Isograft Derived from a Diabetic Rat Does Not Support Inferior Nerve Regeneration Compared to Isograft Obtained from a Healthy Rat
Mackenzie B Grasso, MD1, Moe Al Tekreeti, BS2, Elizabeth Zielinski, MD3, Geetanjali S Bendale, PhD2 and Jonathan Isaacs, MD4, 1Virginia Commonwealth University Health System, Richmond, VA, 2Virginia Commonwealth University, Richmond, VA, 3Summit Health, Berkeley Heights, NJ, 4Department of Orthopaedics, Virginia Commonwealth University, Richmond, VA
Introduction: Nerve injury that results in discontinuity but is not amenable to a primary tensionless end-to-end repair must be bridged using either nerve autograft, acellular nerve allograft (ANA), or conduits. Autologous nerve graft is considered the gold standard due to superior neurotrophic properties. There may be pathologic states in which peripheral nerve autograft loses this biologic advantage and ANA becomes a more appealing option. We sought an appropriate small animal model to test this theory and hypothesized that isograft obtained from a diabetic rat would be biologically compromised.
Methods: 10 inbred male ZDF rats (Obese Fa/Fa) from Charles River Laboratories genetically predisposed to have type 2 diabetes were maintained in a hyperglycemic state for 3 months to induce peripheral neuropathy. 10 inbred male ZDF rats (Lean) were utilized as a healthy control. A 15mm segment of sciatic nerve was harvested bilaterally from the compromised and control groups and was utilized to reconstruct a 15mm defect in lean rodents. 20 nerve reconstructions were performed for each arm. At 16 weeks post operatively, we performed motor testing using ADI Instruments Power Lab system and harvested the nerves for histologic analysis.
Results: There was no statistically significant difference in axonal counts between the compromised (mean 11902, SD 3729) and control groups (mean 10747, SD 3638). The average twitch force in the compromised donor group reached 82% (SD 33%) of the twitch force of the normal contralateral limb, compared to 67% (SD 28%) in the lean isograft group. Tetanic force in the compromised donor group reached 89% (SD 30%) normalized force compared to 74% (SD 29%) for the lean isograft group. Muscle mass and girth were 78% (SD 4%) and 79% (SD 12%) of the control in the gastrocnemius muscles for the compromised donor group, compared to 74% (SD 18%) and 78% (SD 11%) respectively for the lean group.
Conclusion: Isograft obtained from a diabetic donor rat did not demonstrate inferior nerve regeneration compared with “normal” isograft and would not be a suitable model to assess “compromised” donor nerve grafts.
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