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Hip arthroscopy is an effective method for the diagnosis and treatment of hip joint pathologies. However, gaining access to the central and peripheral compartments is challenging. The present study aimed to assess the advantages of using an arthroscopic extra-capsular approach and partial capsulotomy for access and subsequent management of hip diseases. Patients subjected to hip arthroscopy by partial capsulotomy for exposure and treatment of hip diseases between February 2012 and February 2016 were retrospectively analyzed. A total of 32 patients, including 19 males and 13 females, aged 19-48 years (median age, 36 years), had undergone the procedure. Firstly, the distal anterior lateral and anterolateral arthroscopic approach with blunt dissection was performed. Subsequently, a T-shaped partial capsulotomy was established to achieve adequate exposure. The shaver, radiofrequency probe and tissue penetrating suture grasper were then inserted to perform procedures including debridement of the synovium, suturing of the glenoid labrum. During surgery, a probe hook was used to push the capsule section limbs or pull the sutures placed on the capsule section limbs to improve exposure. For patients with pre-operative anterior instability, ligamentous laxity or acetabular dysplasia capsules were sutured to finish capsule closure. The pre-operative and post-operative Visual Analogue Scale (VAS) score and modified Harris hip score (MHHS) were used to assess the effectiveness of the procedure. No obvious post-operative complications were encountered. The mean follow-up time was 22.4 months (range, 18-32 months) and 31 patients completed the follow-up, while 1 patient was lost to follow-up. Compared with the pre-operative score, the MHHS was significantly increased (66.2±6.0 vs. 82.6±5.2; P

The beneficial effects of combined use of mesenchymal stem cells (MSCs) and endothelial progenitor cells (EPCs) on tissue repair and regeneration after injury have been demonstrated, but the underlying mechanism remains incompletely understood. This study aimed to investigate the effects of direct contact coculture of human bone marrow‐derived EPCs (hEPCs)/human bone marrow‐derived MSCs (hMSCs) on their proliferation and angiogenic capacities and the underlying mechanism. hEPCs and hMSCs were cocultured in a 2D mixed monolayer or a 3D transwell membrane cell‐to‐cell coculture system. Cell proliferation was determined by Cell Counting Kit‐8. Angiogenic capacity was evaluated by in vitro angiogenesis assay. Platelet‐derived growth factor‐BB (PDGF‐BB), PDGF receptor neutralizing antibody (AB‐PDGFR), and DAPT (a γ‐secretase inhibitor) were used to investigate PDGF and Notch signaling. Cell proliferation was significantly enhanced by hEPCs/hMSCs 3D‐coculture and PDGF‐BB treatment, but inhibited by AB‐PDGFR. Expression of cyclin D1, PDGFR, Notch1, and Hes1 was markedly enhanced by PDGF‐BB but inhibited by DAPT. In vitro angiogenesis assay showed that hEPCs/hMSCs coculture and PDGF‐BB significantly enhanced angiogenic capacity, whereas AB‐PDGFR significantly reduced the angiogenic capacity. PDGF‐BB increased the expression of kinase insert domain receptor (KDR, an endothelial marker) and activated Notch1 signaling in cocultured cells, while DAPT attenuated the promoting effect of PDGF‐BB on KDR expression of hEPCs/hMSCs coculture. hEPCs/hMSCs coculture enhanced their proliferation and angiogenic capacities. PDGF and Notch signaling pathways participated in the promoting effects of hEPCs/hMSCs coculture, and there was crosstalk between these two signaling pathways. Our findings should aid understanding of the mechanism of beneficial effects of hEPCs/hMSCs coculture.

Background. To assess the clinical outcomes of central tendon-splitting approach and double row anchor suturing for the treatment of insertional Achilles tendinopathy. Methods. 28 patients (28 feet) diagnosed with insertional Achilles tendinopathy were included in this study. The inclusions were symptom of hindfoot pain around the insertion of the Achilles tendon, radiographic demonstration of calcification, or degeneration of the Achilles tendon, showing no symptom improvement even after standard nonsurgical treatment for more than six months. The X-ray revealed that patients had obvious posterior superior calcaneal exostosis with the possibility of friction with the Achilles tendon or intratendinous calcification. Surgical correction by the central tendon-splitting approach and double row Achilles tendon suturing was performed. The ankles were immobilized with plaster for four weeks postoperatively. The American Orthopaedic Foot and Ankle Society (AOFAS) score and visual analogue score (VAS) were assessed preoperatively and at 2 years postoperatively. At final follow-up, the Manchester-Oxford Foot Questionnaire (MOXFQ) as patient-reported outcome measures (PROMs) was also evaluated. Results. No complication, including postoperative wound infection and tendon rupture, was not found. All the patients resumed their daily activities with no high level of daily activities, such as jumping and jogging after 6 weeks postoperatively. 27 patients were available for follow-up for at least 2 years, while only one patient was lost to follow-up. At postoperative 2 years, the postoperative AOFAS score increased significantly, while the VAS score decreased statistically when compared with preoperative values. At final follow-up, 24 patients had complete alleviation of pain, whereas the remaining 3 patients complained of mild heel pain after walking for a long time. The MOXFQ score showed obvious relief of previous symptoms for all included cases. Conclusions. Central tendon-splitting approach and double row Achilles tendon suture provide excellent intraoperative visual field, larger tendon-bone contact area, and stronger pullout strength and, thus, facilitate early rehabilitation. It can be a safe and effective method for the treatment of insertional Achilles tendinopathy.

The present study aimed to evaluate the effect of tissue inhibitor of metalloproteinase-1 (TIMP-1) on the proliferation and osteogenic differentiation potential of human bone marrow-derived MSCs (hBMSCs). hBMSCs with stable TIMP-1 overexpression or TIMP-1 knockdown were generated. Osteogenic differentiation was assessed by Alizarin Red S staining, alkaline phosphatase (ALP) activity and expression of specific markers. Compared with the vehicle controls, TIMP-1 knockdown significantly promoted the growth of hBMSCs. TIMP-1 knockdown up-regulated β-catenin and cyclin D1 proteins. During osteogenic differentiation, TIMP-1 knockdown elevated the deposition of calcium nodules, ALP activity and the mRNA levels of the osteogenic markers sex determining region Y-box 9 (Sox9), CCAAT-enhancer-binding protein and peroxisome proliferator-activated receptor γ. During osteogenic differentiation, TIMP-1 knockdown significantly enhanced the up-regulation of osteocalcin proteins. Meanwhile, TIMP-1 overexpression attenuated the Wnt/activator Wnt3a-induced up-regulation cyclin D1 and Runt-related transcription factor 2 (RUNX-2) (during osteogenic differentiation) proteins, while TIMP-1 knockdown restored the inhibitor Dickkopf 1-induced inhibition effect on the expression of β-catenin, cyclin D1 and RUNX-2. TIMP-1 plays a negative regulatory role in the proliferation and osteogenesis of hBMSCs, at least partially, through Wnt/β-catenin signaling.

Interferon regulatory transcription factor 1 (IRF-1) regulates downstream signals of tumor necrosis factor α (TNF-α). The activity of IRF-1 is mediated by Jak/Stat signaling pathway. In this study, we found that PPAR γ coactivator-1α (PGC-1α) is able to suppress the induction of IRF-1. Treatment with TNF-α in MC3T3 cells leads to a sustainable increase in the expression of IRF-1 and its target gene cyclooxygenase 2 (COX-2). In contrast, TNF-α treatment led to a sustainable reduction in expression of PGC-1α. Interestingly, we found that overexpression of PGC-1α attenuated the induction of IRF-1 and COX-2. However, silence of PGC-1α exacerbated the induction of IRF-1 and COX-2. Importantly, we found that the effect of PGC-1α on repressing IRF-1 expression and activity is facilitated by the reduction in phosphorylation of STAT1 at position 727 (S727P), an essential transcriptional activator of IRF-1. Finally, we found that calyculin A, a pharmacological inhibitor of protein phosphatase 2A (PP2A) and PP1 abolishes the repression of STAT1 phosphorylation mediated by PGC-1α, suggesting a new mechanism of PGC-1α in regulating STAT1/IRF-1 pathway.

The ability of mesenchymal stem cells (MSCs) to differentiate into osteogenic lineages requires management for their future use in treating bone destruction and osteoporosis. Hepcidin is closely associated with bone metabolism, however, it remains to be elucidated whether hepcidin affects osteogenic differentiation in MSCs. The present study demonstrated that hepcidin enhanced osteoblastic differentiation and mineralization, which was manifested by an upregulation in the differentiation markers alkaline phosphatase and osteogenic genes. Furthermore, the expression levels of bone morphogenetic proteins and small mothers against decapentaplegic homologs were concomitantly increased following hepcidin treatment. In addition, the p38 mitogen-activated protein kinase may be an upstream kinase for osteoblastic differentiation. Thus, hepcidin may be important in the osteogenic differentiation of MSCs and may be considered as a target in the development of therapies for pathological bone loss.

Interferon regulatory transcription factor 1 (IRF-1) regulates downstream signals of tumor necrosis factor α (TNF-α). The activity of IRF-1 is mediated by Jak/Stat signaling pathway. In this study, we found that PPAR γ coactivator-1α (PGC-1α) is able to suppress the induction of IRF-1. Treatment with TNF-α in MC3T3 cells leads to a sustainable increase in the expression of IRF-1 and its target gene cyclooxygenase 2 (COX-2). In contrast, TNF-α treatment led to a sustainable reduction in expression of PGC-1α. Interestingly, we found that overexpression of PGC-1α attenuated the induction of IRF-1 and COX-2. However, silence of PGC-1α exacerbated the induction of IRF-1 and COX-2. Importantly, we found that the effect of PGC-1α on repressing IRF-1 expression and activity is facilitated by the reduction in phosphorylation of STAT1 at position 727 (S727P), an essential transcriptional activator of IRF-1. Finally, we found that calyculin A, a pharmacological inhibitor of protein phosphatase 2A (PP2A) and PP1 abolishes the repression of STAT1 phosphorylation mediated by PGC-1α, suggesting a new mechanism of PGC-1α in regulating STAT1/IRF-1 pathway.

Osteosarcoma is a common malignant tumor, which exists widely in the bone of children and adolescents. Protein kinase C gamma (PRKCG) gene, which encodes γPKC, plays important roles in tumor promotion, cell proliferation, differentiation, and migration. The objective of the present study was to investigate the relationship between PRKCG polymorphisms and the risk of osteosarcoma. Five tag single nucleotide polymorphisms (SNPs) of PRKCG were retrieved from the HapMap database and genotyped by the method of SNapShot in a hospital-based study containing 388 patients and 388 healthy individuals. Odds ratios (ORs) and their 95 % confidence intervals (CIs) were used to evaluate the association SPSS 20.0 statistical software package was used to analyze statistical data. Our results suggested that the T/C variant of rs454006 located in the intron 3 region of PRKCG gene was significantly associated with an increased risk of osteosarcoma (CC vs. TT, OR = 1.91; 95 % CI 1.29-2.85; P = 0.001; CC vs. TT+TC, OR = 2.14, 95 % CI = 1.48-3.09, P = 0.001; C vs. T, OR = 1.32, 95 % CI = 1.08-1.62, P = 0.008). Similarly, the rs3745406 T/C variant can also elevate the risk of osteosarcoma in the dominant model (OR = 1.45, 95 % CI = 1.08-1.96, P = 0.014), homozygous model (OR = 1.68, 95 % CI = 1.10-2.59, P = 0.002), and allelic model (OR = 1.31, 95 % CI = 1.07-1.61, P = 0.009). However, there were no significant differences in genotypes and allele frequencies of rs2547362 (T>C), rs8103851 (C>G), and rs2242245 (T>C) SNPs between osteosarcoma patients and healthy controls. The results showed that carrier of rs454006*C allele and rs3745406*C might elevate the risk of osteosarcoma. Further studies are needed to validate the coalition between PRKCG gene polymorphisms and risk of osteosarcoma relying on a larger population that included the participants in different ethnicity and hospital.

Although success of digital replantations in children has been reported by many authors, the very distal fingertip replantation remains technically demanding. The aim of this article is to review our experience with fingertip replantations at or distal to the nail base in pediatric patients and evaluate the clinical outcomes. From October 2000 to May 2007, 12 pediatric fingertips amputated at or distal to the nail base were replanted. Only one artery was anastomosed for revascularization with or without nerve repair; vein drainage was provided by the controlled bleeding technique. Eleven of the 12 replants (91%) survived; one replant of crushed digit failed. An average of 26 month (range, 6 to 36 months) follow-up revealed excellent restoration of finger motion and appearance. The regained static 2-point discrimination (S2PD) sensation was from 3.2 to 5.0 mm (mean, 4.2 mm). Both the parents and the children were satisfied with the final results. In conclusion, fingertip replantation in children allows good functional and esthetical recovery and should be attempted if technically feasible.

To evaluate the feasibility and the value of the layered cylindric collagen-hydroxyapatite composite as a scaffold for the cartilage tissue engineering after an observation of how it absorbs the chondrocytes and affects the cell behaviors.The chondrocytes were isolated and multiplied in vitro, and then the chondrocytes were seeded onto the porous collagen/hydroxyapatite composite scaffold and were cultured in a three-dimensional environment for 3 weeks. The effects of the composite scaffold on the cell adhesivity, proliferation, morphological changes, and synthesis of the extracellular matrix were observed by the phase-contrast microscopy, histology, scanning electron microscopy, and immunohistochemistry.The pore diameter of the upper layer of the collagen-hydroxyapatite composite scaffold was about 147 microm, and the porosity was 89%; the pore diameter of the bottom layer was about 85 microm and the porosity was 85%. The layered cylindric collagen-hydroxyapatite composite scaffold had good hydrophilia. The chondrocytes that adhered to the surface of the scaffold, proliferated and migrated into the scaffold after 24 hours. The chondrocytes attached to the wall of the microholes of the scaffold maintained a rounded morphology and could secrete the extracellular matrix on the porous scaffold.The layered cylindric collagen-hydroxyapatite composite scaffold has a good cellular compatibility, and it is stronger in the mechanical property than the pure collagen. It will be an ideal scaffold for the cartilage tissue engineering.

To develop a novel porous three-dimensional scaffold and to investigate its physico-chemical properties for tissue engineering cartilage.Refined 88% deacetylation degree chitosan was prepared and dissolved in 0.2 mol/L acetate acid and fully mixed with highly purified porcine type II collagen in 0.5 mol/L acetate acid solution in a ratio of 4 to 1 (wt/wt). Freeze-drying process was employed to fabricate the composite scaffold. The construct was cross-linked by use of 1-ethyl-3-(3-dimethyl aminopropyl) carbodiimide (EDC) and N-hydroxysuccinimide (NHS). A mechanical tester was utilized to determine the tensile strength change before and after cross-linking. The microstructure was observed via scanning electron microscopy (SEM). The lysozyme degradation was performed to evaluate the degradability of the scaffold in vitro.A bulk scaffold with desired configuration was obtained. The mechanical test showed that the cross-linking treatment could enhance the mechanical strength of the scaffold. The SEM results revealed that the two constituents evenly distributed in the scaffold and that the matrix was porous, sponge-like with interconnected pore sizing 100-250 microm. In vitro lysozyme degradation indicated that cross-linked or uncross-linked composite scaffolds had faster degradation rate than the chitosan matrix.Chitosan and type II collagen can be developed into a porous three-dimensional scaffold. The related physico-chemical tests suggest that the composite scaffold meets requirements for tissue engineered scaffold and may serve as an alternative cell-carrier for tissue engineering cartilage.