The impact of type 2 diabetes on bone metabolism and growth after spinal fusion

BACKGROUND CONTEXT: 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. PURPOSE: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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. (C) 2018 Elsevier Inc. All rights reserved.