金属破坏脊柱后外侧融合中的骨愈合:金属颗粒对融合完整性影响的体内模型。

The Iowa orthopaedic journal Pub Date : 2026-01-01
Jacob S Fisher, Mitchell C Coleman, Douglas Fredericks, Cale B Dobson, Madeline R Hines, Catherine Olinger
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引用次数: 0

摘要

背景:金属病是已知的关节置换术并发症,但其在脊柱融合术失败中的作用可能仍未得到充分认识。金属碎片从种植体界面释放可能通过引发局部炎症反应而损害成骨。到目前为止,还没有建立体内模型来研究脊柱融合术中的这一过程。使用一个独特的建模系统,我们试图确定高局部浓度的金属颗粒是否损害脊柱融合,以及颗粒负荷是否与炎症反应相关。方法:12只兔采用自体髂骨植骨行后外侧腰椎融合术。术后6周,动物在移植物背侧立即接受双侧椎旁注射高、低或零浓度的Ti/Cr/ Co合金。12周时,对标本实施安乐死,并通过x线摄影、手触诊和组织病理学评估移植物。使用自定义图像分析算法量化组织学切片中的金属碎片,并评估炎症反应。采用非配对t检验比较两组间融合结果和金属负荷。结果:8个可评估的标本中有5个未融合,在组织学分析中,大多数标本含有比融合标本更高水平的可见金属碎片。相比之下,融合移植物表现出最小的颗粒负担和连续的小梁桥接。淋巴细胞被发现定位在金属颗粒附近,纤维化组织被观察到在非融合部位取代骨。各组间炎症细胞计数无明显差异。结论:后外侧融合环境中金属颗粒负荷升高与成骨受损和局部炎症增加有关,特别是在未融合的标本中。这些结果确立了该模型在研究金属作用驱动的脊柱融合失败方面的实用性,并表明其作为评估脊柱内固定中颗粒相关风险的预测平台的潜力。临床意义:本研究提供了一个可重复的体内模型来探讨金属碎片如何导致脊柱融合失败。它为测试脊柱融合手术中金属相关并发症的未来干预措施提供了一个平台。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Metallosis Disrupts Bone Healing in Posterolateral Spinal Fusion: in Vivo Modeling of Metal Particle Effects on Fusion Integrity.

Background: Metallosis is a known complication of joint arthroplasty, but its role in failures of spinal fusion procedures likely remains underrecognized. The release of metallic debris from implant interfaces may impair osteogenesis by triggering local inflammatory responses. To date, no in vivo models have been developed to investigate this process in the context of spinal fusion. Using a unique modelling system, we sought to determine whether high local concentrations of metal particles impair spinal fusion, and whether particle load correlates with inflammatory response.

Methods: Twelve rabbits underwent posterolateral lumbar spinal fusion using autologous iliac crest bone grafts. Six weeks postoperatively, animals received bilateral paraspinal injections of Ti/Cr/ Co alloy at high, low, or zero concentrations immediately dorsal to the graft site. At twelve weeks, specimens were euthanized, and the grafts were assessed by radiography, manual palpation, and histopathology. A custom image analysis algorithm was used to quantify metal debris in histologic sections, and inflammatory responses were evaluated. Fusion outcomes and metal burden were compared between groups using unpaired t-tests.

Results: Five of eight evaluable specimens exhibited non-fusion, most of which contained higher levels of visible metal debris than fused counterparts upon histologic analysis. Fused grafts, in contrast, demonstrated minimal particle burden and continuous trabecular bridging. Lymphocytes were found to be localized near metal particles, and fibrotic tissue was observed to replace bone at non-fused sites. No significant differences in inflammatory cell counts were observed between groups.

Conclusion: Elevated metal particle burden in the posterolateral fusion environment was associated with impaired osteogenesis and increased localized inflammation, particularly in non-fused specimens. These results establish this model's utility for investigating metallosis-driven spinal fusion failure and suggest its potential as a predictive platform for assessing particle-related risk in spinal instrumentation.

Clinical relevance: This study provides a reproducible in vivo model to explore how metallic debris may contribute to spinal fusion failure. It offers a platform for testing future interventions targeting metallosis-related complications in spinal fusion surgery.

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