Osteoarthritis (OA) is mainly caused by ageing, strain, trauma, and congenital joint abnormalities, resulting in articular cartilage degeneration. During the pathogenesis of OA, the changes in subchondral bone (SB) are not only secondary manifestations of OA, but also an active part of the disease, and are closely associated with the severity of OA. In different stages of OA, there were microstructural changes in SB. Osteocytes, osteoblasts, and osteoclasts in SB are important in the pathogenesis of OA. The signal transduction mechanism in SB is necessary to maintain the balance of a stable phenotype, extracellular matrix (ECM) synthesis, and bone remodelling between articular cartilage and SB. An imbalance in signal transduction can lead to reduced cartilage quality and SB thickening, which leads to the progression of OA. By understanding changes in SB in OA, researchers are exploring drugs that can regulate these changes, which will help to provide new ideas for the treatment of OA. Cite this article:
Minimally invasive (MIS) screw fixation for Hangman's fracture can decrease iatrogenic soft-tissue injury compared with conventional open approach, but increase the risk of instrumentation-related complications due to lack of anatomical landmarks. With the advantages, the intra-operative three-dimensional fluoroscopy-based navigation (ITFN) system seems to be an inherent partner for MIS techniques. The purpose of this study was to evaluate the accuracy and feasibility of MIS techniques incorporating with ITFN for treating Hangman's fracture. 20 patients with Hangman's fracture underwent C2-C3 pedicle screw fixation using ITFN. 6 patients used MIS technique, with the other 14 patients using conventional open technique. Preoperative visual analogue score (VAS) was 5.7±1.4 in CAOS-MIS group and 5.5±0.9 in CAOS-open group. Operative time, blood loss and postoperative neurovascular complications were recorded. The accuracy of screw positions was studied by postoperative CT scan. All patients were followed up for at least 6 months and the fusion status was ascertained by dynamic radiographs. The average operative time was 134.2±8.0 min in CAOS-MIS group and 139.3±25.8 min in CAOS-open group, and there was no significant difference between the two (p>0.01). The blood loss was 66.7±25.8 ml in CAOS-MIS group and 250.0±141.4 ml in CAOS-open group. Statistical difference existed with CAOS-MIS group significant less than CAOS-open group (p<0.01). A total of 80 screws were inserted. No screw-related neurovascular injury was observed. Post-operative CT scan revealed 83.3% (20/24) screws of grade 1 and 16.7% screws of grade 2 (4/24) in CAOS-MIS group, meanwhile 89.3% screws of grade 1 (50/56) and 10.7% screws of grade 2 (6/56) in CAOS-open group. There was no grade 3 screw detected. Fisher's exact test showed there was no statistical difference between these two groups (p>0.01). There was no statistical difference in pre-operative VAS between these two groups (p>0.01). Compared with the CAOS-open group (1.7±0.6), neck pain VAS at 6-month follow-up in CAOS-MIS group (0.3±0.5) was significantly lower (p<0.01). Solid fusion was demonstrated in all the cases by dynamic radiographs. So it is feasible and safe for percutaneous minimally invasive C2-C3 pedicle screw fixation for Hangman's fracture using intra-operative three-dimensional fluoroscopy-based navigation, which can also decrease the incidence of post-operative neck pain.
From the many human studies that attempt to identify genes for adolescent idiopathic scoliosis (AIS), the view emerging is that AIS is a complex genetic disorder with many predisposing genes exhibiting complex phenotypes through environmental interactions. Although advancements in genomic technology are transforming how we undertake genetic and genomic studies, only some success has been reached in deciphering complex diseases such as AIS. Moreover, the present challenge in AIS research is to understand the causative and correlative effects of discovered genetic perturbations. An important limitation to such investigations has been the absence of a method that can easily stratify patients with AIS. To overcome these challenges, we have developed a functional test that allows us to stratify patients with AIS into three functional subgroups, representing specific endophenotypes. Interestingly, in families with multiple cases of AIS, a specific endophenotype is shared among the affected family members, indicating that such a transmission is inherited. Moreover, increased vulnerability to AIS could be attributable to sustained exposure to osteopontin (OPN), a multifunctional cytokine that appears to be at the origin of the Gi-coupled receptor signalling dysfunction discovered in AIS. We examined the molecular expression profiles of patients with AIS and their response to OPN. Osteoblasts isolated from patients with AIS were selected for each functional subgroup and compared with osteoblasts obtained from healthy matched controls. We used the latest gene chip human genome array Affymetrix (HuU133 Plus 2.0 array) that allows for the analysis of the expression level of 38 000 well characterised human genes. Raw data were normalised with robust multiarray analysis method. Statistical analysis was done by the EB method with FlexArray software. Selection criteria for in-depth analysis include the magnitude of change in expression (at least □} 3-fold) and 5% false discovery rate as stringency selection. Validation of selected candidate genes was done by qPCR and at the protein level by Western blot and ELISA methods. Plasma OPN concentrations were measured by ELISA on a group of 683 consecutive patients with AIS and were compared with 262 healthy controls and 178 asymptomatic offspring, born from at least one scoliotic parent, and thus considered at risk of developing the disorder. The regulation of OPN signalling pathway in normal and AIS cells were validated in vitro by cellular dielectric spectroscopy (CDS).Introduction
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