined that two-level HS and greater ΔDA were independent preventative and risk factors for BL, respectively. Further analysis revealed that severe BL significantly elevated the risk of implant subsidence compared to non-BL and mild BL.ConclusionsThis study posited bone remodeling and micromotion as potential underlying mechanisms of BL. Subsequent research endeavors should delve into the divergent mechanisms and progression observed between lower- and higher-grade BL, aiming to prevent potential adverse outcomes associated with severe BL.© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.

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