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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.