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Skeletal Injury (skeletal + injury)
Selected AbstractsClinical study of cats injured and killed in road traffic accidents in CambridgeshireJOURNAL OF SMALL ANIMAL PRACTICE, Issue 8 2004I. Rochlitz Data were collected on the injuries, treatment and outcome of 128 cats involved in road accidents and seen as first-opinion cases in veterinary practices in Cambridgeshire. Sixteen cats were dead on arrival; the mortality rate for the remaining cats was 16 per cent. Half of the cats were aged between seven months and two years, with more males than females affected. Most cats had moderate injuries; strays had more severe injuries than owned cats. Areas of the body most often injured were the extremities, head and neck, pelvis and thorax. Skeletal injuries were present in 67 cats and neurological signs in 29. Diagnostic procedures and medical treatment were necessary for the majority of cats; surgery was required in 51 cases. Most cats were hospitalised for between two and seven days and some required up to one month of treatment. The cost of treatment was less than £400 for 84 per cent of cats. [source] rBMP represses Wnt signaling and influences skeletal progenitor cell fate specification during bone repairJOURNAL OF BONE AND MINERAL RESEARCH, Issue 6 2010Steve Minear Abstract Bone morphogenetic proteins (BMPs) participate in multiple stages of the fetal skeletogenic program from promoting cell condensation to regulating chondrogenesis and bone formation through endochondral ossification. Here, we show that these pleiotropic functions are recapitulated when recombinant BMPs are used to augment skeletal tissue repair. In addition to their well-documented ability to stimulate chondrogenesis in a skeletal injury, we show that recombinant BMPs (rBMPs) simultaneously suppress the differentiation of skeletal progenitor cells in the endosteum and bone marrow cavity to an osteoblast lineage. Both the prochondrogenic and antiosteogenic effects are achieved because rBMP inhibits endogenous ,-catenin-dependent Wnt signaling. In the injured periosteum, this repression of Wnt activity results in sox9 upregulation; consequently, cells in the injured periosteum adopt a chondrogenic fate. In the injured endosteum, rBMP also inhibits Wnt signaling, which results in the runx2 and collagen type I downregulation; consequently, cells in this region fail to differentiate into osteoblasts. In muscle surrounding the skeletal injury site, rBMP treatment induces Smad phosphorylation followed by exuberant cell proliferation, an increase in alkaline phosphatase activity, and chondrogenic differentiation. Thus different populations of adult skeletal progenitor cells interpret the same rBMP stimulus in unique ways, and these responses mirror the pleiotropic effects of BMPs during fetal skeletogenesis. These mechanistic insights may be particularly useful for optimizing the reparative potential of rBMPs while simultaneously minimizing their adverse outcomes. © 2010 American Society for Bone and Mineral Research [source] Stem cell-mediated accelerated bone healing observed with in vivo molecular and small animal imaging technologies in a model of skeletal injuryJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 3 2009Sheen-Woo Lee Abstract Adult stem cells are promising therapeutic reagents for skeletal regeneration. We hope to validate by molecular imaging technologies the in vivo life cycle of adipose-derived multipotent cells (ADMCs) in an animal model of skeletal injury. Primary ADMCs were lentivirally transfected with a fusion reporter gene and injected intravenously into mice with bone injury or sham operation. Bioluminescence imaging (BLI), [18F]FHBG (9-(fluoro-hydroxy-methyl-butyl-guanine)-micro-PET, [18F]Fluoride ion micro-PET and micro-CT were performed to monitor stem cells and their effect. Bioluminescence microscopy and immunohistochemistry were done for histological confirmation. BLI showed ADMC's traffic from the lungs then to the injury site. BLI microscopy and immunohistochemistry confirmed the ADMCs in the bone defect. Micro-CT measurements showed increased bone healing in the cell-injected group compared to the noninjected group at postoperative day 7 (p,<,0.05). Systemically administered ADMC's traffic to the site of skeletal injury and facilitate bone healing, as demonstrated by molecular and small animal imaging. Molecular imaging technologies can validate the usage of adult adipose tissue-derived multipotent cells to promote fracture healing. Imaging can in the future help establish therapeutic strategies including dosage and administration route. © 2008 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 27:295,302, 2009 [source] Locally delivered rhTGF-,2 enhances bone ingrowth and bone regeneration at local and remote sites of skeletal injuryJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 1 2001Dr. Sumner The purposes of the present study were to determine if recombinant human transforming growth factor-beta-2 (rhTGF-,2) enhances bone ingrowth into porous-coated implants and bone regeneration in gaps between the implant and surrounding host bone. The implants were placed bilaterally for four weeks in the proximal humeri of skeletally mature, adult male dogs in the presence of a 3-mm gap. In three treatment groups of animals, the test implant was treated with hydroxyapatite/tricalcium phosphate (HA/TCP) and rhTGF-,2 in buffer at a dose per implant of 1.2 ,g (n = 6), 12 ,g (n = 7), or 120 ,g (n = 7) and placed in the left humerus. In these same animals, an internal control implant treated only with HA/TCP and buffer was placed in the right humerus. In a non-TGF-, treated external control group of animals (n = 7), one implant was treated with HA/TCP while the contralateral implant was not treated with the ceramic. In vitro analyses showed that approximately 15% of the applied dose was released within 120 h with most of the release occurring in the first 24 h. The TGF-, treated implants had significantly more bone ingrowth than the controls with the greatest effect in the 12 ,g/implant group (a 2.2-fold increase over the paired internal control (P = 0.004) and a 4-fold increase over the external control (P < 0.001)). The TGF-, treated implants had significantly more bone formation in the gap than the controls with the greatest effect in the 12 and 120 ,g groups (1.8-fold increases over the paired internal controls (P = 0.003 and P = 0.012, respectively) and 2.8-fold increases over the external controls (P < 0.001 and P = 0.001, respectively)). Compared to the external controls, the internal control implants tended to have more bone ingrowth (1.9-fold increase, P = 0.066) and had significantly more bone formation in the gap (1.7-fold increase, P = 0.008). Thus, application of rhTGF-,2 to a porous-coated implant-stimulated local bone ingrowth and gap healing in a weakly dose-dependent manner and stimulated bone regeneration in the 3-mm gap surrounding the contralateral control implant, a site remote from the local treatment with the growth factor. © 2001 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved. [source] Popliteal artery injury: Royal Perth experience and literature reviewANZ JOURNAL OF SURGERY, Issue 10 2005Mazri M. Yahya Background: Popliteal artery injury is uncommon but poses a significant challenge in Australian trauma care. Blunt trauma and knee dislocations appear to be associated with higher amputation rates. The aim of the present study was to review the authors' experience with this condition and discuss the best approach to investigation and management. Methods: The medical records of all patients with popliteal artery injury (n = 19) who were entered prospectively onto the Royal Perth Hospital Trauma Registry from 1995 to 2003 were reviewed. Their demographic data, investigations, primary operative procedures, fasciotomy, primary and secondary amputation rates and mortality were determined. Results: There were 17 male and two female patients with a median age of 34 years (range 17,62 years). Most patients (84%) were under 40 years in age. Blunt trauma was the commonest cause of popliteal artery injury (68.4%), and 84.6% of the patients had associated skeletal injury. The amputation rate in the present study was 26.3% (5/19). There were no intraoperative or in-hospital deaths. Three of 13 patients (23%) with blunt trauma underwent amputation, compared to two of six (33.3%) with penetrating injury. Two of three amputee patients in the blunt trauma group had dislocated knees. Conclusion: Despite technical improvements in management of popliteal artery injury, a high amputation rate is still seen, especially in patients with one or more of the following factors: extensive soft-issue injury, associated skeletal trauma, knee dislocation, and prolonged ischaemia time. Measures to reduce the amputation rate, ranging from more prompt diagnosis to modified surgical treatment techniques, are discussed. [source] A role for ,/, T cells in a mouse model of fracture healingARTHRITIS & RHEUMATISM, Issue 6 2009Nona T. Colburn Objective Fractures can initiate an immune response that disturbs osteoblastic and osteoclastic cellular homeostasis through cytokine production and release. The aim of our study was to investigate ,/, T cells, innate lymphocytes known to be involved in tissue repair, as potential cellular components of the osteoimmune system's response to an in vivo model of bone injury. The absence of such cells or their effector cytokines influences the fate of other responder cells in proliferation, differentiation, matrix production, and ultimate callus formation. Methods Tibia fractures were created in 60 ,/, T cell,deficient mice (also called , T cell receptor [TCR],knockout mice) and 60 control C57BL/6 mice. Analysis included radiographs, basic histology, mechanical testing, flow cytometry, and immunohistochemical localization of ,/, TCR,positive subsets from control animals and of CD44 expression from both groups, as well as enzyme-linked immunosorbent assay for the effector cytokines interleukin-2 (IL-2), interferon-, (IFN,), and IL-6. Results Animals deficient in ,/, T cells demonstrated more mature histologic elements and quantitative increases in the expression of major bone (bone sialoprotein) and cartilage (type II collagen) matrix proteins and in the expression of bone morphogenetic protein 2 at a critical reparative phase. Moreover, only ,/, T cell,deficient animals had a decrease in the osteoprogenitor antiproliferative cytokines IL-6 and IFN, at the reparative phase. The result was improved stability at the repair site and an overall superior biomechanical strength in ,/, T cell,deficient mice compared with controls. Conclusion The evidence for a role of ,/, T cells in the context of skeletal injury demonstrates the importance of the immune system's effect on bone biology, which is relevant to the field of osteoimmunology, and offers a potential molecular platform from which to develop essential therapeutic strategies. [source] | ||||||||||