Long-Segment or Bone Cement-Augmented Short-Segment Fixation for Kummell Disease with Neurologic Deficits? A Comparative Cohort Study.

BACKGROUND: The standard treatment for Kummell disease with neurologic deficit remains controversial. Traditional posterior long-segment fixation (LSF) has been widely used, but the procedure results in significant trauma and carries the risk of multiple complications. Therefore, bone cement-augmented short-segment fixation (BCASSF) has been recommended for this condition. METHODS: The study included 36 patients treated with LSF or BCASSF between January 2012 and June 2015. The visual analog scale (VAS), Oswestry Disability Index (ODI) score, anterior height of fractured vertebrae, kyphotic Cobb angle, and neurologic function by the Frankel classification were evaluated and compared, and duration of operation, blood loss, length of hospital stay, and complications were recorded. RESULTS: Significant differences were observed in the VAS, ODI, anterior height of affected vertebrae, and kyphotic Cobb angle between preoperatively and 7 days postoperatively and between preoperatively and at the final follow-up, whereas no significant differences were observed between 7 days postoperatively and at final follow-up. No significant differences in the aforementioned parameters were observed between the groups at 7 days postoperatively and at the final follow-up. Neurologic function was improved in both groups; however, no significant differences were observed between the 2 groups either preoperatively or postoperatively. Blood loss and length of hospital stay were significantly lower in the BCASSF group compared with the LSF group, but no significant between-group differences were observed in operation time and complications. CONCLUSIONS: Lower blood loss and shorter hospital stay were associated with BCASSF compared with LSF; the 2 techniques had similar clinical outcomes and radiographic findings. Therefore, we recommend BCASSF for treating patients with Kummell disease with neurologic deficits.

[Clinical observation of axial offset after treatment by Ilizarov bone transport technology].

OBJECTIVE: To observe the incidence, causes and deviation angle of axial offset in patients with fracture ununited treated by Ilizarov bone transport technology. METHODS: From January 2007 to December 2012, 10 patients with fracture ununited were treated by Ilizarov bone transport including 8 males and 2 females with an average age of (30.3 ± 10.6) years old ranging from 18 to 49 years old. The segment of bone defect involved upper tibial in 2 cases, medial tibia in 2 cases, lower tibial in 5 cases, upper femoral in 1 case. For Paley type of bone defect, 6 cases were type B1, 4 cases were B3. The incidence and deviation angle of axial offset after Ilizarov bone transport technology were observed and evaluated on bone result by Paley assessment. RESULTS: All patients were followed up from 19 to 32 months with an average of (22.0 ± 5.6) months. Three cases were natural healed at fracture ends, the other 7 cases were healed after bone graft. The time of external fixator was 16 to 28 months. At the last follow-up, there were 3 cases occurred coronal angulation of angle 5° to 11° with an average of (8.7 ± 3.2). Sagittal angulation was in 4 cases, angle 6° to 9° with an average of (8.5 ± 2.1)°. There were 4 cases occurred axial offset. In the last follow-up, according to Paley evaluation criteria, osseous results were excellent in 7 cases, good in 3 cases; functional results were excellent in 6 cases, good in 4 cases. CONCLUSION: Axial deviation after the Ilizarov bone transport treatment is relatively common, which will result in delayed healing of bone and poor limb alignment. In order to improve the bone healing, corresponding measurements should be taken to avoid or reduce the incidence of axial deviation during and after the operation.

Asiatic acid inhibits adipogenic differentiation of bone marrow stromal cells.

Bone marrow mesenchymal stromal cells (BMSCs) are the common precursors for both osteoblasts and adipocytes. With aging, BMSC osteoblast differentiation decreases whereas BMSC differentiation into adipocytes increases, resulting in increased adipogenesis and bone loss. In the present study, we investigated the effect of asiatic acid (AA) on adipocytic differentiation of BMSCs. AA inhibited the adipogenic induction of lipid accumulation, activity of glycerol-3-phosphate dehydrogenase, and expression of marker genes in adipogenesis: peroxisome proliferation-activated receptor (PPAR)γ, adipocyte fatty acid-binding protein (ap) 2, and adipsin. Further, we found that AA did not alter clonal expansion rate and expression of C/EBPß, upstream key regulator of PPARγ, and binding activity of C/EBPß to PPARγ promoter was not affected by AA as well. These findings suggest that AA may modulate differentiation of BMSCs to cause a lineage shift away from the adipocytes, and inhibition of PPARγ by AA is through C/EBPß-independent mechanisms. Thus, AA could be a potential candidate for a novel drug against osteoporosis.

Inhibition of Nogo expression to promote repair after spinal cord injury.

BACKGROUND: One of the reasons for poor neuroregeneration after central nervous system injury is the presence of inhibitory factors such as Nogo. Here, we tested the inhibition of Nogo by RNA interference both in vitro and in vivo, using recombinant adenovirus-mediated transfection of short hairpin RNAs, to explore a new method of treatment for spinal cord injury. METHODS: We designed and cloned two Nogo-specific short hairpin RNAs and an unrelated short hairpin RNA, packaged the clones into adenovirus, and amplified the recombinant virus in 293 cells. We then tested the inhibition of Nogo expression both in vitro in adenovirus-transfected oligodendrocytes and in vivo in spinal cord tissue from adenovirus-transfected spinal cord injury model rats. We tested Nogo expression at the mRNA level by reverse-transcription PCR and at the protein level by Western blotting and immunohistochemistry. RESULTS: In vitro, the two specific Nogo short hairpin RNAs decreased Nogo mRNA expression by 51% and 49%, respectively, compared with Nogo expression in cells transfected with the unrelated control small hairpin RNA (P < 0.005). Similarly, Nogo protein expression decreased by 50% and 48%, respectively (P < 0.005). In vivo, in spinal cord injury model rats, the two specific Nogo short hairpin RNAs decreased Nogo mRNA expression by 45% and 40%, respectively, compared with Nogo expression in spinal cord injury model rats transfected with the unrelated control short hairpin RNA (P < 0.005). The Nogo protein level was similarly decreased. CONCLUSIONS: We were successful in specifically downregulating Nogo at the mRNA and protein levels by adenovirus-mediated delivery of short hairpin RNAs, both in vitro and in vivo. This confirms the effectiveness of RNA interference for the inhibition of Nogo gene expression and the efficiency of using adenovirus for delivery. Thus gene therapy may be an effective treatment for spinal cord injury.

Establishment and characterization of human osteosarcoma cell lines with different pulmonary metastatic potentials.

To develop an investigative tool for the study of human osteosarcoma (OSA), we established a human OSA cell line, namely, SOSP-9607, which exhibits a potential for spontaneous pulmonary metastasis. Subsequently, we screened two related sublines (F5M2 and F4) that have different pulmonary metastatic potentials. An in vivo orthotopic transplantation assay confirmed spontaneous pulmonary metastasis in all mice (100%) transplanted with the more aggressive OSA cells (F5M2) and a lesser degree of metastases with smaller nodules in 33.3% mice transplanted with the less aggressive OSA cell subline (F4). In mice transplanted with F5M2 cells, death from metastasis occurred at a median of 71 days; however, in mice transplanted with F4, no death occurred even after 120 days. Therefore, the F5M2 and F4 sublines, which originated from the same parent cell line, differed with respect to metastasis-related properties such as proliferating ability and invasiveness. Hence, these well-characterized human OSA sublines can be used as valuable models for comparative studies of genetic determinants of OSA in the future.

[Application of external skin expansion in repair of massive skin and soft tissue defects].

OBJECTIVE: To evaluate the clinical effect of external tissue expansion in the repair of massive skin and soft tissue defects. METHODS: From August 1998 to January 2004, 10 patients with massive skin and soft tissue defects ( the area ranging from 10 cm x 4 cm to 24 cm x 15 cm) , including 7 with wounds in the leg, 2 with wounds in knee region, and 1 with wounds in the forearm, were enrolled in the study. All patients were subjected to external tissue expansion together with external skeletal fixation for 2 -3 weeks, then the wounds were closed with suturing or supplemented with skin flaps. RESULTS: The defects were closed completely after external expansion in 4 cases, and in other 5 cases the wounds were significantly decreased in area, and the residual wounds were covered with free skin grafting. In I case the wound could only be reduced in size, and the residual wound was closed with a local flap. Follow-up from 1 to 12 months showed that the wounds were closed with normal cutaneous sensation and good appearance. CONCLUSION: External skin expansion is a simple, economical method for repair of massive skin soft-tissue defect, which can significantly be reduced or entirely closed.