Posterior Only Vertebral Column Resection for the Treatment of Severe Spinal Deformities in Pediatric Patients: A Retrospective Case Series.

OBJECTIVE: The treatment of severe spinal deformities in pediatric patients is very challenging. Posterior only vertebral column resection (PVCR) allows for correcting of severe deformities of the vertebral column via a posterior only procedure. We analyzed radiologic outcome of PVCR performed on a series of pediatric patients with severe congenital and acquired spinal deformities. METHODS: A case series of 11 pediatric patients with severe spinal deformity who were treated by PVCR between 2009 and 2013 were retrospectively analyzed. All patients had posterior instrumentation and reconstruction of the anterior column with titanium cages filled with autologous bone. Seven patients had pure kyphosis or kyphoscoliosis, whereas 4 patients were treated because of scoliotic deformities. The patient records were reviewed for demographic and general clinical data. Complications and adverse events, transfusion rates, and surgical time were recorded. Radiologic analysis included Cobb angles and percentage of correction, analysis of sagittal profile, time to fusion, and possible complications related to instrumentation. RESULTS: Average preoperative scoliosis of 61° was corrected to 32°, resulting in a 50% correction at final follow-up. Coronal imbalance was improved to 36% at the most recent follow-up. Mean preoperative kyphotic deformity was 90° and was corrected to 43° at the last follow-up evaluation. Intraoperative complications included loss of the neuromonitoring signals in 2 cases and pleural laceration in 1 case. CONCLUSIONS: PVCR for children is an effective and safe technique providing a successful correction of complex pediatric spinal deformities. Nevertheless, it remains a technically highly demanding procedure, implying the possibility of severe complications.

Interleukin-33 is expressed in differentiated osteoblasts and blocks osteoclast formation from bone marrow precursor cells.

Since the hematopoetic system is located within the bone marrow, it is not surprising that recent evidence has demonstrated the existence of molecular interactions between bone and immune cells. While interleukin 1 (IL-1) and IL-18, two cytokines of the IL-1 family, have been shown to regulate differentiation and activity of bone cells, the role of IL-33, another IL-1 family member, has not been addressed yet. Since we observed that the expression of IL-33 increases during osteoblast differentiation, we analyzed its possible influence on bone formation and observed that IL-33 did not affect matrix mineralization but enhanced the expression of Tnfsf11, the gene encoding RANKL. This finding led us to analyze the skeletal phenotype of Il1rl1-deficient mice, which lack the IL-33 receptor ST2. Unexpectedly, these mice displayed normal bone formation but increased bone resorption, thereby resulting in low trabecular bone mass. Since this finding suggested a negative influence of IL-33 on osteoclastogenesis, we next analyzed osteoclast differentiation from bone marrow precursor cells and observed that IL-33 completely abolished the generation of TRACP(+) multinucleated osteoclasts, even in the presence of RANKL and macrophage colony-stimulating factor (M-CSF). Although our molecular studies revealed that IL-33 treatment of bone marrow cells caused a shift toward other hematopoetic lineages, we further observed a direct negative influence of IL-33 on the osteoclastogenic differentiation of RAW264.7 macrophages, where IL-33 repressed the expression of Nfatc1, which encodes one of the key transciption factors of osteoclast differentiation. Taken together, these findings have uncovered a previously unknown function of IL-33 as an inhibitor of bone resorption.