• Fabrizio Russo, Luca Ambrosio, Kevin Ngo, Gianluca Vadalà, Vincenzo Denaro, Yong Fan, Gwendolyn Sowa, James D Kang, and Nam Vo.
• Department of Orthopaedic and Trauma Surgery, Campus Bio-Medico University of Rome, Rome, Italy.
• Spine. 2019 Sep 1; 44 (17): 1177-1185.

Study DesignAn experimental laboratory study.ObjectiveTo investigate the pathogenesis of intervertebral disc degeneration (IDD) in a murine model of type 1 diabetes mellitus (DM), namely nonobese diabetic (NOD) mouse.Summary Of Background DataIDD is a leading contributor of low back pain, which represents one of the most disabling symptoms within the adult population. DM is a chronic metabolic disease currently affecting one in 10 adults in the United States. It is associated with an increased risk of developing IDD, but the underlying process remains poorly understood.MethodsTotal disc glycosaminoglycan content, proteoglycan synthesis, aggrecan fragmentation, glucose transporter gene expression, and apoptosis were assessed in NOD mice and wild-type euglycemic control mice. Spinal structural and molecular changes were analyzed by micro-computed tomography, histological staining (Safranin-O and fast green), and quantitative immunofluorescence (anti-ADAMTS-4 and -5 antibodies).ResultsCompared with euglycemic controls, NOD mice showed increased disc apoptosis and matrix aggrecan fragmentation. Disc glycosaminoglycan content and histological features of NOD mice did not significantly differ from those of euglycemic littermates.ConclusionThese data demonstrate that DM may contribute to IDD by increasing aggrecan degradation and promoting cell apoptosis, which may represent early indicators of the involvement of DM in the pathogenesis of IDD.Level Of EvidenceN/A.

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