• Young-Hoon Kim, Genriech N Reoyan, Kee-Yong Ha, and Chul-Kyu Kim.
• Department of Orthopedic Surgery, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea.
• Spine. 2016 Nov 15; 41 (22): E1372E1378E1372-E1378.

Study DesignA case report and literature review.ObjectiveTo report a late dislocation of the vertebra caused by progressive dural ectasia combined with type-1 neurofibromatosis (NF-1) and the clinical results of pseudarthrosis repairs using autologous cultured osteoblasts.Summary Of Background DataNF-1 is a well-known genetic disorder that is commonly characterized by spinal deformities including kyphoscoliosis. Late dislocation of the vertebra resulting from progressive dural ectasia after surgical correction of NF-1 scoliosis is a very rare occurrence, and pseudarthrosis frequently develops after surgical intervention for this complex spinal deformity.MethodsA 32-year-old female patient with NF-1 scoliosis underwent surgical correction with posterior instrumented fusion. Seventeen years later, dislocation of the lumbar spine with implant failure resulting from massive progressive dural ectasia was observed. She underwent anterior interbody fusion three times and posterior instrumented fusion four times for pseudarthrosis followed by surgical deformity correction. For the last operation, autologous cultured osteoblasts were used as a therapeutic approach to repair the pseudarthrosis, and a three-dimensional printing technique was used to understand the surgical anatomy of the dislocated lumbar spine in detail.ResultsAfter the final operation, bone union was achieved and confirmed by clinical and radiological examination.ConclusionSpine surgeons should be knowledgeable about the possibility of late destabilization of the spine, due to pulsatile dural ectasia, and a high rate of pseudarthrosis in neurofibromatosis. Autologous cultured osteoblasts may prove to be a modality that can be applied pseudarthrosis repair to treat complex spinal deformity.Level Of Evidence5.

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