C-arm Free O-arm Navigated Posterior Atlantoaxial Fixation in Down Syndrome: A Technical Note.

The surgical treatment of pediatric atlantoaxial subluxation (AAS) in Down syndrome (DS) remains technically challenging due to radiation exposure and complications such as vertebral artery injury and nonunion. The established treatment is fixation with a C1 lateral mass screw and C2 pedicle screw (modified Goel technique). However, this technique requires fluoroscopy for C1 screw insertion. To avoid exposing the operating team to radiation we present here a new C-arm free O-arm navigated surgical procedure for pediatric AAS in DS. A 5-year-old male DS patient had neck pain and unsteady gait. Radiograms showed AAS with an atlantodental interval of 10 mm, and irreducible subluxation on extension. CT scan showed Os odontoideum and AAS. MRI demonstrated spinal cord compression between the C1 posterior arch and odontoid process. We performed a C-arm free O-arm navigated modified Goel procedure with postoperative halo-vest immobilization. At oneyear follow-up, good neurological recovery and solid bone fusion were observed. The patient had no complications such as epidural hematoma, infection, or nerve or vessel injury. This novel procedure is a useful and safe technique that protects surgeons and staff from radiation risk.

MicroRNA­25­3p regulates human nucleus pulposus cell proliferation and apoptosis in intervertebral disc degeneration by targeting Bim.

Intervertebral disc degeneration (IDD) is a degenerative disease of the spine originating from the intervertebral disc. MicroRNAs (miRNAs or miRs) are a group of endogenous small non­coding RNAs that act on target genes and play a critical role in numerous biological processes. However, the underlying mechanism of miR­25­3p in IDD remains unclear. Therefore, the present study aimed to explore the role of miR­25­3p in the pathogenesis of IDD. The results demonstrated that miR­25­3p was downregulated in rat degenerative nucleus pulposus (NP) cells and that Bcl­2 interacting mediator of cell death (Bim) was a direct target of miR­25­3p. Next, to investigate the effect of miR­25­3p on normal NP cell proliferation and apoptosis, NP cells were transfected with an miR­25­3p inhibitor, a negative control of miR­25­3p inhibitor, miR­25­3p inhibitor + control­small interference RNA (siRNA) or miR­25­3p inhibitor + Bim­siRNA for 48 h and cell proliferation and apoptosis were then analyzed. The results demonstrated that the miR­25­3p inhibitor could decrease NP cell proliferation and induce cell apoptosis, and these effects were reversed by Bim­siRNA. In addition, an in vitro cell model of IDD was established by subjecting NP cells to 10 ng/ml interleukin (IL)­1ß for 24 h. Further experiments suggested that IL­1ß treatment induced a reduction in NP cell proliferation and an increase in cell apoptosis, which were prevented by the miR­25­3p mimic. All the effects of miR­25­3p mimic on IL­1ß­treated NP cells were significantly reversed by Bim upregulation. These findings suggested that miR­25­3p may be a novel therapeutic target for IDD prevention.