Orthopaedic Department, Cedars-Sinai, 444 S San Vicente Blvd., Los Angeles, CA, USA.
Orthopedic Stem Cell Research Laboratory, Cedars-Sinai Medical Center, 127 S. San Vicente Blvd., A8308 Los Angeles, CA, USA.
Spine J. 2019 Jun;19(6):1085-1093. doi: 10.1016/j.spinee.2018.12.003. Epub 2018 Dec 7.
Some clinical reports suggest diabetes may have a negative effect on spinal fusion outcomes, although no conclusive experimental research has been conducted to investigate the causality, impact, and inherent risks of this growing patient population.
To analyze the hypothesis that type 2 diabetes (T2DM) inhibits the formation of a solid bony union after spinal fusion surgery by altering the local microenvironment at the fusion site through a reduction in growth factors critical for bone formation.
STUDY DESIGN/SETTING: In vivo rodent model of type 2 diabetes.
Twenty control (Sprague Dawley, SD) and 30 diabetic (Zucker Diabetic Sprague Dawley, ZDSD) rats underwent posterolateral and laminar fusion surgery using a tailbone autograft implanted onto the L4/L5 transverse processes. A subset of animals was sacrificed 1-week postsurgery for growth factor analysis. Remaining rats were sacrificed 3-month postsurgery for fusion evaluation via manual palpation, micro-CT, and histology.
There was no significant difference in the manual palpation fusion rate between ZDSD rats and SD control rats. Growth factor assay of fusion site explants at early sacrifice demonstrated PDGF was upregulated in the ZDSD rats. TGFB, IGF, and VEGF were not statistically different between groups. Bone mineral density as determined by micro-CT was significantly lower in ZDSD rats compared to SD controls and was a significant function of HbA1c.
Data generated in this in vivo rat model of T2DM demonstrate that the metabolic dysregulation associated with the diabetic condition negatively impacts the quality and density of the formed fusion mass. Increased measures of diabetic status, as determined by blood glucose and HbA1c, were correlated with decreased quality of formed fusion, highlighting the importance of diabetic status monitoring and regulation to bone health, particularly during bone healing.
T2DM rats demonstrated increased rates of infection, metabolic dysregulation, and a reduction in spinal fusion consolidation. Clinicians should consider these negative effects during preoperative care and treatment of this growing patient population.
一些临床报告表明，糖尿病可能对脊柱融合结果产生负面影响，尽管没有确凿的实验研究来调查这种不断增长的患者群体的因果关系、影响和固有风险。
通过分析 2 型糖尿病（T2DM）是否通过减少对骨形成至关重要的生长因子来改变融合部位的局部微环境，从而抑制脊柱融合手术后固体骨性融合的形成，从而验证假设。
研究设计/设置：2 型糖尿病的体内啮齿动物模型。
20 只对照（Sprague Dawley，SD）和 30 只糖尿病（Zucker Diabetic Sprague Dawley，ZDSD）大鼠接受尾骨自体移植物植入 L4/L5 横突的后路和层间融合手术。部分动物在手术后 1 周进行生长因子分析时被处死。其余大鼠在手术后 3 个月进行融合评估，通过手动触诊、微 CT 和组织学进行。
ZDSD 大鼠与 SD 对照大鼠的手动触诊融合率无显著差异。早期融合部位标本生长因子测定显示 PDGF 在 ZDSD 大鼠中上调。TGFB、IGF 和 VEGF 在组间无统计学差异。微 CT 测定的骨矿物质密度在 ZDSD 大鼠中明显低于 SD 对照大鼠，且与 HbA1c 显著相关。
在 2 型糖尿病的体内大鼠模型中生成的数据表明，与糖尿病状态相关的代谢失调会对形成的融合质量和密度产生负面影响。血糖和 HbA1c 确定的糖尿病状态增加与形成融合的质量降低相关，这突出了监测和调节糖尿病状态对骨骼健康的重要性，特别是在骨愈合期间。
T2DM 大鼠表现出更高的感染率、代谢失调和脊柱融合巩固减少。临床医生在进行术前护理和治疗这一不断增长的患者群体时，应考虑到这些负面影响。
