Academic literature on the topic 'Autologous chondrocyte implantation'

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Journal articles on the topic "Autologous chondrocyte implantation":

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Jones, Deryk G., and Lars Peterson. "Autologous Chondrocyte Implantation." Journal of Bone & Joint Surgery 88, no. 11 (November 2006): 2501–20. http://dx.doi.org/10.2106/00004623-200611000-00025.

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Minas, Tom, Takahiro Ogura, and Tim Bryant. "Autologous Chondrocyte Implantation." JBJS Essential Surgical Techniques 6, no. 2 (June 22, 2016): e24. http://dx.doi.org/10.2106/jbjs.st.16.00018.

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Harris, Joshua D., Robert A. Siston, Xueliang Pan, and David C. Flanigan. "Autologous Chondrocyte Implantation." Journal of Bone and Joint Surgery-American Volume 92, no. 12 (September 2010): 2220–33. http://dx.doi.org/10.2106/jbjs.j.00049.

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Cole, Brian J., and Mike D'Amato. "Autologous chondrocyte implantation." Operative Techniques in Orthopaedics 11, no. 2 (April 2001): 115–31. http://dx.doi.org/10.1016/s1048-6666(01)80021-5.

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Henderson, Ian, Patrick Lavigne, Herminio Valenzuela, and Barry Oakes. "Autologous Chondrocyte Implantation." Clinical Orthopaedics and Related Research 455 (February 2007): 253–61. http://dx.doi.org/10.1097/01.blo.0000238829.42563.56.

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Min, Byoung-Hyun, and Kyung-Soo Oh. "Autologous Chondrocyte Implantation." Techniques in Knee Surgery 9, no. 2 (June 2010): 66–79. http://dx.doi.org/10.1097/btk.0b013e3181e0e349.

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Cluett, Jonathan C., James C. Kasper, Bert R. Mandelbaum, and Kai Mithoefer. "Autologous Chondrocyte Implantation." Techniques in Knee Surgery 5, no. 3 (September 2006): 158–64. http://dx.doi.org/10.1097/01.btk.0000234077.86516.80.

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Browne, Jon E., Thomas M. Sasser, and Thomas P. Branch. "Autologous Chondrocyte Implantation." Techniques in Knee Surgery 5, no. 4 (December 2006): 238–51. http://dx.doi.org/10.1097/01.btk.0000236411.77051.81.

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Williams, Joseph J. "AUTOLOGOUS CHONDROCYTE IMPLANTATION." Southern Medical Journal 91, Supplement (October 1998): S71. http://dx.doi.org/10.1097/00007611-199810001-00175.

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Goldberg, A. J., D. A. Lee, D. L. Bader, and G. Bentley. "Autologous chondrocyte implantation." Journal of Bone and Joint Surgery. British volume 87-B, no. 1 (January 2005): 128–34. http://dx.doi.org/10.1302/0301-620x.87b1.14154.

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Dissertations / Theses on the topic "Autologous chondrocyte implantation":

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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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Kobayashi, Tomohito. "A-674563 increases chondrocyte marker expression in cultured chondrocytes by inhibiting Sox9 degradation." Kyoto University, 2018. http://hdl.handle.net/2433/232130.

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Briggs, T. W. R. "Autologous chondrocyte implantation of the knee using an inert collagen membrane." Thesis, University College London (University of London), 2009. http://discovery.ucl.ac.uk/17271/.

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The hypothesis for this thesis was that using cultured autologous chondrocytes would lead to repair of full thickness defects with a hyaline type cartilage reparative tissue producing a significant improvement in pain and joint function in both the short and medium term. It was also hypothesised that the cover to contain the implanted cells is only a containment device so can be biologically inert resulting in no difference between Autologous Chondrocyte Implantation (ACI) and Matrix Assisted Chondrocyte Implantation (MACI). For this study autologous cultured chondrocytes were re-implanted under (ACI) or within (MACI) an inert type I/III collagen membrane. Patients were clinically assessed for up to seven years by standardised objective and subjective scores, as well as undergoing a second arthroscopy at one year to assess the regenerating tissue within the defect. All patients treated had full thickness chondral defects (1-12 cm^2).and were aged between .15-55 years age. The majority of patients had undergone at least one surgical procedure prior to referral for this technique, most commonly arthroscopy. The objective and subjective scores used showed a significant improvement post-surgery and the Short Form 36 proved to be sufficiently sensitive to demonstrate perceived health benefit from ACI at one year. ACI also resulted in an increase in post-operative score in patient previously treated with microfracture. The study showed that defect site, duration of symptoms, gender, defect size, and pre-operative score all affected the post-operative score. Histological assessment of the repair tissue showed that the regenerate is fibrocartilaginous but continues to adapt with time post-surgery resulting in a tissue more like normal articular cartilage. However, the type of regenerate does not significantly affect the post-operative patient score. Standard histological techniques showed that the regenerate contained collagen type IIA and B, collagen X, proteoglycans and S100. The results showed that the reparative tissue is showing features of hyaline cartilage but its architectural structure is not yet formed and the on the superficial surface only fibrous tissue is found architectural structure is not yet formed and the on the superficial surface only fibrous tissue is found. Both ACI and MACI produced significant improvements in knee function when compared to pre-operative levels (p<0.0001), with continued improvement in outcome for up to seven years, but the rate of clinical improvement in the MACI group was superior. There was, however, a greater tendency in the MACI group for fibrocartilaginous repair. This may be the reason why the MACI group had an inferior post-operative score at one year post-implantation compared to ACI group. However, by two years the MACI score surpassed the ACI group, possibly indicating a slower rate of maturation of the MACI regenerate. In summary, ACI for the repair of full thickness defects of the knee produces a repair with a tendency to form hyaline-like articular cartilage. Subjective and objective scores demonstrate sequential improvement for up to seven years demonstrating the durability of this technique in this group of patients.
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Walker, Robert William. "The contact stress in the natural knee following autologous chondrocyte implantation." Thesis, Anglia Ruskin University, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.440249.

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Bhosale, Abjijit. "Assessment of outcome measure of autologous chondrocyte implantation of the knee joint." Thesis, Keele University, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.540618.

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Gooding, Christopher Rees. "A clinical and histopathological review of autologous chondrocyte implantation in the knee." Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1444392/.

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Osteochondral defects in the knee can be disabling causing persistent pain, giving way, locking, catching and swelling and a reduction in activities including sport. Traditionally symptomatic defects were treated with marrow stimulation techniques such as drilling, abrasion and microfracture of the subchondral bone which have had limited success with usually the production of a fibrocartilage repair. This repair tissue tends to be soft and degenerates over a period of time. Autologous chondrocyte implantation (ACI) has produced hyaline or hyaline-like repair tissue in experimental models and in the clinical setting in early studies, with the potential for permanent regeneration of articular cartilage, thus preventing early onset osteoarthritis. This study reviews the clinical results of 3 techniques of autologous chondrocyte implantation (ACI): the more traditional periosteum covered ACI (ACI-P) implant, the collagen-covered ACI (ACI-C) and the matrix carried autologous chondrocyte implantation (MACI). Single cohort studies of ACI-P and ACI-C over a 4 year period were made together with the provisional results of the MACI procedure at 1 year. Then 2 prospectively randomized studies were performed to compare ACI-C with ACI-P and MACI with ACI-C. Finally a small series of patients were reviewed who had a chondrocyte implantation combined with other surgical techniques such as an anterior cruciate ligament reconstruction or tibial osteotomy. A review of these patients revealed a significant improvement in their clinical scores over 4 years for the ACI-C and ACI-P technique in keeping with previously published data and also for the MACI technique at 1 year. Interestingly, a large number of the ACI-P patients developed graft hypertrophy which required arthroscopic debridement since patients complained of pain and catching. However, the ACI-C and MACI patients rarely developed this problem. The prospectively randomised study did not show any difference in terms of clinical and histological assessment at 2 years between the ACI-C and ACI-P patients. The early results for the MACI technique are also comparable. Based on this data it is proposed that collagen-covered ACI is the present 'gold standard' in chondrocyte implantation rather than periosteum-covered ACI.
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Willers, Craig Robert. "Matrix-induced autologous chondrocyte implantation for articular cartilage injury : biology, histology and clinical outcomes." University of Western Australia. School of Surgery, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0227.

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[Truncated abstract] Articular cartilage has no vascular, neural, or lymphatic supply, and hence no intrinsic capacity to self-repair following injury. These physiological limitations, combined with the inability of local chondrocytes to contribute to the repair process, translate to poor structural and functional outcomes in these troublesome defects, and osteoarthritic deterioration with time. Subsequently, many surgical therapies have been trialed to stimulate cartilage repair, but none have produced reliable outcomes. Hence, cartilage repair research has been broadened, with many investigators now focused on cell-based treatment. Smith began a revolution of autologous cell research when in 1965 she isolated chondrocytes from articular cartilage and transplanted them into fresh cartilage nodules (Smith, 1965). Since, new technologies and improved techniques have seen autologous chondrocyte implantation (ACI) widely accepted for use in clinical orthopaedics (Bentley et al., 2003; Brittberg et al., 1994; Grande et al., 1989; Peterson et al., 2002). At present, matrix-induced autologous chondrocyte implantation (MACI) is the most surgically simple form of ACI, boasting clinical outcomes comparable to any technique on the market, and far less complications compared to the first generation of ACI - periosteal ACI (Bartlett et al., 2005; Behrens et al., 2006; Gigante et al., 2006; Henderson et al., 2004; Marlovits et al., 2005; Minas, 2001; Willers et al., 2007; Zheng et al., 2007). But whilst MACI has been adopted by the orthopaedic surgeon for articular cartilage repair, many of the molecular, histological, and clinical factors governing patient outcomes are still largely understudied. Firstly we assessed the bioactivity of fibrin sealant (FS - Tisseel®), a critical component of MACI, on the migration and proliferation of human articular chondrocytes in vitro. We also looked to elucidate the associated molecular mechanisms of thrombin, a key active ingredient in FS, by examining the expression and activation of proteaseactivated receptors (PARs), established thrombin receptors. All four PAR isoforms were detected in human chondrocytes, with PAR-1 being the major isoform expressed. '...' This thesis has demonstrated biological, histological, and clinical features of the MACI technique. Our in vitro has supported the use of fibrin sealant and collagen membrane as the major material components of MACI, illustrating improved chondrocyte proliferation, migration, and chondrogenic differentiation. We have evidenced that MACI stimulates successful production of hyaline-like cartilage by 6 months, while also showing that revised and clinically failed repair tissues are predominantly hyaline-like and fibrocartilage with inferior composition. Clinically, we have documented significant improvements in patient repair structure, function, symptoms, quality of life, and satisfaction, whilst concurrently confirming sentiment within the literature regarding the importance of exercise/ rehabilitation for maximising MACI outcome. In summary, the findings presented in this thesis suggest that MACI is a biologically sound and clinically efficacious cell-based treatment option for repairing articular cartilage defects.
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Steika, Nils A. "A Comparison of the Wear Resistance of Normal, Degenerate, and Repaired Human Articular Cartilage." Thesis, Virginia Tech, 2004. http://hdl.handle.net/10919/35664.

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In our aging population, arthritis is becoming an increasingly common problem. Pain, loss of joint function and other negative affects make arthritis a major health problem. The most common form of arthritis, osteoarthritis, is caused by the "wear and tear" of articular cartilage on the surface of bones in synovial joints. It is a chronic problem that is slowed with different types of therapies, including pharmaceutical, nutritional and surgical, but to date the wearing down of the cartilage cannot be stopped or reversed. Normal, mature, articular cartilage does not spontaneously repair itself after an injury. In light of this, several surgical techniques are being developed to repair degenerate and/or osteoarthritic cartilage. One such approach uses Autologous Chondrocyte Implantation (ACI). Dr. Mats Brittberg, and associates at Goteborg University in Sweden began using this cartilage repair procedure in 1987. Other techniques attempt to stimulate the subchondral bone to generate cartilage, such as Abrasion Arthroplasty. Still others use tissue grafts to attempt to repair lesions in cartilage. The surface biomechanics of these repaired tissues have not yet been studied. How well does the repaired cartilage resist wear? How long will it last? How does the repaired cartilage compare to "normal" cartilage in terms of wear-resistance? It is the goal of this research to gain initial knowledge to help answer these questions. Dr. Brittberg has provided 17 sample of cartilage, from 9 Swedish patients, including repaired and normal pairs using the aforementioned repair techniques and others, as well as a degenerate and normal cartilage pair. The intention of this paper is to report the findings of experiments performed using these samples, and compare the wear-resistance of repaired and degenerate cartilage to that of normal cartilage. Wear and friction tests were carried out on 2 mm diameter specimens using a biotribology device and a new, modified technique developed specifically for these small samples. The cartilage samples were mounted, using specially designed adapters, in our biotribology device for oscillating contact against polished stainless steel disks at a constant applied normal load, oscillating frequency, and test time. A buffered saline solution was used as the lubricant. Cartilage wear was determined from hydroxyproline analysis of the test fluid and washings from the wear test. Thin layers of transferred cartilage-like films to the stainless steel disks were also analyzed. Also, friction data was recorded throughout the tests. The results of these experiments show that: 1)For the two pairs of ACI repaired cartilage, the repaired cartilage gave substantially less wear than that of normal cartilage. 2)For all other repair techniques tested, the repaired cartilage produced more wear than normal cartilage. 3)The single osteoarthritic cartilage tested produced similar wear to that of normal cartilage. This is surprising since the current thought is osteoarthritic cartilage is more susceptible to wear. 4)The hydroxyproline concentration, by weight, of cartilage increases after the wear test. 5)Friction levels were in the boundary lubrication regime, and had no correlation with the amount of wear. To our knowledge, this research represents the first controlled "in vitro" study of an important unknown in cartilage repair, i.e., the wear-resistance of the repaired cartilage. It shows that ACI produces a cartilage with very good wear-resistance, better than that of other repair techniques, and possibly better than normal, healthy cartilage. ACI and its applications to the treatment of degenerate and osteoarthritic joints are promising, and studies will continue to investigate this and other types of cartilage repair.
Master of Science
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Jaiswal, P. K. "Factors affecting outcome after autologous chondrocyte implantation for the treatment of osteochondral defects of the knee." Thesis, University College London (University of London), 2015. http://discovery.ucl.ac.uk/1467124/.

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Some studies on autologous chondrocyte implantation (ACI) have demonstrated little benefit over other techniques and few have demonstrated a lasting benefit. A number of factors can contribute to failure and a scientific approach to elucidate these variables has not been reported. This thesis reports on the use of a statistical approach - the Generalised Linear Model (GLM) to quantify the effect each factor has whilst considering the interplay of other variables. Data from a randomised controlled trial and several case-controlled studies will assess the efficacy of 2 different types of ACI, the influence of smoking, BMI, and physical activity. Non-modifiable risk factors that were assessed include the aetiology, site and size of the lesion, the duration of symptoms and number of previous operations prior to the index procedure and the presence of early osteoarthritis. Site had a significant effect on outcome but size did not. The GLM predicted a point increase in the Modified Cincinnati Score (MCS) before surgery (MCS 0) would lead to a further 0.5 point increase in MCS 2 years postoperatively (MCS 24) (p=0.001). Other significant non-modifiable risk factors include age and sex of the patient. When treating lesions in the patella, duration of symptoms was a significant factor, but age was not. The GLM predicted that smokers’ MCS 24 (the Modified Cincinnati Score 2 years after surgery) was likely to be 15 less than non-smokers (p=0.002). Patients playing no sports experienced an 11.4 point decrease. For each increase in BMI, the MCS 24 was 2.4 less (p=0.001). Factors that optimise outcome following surgery are; avoidance of numerous procedures prior to ACI and delay of more than one year before undergoing ACI. Current NICE guidelines prohibit the use of ACI as the first-line surgical procedure and prevent addressing the above 2 issues. Poorer results were observed in obese patients. Weight loss and active lifestyle are essential pre-operatively. Furthermore, we recommend that pre-operative counselling for smokers is essential and that all smokers be offered a cessation programme.
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ISHIGURO, NAOKI, HIROHITO MITSUYAMA, YOHEI ONO, MOTOSHIGE NAKASHIMA, HIDEKI HIRAIWA, TADAHIRO SAKAI, and TAKASHI HAMADA. "Surface Markers and Gene Expression to Characterize the Differentiation of Monolayer Expanded Human Articular Chondrocytes." Nagoya University School of Medicine, 2013. http://hdl.handle.net/2237/17606.

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Book chapters on the topic "Autologous chondrocyte implantation":

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Gómez-Cardero, Primitivo, E. Carlos Rodríguez-Merchán, and Ángel Martínez-Lloreda. "Autologous Chondrocyte Implantation." In Articular Cartilage Defects of the Knee, 67–78. Milano: Springer Milan, 2012. http://dx.doi.org/10.1007/978-88-470-2727-5_8.

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Jones, Deryk G., and Lars Peterson. "Autologous Chondrocyte Implantation." In Cartilage Repair Strategies, 137–65. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-343-1_10.

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Gomoll, Andreas H., and Jack Farr. "Autologous Chondrocyte Implantation (ACI)." In Cartilage Restoration, 265–74. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-77152-6_21.

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Gomoll, Andreas H., and Jack Farr. "Autologous Chondrocyte Implantation (ACI)." In Cartilage Restoration, 143–52. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-0427-9_13.

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Johnston, L., M. Faimali, P. D. Gikas, and Timothy W. R. Briggs. "Matrix-Induced Autologous Chondrocyte Implantation." In Techniques in Cartilage Repair Surgery, 237–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-41921-8_20.

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Wood, David, and Ming Hao Zheng. "Matrix-Induced Autologous Chondrocyte Implantation." In Cartilage Repair Strategies, 193–206. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-343-1_12.

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Guzman, Maurice S., Thomas Bucher, Jay R. Ebert, and Gregory C. Janes. "Arthroscopic Matrix-Induced Autologous Chondrocyte Implantation." In Cartilage Restoration, 275–85. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-77152-6_22.

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Bucher, Thomas A., Jay Robert Ebert, and Gregory C. Janes. "Arthroscopic Matrix-Induced Autologous Chondrocyte Implantation." In Cartilage Restoration, 153–60. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-0427-9_14.

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Gillogly, Scott D., and Mats Brittberg. "Autologous Chondrocyte Implantation for Focal Chondral Lesions." In Articular Cartilage Lesions, 95–104. New York, NY: Springer New York, 2004. http://dx.doi.org/10.1007/978-0-387-21553-2_10.

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Minas, Tom. "Autologous Chondrocyte Implantation in the Osteoarthritic Knee." In Articular Cartilage Lesions, 105–18. New York, NY: Springer New York, 2004. http://dx.doi.org/10.1007/978-0-387-21553-2_11.

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Conference papers on the topic "Autologous chondrocyte implantation":

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Gupta, Akash, Kyung Chil Chung, Ryan J. Quigley, Bong Jae Jun, and Thay Q. Lee. "Evaluation of Scaffold Fixation for Treatment of Osteochondral Defects of the Knee." In ASME 2010 5th Frontiers in Biomedical Devices Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/biomed2010-32050.

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Articular cartilage damage is a common source of knee pain that can be treated with autologous chondrocyte implantation (ACI). Fixation of the scaffolds can be accomplished by various means with bone sutures being the most effective. The purpose of this study was to evaluate the fixation of a new scaffold with three bone sutures after cycling with continuous passive motion (CPM). Two defects, each of 20mm diameter and 5mm depth, were created per knee and the scaffold was fixed with three bone sutures at the 12 o’clock, 4 o’clock and 8 o’clock positions. Knees were then cycled from 0 degrees to 74 degrees to 0 degrees on a CPM machine for a total of 210 cycles and the scaffolds were then evaluated for fixation, fraying and delaminations. All scaffolds were noted to have remained fixed inside the defect. Fraying occurred in 16 out of the 20 scaffolds and delaminations occurred in 12 out of the 20. Only two scaffolds were completely free of both fraying and delaminations. Fraying occurred in 32.5% of the circumference of medial scaffolds while only 15.0% in lateral scaffolds. Fraying occurred mostly over flush areas and the least over recessed areas. Overall, three bone sutures provided excellent fixation of this scaffold. If at all possible, the scaffold should be recessed into the defect to minimize the amount of fraying that occurs.
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Steika, Nils A., Michael J. Furey, Hugo P. Veit, and Mats Brittberg. "Biotribology: The Wear Resistance of Repaired Human Articular Cartilage." In World Tribology Congress III. ASMEDC, 2005. http://dx.doi.org/10.1115/wtc2005-63304.

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Normal, mature articular cartilage does not spontaneously repair itself back to hyaline cartilage after an injury or degenerative disease (e.g., osteoarthritis)—problems of increasing importance in an aging population. A promising new approach is to repair damaged cartilage by a method known as Autologous Chondrocyte Implantation (ACI)—a technique pioneered and further developed by the Cartilage Research Unit at Goteborg University in Sweden. However, the tribological properties of the repaired cartilage, including the important property wear-resistance, are unknown. How durable is the repaired cartilage? How long will it last? One of the co-authors, Dr. Mats Brittberg, has provided 16 samples of 2mm diameter human biopsies from the knees of eight Swedish patients for testing in our biotribology device. This paper presents results of wear experiments on cartilage repaired by Brittberg’s ACI technique and, for comparison, two other methods. Four of these samples (2 pairs) were from patients who had undergone the ACI procedure while another four were from those who had other methods of repair. A pair consists of a biopsy from the repaired area of the joint along with a sample from nearby “healthy” cartilage from the same joint. Thus, each pair allowed for a direct comparison of the tribological properties of the repaired cartilage to those of “normal” cartilage from the same joint. The results of this study show that the ACI method of cartilage repair gave substantially less wear than that of normal cartilage while spontaneous repair and abrasion arthroplasty produced higher wear. Friction levels were in the boundary lubrication regime and, in line with our previous experience, had no correlation with wear. Results obtained with cartilage from the remaining patients will be discussed in future papers.

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