: Tail disc percutaneous needle puncture is a simple method for inducing disc degeneration and the rate of degeneration is positively related to the depth of needle puncture. This model still has some limitations that should be taken into consideration when results of disc regeneration research in this model are interpreted and extrapolated to human.

Object The authors evaluated different surgical methods used to treat thoracic ossification of the ligamentum flavum (OLF). Methods Data obtained in 40 patients who underwent posterior decompression for thoracic myelopathy caused by thoracic OLF were studied retrospectively. There were 32 men and eight women. All patients underwent posterior decompression in which laminoplasty was performed or laminectomy combined with lateral fusion. Every surgical specimen was stained with H & E, and scanning electron microscopy was performed in 20 cases. The mean follow-up period was 28 months. Postoperative outcomes were evaluated using a recovery scale based on the Japanese Orthopaedic Association classification. There were a total of 168 ossified segments in this series, 77.4% of which were located in the lower thoracic spine. Marginal osteophyte formation was found in 36 patients; in 32 of the 36 patients, these marginal osteophytes were located at the intervertebral space either higher or lower than the ossified segment. Scanning electron microscopy showed elastic fiber breakdown, proliferation of collagenous fibers, calcification, and OLF in the same microscopy region. Laminoplasty was performed in four patients. In three cases surgery resulted in unchanged or worse outcome (increased kyphotic deformity in two), and in one it resulted in good outcome. Laminectomy combined with lateral fusion was performed in 36 patients, in 30 cases of which it resulted in a good or fair outcome, and increased kyphotic deformity in only one. Of these 36 laminectomy-treated patients, an en bloc laminectomy-treated procedure was performed in 16 patients; in 11 of the 12 patients with lateral or diffuse-type lesions the surgery resulted in a good or fair outcome. En bloc laminectomy, however, seems ineffective in the treatment of patients with thickened, nodular-type thoracic OLF, as the procedure resulted in worse outcome in two of the four patients. The authors have thus developed a new modality of laminectomy that they have termed “separating laminectomy,” which they performed in 16 patients with thickened, nodular-type OLF; in 13 cases it resulted in a good or fair outcome, and in only one case did it result in a worse outcome. Conclusions The pathogenesis of thoracic OLF is mainly due to the localized mechanical stress on the ligament. Laminectomy combined with lateral fusion is the treatment of choice for thoracic OLF; furthermore, in terms of the configuration of the ossified lesion, en bloc laminectomy is suitable for the treatment of lateral-type and diffuse-type OLF, and the separating laminectomy is suitable for the thickened, nodular-type OLF.

The aim of our study was to evaluate if Sirt6, a NAD + dependent histone deacetylase, plays a protective role in cartilage degeneration by suppressing cellular senescence and inflammatory responses. The expression level of sirt6 in normal and OA human knee articular cartilage was compared by immunofluorescence and western blotting. The effect of sirt6 overexpression on replicative senescence of chondrocytes and NF-κB target genes expression was evaluated. Histological assessment of OA mice knee joint was carried out to assess the in vivo effects of sirt6 overexpression on mice chondrocytes. We found sirt6 level was significantly decreased in the articular chondrocytes of OA patients compare to normal human. SA-β-gal staining revealed that overexpression of sirt6 suppressed replicative senescence of chondrocytes. Meanwhile, the expression of NF-κB dependent genes were significantly attenuated by sirt6 overxpression. Safranin-O staining and OARSI score of knee joint cartilage in OA mice revealed that Lenti-Sirt6 intraarticular injection could protect mice chondrocytes from degeneration. These data strongly suggest that overexpression of Sirt6 can prevent OA development by reducing both the inflammatory response and chondrocytes senescence. Therefore, the development of specific activators of Sirt6 may have therapeutic potential for the treatment of OA.

BackgroundHuman adipose-derived mesenchymal stem cells (ADMSCs) may be ideal source of cells for intervertebral disc (IVD) regeneration, but the harsh chemical microenvironment of IVD may significantly influence the biological and metabolic vitality of ADMSCs and impair their repair potential. This study aimed to investigate the viability, proliferation and the expression of main matrix proteins of ADMSCs in the chemical microenvironment of IVD under normal and degeneration conditions.MethodsADMSCs were harvested from young (aged 8-12 years, n = 6) and mature (aged 33-42 years, n = 6) male donors and cultured under standard condition and IVD-like conditions (low glucose, acidity, high osmolarity, and combined conditions) for 2 weeks. Cell viability was measured by annexin V-FITC and PI staining and cell proliferation was measured by MTT assay. The expression of aggrecan and collagen-I was detected by real-time quantitative polymerase chain reaction and Western blot analysis.ResultsIVD-like glucose condition slightly inhibited cell viability, but increased the expression of aggrecan. In contrast, IVD-like osmolarity, acidity and the combined conditions inhibited cell viability and proliferation and the expression of aggrecan and collagen-I. ADMSCs from young and mature donors exhibited similar responses to the chemical microenvironments of IVD.ConclusionIVD-like low glucose is a positive factor but IVD-like high osmolarity and low pH are deleterious factors that affect the survival and biological behaviors of ADMSCs. These findings may promote the translational research of ADMSCs in IVD regeneration for the treatment of low back pain.

Adolescent idiopathic scoliosis (AIS) is a structural deformity of the spine affecting millions of children. As a complex disease, the genetic aetiology of AIS remains obscure. Here we report the results of a four-stage genome-wide association study (GWAS) conducted in a sample of 4,317 AIS patients and 6,016 controls. Overall, we identify three new susceptibility loci at 1p36.32 near AJAP1 (rs241215, Pcombined=2.95 × 10−9), 2q36.1 between PAX3 and EPHA4 (rs13398147, Pcombined=7.59 × 10−13) and 18q21.33 near BCL-2 (rs4940576, Pcombined=2.22 × 10−12). In addition, we refine a previously reported region associated with AIS at 10q24.32 (rs678741, Pcombined=9.68 × 10−37), which suggests LBX1AS1, encoding an antisense transcript of LBX1, might be a functional variant of AIS. This is the first GWAS investigating genetic variants associated with AIS in Chinese population, and the findings provide new insight into the multiple aetiological mechanisms of AIS.