RESUMEN
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.
Asunto(s)
Articulación Atlantoaxoidea/cirugía , Síndrome de Down/cirugía , Luxaciones Articulares/cirugía , Dispositivos de Fijación Ortopédica , Procedimientos Ortopédicos/instrumentación , Vértebras Cervicales/cirugía , Preescolar , Humanos , Imagenología Tridimensional , Imagen por Resonancia Magnética , Masculino , Tornillos Pediculares , Compresión de la Médula Espinal/cirugía , Fusión Vertebral/métodos , Cirugía Asistida por Computador , Tomografía Computarizada por Rayos XRESUMEN
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.