Academic literature on the topic 'Articular cartilage – Surgery'

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Journal articles on the topic "Articular cartilage – Surgery"

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Gong, Huchen, Yutao Men, Xiuping Yang, Xiaoming Li, and Chunqiu Zhang. "Experimental Study on Creep Characteristics of Microdefect Articular Cartilages in the Damaged Early Stage." Journal of Healthcare Engineering 2019 (November 13, 2019): 1–9. http://dx.doi.org/10.1155/2019/8526436.

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Traumatic joint injury is known to cause cartilage deterioration and osteoarthritis. In order to study the mechanical mechanism of damage evolution on articular cartilage, taking the fresh porcine articular cartilage as the experimental samples, the creep experiments of the intact cartilages and the cartilages with different depth defect were carried out by using the noncontact digital image correlation technology. And then, the creep constitutive equations of cartilages were established. The results showed that the creep curves of different layers changed exponentially and were not coincident for the cartilage sample. The defect affected the strain values of the creep curves. The creep behavior of cartilage was dependent on defect depth. The deeper the defect was, the larger the strain value was. The built three-parameter viscoelastic constitutive equation had a good correlation with the experimental results and could predict the creep performance of the articular cartilage. The creep values of the microdefective cartilage in the damaged early stage were different from the diseased articular cartilage. These findings pointed out that defect could accelerate the damage of cartilage. It was helpful to study the mechanical mechanism of damage evolution.
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Weitzel, Paul P. "Complications of Articular Cartilage Surgery." Sports Medicine and Arthroscopy Review 12, no. 3 (September 2004): 160–66. http://dx.doi.org/10.1097/01.jsa.0000131857.12698.65.

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Erggelet, Christoph, and Matthias Steinwachs. "Articular cartilage regeneration techniques." Current Opinion in Orthopedics 10, no. 6 (December 1999): 452–57. http://dx.doi.org/10.1097/00001433-199912000-00006.

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Ulrich-Vinther, Michael, Michael D. Maloney, Edward M. Schwarz, Randy Rosier, and Regis J. OʼKeefe. "Articular Cartilage Biology." Journal of the American Academy of Orthopaedic Surgeons 11, no. 6 (November 2003): 421–30. http://dx.doi.org/10.5435/00124635-200311000-00006.

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Trice, Michael E. "Articular cartilage surgery for the athlete." Current Orthopaedic Practice 19, no. 3 (May 2008): 299–307. http://dx.doi.org/10.1097/bco.0b013e32830349b5.

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Rosenberg, Lawrence C. "Articular Cartilage Lesions." Journal of Bone & Joint Surgery 87, no. 4 (April 2005): 921–22. http://dx.doi.org/10.2106/00004623-200504000-00033.

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Dziak, Rosemary. "Articular cartilage and osteoarthritis." Bone and Mineral 19, no. 1 (October 1992): 99–100. http://dx.doi.org/10.1016/0169-6009(92)90848-8.

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Sah, Robert L., David Amiel, and Richard D. Coutts. "Tissue engineering of articular cartilage." Current Opinion in Orthopaedics 6, no. 6 (December 1995): 52–60. http://dx.doi.org/10.1097/00001433-199512000-00011.

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Vogt, Stephan, and Andreas B. Imhoff. "Injuries to the Articular Cartilage." European Journal of Trauma 32, no. 4 (August 2006): 325–31. http://dx.doi.org/10.1007/s00068-006-6096-z.

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Karpie, John C., and Constance R. Chu. "Imaging of Articular Cartilage." Operative Techniques in Orthopaedics 16, no. 4 (October 2006): 279–85. http://dx.doi.org/10.1053/j.oto.2006.09.005.

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Dissertations / Theses on the topic "Articular cartilage – Surgery"

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Brockmeier, Peter Macy. "Surgical Navigation for Articular Cartilage Repair: Motivation, Development, and Validation." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1250219405.

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Benaroch, Thierry Ezer. "Biosynthetic response of young and adult human articular cartilage to growth factors." Thesis, McGill University, 1990. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=59530.

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Adult articular cartilage of many species including humans has a limited capacity for repair following injury. The hypothesis that this might be related to a lack of responsiveness to growth factors involved in growth was investigated. Cartilage explants from 4 child and 5 adult human donors were cultured in the presence of various growth factors. Incorporation of $ sp{35}$SO$ sb4$ into proteoglycans and $ sp3$H-thymidine into deoxyribonucleic acid used as measures of the biosynthetic response of cartilage.
Young cartilage showed the ability to behave in an autocrine or paracrine manner to stimulate its basal biosynthetic rate. Immature chondrocytes respond well to somatomedin C (insulin-like growth factor, IGF-I) and insulin but there was no significant stimulation in old cartilage. This data suggests a specific loss of responsiveness to IGF-I in mature cartilage. However, adult cartilage was stimulated by IGF-I and insulin after prolonged incubation times. Adult cartilage could also be stimulated by the addition of fetal calf serum and to some degree by platelet derived growth factor, indicating that adult chondrocytes still have the capacity to respond to external stimuli. The relevance of these results is discussed.
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Esa, Adam. "Characterising the role of articular cartilage progenitor cells in osteoarthritis." Thesis, Cardiff University, 2015. http://orca.cf.ac.uk/90195/.

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Osteoarthritis (OA) is a chronic and highly prevalent degenerative disease of the synovial joint leading to cartilage destruction and bone remodelling. The current management of end-stage OA is joint replacement, however, this procedure is not suitable for a subset of patients hence there is a growing need for alternative treatments and technologies to address this limitation. One such approach to this problem is the application of cell-based therapies that regenerate areas of damaged cartilage. Recently discovered articular cartilage progenitor cells (CPC) have been hallmarked as a potential cell source for repair and/or regeneration of damaged articular cartilage. Initial focus was on the characterisation of human CPC isolated from healthy donors and compared with OA derived CPC and patient matched OA Bone Marrow Mesenchymal Stem Cells (BM-MSCs). Comparison of all cell types showed similar morphology and proliferative capacity. In addition, all cell types isolated showed positive expression of the putative mesenchymal stem cell makers; CD-90, CD-105 and CD-166 while lacking expression of CD-34. All cell types investigated showed successful osteogenic, chondrogenic and adipogenic differentiation, hence providing evidence of the mesenchymal stem cell properties of isolated CPC. A gene profiler array was used to identify the expression of Wnt pathway genes from RNA isolated from CPC cell lines originating from healthy and OA cartilage. Interestingly, the expression of Dkk-1 was observed to have the highest up-regulation in OA-derived CPC. The role of Dkk-1 was further studied in a number of CPC and chondrocyte cell lines from healthy and OA cartilage. It was found that normal CPC cell lines showed homogenously low expression and secretion of Dkk-1, however, OA-derived CPC cell lines exhibited a heterogeneous expression and secretion of Dkk-1. In a pellet culture model of chondrogenic differentiation, CPC cell lines secreting high levels of Dkk-1 failed to undergo chondrogenic differentiation, measured by diminished expression of chondrogenic differentiation markers, Type II collagen, ACAN and Sox-9 at both molecular and protein levels. Immunolocalisation of Dkk-1 in OA osteochondral plugs showed peri-cellular expression in chondrocytes located in all zones and around migratory endothelial cells invading articular cartilage where there was a quantifiable increase of blood vessel invasion. This later observation was further studied through a series of experiments to investigate the role of Dkk-1 in relation to endothelial cell migration and angiogenesis using an in vitro model of angiogenesis and migration/invasion assays. A novel finding emerged from these studies, which provides evidence for a pro-angiogenic and pro-migratory role of Dkk-1 and to a lesser extent Dkk-2 in human endothelial cell lines. A novel in vitro Transwell co-culture model was developed to study the interaction between chondrocytes and endothelial cells mimicking the osteochondral interface. A novel finding from these studies included the observation that normal or OA-derived chondrocytes appeared to induce an endothelial to mesenchymal transformation (EndMT) of the co-culture endothelial cells. This was assessed by a loss of the endothelial cobble stone morphology and a down-regulation of key factors implicated in endothelial cell phenotype, including VE-cadherin, Tie-2, e-NOS, PDGF-AA and PECAM-1. As endothelial cells lost their phenotype they adopted a spindle morphology and expressed mesenchymal cell markers including: Lumican, Snail, α-SMA, Vimentin and MMPs. Interestingly, this was also associated with an increase in Dkk-1 expression. To confirm a role for Dkk-1 in this process endothelial cells were cultured in the presence of Dkk-1 and were found to undergo EndMT when compared to the control. In summary, this thesis has uncovered several interesting differences in CPC phenotype. In addition, my results suggest that Dkk-1 has potential as a biomarker of OA pathology. This thesis highlights further the complex role of the Wnt Pathway and in particular Dkk-1 may play a role in the pathogenesis of osteoarthritis.
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Silva, Anderson Coutinho da. "Estudo da osteoartrose em joelhos de cães secundária à ruptura do ligamento cruzado cranial." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/5/5145/tde-09062009-165130/.

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INTRODUÇÃO e OBJETIVO: A osteoartrite (OA) embora frequente tem patogênese incerta em humanos. Descrevemos modelo experimental original de OA em cães, analisando em dois tempos diferentes as consequências da Ruptura Espontânea do Ligamento Cruzado Cranial (RLCCr). MÉTODOS: Vinte animais machos com menos de 5 anos ( 20 a 45 Kg) com RLCCr submetidos à artrotomia para estabilização articular tiveram fragmentos articulares removidos para análise. O grupo RLCCr < 20 (10 animais) foi operado antes dos vinte dias e o grupo > 20 (10 animais) após 20 dias do início da lesão. Sete animais com OA pré-existente (OA) que morreram por quaisquer motivos e 7 animais normais (NC) provenientes do C.C.Z., serviram de grupos controles. Os animais foram avaliados clinica e radiologicamente. Foi colhido líquido sinovial dos animais operados e de outros 20 cães controles submetidos às cirurgias por diferentes causas. Para estudo morfológico, os fragmentos de cartilagens foram corados com H&E e Picrossirius. A gravidade do escore histológico da OA foi quantificada através da coloração com Safranina O. Analisou-se citocinas próinflamatórias (IL-6, TNF-alfa) e a quimiocina CCL2/MCP-1 nos líquidos sinoviais. RESULTADOS: Todos os cães tinham o teste de movimento da gaveta e exame de compressão da mesa tibial positivos. Achados radiográficos correlacionaram-se com maior tempo de RLCCr. Cartilagem articular de animais normais (NC) exibiram superfície preservada, disposição ordenada dos condrócitos e integridade da rede de colágeno. Exames histológicos em animais do grupo RLCCr < 20 mostraram irregularidades na superfície articular, diminuição no número de condrócitos e remodelamento de fibras de colágeno. No grupo > 20, observou-se osteófitos e irregularidades evidentes nas superfícies articulares. A gravidade do escore de acometimento histológico traduziu-se por intensa diminuição celular na superfície articular, com presença de clusters de condrócitos na região intermediária da cartilagem e total desorganização da rede de fibras de colágeno. A quimiocina CCL2/MCP-1 esteve aumentada no grupo com menos de 20 dias de lesão, enquanto a IL-6 foi mais expressiva nos animais operados tardiamente. CONCLUSÃO: O modelo experimental espontâneo de OA canino, estudado em dois tempos, é um instrumento original e útil para estudo da patogênese da osteoartrite, além de ter o mérito de preservar a integridade física dos animais de laboratório
INTRODUCTION and OBJECTIVE: Osteoarthritis (OA) is a frequent and severe rheumatic disease of unknown pathogenesis. We described an original experimental model of OA, analyzing the consequences of spontaneous cranial cruciate ligament rupture (RLCCr), occurred at two different times. METHOD: Twenty male animals, younger than 5 years old (20 to 45kg) with RLCCr were submitted to arthrotomy for articular stability and had cartilage fragments removed for analysis. The Group RLCCR < 20 (10 animals) was operated before 20 days and Group RLCCR > 20 (10 animals) after 20 days of beginning of lesion. Seven animals with pre-existent OA which died without any reason, and 7 normal animals (NC) from Service of Zoonosis Control were the control groups. The animals were submitted to clinical and radiological evaluations. Synovial fluid were collected from operated dogs and from another 20 control animals, submitted for surgical procedures for any reason. For the morphological study, the cartilage fragments were stained with H&E and Picrossirus. The score for OA severity was quantified using Safranin-O staining. Inflammatory cytokines (IL-6 and TNF alfa) and chemiokine CCL2/MCP-1 were measured in sinovial fluid. RESULTS: At physical examination, all the dogs had positive drawer and the tibial plateau compression tests. Knee Radiographic data showed that narrowing of joint space, osteophytes and erosions were more prominent in Group RLCCr> 20 animals. Articular cartilage of normal animals (NC) revealed preserved cartilage surface, organized disposition of chondrocytes and integrity of collagen net. Histological exams done in animals from Group RLLCr > 20 showed irregularities on articular surface, reduction of the number of chondrocytes and collagen fibers remodeling. Animals from Group RLCCR > 20 exhibited deep fibrillations, presence of chondrocytes clusters at intermediate area of cartilage, osteophytes and and total disorganization of the collagen fibers net. Chemiokine CCL2/MCP-1 was found overexpressed in dogs operated less than 20 days, while IL-6 was increased in late surgical group. CONCLUSION: The spontaneous model of canine RLCCr, studied at two distinct times, is an original and useful tool to understand pathogenesis of OA. Furthermore, the procedure preserves the animal integrity, becoming an Ethical laboratorial procedure
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Nguỹên, Quang. "Characterization of proteolytic agents involved in the degradation of human articular cartilage proteoglycan during aging and arthritis." Thesis, McGill University, 1990. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=74620.

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Some of the age-related changes in the structure of human proteoglycan aggregate, and the depletion of proteoglycan in arthritic cartilage have been attributed to the action of proteolytic agents. However, the identity of these agents is still uncertain. In this study, the cartilage matrix protein, link protein, has been used as an in situ probe of endogenous proteolysis, due to its relative resistance to proteolysis and the accumulation of its proteolytically-modified form with age in the matrix. Stromelysin, a metalloproteinase secreted in a latent form by human articular cartilage in organ culture, was shown to play a major role in the matrix degradation of neonatal cartilage. In adult cartilage, additional proteolytic agents, besides stromelysin, are involved. The data are compatible with the action of cathepsins B and G, and probably cathepsin L and hydroxyl radicals. The same multiple proteolytic agents appear to have acted on the cartilage remaining in both osteoarthritic and rheumatoid arthritic joints. To further investigate the role of the stromelysin in the degradation of arthritic cartilage, relative steady-state mRNA levels of prostromelysin in normal and arthritic cartilage were also examined. Northern blots indicated that abundant amounts of prostromelysin mRNA were present in normal adult cartilage, whereas relatively lower levels were found in arthritic and neonatal cartilage. Relative to prostromelysin mRNA, little procollagenase and tissue inhibitor of metalloproteinases (TIMP) mRNA were expressed in vivo by chondrocytes in human articular cartilage. In situ hybridization revealed that the metalloproteinase message was being expressed predominantly in the superficial chondrocytes of normal adult and osteoarthritic cartilage. If the observed low levels of latent metalloproteinase precursor are characteristic of all phases of the disease process, then it would appear that the level of activation rather than the amount of the metalloproteinase pre
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Whale, Conley Caitlin E. "EFFECT OF A 12-WEEK HOME-BASED NEUROMUSCULAR ELECTRICAL STIMULATION TREATMENT ON CLINICAL OUTCOMES FOLLOWING ARTICULAR CARTILAGE KNEE SURGERY." UKnowledge, 2017. http://uknowledge.uky.edu/rehabsci_etds/40.

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Articular cartilage defects in the knee are common, and can result in pain, decreased function and decreased quality of life. Untreated defects are considered to be a risk factor for developing osteoarthritis, a progressive degenerative joint disease with minimal treatment options. To address these issues, various surgical procedures are available to treat articular cartilage defects in the knee. While these procedures overall have positive results, after surgery patients experience large and persistent deficits in quadriceps strength. A contributing factor to this post-surgical weakness is believed to be the extended post-operative non-weight bearing period, with full weight bearing not initiated until approximately 4 – 6 weeks after surgery. During this non-weight bearing period a minimal amount of demand is placed upon the muscle. Subsequently, the quadriceps muscle undergoes a large degree of atrophy with a significant decrease in muscle strength. Muscular strength deficits reduce the knee joint stability, also increasing the risk of osteoarthritis development. Interventions that can be used to facilitate quadriceps strength while protecting the articular cartilage repair are needed. Neuromuscular electrical stimulation (NMES) is an effective post-knee surgery rehabilitation technique to regain quadriceps musculature. In recent years manufactures have been developing knee sleeve garments integrated with NMES allowing for portability of the NMES treatment. The primary aim of this study was to evaluate the effectiveness of a 12-week home-based neuromuscular electrical stimulation treatment on post-surgical clinical outcomes (quadriceps strength, lower extremity function, and patient reported outcomes) after articular cartilage knee surgery. Patients were randomized between a standard of care home-treatment group and a NMES home-treatment group. Patients completed isometric quadriceps strength testing, the Y-balance test, and the Knee Injury and Osteoarthritis Outcome Score (KOOS) before surgery and at 3-months after surgery. The secondary aims of this study were to determine the most effective NMES parameters for post-surgical quadriceps strength; and to develop a framework to identify factors that may influence a patient’s adherence to a prescribed therapy program. From our results we can make several conclusions. First, we found only a small number of studies utilize similar parameters for post-surgical quadriceps strength treatments. The majority of the parameters reported in the literature were highly variable between studies. Second, clinicians can utilize the expanded Health Belief Model to identify situational and personal factors unique to a patient that may impact adherence to a prescribed treatment. Clinicians can then implement the proposed interventional strategies to address the identified situational and personal factors. Finally, there was no difference in quadriceps strength, lower extremity function, or self-reported scores at 3-month between a home-based NMES treatment and a standard of care home-based treatment. Patients’ adherence to the treatment protocols may have been a major factor contributing to these results. Utilizing a model, such as the proposed expanded Health Belief Model, may assist clinicians in improving a patients’ adherence to future prescribed home-treatment programs.
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Ebert, Jay Robert. "Post-operative load bearing rehabilitation following autologous chondrocyte implantation." University of Western Australia. School of Sport Science, Exercise and Health, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0196.

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[Truncated abstract] Autologous Chondrocyte Implantation (ACI) has shown early clinical success as a repair procedure to address focal articular cartilage defects in the knee, and involves isolating and culturing a patient's own chondrocytes in vitro and re-implantation of those cells into the cartilage defect. Over time, repair tissue can develop and remodel into hyaline-like cartilage. A progressive partial weight bearing (PWB) program becomes the critical factor in applying protection and progressive stimulation of the implanted cells, to promote best chondrocyte differentiation and development, without overloading the graft. The aim of this thesis was to investigate whether patients could replicate this theoretical load bearing model to possibly render the best quality tissue development. In addition, this proposed external load progression is only a means to loading the articular surface. Several factors, including those that may result from pathology, have the potential to influence gait patterns, and therefore, articular loading. The association between increasing external loads (ground reaction forces - GRF) and knee joint kinetics during partial and full weight bearing gait was, therefore, investigated in the ACI patient group, as was the contribution of other gait variables to these knee joint kinetics which may be modified by the clinician. Finally, current weight bearing (WB) protocols have been based on early ACI surgical techniques. With advancement in the surgical procedure and ongoing clinical experience, we employed a randomised controlled clinical trial to assess the effectiveness of an 'accelerated' load bearing program, compared with the traditionally 'conservative' post-operative protocol. ... Although similar spatio-temporal, knee kinematic and external loading parameters were observed between the traditional and accelerated rehabilitation groups, the accelerated group was 'more comparable' to the controls in their external knee adduction and flexion moments, where the traditional group had lower knee moments. Knee moments greatly affect knee articular loading, and large adduction moments have been related to poor clinical outcomes after surgery. Therefore, the return of normal levels may be ideal for graft stimulation, however, may overload the immature chondrocytes. Acceleration of the intensive rehabilitation program will enable the patient to return to normal activities earlier, whilst reducing time and expenses associated with the rehabilitative process, and may enhance long-term tissue development. However, continued follow-up is required to determine if there are any detrimental effects that may emerge as a result of the accelerated load bearing program, and assess the recovery of normal gait patterns and whether longer term graft outcomes are affected by the recovery time course of normal gait function, and/or abnormal loading mechanics in gait. Furthermore, analysis at all levels of PWB is needed to identify a more complete set of variables attributing to the magnitude of external knee joint kinetics and, therefore, knee articular loading, while the influence muscle activation patterns may have on articular loading needs to be investigated. This becomes critical when you consider loads experienced by the articular surface throughout the early post-operative period following ACI may be important to short- and long-term graft development.
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Chen, Rebecca Y. "Attenuation of the Progression of Articular Cartilage Degeneration by Inhibition of Tgf-β1 Signaling in a Mouse Model of Osteoarthritis." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:17331955.

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Background The goal of this study is to understand role of transforming growth factor beta 1 (TGF-β1) in development of osteoarthritis (OA). Results from studies indicate that the genetic inactivation of Smad-3, or the disruption of the interaction of Tgf-β1 with its receptor Tgf-β type II receptor (Tgfbr2), in germline cells results in OA-like knee joints in mice at one month of age. However, other studies suggest that the increased expression of Tgf-β1 in mature knee joints causes OA in animal models. A human genetic study reports that a two-nucleotide deletion, 741-742del AT, and/or a nucleotide change, 859C>T or 782C>T in SMAD-3 are associated with early-onset OA. This observation is consistent with the finding that the lack of Tgf-β1 signaling in the germline cell results in OA in developing joints and that increased Tgf-β1 signaling causes OA in mature joints. The plausible explanation for this “conflicting” role of TGF-β1 in the pathogenesis of OA is that the effective TGF-β1 signaling acts in either a dose-dependent or a developmental stage-dependent manner. The present study addresses the question as to whether inhibition of Tgf-β1 signaling prevents mature knee joints from being degenerated in mouse models of OA. Methods 1) Using conditional knock out techniques with aggrecan-CreERt2 mice and floxed Tgfbr2 mice, Tgfbr2 was removed from articular cartilage of knee joints in 2-month-old mice. Mice without Tgfbr2 were kept for another 6 months or longer. Knee joints from the mice (n=8) and their corresponding control (n=4) were collected for morphological analysis. 2) Mice without Tgfbr2 at two months old were subjected to DMM to induce articular cartilage degeneration. Knee joints from the mice at 4 and 8 weeks post surgery (n=8 in each group) were collected for morphological analysis. Results 1) We did not find the initiation and acceleration of articular cartilage degeneration by the genetic inactivation of Tgfbr2 in knee joints of mice at the age of 9 months or older. We also did not find hypertrophic chondrocytes in the articular cartilage of the mice. 2) We found that removal of Tgfbr2 in articular cartilage of knee joints delayed articular cartilage degeneration, at least 6 weeks, compared to that in wild-type littermates. Conclusion Inhibition of Tgf-β1 signaling attenuated articular cartilage degeneration in mature knee joints of mouse models of OA. Therefore, inhibition activity of TGF-β1, not application of TGF-β1, may be considered in treatment of OA in mature joints.
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Robertson, William Brett. "Functional and radiological evaluation of autologous chondrocyte implantation using a type I/III collagen membrane: from single defect treatment to early osteoarthritis." University of Western Australia. Orthopaedics Unit, 2007. http://theses.library.uwa.edu.au/adt-WU2007.0172.

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[Truncated abstract] Hyaline articular cartilage is a highly specialised tissue consisting of chondrocytes embedded in a matrix of proteoglycan and collagens. Hyaline articular cartilage withstands high levels of mechanical stress and continuously renews its extracellular matrix. Despite this durability, mature articular cartilage is vulnerable to injury and disease processes that cause irreparable tissue damage. Native hyaline articular cartilage has poor regenerative capacity following injury, largely due to the tissue's lack of blood and lymphatic supply, as well as the inability of native chondrocytes to migrate through the dense extracellular matrix into the defect site. Articular cartilage injuries that fail to penetrate the subchondral bone plate evoke only a short-lived metabolic and enzymatic response, which fails to provide sufficient new cells or matrix to repair even minimal damage. Clinically, it has previously been accepted that treatment of such defects does not result in the restoration of normal hyaline articular cartilage, which is able to withstand the mechanical demands that are placed on the joint during every day activities of daily living. ... Historically, rehabilitation following ACI has not kept pace with the advances in cell culture and surgical technique. Subsequently, there exists a significant gap in knowledge regarding `best practice' in post operative rehabilitation following ACI. The importance of structured rehabilitation in ACI should not be underestimated when evaluating the clinical success of this chondral treatment. Patients should not be left to their own devices following ACI surgery, as the risk of damage to their implant (via delamination) is high if immediate postoperative movement is not controlled. Furthermore, the biological longevity and clinical success of the graft is dependent on a controlled and graduated return to ambulation and physical activity, and the biomechanical stimulation of the implanted chondrocytes.
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Rizkalla, Geihan. "Immunochemical studies of aggregating proteoglycans in normal and osteoarthritic human articular cartilages." Thesis, McGill University, 1990. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=59642.

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The aim of the present investigation was to study the structural variability of osteoarthritic human femoral condylar cartilage proteoglycans that can aggregate with hyaluronic acid as compared with site and age matched normal adult cartilage proteoglycans. Using specific antibodies to different parts of the proteoglycan molecule in radioimmunoassays, we were able to detect four proteoglycan populations of different hydrodynamic sizes in normal, as well as in osteoarthritic articular cartilage. These populations were: a large chondroitin 6-sulfate, a smaller chondroitin 4-sulfate, and an even smaller keratan sulfate population together with the hyaluronic acid-binding region. Osteoarthritic articular cartilage contained increased amounts of a foetal-specific epitope, 846, and a decrease in the characteristic adult cartilage proteoglycans. As determined histologically, using a grading system for cartilage degeneration, early in the disease (phase I), the proteoglycans appear to be smaller in size than in normal adult cartilage, while in the later stages of the disease (phase II) they appear to be larger in their hydrodynamic size. The hyaluronic acid-binding region appeared to be functional and proteoglycan aggregation with hyaluronic acid was not altered in osteoarthritis. The data indicate an attempt by the osteoarthritic cartilage at remodeling and repair by making an immature type of proteoglycan.
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Books on the topic "Articular cartilage – Surgery"

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Cartilage tympanoplasty. Stuttgart: Thieme, 2009.

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Minas, Tom. A primer in cartilage repair and joint preservation of the knee. Philadelphia, PA: Elsevier/Saunders, 2011.

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European Congress of Knee Surgery and Arthroscopy (1st 1984 Berlin, Germany). Surgery and arthroscopy of the knee: First European Congress of Knee Surgery and Arthroscopy, Berlin, 9-14.4.1984. Berlin: Springer-Verlag, 1986.

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Bristol-Myers/Zimmer Orthopaedic Symposium (4th 1988 Chicago, Ill.). Articular cartilage and knee joint function: Basic science and arthroscopy. Edited by Ewing J. Whit, Arthroscopy Association of North America., and Bristol-Myers/Zimmer (Firm). New York: Raven Press, 1990.

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1964-, Hendrich Christian, Nöth Ulrich 1967-, and Eulert Jochen, eds. Cartilage surgery and future perspectives. Berlin: Springer, 2003.

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Farr, Jack, and Andreas H. Gomoll. Cartilage Restoration: Practical Clinical Applications. Springer, 2016.

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Farr, Jack, and Andreas H. Gomoll. Cartilage Restoration: Practical Clinical Applications. Springer, 2013.

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Farr, Jack, and Andreas H. Gomoll. Cartilage Restoration: Practical Clinical Applications. Springer, 2018.

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Cartilage surgery: An operative manual. Philadelphia, PA: Elsevier Saunders, 2011.

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F, Houlton John E., and British Small Animal Veterinary Association., eds. BSAVA manual of canine and feline musculoskeletal disorders. Gloucester [England]: British Small Animal Veterinary Association, 2006.

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Book chapters on the topic "Articular cartilage – Surgery"

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van der Linden, A. J. "Repair of articular cartilage." In Surgery and Arthroscopy of the Knee, 27–30. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71022-3_13.

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Tomford, William W., Christian Ohlendorf, and Henry J. Mankin. "Articular Cartilage Cryopreservation and Transplantation." In Orthopaedic Allograft Surgery, 269–73. Vienna: Springer Vienna, 1996. http://dx.doi.org/10.1007/978-3-7091-6885-1_31.

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Jung, Chan Kwon. "Articular Cartilage: Histology and Physiology." In Techniques in Cartilage Repair Surgery, 17–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-41921-8_2.

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Geesink, R. G. T. "Stress response of articular cartilage." In Surgery and Arthroscopy of the Knee, 23–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71022-3_11.

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Lansdown, Drew A., Kevin C. Wang, and Brian J. Cole. "Defining Failure in Articular Cartilage Surgery." In Joint Preservation of the Knee, 69–82. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-01491-9_5.

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Aigner, Thomas, and Zhiyong Fan. "Anatomy and Biochemistry of Articular Cartilage." In Cartilage Surgery and Future Perspectives, 3–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-19008-7_1.

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Nöth, Ulrich, Arne Berner, Richard Tuli, Achim Battmann, Christian Hendrich, Jochen Eulert, and Rocky S. Tuan. "Fabrication of Cartilage-Polymer Constructs for Articular Cartilage Repair." In Cartilage Surgery and Future Perspectives, 165–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-19008-7_19.

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Cavanaugh, John T. "Rehabilitation Strategies Following Articular Cartilage Surgery in the Knee." In Cartilage Repair Strategies, 343–69. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-343-1_20.

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Kim, Seok-Jung, Asode Ananthram Shetty, and Vishvas A. Shetty. "Gel ACI (GACI): Articular Cartilage Repair Technique." In Techniques in Cartilage Repair Surgery, 175–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-41921-8_15.

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Bauer, M., R. W. Jackson, and D. Ogilvie-Harris. "Articular cartilage lesions of the femoral condyles." In Surgery and Arthroscopy of the Knee, 31–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71022-3_14.

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Conference papers on the topic "Articular cartilage – Surgery"

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Jaumard, Nicolas V., Joel A. Bauman, William C. Welch, and Beth A. Winkelstein. "Biomechanical Comparison of Contact Pressure in the Cervical Facet Joint During Bending Using a Probe and Pressure-Sensitive Paper." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19498.

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Non-physiologic loading of the facet joint is a potential cause of facet joint pain in the cervical spine [1]. When the local biomechanical environment of the facet joint is altered, like with trauma or after surgery [2], the cartilaginous articular surfaces of the facets can also be damaged. Defining articular contact pressure can provide a metric of altered joint mechanics and the local mechanical environment of the cartilage in the facet joint. However, accessing the articular surface to make such measurements without altering the overall mechanics of the joint remains a substantial challenge.
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Linder-Ganz, Eran, Gal Zur, Jonathan Shani, Jonathan J. Elsner, Ori Brenner, Steven P. Arnoczky, Gabriel Agar, Elliott B. Hershman, and Avi Shterling. "Can a Polycarbonate-Urethane Meniscal Implant Protect Articular Cartilage? Histopathological Results in a Sheep Model." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-204860.

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The menisci play an important role in the knee joint biomechanics [1]. Clinical studies have shown that the loss of the meniscus leads to degenerative arthritis attributed to the changes in load distribution and the loss of proprioception [2]. Clearly, there is a substantial need to protect the articular cartilage by either repairing or replacing the menisci. There are many difficulties dealing with both fresh frozen or cryopreserved allograft menisci, and the complexities of meniscal repairs may contribute to uneven distribution of load, instability and recurrence of degenerative damage. Hence there is a need for the development of an artificial meniscus that is available at the time of surgery in several sizes that can accommodate most patients.
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Linder-Ganz, Eran, Jonathan J. Elsner, Gal Zur, Jonathan Shani, Ori Brenner, Elliott Hershman, Avi Shterling, and Farshid Guilak. "Chondroprotective Effects of a Polycarbonate-Urethane Meniscal Implant: Semi-Quantitative Results in a Sheep Model." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19048.

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The menisci play a critical role in load-bearing and stability of the knee joint [1]. Damage or removal of the meniscus leads to alterations in the magnitude and distribution of stresses in the knee, which have been associated with degenerative osteoarthritis [2]. Clearly, there remains a need to develop means of protecting the articular cartilage following meniscal injury by either repairing or replacing the menisci. While allograft meniscal replacements can improve joint stability and function, they often provide little benefit in preventing osteoarthritic changes [3]. The development of an artificial meniscus that is available at the time of surgery in several sizes that can accommodate most patients would provide important therapeutic potential for treatment meniscal injury.
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Baer, Thomas, Ryan Frisbie, Michael Willey, and Jessica Goetz. "Development of a Simplified Ankle Distractor." In 2017 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/dmd2017-3438.

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The physical impairment caused by OA of a single lower extremity joint is comparable to that reported for major life-altering disorders such as end-stage kidney disease and heart failure. (Buckwalter, et al) [1] Ankle distraction arthroplasty has been shown to greatly decrease pain due to end-stage ankle arthritis. Unlike arthrodesis (fusion of the joint), distraction arthroplasty maintains the joint’s natural movement, and it is far less complicated than total joint replacement surgery. There is a considerable body of research supporting the idea that distraction of an end-stage arthritic joint (most of the work thus far has been done on ankles, although there has also been some investigation of the efficacy of the treatment for knee arthritis) for a period of weeks allows the growth of new tissue in the joint. Although this tissue is not true articular cartilage, distraction arthroplasty has been shown to significantly decrease pain and, in the majority of cases, to be a long lasting remedy for a condition that would otherwise commonly be treated with arthrodesis. [2] Devices currently available for this procedure are generally quite complicated because they are designed for a wide range of functions related to bone fixation. This versatility also tends to make those systems larger and more expensive, and their aggressively mechanical appearance makes potential joint distraction patients hesitant to select the procedure. While fracture patients may not have a choice about being treated with such devices, elective patients are instinctively resistant to their use, even when assured that the end result will most likely significantly improve in the quality of their lives.
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Meyer, Eric G., Conor T. Buckley, and Daniel J. Kelly. "The Effect of Cyclic Hydrostatic Pressure on the Functional Development of Cartilaginous Tissues Engineered Using Bone Marrow Derived Mesenchymal Stem Cells." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53634.

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Articular cartilage has a poor capacity for repair. Of the many procedures available to the orthopaedic surgeon, osteochondral grafting is the only technique which reliably produces hyaline cartilage within a defect.1 Bone marrow derived mesenchymal stem cells (MSCs) are an interesting alternative to harvesting cartilage grafts for chondrocytes as they also have the ability to produce cartilaginous tissues in vitro. This suggests that if tissue engineering strategies could be used to develop cartilaginous grafts with mechanical properties approaching that of normal articular cartilage, then hyaline tissue could be regenerated. Of concern with such approaches are reports that the mechanical properties of cartilaginous tissues engineered using MSCs are inferior to that engineered using chondrocytes derived from articular cartilage, although recent studies have demonstrated that adult equine MSCs produce a cartilaginous tissue mechanically superior to that derived using animal-matched adult chondrocytes.2
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Martínez Bocanegra, Marco A., Javier Bayod Lopez, A. Vidal-Lesso, Ricardo Becerro de Bengoa Vallejo, Raúl Lesso Arroyo, and Humberto Corro Hernández. "Biomechanics Aspects for Silastic Implant Arthroplasty Simulation of the First Metatarsophalangeal Joint." In ASME 2015 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/imece2015-53525.

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This work focuses on the biomechanical simulation of surgery for total replacement of the first metatarsophalangeal joint (MTPJ) allowed us to identify and analyze several key aspects for finite element simulation of hallux rigidus pathology. Predicting the optimal response of a finite element model (FEM) depends on proper characterization. At this part of the work, those conditions that have a direct or indirect influence on the model that can change its behavior should be considered. For this purpose, we presented in this work a finite element model which include 26 bones: 14 phalanges, 5 metatarsals, 3 cuneiform bones, 1 cuboid, 1 navicular, 1 talus and 1 calcaneus, all of them include articular cartilage. In addition, the model also considers: thin ligaments, long ligaments, muscles and a joint implant. Loads and boundary conditions included: a pretension in the flexor caused by position analysis, a distributed load in the talus in its normal and tangential component, a restriction of movement of some points in the phalanges and calcaneus and the contact conditions between flexor and extensor created from surfaces in the bone volumes. Moreover, the selection of support and constrains regions in the phalanges and calcaneus area must be carefully selected to reproduce the conditions of real support and interaction with adjacent tissues not simulated. These conditions have influence in the structural biomechanical response of each tissue and in contact regions, leading to unexpected behavior if they are wrong selected. In addition, results showed that care must be taken in the mechanical characterization of each tissue, selecting the mechanical properties, pretension, geometry and critical position according to in vitro results or MRIs. Biomechanical aspects reported in this work allow to take into account fundamental details to improve future simulations of this pathology as well as to improve the correlation with experimental results. These biomechanical aspects provide knowledge for finite element simulation of the arthroplasty for the first metatarsophalangeal joint, this allow us to generate a virtual model for arthroplasty of the hallux rigidus to predict, prevent and improve surgical techniques for implantation of prostheses in the first metatarsophalangeal joint.
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