The purpose of this study was to investigate the survival and differentiation status of MSCs transplanted to ONFH. Traumatic ONFH was surgically produced in skeletally mature mongrel dogs. Osteonecrosis was treated with either saline (control) or autologous mesenchymal stem cells (MSCs) transplantation after decompression. Green fluorescent protein (GFP) was used to track the transplanted MSCs, the differentiation of MSCs were evaluated by fluorescent double-labeling with GFP between osteocalcin or von Willebrand factor (vWF) at 2nd, 8th, and 12th week after the transplantation. It was demonstrated that GFP-positive cells were present in the necrotic area up to 12 weeks after the transplantation, their number increased from 15% at 2nd week to 38% at 12th week (p < 0.05). Neither osteocalcin nor vWF was detected by immunocytochemistry in GFP-labeled MSCs in vitro, but osteocalcin was immunohistochemically positive in 90% of the GFP-labeled MSCs in vivo, while vWF was still negative. The vWF expression was of no significant difference between the control group and MSCs-transplanted group. The percentages of trabeculae bone volume were 9.36% and 8.42% at 2nd week (p > 0.05), 22.82% and 14.72% at 8th week, and 31.08% and 20.66% at 12th week (p < 0.05) in MSCs-transplanted group and control group, respectively; new trabeculae bone in MSCs-transplanted group was significantly increased as compared to that of control group at 8th and 12th week. The results demonstrated that the transplanted MSCs could survive, proliferate, and differentiate into osteoblasts directly, which contributed to the accelerated repair process. The possible mechanism is site-dependant differentiation. ß

We evaluated the efficacy of vascular endothelial growth factor 165 (VEGF₁₆₅) transgenic bone marrow mesenchymal stem cells (BMSCs) for the repair of early-stage osteonecrosis of the femoral head (ONFH) in mature mongrel dogs. This animal model was surgically established by femoral neck osteotomy and subsequent repinning. Twenty-seven dogs (54 hips) were divided into 3 equal-sized groups: a pCI-neo-VEGF₁₆₅ BMSC group, a pCI-neo BMSC group and a core decompression-alone group. The lipofectamine was used to introduce the VEGF₁₆₅ gene into the BMSCs. After core decompression, transgenic and non-transgenic autologous BMSCs were implanted. Therapeutic efficacy, including new bone formation and neovascularization in the femoral head, was examined by computed radiography, single-photon emission computed tomography, histological and histomorphometric analysis and immunofluorescent staining for von Willebrand factor in pathological sections. The femoral osteotomy site healed completely by the 4th week after the osteotomy surgery and regions of histologically evident osteonecrosis were found 12 weeks later. A regular arrangement of trabeculae and obvious bone regeneration were observed in the animals receiving implanted VEGF-transgenic BMSCs. The quantity of newly generated capillaries was significantly increased in the pCI-neo-VEGF₁₆₅ BMSC group, but there was no significant difference between the pCI-neo BMSC group and the core decompression-alone group. These results demonstrated that VEGF₁₆₅ transgenic autologous BMSCs enhanced bone reconstruction and blood vessel regeneration in the ONFH model. Compared with non-transgenic BMSCs, this approach could provide advanced benefits in the treatment of ONFH.

Results: 33 patients sustained type I, 18 type II, and 7 type III fractures. All patients were treated conservatively at first instance. The treatment included soft dressings with or without hard sole shoe in 21 patients with type I and 5 patients with type II fractures. 12 patients with type I, 13 patients with type II and all type III were treated with below knee plaster. The duration of immobilization was 3-6 weeks in type I and 6-12 weeks in type II and III fractures.All type I fractures healed at 3 months follow-up. 4 patients with type II and 2 patients with type III fractures had non-union even after prolonged immobilisation and one re-fracture occurred in type III fracture, which were successfully treated with cannulated screws. The average number of days absent from work was 26 days (7-51 days) in type I fractures and 78 days (28-213 days) in type II and III fractures. Conclusion: Fracture base of fifth metatarsal fractures are potential source of lost work productivity. Type II and III fractures are of particular risk with high incidence of non-union and re-fracture even after prolonged immobilization. We suggest that in active working individual with type II and III fractures should be treated primarily with cannulated screw or tension-band-wiring. This enables them to return to work earlier and prevent the incidence of non-union and re-fracture.Introduction: The management of periprosthetic fractures principally influenced by factors like nature of prosthesis in situ, type of fracture and quality of bone. Surgical treatment of these injuries includes either changing the prosthesis to a long stemmed implant or open reduction and internal fixation using various types of plates and screws, strut allografts alone or in combination with plates and circlage wires. The choice of implant is determined by fracture configuration, quality of bone and stem and or cement and bone interface. We present our experience in treating these fractures, using locking plates. Method: All patients who had undergone open reduction and internal fixation of periprosthetic fractures were identified from theatre records and a retrospective case note review was performed. Results: Six consecutive patients with periprosthetic fractures were treated with locking plates. There were one man and five women with a mean age of 71 years. The patients were assessed clinically and radio logically. We are presenting the outcomes of these cases including per operative and post-operative complications, fracture union, follow up and walking abilities. We achieved union and pre operative walking abilities in all of our cases. Discussion: These are technically challenging procedures, as fixation has to be achieved in the presence of preexisting implant, which significantly reduces surface area available for fixation, and poor quality of bone. Locking plates, with their unique qualities like uni cortical fixation, and more angular stability addressing these clinically challenging situations in an efficient manner. We were able to successfully prod...

BackgroundOur purpose was to investigate the clinical efficacy of arthroscope-assisted acromioclavicular ligament reconstruction in combination with double endobutton coracoclavicular ligament reconstruction for the treatment of complete acromioclavicular joint dislocation.MethodsDuring the period from February 2010 to October 2012, ten patients with Rockwood types IV and V acromioclavicular joint dislocation were hospitalized and nine were treated with acromioclavicular ligament reconstruction combined with double endobutton of coracoclavicular ligament reconstruction. The improvement in shoulder functions was assessed using a Constant score and visual analog scale (VAS) system.ResultsThe mean follow-up period was 33.6 ± 5.4 months. The mean Constant scores improved from 25.2 ± 6.6 preoperatively to 92.4 ± 6.5 postoperatively, while the mean VAS score decreased from 5.9 ± 1.4 to 1.2 ± 0.9; significant differences were observed. The final follow-up revealed that excellent outcomes were achieved in eight patients and good outcome in two patients.ConclusionArthroscope-assisted acromioclavicular ligament reconstruction in combination with double endobutton of coracoclavicular ligament reconstruction is an effective approach for treatment of acute complete acromioclavicular joint dislocation.

Serine/threonine kinase 39 (STK39) is associated with hypertension, autism, Parkinson's disease and various types of cancer in recent years. This study investigated STK39 expression and possible roles in osteosarcoma using qPCR and western blot analysis. Compared to normal bone tissues, the mRNA and protein expression of STK39 was found to be upregulated in osteosarcoma. Using small interfering RNA transfection, STK39 was knocked down into two cell lines of osteosarcoma, U2OS and MG63, and the effects exerted on cell functioning were examined. The results showed that STK39 downregulation inhibited ostesarcoma cell proliferation and invasion. Moreover, STK39 knockdown in osteosarcoma cells significantly affected the expression of proteins connected to cell proliferation (proliferating cell nuclear antigen and p21) and invasion [Twist1, matrix metalloproteinase (MMP)2 and MMP9]. Phosphorylation of Smad2/3 was reduced by STK39 knock down. In conclusion, our data provide evidence that STK39 was overexpressed in osteosarcoma. STK39 may serve as an oncogene by adjusting the proliferation and invasion of osteosarcoma cells.

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Long non-coding RNAs (lncRNA) CASC2 is a key player in cancer biology. Our new findings showed that both lncRNA CASC2 and IL-17 were up-regulated in plasma of osteoarthritis patients. Plasma levels of lncRNA CASC2 and IL-17 were significantly and positive correlated only in osteoarthritis patients. Overexpression of lncRNA CASC2 led to up-regulated expression of IL-17 in cells of human chondrocyte cell line CHON-001 (ATCC® CRL-2846™). In addition, overexpression of lncRNA CASC2 inhibited the proliferation, and promoted the apoptosis of chondrocyte. Therefore, lncRNA CASC2 is up-regulated in osteoarthritis and participates in the regulation of IL-17 expression and chondrocyte proliferation and apoptosis.

Intervertebral disc degeneration (IVDD) is a major health problem. Although mesenchymal stem cells (MSCs) have been used to promote IVD regeneration, the actual survival time of implanted MSCs in IVDs has never been studied noninvasively and continuously in vivo. To investigate survival of implanted MSCs in vivo, this study used a canine model of degenerated IVD and MSCs transfected with a mutant herpes simplex type-1 virus thymidine kinase and labeled with magnetic iron oxide nanoparticles (MION). One-stage positron emission tomography (PET) and magnetic resonance (MR) imaging were carried out 3 days and 2 weeks, 3 weeks, and 4 weeks after implantation of MSCs into IVDs with surgically induced degeneration. Pfirrmann disc degeneration grade determined from the MR images indicated that the repair progress of degenerated IVD stopped 3 weeks after MSC implantation. Meanwhile, MION signal strength, signal contrast ratio (%), and low signal area (mm) did not change significantly from that seen 3 days after cell implantation until 4 weeks [751.43 (4 weeks) ±52.67 (3 days) vs. 225.34 ± 35.62; 47.37 ± 5.01 vs. 85.37 ± 10.54; 1.78 ± 0.31 vs. 5.29 ± 1.35; P < 0.01, respectively]. Accumulation of the PET reporter probe, 9-(4-[F]-fluoro-3-hydroxymethylbutyl)-guanine, was dramatically decreased at 3 weeks after MSC implantation. These results demonstrated that MSCs could survive no more than 3 weeks after implantation into IVDs with surgically induced degeneration, suggesting that MSCs could contribute to IVD repair for the first 3 weeks after implantation. The results also indicate that PET imaging could be used reliably to quantify the survival of implanted MSCs, whereas MION with MR imaging would likely be unsuitable for long-term tracking of MSCs in IVDs.