PURPOSE: A series of electrophysiologic studies were performed in a canine model to evaluate inferior alveolar nerve (IAN) function during distraction osteogenesis of the mandible. MATERIALS AND METHODS: Fourteen dogs, including two controls, were used in the study. Twelve dogs underwent a 10-mm bilateral mandibular lengthening with an intraoral bone-borne appliance and midbody osteotomy. By using sensory nerve action potentials, IAN function was assessed before and immediately after surgery, before and at the completion of distraction, and before necropsy after 4, 6, or 8 weeks of fixation. RESULTS: Twelve of the 24 nerves showed a complete loss of evoked potential after surgery without recovery at any point throughout the study. Acute nerve injury caused by either the osteotomy or screw encroachment was identified at necropsy. The other 12 nerves showed reproducible responses after surgery. Eight of these nerves had significant amplitude attenuation of the evoked potentials, which was identified at necropsy as a result of acute injury. The remaining four nerves did not show significant evoked potential abnormalities and appeared to be grossly normal at necropsy. During distraction, the amplitude of evoked potentials in all 12 nerves remained at the postoperative level, whereas latency showed a significant delay. In 7 of these 12 nerves, various degrees of evoked potential recovery were identified at the completion of the study. CONCLUSIONS: The high incidence of acute IAN injury in the current study was primarily related to device construction and osteotomy technique. If acute nerve injury is avoided at surgery, distraction osteogenesis with 10 mm mandibular lengthening appears to produce minimal deleterious effect on IAN function.
PURPOSE: A series of electrophysiologic studies were performed in a canine model to evaluate inferior alveolar nerve (IAN) function during distraction osteogenesis of the mandible. MATERIALS AND METHODS: Fourteen dogs, including two controls, were used in the study. Twelve dogs underwent a 10-mm bilateral mandibular lengthening with an intraoral bone-borne appliance and midbody osteotomy. By using sensory nerve action potentials, IAN function was assessed before and immediately after surgery, before and at the completion of distraction, and before necropsy after 4, 6, or 8 weeks of fixation. RESULTS: Twelve of the 24 nerves showed a complete loss of evoked potential after surgery without recovery at any point throughout the study. Acute nerve injury caused by either the osteotomy or screw encroachment was identified at necropsy. The other 12 nerves showed reproducible responses after surgery. Eight of these nerves had significant amplitude attenuation of the evoked potentials, which was identified at necropsy as a result of acute injury. The remaining four nerves did not show significant evoked potential abnormalities and appeared to be grossly normal at necropsy. During distraction, the amplitude of evoked potentials in all 12 nerves remained at the postoperative level, whereas latency showed a significant delay. In 7 of these 12 nerves, various degrees of evoked potential recovery were identified at the completion of the study. CONCLUSIONS: The high incidence of acute IAN injury in the current study was primarily related to device construction and osteotomy technique. If acute nerve injury is avoided at surgery, distraction osteogenesis with 10 mm mandibular lengthening appears to produce minimal deleterious effect on IAN function.