subject:(Cartilage)

Mississippi State University

1. Gilbert, Eric Andrew. Efficacy of a novel through-thickness perfusion bioreactor to create scaffold-free tissue engineered cartilage.

Degree: MS, Agricultural and Biological Engineering, 2013, Mississippi State University

URL: http://sun.library.msstate.edu/ETD-db/theses/available/etd-10262013-234246/ ;

► Articular cartilage is an avascular, aneural tissue that covers the ends of diarthroidal joints. Once damaged by disease or injury, cartilage lacks the ability… (more)

Subjects/Keywords: neonatal porcine cartilage; cartilage bioreactor

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APA (6^th Edition):

Gilbert, E. A. (2013). Efficacy of a novel through-thickness perfusion bioreactor to create scaffold-free tissue engineered cartilage. (Masters Thesis). Mississippi State University. Retrieved from http://sun.library.msstate.edu/ETD-db/theses/available/etd-10262013-234246/ ;

Chicago Manual of Style (16^th Edition):

Gilbert, Eric Andrew. “Efficacy of a novel through-thickness perfusion bioreactor to create scaffold-free tissue engineered cartilage.” 2013. Masters Thesis, Mississippi State University. Accessed March 07, 2021. http://sun.library.msstate.edu/ETD-db/theses/available/etd-10262013-234246/ ;.

MLA Handbook (7^th Edition):

Gilbert, Eric Andrew. “Efficacy of a novel through-thickness perfusion bioreactor to create scaffold-free tissue engineered cartilage.” 2013. Web. 07 Mar 2021.

Vancouver:

Gilbert EA. Efficacy of a novel through-thickness perfusion bioreactor to create scaffold-free tissue engineered cartilage. [Internet] [Masters thesis]. Mississippi State University; 2013. [cited 2021 Mar 07]. Available from: http://sun.library.msstate.edu/ETD-db/theses/available/etd-10262013-234246/ ;.

Council of Science Editors:

Gilbert EA. Efficacy of a novel through-thickness perfusion bioreactor to create scaffold-free tissue engineered cartilage. [Masters Thesis]. Mississippi State University; 2013. Available from: http://sun.library.msstate.edu/ETD-db/theses/available/etd-10262013-234246/ ;

2. Stone, Austin V. A potential biologic role for the meniscus in the development of osteoarthritis.

Degree: 2013, Wake Forest University

URL: http://hdl.handle.net/10339/39030

► The overarching goal of this research is to identify the biologic role of the meniscus in the development of osteoarthritis. We hypothesized that inflammatory factors… (more)

Subjects/Keywords: cartilage

…monkey menisci. ....................................... 35 Table S1: Vervet knee cartilage and… …72 Figure 3: Comparison of osteoarthritic meniscus and cartilage cells in response to… …78 Table S1: Grading system used for cartilage and meniscus specimens… …120 Table S1: Grading system for cartilage and meniscus specimens… …leads to a compromise of the structural integrity of the cartilage, subchondral bone, and the…

11 more images…

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APA (6^th Edition):

Stone, A. V. (2013). A potential biologic role for the meniscus in the development of osteoarthritis. (Thesis). Wake Forest University. Retrieved from http://hdl.handle.net/10339/39030

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Stone, Austin V. “A potential biologic role for the meniscus in the development of osteoarthritis.” 2013. Thesis, Wake Forest University. Accessed March 07, 2021. http://hdl.handle.net/10339/39030.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Stone, Austin V. “A potential biologic role for the meniscus in the development of osteoarthritis.” 2013. Web. 07 Mar 2021.

Vancouver:

Stone AV. A potential biologic role for the meniscus in the development of osteoarthritis. [Internet] [Thesis]. Wake Forest University; 2013. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/10339/39030.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Stone AV. A potential biologic role for the meniscus in the development of osteoarthritis. [Thesis]. Wake Forest University; 2013. Available from: http://hdl.handle.net/10339/39030

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

3. Mandl, Erik. Advances in cartilage tissue engineering : in vitro.

Degree: 2004, Erasmus University Medical Center

URL: http://hdl.handle.net/1765/39804

► textabstractWithin the body three subtypes of cartilage can be distinguished: hyaline cartilage, elastic cartilage and fibrocartilage. Hyaline cartilage is the predominant subtype and is mainly… (more)

▼ textabstractWithin the body three subtypes of cartilage can be distinguished: hyaline cartilage, elastic cartilage and fibrocartilage. Hyaline cartilage is the predominant subtype and is mainly located in articular joints and in less extent in the nasal septum and cricoid. Elastic cartilage can be found in the outer ear and in parts of the respiratory tract. The menisci and intervertebral discs are made from the third subtype: fibrocartilage. Hyaline cartilage in joints, further refered to as articular cartilage, is a highly specialized tissue that ensures low-friction movement of articulating bones, whilst transmitting load. The only cell-type present in articular cartilage is the chondrocyte, which only composes less than 5% of the total tissue volume. Water (up to 80% wet weight) is the predominant molecule in cartilage, followed by different collagens (10-20% wet weight) and the group of GAG (GlycosAminoGlycan, 4-7% wet weight) 181. From the latter two groups, collagen type II and aggrecan are the most prominent respectively. A simplified reflection of the cartilage structure and function would be as follows. The collagen molecules form a tightly woven network in which the GAG are contained (Figure I-1 next page). In solution, the GAG is negatively charged and creates an osmotic pressure via attraction of positive counter-ions. This osmotic pressure, together with repulsive forces of the negatively charged GAG, result in a swelling pressure within the matrix that accounts for the excellent capabilities of cartilage to absorb and transmit forces during joint movement and loading. Several smaller molecules also play a crucial role in the extracellular matrix of articular cartilage: decorin, anchorin, collagen type VI, IX and XI. Articular cartilage lacks blood vessels; chondrocytes receive oxygen and nutrients through diffusion from the synovium and the underlying bone. Articular cartilage can be divided in four zones with respect to the architecture 68, 181, 213 (Figure I-2, next page). The superficial zone comprises approximately 10% of the cartilage and is characterized by a high cell density, flattened chondrocytes and thin collagen fibers that are oriented tangential to the articular surface. The middle zone or intermediate zone has randomly orientated collagen fibers and chondrocytes with a more spherical configuration.

Subjects/Keywords: cartilage

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APA (6^th Edition):

Mandl, E. (2004). Advances in cartilage tissue engineering : in vitro. (Doctoral Dissertation). Erasmus University Medical Center. Retrieved from http://hdl.handle.net/1765/39804

Chicago Manual of Style (16^th Edition):

Mandl, Erik. “Advances in cartilage tissue engineering : in vitro.” 2004. Doctoral Dissertation, Erasmus University Medical Center. Accessed March 07, 2021. http://hdl.handle.net/1765/39804.

MLA Handbook (7^th Edition):

Mandl, Erik. “Advances in cartilage tissue engineering : in vitro.” 2004. Web. 07 Mar 2021.

Vancouver:

Mandl E. Advances in cartilage tissue engineering : in vitro. [Internet] [Doctoral dissertation]. Erasmus University Medical Center; 2004. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/1765/39804.

Council of Science Editors:

Mandl E. Advances in cartilage tissue engineering : in vitro. [Doctoral Dissertation]. Erasmus University Medical Center; 2004. Available from: http://hdl.handle.net/1765/39804

Cornell University

4. Griffin, Darvin. Assessing The Mechanical Behavior Of Treatments For Focal Articular Cartilage Lesions.

Degree: PhD, Biomedical Engineering, 2016, Cornell University

URL: http://hdl.handle.net/1813/43588

► In a healthy knee joint, articular cartilage (AC) supports loads, dissipates energy, and lubricates with little to no signs of wear or damage. With injury… (more)

▼ In a healthy knee joint, articular cartilage (AC) supports loads, dissipates energy, and lubricates with little to no signs of wear or damage. With injury or degeneration related to osteoarthritis (OA), cartilage changes occur leading to significant loss of mechanical function, with the potential to cause further progressive degeneration of cartilage. While the connection between mechanical changes and arthritis progression is well known, previous work has focused primarily on bulk, tissue-scale ([ALMOST EQUAL TO]1mm) behavior. What is less clear is how mechanical behavior changes on the microscale (e.g. [ALMOST EQUAL TO]10-20[MICRO SIGN]m) during cartilage degradation. Previous work in our lab has developed techniques for measuring local strains in healthy cartilage via confocal elastography. This work focuses on applying traditional and novel techniques to understand the mechanical behavior at degraded and repaired articular cartilage. The first aim elucidates the fundamental relationships between the composition and structure of degraded cartilage and its local mechanical behavior, specifically its viscoelastic response with degeneration. This study combined state of the art techniques for analyzing cartilage structure, and high resolution mapping of mechanical properties on the microscale([ALMOST EQUAL TO]20[MICRO SIGN]m). This work provided new insight into structural and local mechanical changes that occur in cartilage during the early stages of OA. Due to its avascular nature, articular cartilage exhibits an extremely limited capacity to heal when damaged. Consequently, research dealing with cartilage repair strategies is of elevated importance. Restoring the mechanical properties of tissue at the repair site is a common problem in tissue engineering techniques aimed at repairing cartilage defects. Therefore, the second and third aims investigated the mechanical performance of repaired cartilage treated with either matrix membranes or growth factors to assist in tissue formation within a defect site and surrounding AC. The present work has developed into an innovative mechanical characterization technique. Specifically, combining the confocal elastography technique, with the unique sample populations from second and third aim to tackle a problem that has faced the orthopedic research field for more than two decades: understanding the mechanics of the interface between native and repaired cartilage. I've identified two distinct error modes of failure for this interface - sliding and peeling. As such, understanding the structure function relationship in healthy, damaged, and repaired cartilage, is critical for devising strategies to restore tissue impaired by injury or disease and can provide a template for successful implant design. Advisors/Committee Members: Bonassar,Lawrence (chair), Cohen,Itai (committee member), Nixon,Alan J (committee member).

Subjects/Keywords: Articular Cartilage; Cartilage Repair; Confocal Elastography

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APA (6^th Edition):

Griffin, D. (2016). Assessing The Mechanical Behavior Of Treatments For Focal Articular Cartilage Lesions. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/43588

Chicago Manual of Style (16^th Edition):

Griffin, Darvin. “Assessing The Mechanical Behavior Of Treatments For Focal Articular Cartilage Lesions.” 2016. Doctoral Dissertation, Cornell University. Accessed March 07, 2021. http://hdl.handle.net/1813/43588.

MLA Handbook (7^th Edition):

Griffin, Darvin. “Assessing The Mechanical Behavior Of Treatments For Focal Articular Cartilage Lesions.” 2016. Web. 07 Mar 2021.

Vancouver:

Griffin D. Assessing The Mechanical Behavior Of Treatments For Focal Articular Cartilage Lesions. [Internet] [Doctoral dissertation]. Cornell University; 2016. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/1813/43588.

Council of Science Editors:

Griffin D. Assessing The Mechanical Behavior Of Treatments For Focal Articular Cartilage Lesions. [Doctoral Dissertation]. Cornell University; 2016. Available from: http://hdl.handle.net/1813/43588

University of Sydney

5. Biasutti, Sara. Experimental Studies in Tendinopathy and Use of a Novel Tendon Autograft for Cartilage Resurfacing: An Ovine Model .

Degree: 2018, University of Sydney

URL: http://hdl.handle.net/2123/18621

► Cartilage damage and osteoarthritis are enormous medical problems in humans and animals. The inherent poor regenerative capacity of articular cartilage after injury results in loss… (more)

Subjects/Keywords: Cartilage; tendon; tendinopathy; osteoarthritis; cartilage resurfacing

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APA (6^th Edition):

Biasutti, S. (2018). Experimental Studies in Tendinopathy and Use of a Novel Tendon Autograft for Cartilage Resurfacing: An Ovine Model . (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/18621

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Biasutti, Sara. “Experimental Studies in Tendinopathy and Use of a Novel Tendon Autograft for Cartilage Resurfacing: An Ovine Model .” 2018. Thesis, University of Sydney. Accessed March 07, 2021. http://hdl.handle.net/2123/18621.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Biasutti, Sara. “Experimental Studies in Tendinopathy and Use of a Novel Tendon Autograft for Cartilage Resurfacing: An Ovine Model .” 2018. Web. 07 Mar 2021.

Vancouver:

Biasutti S. Experimental Studies in Tendinopathy and Use of a Novel Tendon Autograft for Cartilage Resurfacing: An Ovine Model . [Internet] [Thesis]. University of Sydney; 2018. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2123/18621.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Biasutti S. Experimental Studies in Tendinopathy and Use of a Novel Tendon Autograft for Cartilage Resurfacing: An Ovine Model . [Thesis]. University of Sydney; 2018. Available from: http://hdl.handle.net/2123/18621

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Cornell University

6. Galley, Natalie. Alterations In Tribologic Behavior Of Cartilage During Tissue Degeneration And Repair.

Degree: PhD, Mechanical Engineering, 2012, Cornell University

URL: http://hdl.handle.net/1813/29437

► Osteoarthritis is the leading cause of disability in the United States, associated with joint pain and loss of mobility of an increasing proportion of the… (more)

Subjects/Keywords: cartilage; friction; osteoarthritis

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APA (6^th Edition):

Galley, N. (2012). Alterations In Tribologic Behavior Of Cartilage During Tissue Degeneration And Repair. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/29437

Chicago Manual of Style (16^th Edition):

Galley, Natalie. “Alterations In Tribologic Behavior Of Cartilage During Tissue Degeneration And Repair.” 2012. Doctoral Dissertation, Cornell University. Accessed March 07, 2021. http://hdl.handle.net/1813/29437.

MLA Handbook (7^th Edition):

Galley, Natalie. “Alterations In Tribologic Behavior Of Cartilage During Tissue Degeneration And Repair.” 2012. Web. 07 Mar 2021.

Vancouver:

Galley N. Alterations In Tribologic Behavior Of Cartilage During Tissue Degeneration And Repair. [Internet] [Doctoral dissertation]. Cornell University; 2012. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/1813/29437.

Council of Science Editors:

Galley N. Alterations In Tribologic Behavior Of Cartilage During Tissue Degeneration And Repair. [Doctoral Dissertation]. Cornell University; 2012. Available from: http://hdl.handle.net/1813/29437

University of Illinois – Chicago

7. Stoia, Jonathan L. Cartilage-on-Cartilage Articulating System as a Wear Benchmark for Artificial Replacement Materials.

Degree: 2012, University of Illinois – Chicago

URL: http://hdl.handle.net/10027/9057

► A multidisciplinary study – with applications in engineering, tribology, biomechanics, orthopedics, biochemistry and biology – was conducted to establish a wear system that could be… (more)

▼ A multidisciplinary study – with applications in engineering, tribology, biomechanics, orthopedics, biochemistry and biology – was conducted to establish a wear system that could be used to critically evaluate candidate artificial materials for clinical application in diarthrodial joint rehabilitation. More specifically, this study was conducted to examine the effects of articulating artificial materials against live cartilage by direct comparison to a model that articulated cartilage on cartilage. The goal of this study was met by addressing the following specific aims: 1) To modify the current material-on-cartilage setup to accommodate a cartilage-on-cartilage articulating system; 2) To investigate the effects of using synovial fluid as a lubricant in material-on-cartilage wear experiments as opposed to culture media; 3) To establish a cartilage-on-cartilage articulating system as a benchmark for material-on-cartilage wear experiments. Wear testing was performed in which cobalt chromium alloy (CoCrMo) balls or cartilage strips secured to polymer adapters were articulated against flat cartilage explants. All samples were cultured in constant temperature (37 ºC), humidity (95%) and CO2 level (5%) five days prior to wear testing. In order to apply load (40 N) and motion (±30° ball rotation; 5.2 mm migrating contact) a joint-motion simulator was used. A total of 16200 cycles at 0.5 Hz equally spread over three testing days was applied. A current method of articulating material on cartilage was modified to accommodate articulation of cartilage strips against flat cartilage explants. It was observed that synovial fluid performed significantly better than culture media as a lubricant with respect to maintaining the integrity of the cartilage matrix. It was also observed that cell viability of the explants significantly decreased when synovial fluid was used as the lubricant. The cartilage-on-cartilage model performed significantly better than the material-on-cartilage model with respect to maintaining matrix integrity, cell viability and surface topography characteristics during wear testing. Overall, the findings of this study have improved the current tribological methods of evaluating articular cartilage as well as candidate artificial materials for use in clinical joint rehabilitation treatments. Specifically, this study is directly applicable to clinical studies that facilitate hemiarthroplasties. The findings of this study may also lead to further development of critical evaluation methods and treatments involving articular cartilage and artificial materials. Advisors/Committee Members: Wimmer, Markus (advisor).

Subjects/Keywords: Articular cartilage; biotribology

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APA (6^th Edition):

Stoia, J. L. (2012). Cartilage-on-Cartilage Articulating System as a Wear Benchmark for Artificial Replacement Materials. (Thesis). University of Illinois – Chicago. Retrieved from http://hdl.handle.net/10027/9057

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Stoia, Jonathan L. “Cartilage-on-Cartilage Articulating System as a Wear Benchmark for Artificial Replacement Materials.” 2012. Thesis, University of Illinois – Chicago. Accessed March 07, 2021. http://hdl.handle.net/10027/9057.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Stoia, Jonathan L. “Cartilage-on-Cartilage Articulating System as a Wear Benchmark for Artificial Replacement Materials.” 2012. Web. 07 Mar 2021.

Vancouver:

Stoia JL. Cartilage-on-Cartilage Articulating System as a Wear Benchmark for Artificial Replacement Materials. [Internet] [Thesis]. University of Illinois – Chicago; 2012. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/10027/9057.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Stoia JL. Cartilage-on-Cartilage Articulating System as a Wear Benchmark for Artificial Replacement Materials. [Thesis]. University of Illinois – Chicago; 2012. Available from: http://hdl.handle.net/10027/9057

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Queen Mary, University of London

8. Thomas, Bethan. WNT16 in chondrocyte biology and lineage determination.

Degree: PhD, 2015, Queen Mary, University of London

URL: http://qmro.qmul.ac.uk/xmlui/handle/123456789/9870 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.775127

► Background. During development WNT16 is a specific marker of the superficial zone of the developing articular cartilage. In adult joints WNT16 is no longer expressed,… (more)

▼ Background. During development WNT16 is a specific marker of the superficial zone of the developing articular cartilage. In adult joints WNT16 is no longer expressed, but it becomes rapidly upregulated in the articular cartilage following injury and in osteoarthritis. Unpublished data from our laboratory show that WNT16 deficient mice are more susceptible to instability-induced osteoarthritis. The superficial zone of the articular cartilage contains chondrogenic progenitor cells which are essential for the long-term maintenance of cartilage homeostasis. These cells express WNT16 and also specifically express Lubricin. Lubricin, in adulthood, is essential for joint lubrication and in its absence, mice develop spontaneous osteoarthritis. Results. Exogenous WNT16 dose-dependently increased Lubricin expression in wnt16-/- superficial zone cells and primary bovine chondrocytes. WNT16 treatment also dose-dependently modulated Axin2, a transcriptional target of the canonical Wnt pathway. At low concentration Wnt16 downregulated axin2 expression, while higher concentrations caused upregulation compared to control. WNT16 also caused a dose-dependent phosphorylation of c-Jun transcription factor. In keeping with my data in chondrocytes, in xenopus laevis experiments, WNT16 had a limited capacity to induce features of axis duplication, but could efficiently inhibit axis duplication induced by WNT8. Importantly, both DKK1 and TCS (inhibitors of the canonical Wnt pathway and of the JNK pathways, respectively) prevented the WNT16-induced Lubricin upregulation, thereby demonstrating that modulation of the gene by WNT16 requires both the canonical Wnt pathway and the JNK pathways. WNT16 supported the phenotype of superficial zone cells by enhancing Lubricin expression and by preventing their full chondrocytic maturation: extracellular matrix production was increased in wnt16-/- superficial zone cells and chondrocyte specific marker were lost upon WNT16 stimulation in these cells as well as in bovine primary chondrocytes. Conclusion. WNT16 is a weak activator of the canonical Wnt pathway which supports lubricin expression and the phenotype of the cartilage superficial zone cells.

Subjects/Keywords: WNT16; Articular cartilage

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APA (6^th Edition):

Thomas, B. (2015). WNT16 in chondrocyte biology and lineage determination. (Doctoral Dissertation). Queen Mary, University of London. Retrieved from http://qmro.qmul.ac.uk/xmlui/handle/123456789/9870 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.775127

Chicago Manual of Style (16^th Edition):

Thomas, Bethan. “WNT16 in chondrocyte biology and lineage determination.” 2015. Doctoral Dissertation, Queen Mary, University of London. Accessed March 07, 2021. http://qmro.qmul.ac.uk/xmlui/handle/123456789/9870 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.775127.

MLA Handbook (7^th Edition):

Thomas, Bethan. “WNT16 in chondrocyte biology and lineage determination.” 2015. Web. 07 Mar 2021.

Vancouver:

Thomas B. WNT16 in chondrocyte biology and lineage determination. [Internet] [Doctoral dissertation]. Queen Mary, University of London; 2015. [cited 2021 Mar 07]. Available from: http://qmro.qmul.ac.uk/xmlui/handle/123456789/9870 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.775127.

Council of Science Editors:

Thomas B. WNT16 in chondrocyte biology and lineage determination. [Doctoral Dissertation]. Queen Mary, University of London; 2015. Available from: http://qmro.qmul.ac.uk/xmlui/handle/123456789/9870 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.775127

Universiteit Utrecht

9. Rijswijk, J.W. van. Soluble Mediators in Cartilage Regeneration.

Degree: 2013, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/278456

► Osteoarthritis (OA) is an increasing problem in orthopedics. Many factors may contribute to its development, including mechanically induced impact trauma, normal wear and tear, joint… (more)

Subjects/Keywords: Articular cartilage; Osteoarthritis; Regeneration; Cartilage repair; Cartilage biology; Soluble mediators; Stem cells

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APA (6^th Edition):

Rijswijk, J. W. v. (2013). Soluble Mediators in Cartilage Regeneration. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/278456

Chicago Manual of Style (16^th Edition):

Rijswijk, J W van. “Soluble Mediators in Cartilage Regeneration.” 2013. Masters Thesis, Universiteit Utrecht. Accessed March 07, 2021. http://dspace.library.uu.nl:8080/handle/1874/278456.

MLA Handbook (7^th Edition):

Rijswijk, J W van. “Soluble Mediators in Cartilage Regeneration.” 2013. Web. 07 Mar 2021.

Vancouver:

Rijswijk JWv. Soluble Mediators in Cartilage Regeneration. [Internet] [Masters thesis]. Universiteit Utrecht; 2013. [cited 2021 Mar 07]. Available from: http://dspace.library.uu.nl:8080/handle/1874/278456.

Council of Science Editors:

Rijswijk JWv. Soluble Mediators in Cartilage Regeneration. [Masters Thesis]. Universiteit Utrecht; 2013. Available from: http://dspace.library.uu.nl:8080/handle/1874/278456

University of Kansas

10. Beck, Emily Claire. Development of Chondroinductive Hydrogel Pastes from Naturally Derived Cartilage Matrix.

Degree: PhD, Bioengineering, 2015, University of Kansas

URL: http://hdl.handle.net/1808/20930

► The main focus of hydrogel technology is on hydrogels in their crosslinked form. Although hydrogels are promising materials for cartilage tissue engineering, the clinical translation… (more)

▼ The main focus of hydrogel technology is on hydrogels in their crosslinked form. Although hydrogels are promising materials for cartilage tissue engineering, the clinical translation of these materials are hindered because they lack the ability to be molded into a defect site by a surgeon due to hydrogel precursors being liquid solutions that are prone to leaking from the implantation site during placement. Therefore, the current thesis work focuses on the hydrogels in their precursor form prior to crosslinking and describes the development of creating hydrogel pastes that have the potential to be clinically translatable. The current thesis first developed a platform hydrogel paste composed of methacrylated hyaluronic acid (MeHA), which is a more traditional hydrogel material, and hyaluronic acid nanoparticles. The hyaluronic acid nanoparticles were shown to impart a yield stress on the hydrogel precursors, allowing the precursors to be molded and shaped prior to crosslinking. Furthermore, the mixtures containing hyaluronic acid nanoparticles were able to be crosslinked and further characterized as solids and they could encapsulate bone marrow-derived stem cells that remained viable. The next major focus of the thesis was tailoring the platform system for cartilage tissue specifically, by gradually replacing each of the two components of the platform system with naturally derived cartilage extracellular matrix, to create a chondroinductive material. Devitalized (DVC) and decellularized cartilage (DCC) particles were found to impart paste-like behavior in MeHA gels, where DVC significantly upregulated chondrogenic gene expression. DCC that was solubilized and methacrylated (MeSDCC) was created and crosslinked, which formed hydrogels with a compressive modulus in the range of native cartilage tissue. Finally, DVC particles mixed in with solubilized and methacrylated DVC created pastes that significantly upregulated chondrogenic gene expression compared to gels without DVC particles. The important next steps will be to further evaluate these MeSDVC and DVC particle pastes in an in vivo model, and further explore whether decellularization of the tissue is necessary. Ultimately, this thesis successfully developed a hydrogel paste that is inherently chondroinductive and promising for future cartilage tissue engineering applications. Advisors/Committee Members: Detamore, Michael S. (advisor), Berkland, Cory J. (cmtemember), Gerke, Stevin H. (cmtemember), Kieweg, Sarah L. (cmtemember), Andrews, Brian T. (cmtemember).

Subjects/Keywords: Biomedical engineering; cartilage matrix; chondroinduction; decelluarized cartilage; devitalized cartilage; hydrogel paste; tissue engineering

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APA (6^th Edition):

Beck, E. C. (2015). Development of Chondroinductive Hydrogel Pastes from Naturally Derived Cartilage Matrix. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/20930

Chicago Manual of Style (16^th Edition):

Beck, Emily Claire. “Development of Chondroinductive Hydrogel Pastes from Naturally Derived Cartilage Matrix.” 2015. Doctoral Dissertation, University of Kansas. Accessed March 07, 2021. http://hdl.handle.net/1808/20930.

MLA Handbook (7^th Edition):

Beck, Emily Claire. “Development of Chondroinductive Hydrogel Pastes from Naturally Derived Cartilage Matrix.” 2015. Web. 07 Mar 2021.

Vancouver:

Beck EC. Development of Chondroinductive Hydrogel Pastes from Naturally Derived Cartilage Matrix. [Internet] [Doctoral dissertation]. University of Kansas; 2015. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/1808/20930.

Council of Science Editors:

Beck EC. Development of Chondroinductive Hydrogel Pastes from Naturally Derived Cartilage Matrix. [Doctoral Dissertation]. University of Kansas; 2015. Available from: http://hdl.handle.net/1808/20930

Universiteit Utrecht

11. Goversen, B. Mechanics in articular cartilage regeneration.

Degree: 2015, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/307805

► Articular cartilage is an avascular load-bearing tissue lining the surface of long bones where it serves for the absorbance of shocks as well as the… (more)

Subjects/Keywords: Cartilage; tissue engineering; mechanics; biofabrication

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APA (6^th Edition):

Goversen, B. (2015). Mechanics in articular cartilage regeneration. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/307805

Chicago Manual of Style (16^th Edition):

Goversen, B. “Mechanics in articular cartilage regeneration.” 2015. Masters Thesis, Universiteit Utrecht. Accessed March 07, 2021. http://dspace.library.uu.nl:8080/handle/1874/307805.

MLA Handbook (7^th Edition):

Goversen, B. “Mechanics in articular cartilage regeneration.” 2015. Web. 07 Mar 2021.

Vancouver:

Goversen B. Mechanics in articular cartilage regeneration. [Internet] [Masters thesis]. Universiteit Utrecht; 2015. [cited 2021 Mar 07]. Available from: http://dspace.library.uu.nl:8080/handle/1874/307805.

Council of Science Editors:

Goversen B. Mechanics in articular cartilage regeneration. [Masters Thesis]. Universiteit Utrecht; 2015. Available from: http://dspace.library.uu.nl:8080/handle/1874/307805

University of Rochester

12. Gao, Lin (1976 - ). The Role of TAK1 Mediated Signaling in Cartilage Development and Disease.

Degree: PhD, 2012, University of Rochester

URL: http://hdl.handle.net/1802/25536

► Cartilage is a connective tissue required for the growth of a developing animal and serves as the cushion for joints. In longitudinal bone development, endochondral… (more)

▼ Cartilage is a connective tissue required for the growth of a developing animal and serves as the cushion for joints. In longitudinal bone development, endochondral ossification converts cartilage anlagen into bone through sequential stages from mesenchymal cell condensation to chondrocyte proliferation, hypertrophy and terminal maturation, followed by osteoblasts invasion and bone matrix deposition. Disruption of any of these developmental stages leads to cartilage and bone defects. Better understanding of the mechanisms underlying cartilage development and maintenance will make it possible for better medical care for cartilage and skeletal disease. Tgfβ and BMP are secreted ligands belonging to the Tgfβ superfamily growth factors, and have various roles in cartilage physiological and pathological processes. Tgfβ superfamily members bind to serine/threonine kinase type I and type II receptors and signal through canonical and noncanonical signaling pathways. This dissertation aims to define the roles of noncanonical Tgfβ and BMP signal transduction in postnatal cartilage development and homeostasis. To achieve this goal, BMP type I receptors were assessed, in which Alk3 shows the potential to mediate BMP and Tgfβ induced TAK1-P38-ATF2 signaling pathway and has an effect on canonical BMP and Tgfβ signaling, which argues that in addition to being a BMP type I receptor, Alk3 bridges both Tgfβ and BMP to cytoplasmic signals. In a second set of experiments, cartilage specific, inducible TAK1 loss of function mice were generated. Loss of TAK1 at one week shows severe growth retardation at one month. Analysis of the knee joint cartilage shows loss of proteoglycans, decreased Type II collagen and Aggrecan I expression and reduced chondrocyte proliferation. Additionally, expression of Sox9, Sox5 and Sox6, master regulators of chondrogenesis and chondrocyte proliferation was suppressed upon deletion of TAK1. The signaling mechanism by which TAK1 regulates Sox9 expression was also assessed. The TAK1-P38-ATF2 signaling pathway works synergistically with the canonical Smad-dependent BMP signaling pathway on the regulation of Sox9 gene expression. Overall, this dissertation sheds lights on the mechanism of TAK1 mediated signaling in postnatal cartilage development and homeostasis and may contribute to the development of novel therapeutics for cartilage diseases such as chondrodysplasisa and osteoarthritis (OA).

Subjects/Keywords: TAK1; Cartilage; Development; Disease

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APA (6^th Edition):

Gao, L. (. -. ). (2012). The Role of TAK1 Mediated Signaling in Cartilage Development and Disease. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/25536

Chicago Manual of Style (16^th Edition):

Gao, Lin (1976 - ). “The Role of TAK1 Mediated Signaling in Cartilage Development and Disease.” 2012. Doctoral Dissertation, University of Rochester. Accessed March 07, 2021. http://hdl.handle.net/1802/25536.

MLA Handbook (7^th Edition):

Gao, Lin (1976 - ). “The Role of TAK1 Mediated Signaling in Cartilage Development and Disease.” 2012. Web. 07 Mar 2021.

Vancouver:

Gao L(-). The Role of TAK1 Mediated Signaling in Cartilage Development and Disease. [Internet] [Doctoral dissertation]. University of Rochester; 2012. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/1802/25536.

Council of Science Editors:

Gao L(-). The Role of TAK1 Mediated Signaling in Cartilage Development and Disease. [Doctoral Dissertation]. University of Rochester; 2012. Available from: http://hdl.handle.net/1802/25536

University of Rochester

13. Kohn, Anat. The Role of RBPjκ-Dependent Notch Signaling During Cartilage Development of the Limb Skeleton.

Degree: PhD, 2013, University of Rochester

URL: http://hdl.handle.net/1802/27308

► Cartilage development within the limb skeleton is initiated by the condensation of mesenchymal progenitor cells within the developing limb bud. These progenitors undergo chondrogenesis to… (more)

▼ Cartilage development within the limb skeleton is initiated by the condensation of mesenchymal progenitor cells within the developing limb bud. These progenitors undergo chondrogenesis to generate immature chondrocytes and the cartilage template from which individual skeletal elements form. Chondrocytes must undergo a highly organized process of proliferation, differentiation, and cell death in order to achieve normal skeletal growth and function. These processes of chondrocyte proliferation, hypertrophic and terminal hypertrophic differentiation, and cartilage matrix turnover are intricately regulated by developmental signaling pathways that include: Ihh/PTHrP, Wnt/β-catenin, BMPs and FGFs. Importantly, many of these genetic pathways are defective in congenital and age related cartilage diseases (ie. chondrodysplasias and osteoarthritis), and therefore elucidating the molecular mechanisms by which cartilage develops is crucial to our understanding of cartilage disorders, the repair response to cartilage injury, and age associated changes observed in growth plate and joint cartilages. Recently, our group and others identified the Notch signaling pathway as yet another important regulator of cartilage development. The work presented here set out to determine the molecular mechanisms by which Notch signaling regulates chondrocyte proliferation, hypertrophic differentiation, and terminal chondrocyte maturation using both in vivo and in vitro approaches. Specifically, we relied heavily upon mouse genetic approaches using the Cre/loxP system to generate various Notch-related gain- and loss-of-function mouse models for our analyses. Our studies established, for the first time, that RBPjκ-dependent Notch signaling regulates both the onset of chondrocyte hypertrophy and terminal chondrocyte maturation. Surprisingly, the RBPjκ-independent pathway was identified as a regulator of chondrocyte proliferation, and a long-range, cell non-autonomous regulator of perichondral bone formation. Further studies established Sox9, the master transcriptional regulator of chondrogeneis, as a target of RBPjκ-dependent Notch signaling important for Notch-mediated regulation of chondrocyte hypertrophy. Finally, HES1 was identified as at least one of the mediators of RBPjκ-dependent Notch signaling in the regulation of Sox9 and the initiation of hypertrophy. Taken together, this work provides a strong foundation for our molecular understanding of how Notch signaling regulates cartilage development, allowing future studies to bring even further clarification to the role of Notch signaling in both normal cartilage development and disease.

Subjects/Keywords: NOTCH; Cartilage; Endochondral; Bone; Development

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APA (6^th Edition):

Kohn, A. (2013). The Role of RBPjκ-Dependent Notch Signaling During Cartilage Development of the Limb Skeleton. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/27308

Chicago Manual of Style (16^th Edition):

Kohn, Anat. “The Role of RBPjκ-Dependent Notch Signaling During Cartilage Development of the Limb Skeleton.” 2013. Doctoral Dissertation, University of Rochester. Accessed March 07, 2021. http://hdl.handle.net/1802/27308.

MLA Handbook (7^th Edition):

Kohn, Anat. “The Role of RBPjκ-Dependent Notch Signaling During Cartilage Development of the Limb Skeleton.” 2013. Web. 07 Mar 2021.

Vancouver:

Kohn A. The Role of RBPjκ-Dependent Notch Signaling During Cartilage Development of the Limb Skeleton. [Internet] [Doctoral dissertation]. University of Rochester; 2013. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/1802/27308.

Council of Science Editors:

Kohn A. The Role of RBPjκ-Dependent Notch Signaling During Cartilage Development of the Limb Skeleton. [Doctoral Dissertation]. University of Rochester; 2013. Available from: http://hdl.handle.net/1802/27308

University of Rochester

14. Nowacki, Sara Monica. Effects of intermittent parathyroid hormone treatment on human mesenchymal stem cells and in cartilage-derived matrix-augmented repair of osteochondral defects.

Degree: PhD, 2018, University of Rochester

URL: http://hdl.handle.net/1802/33314

► Microfracture (μFx) is the gold-standard for small lesion cartilage repair due to its simplicity as a surgical procedure, however this repair results in a compositionally… (more)

▼ Microfracture (μFx) is the gold-standard for small lesion cartilage repair due to its simplicity as a surgical procedure, however this repair results in a compositionally and mechanically inferior cartilage tissue termed fibrocartilage that results in long-term failure. We proposed a dual-treatment method of a cartilage-derived matrix (CDM) in conjunction with parathyroid hormone (1-34) (PTH(1-34)) to improve the compositional quality of microfracture repair tissue in an osteochondral defect in rabbit medial femoral condyles, and explored how PTH(1-34) modulated chondroregeneration of mesenchymal stem cells (MSC) embedded in CDM in vitro over the course of 28 days. The CDM in conjunction with chondrogenic factors upregulated MSC aggrecan gene expression and proteoglycan deposition, however there was also upregulation of hypertrophic markers MMP13 and COL10A1 compared to MSCs embedded in a type I collagen matrix in vitro. There was suppression of chondrogenic as well as fibrotic and hypertrophic gene expression regardless of PTH(1-34) dosing in MSCs concurrently treated with chondrogenic factors, namely TGF-β3. Osteochondral defects treated with two weeks of PTH(1-34) showed improved repair immediately after treatment, however these effects subsided and by later time points there was no difference in repair tissue composition or Pineda score. The addition of CDM resulted in a delayed healing response regardless of PTH(1-34) treatment, however due to poor CDM cell infiltration there was suboptimal repair in these defects. We introduced a novel shear testing method that quantified depth-dependent shear strain and assessed quality of integration between healthy cartilage and repair tissue at the integration sites. Depth-dependent shear strain was found in both saline- and PTH-treated μFx defects, as well as saline- and PTH-treated μFx+CDM defects, however the rate of change of shear strain throughout the depth was significantly lower in all groups compared to healthy controls. Peeling strain (εxx) and sliding strain (εxy) were quanitifed to assess quality of integration. Integration between healthy and repair tissue was found in all treatment groups, however the addition of CDM did not provide any mechanical or structural benefits to the resulting repair tissue. All groups had εxx and εxy values higher than healthy controls, indicating that the integrated tissue had not attained native articular cartilage composition. Based on improvement in early repair, as well as promising results on high quality of integration between the defect and healthy tissue, these results suggest that PTH treatment has potential as a surgical adjuvant, and work on matrix optimization and future dosing regimens, including long-term PTH treatment, should be further explored.

Subjects/Keywords: Parathyroid hormone; Cartilage; Microfracture

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APA (6^th Edition):

Nowacki, S. M. (2018). Effects of intermittent parathyroid hormone treatment on human mesenchymal stem cells and in cartilage-derived matrix-augmented repair of osteochondral defects. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/33314

Chicago Manual of Style (16^th Edition):

Nowacki, Sara Monica. “Effects of intermittent parathyroid hormone treatment on human mesenchymal stem cells and in cartilage-derived matrix-augmented repair of osteochondral defects.” 2018. Doctoral Dissertation, University of Rochester. Accessed March 07, 2021. http://hdl.handle.net/1802/33314.

MLA Handbook (7^th Edition):

Nowacki, Sara Monica. “Effects of intermittent parathyroid hormone treatment on human mesenchymal stem cells and in cartilage-derived matrix-augmented repair of osteochondral defects.” 2018. Web. 07 Mar 2021.

Vancouver:

Nowacki SM. Effects of intermittent parathyroid hormone treatment on human mesenchymal stem cells and in cartilage-derived matrix-augmented repair of osteochondral defects. [Internet] [Doctoral dissertation]. University of Rochester; 2018. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/1802/33314.

Council of Science Editors:

Nowacki SM. Effects of intermittent parathyroid hormone treatment on human mesenchymal stem cells and in cartilage-derived matrix-augmented repair of osteochondral defects. [Doctoral Dissertation]. University of Rochester; 2018. Available from: http://hdl.handle.net/1802/33314

University of Alberta

15. Hahn, Joshua N. Optimization of Vitrification for Human Articular Cartilage.

Degree: MS, Department of Surgery, 2015, University of Alberta

URL: https://era.library.ualberta.ca/files/2b88qg163

► Osteoarthritis, a disease resulting in the breakdown of cartilage and bone within joints, is a global burden that is growing in scope. There is no… (more)

▼ Osteoarthritis, a disease resulting in the breakdown of cartilage and bone within joints, is a global burden that is growing in scope. There is no cure for osteoarthritis, and the current treatments are all lacking in some form or another. One treatment which attempts to prevent degeneration of cartilage injury into osteoarthritis is osteochondral allografting. This surgery involves the transplantation of healthy bone and cartilage to replace damaged and diseased areas. Osteochondral allografting application is limited primarily by the supply of fresh, healthy tissue and the lack of a long-term storage method that maintains cell viability within cartilage. Vitrification is a method of cryopreservation that preserves cells and tissues at temperatures low enough to halt all biological activity while maintaining cell health when applied properly. Previous work within this lab resulted in successful vitrification of human articular cartilage, but there is room for improvement. The current research was performed to explore the use of additive compounds as well as the use of a vitrification protocol with altered cryoprotectant exposure criteria in an attempt to improve the post-warmed health of the cryopreserved cartilage tissue. The use of chondroitin sulphate, tetramethylpyrazine, a combination of these two, ascorbic acid, and glucosamine was investigated in a set of cryoprotectant toxicity mitigation experiments. We found that when evaluating the effect of exposure to these compounds in a toxic cryoprotectant solution coupled with a two-day incubation, that all but the chondroitin sulphate alone were capable of improving tissue health, while there were no benefits seen when evaluated before the incubation period. The use of additive compounds has been shown to reduce long-term deleterious effects of CPA exposure, indicating that their use may be beneficial to a vitrification application due to the high CPA concentrations involved. This thesis also experimentally explored an altered cryoprotectant protocol proposed by another student, Nadia Shardt, who used Fick’s 1-D law of diffusion to determine the minimum time required for the diffusion of cryoprotectants into articular cartilage in concentrations that were adequate for vitrification. These modifications reduced the protocol length by one and a half hours, but did not result in viability results that were significantly improved over the standard protocol. As the experimental trials in this thesis work all produced a recovery cell viability that is much lower than the previously published results for the standard vitrification protocol, no conclusions can be made regarding which protocol to use based on these data. The experimental groups did not have an obvious deleterious effect on cell viability and, therefore, the reduction in protocol time may be beneficial. The standard vitrification protocol for articular cartilage has shown good results. The experiments performed here demonstrate that there are two potential avenues that may be exploited to enhance cell…

Subjects/Keywords: Articular Cartilage; Vitrification; Cryopreservation

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APA (6^th Edition):

Hahn, J. N. (2015). Optimization of Vitrification for Human Articular Cartilage. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/2b88qg163

Chicago Manual of Style (16^th Edition):

Hahn, Joshua N. “Optimization of Vitrification for Human Articular Cartilage.” 2015. Masters Thesis, University of Alberta. Accessed March 07, 2021. https://era.library.ualberta.ca/files/2b88qg163.

MLA Handbook (7^th Edition):

Hahn, Joshua N. “Optimization of Vitrification for Human Articular Cartilage.” 2015. Web. 07 Mar 2021.

Vancouver:

Hahn JN. Optimization of Vitrification for Human Articular Cartilage. [Internet] [Masters thesis]. University of Alberta; 2015. [cited 2021 Mar 07]. Available from: https://era.library.ualberta.ca/files/2b88qg163.

Council of Science Editors:

Hahn JN. Optimization of Vitrification for Human Articular Cartilage. [Masters Thesis]. University of Alberta; 2015. Available from: https://era.library.ualberta.ca/files/2b88qg163

Cornell University

16. Novakofski, Kira. High Resolution Imaging Of Early, Subclinical Cartilage Injuries: Implications For The Diagnosis And Treatment Of Post-Traumatic Osteoarthritis.

Degree: PhD, Veterinary Medicine, 2014, Cornell University

URL: http://hdl.handle.net/1813/36101

► Osteoarthritis (OA) is a degenerative disease. Currently, there are no treatments to restore damaged cartilage to its native state. Joint injury increases the risk of… (more)

▼ Osteoarthritis (OA) is a degenerative disease. Currently, there are no treatments to restore damaged cartilage to its native state. Joint injury increases the risk of developing post-traumatic OA (PTOA). Subtle cartilage injury that may progress to PTOA cannot be detected with current clinical imaging modalities. If subtle cartilage injury is detectable, PTOA can be better understood to develop treatments targeting early disease progression. The goal of this dissertation was to evaluate methods for detecting, characterizing, and treating early cartilage injury. Multiphoton microscopy (MPM) can provide high resolution details of live, intact tissue. The purpose of the first study was to validate the use of MPM to detect subtle cartilage damage. The results confirmed the ability of MPM to resolve structural changes and cell death in cartilage immediately after injury. This suggests future application of MPM in the clinic for early diagnosis or in the laboratory to perform longitudinal studies not currently possible due to the necessity of histological processing. In the second study, cartilage and its resiliency to injury were evaluated among eight major joints to determine if there are different susceptibilities to injury in different joints. The structure of articular cartilage and prevalence of OA vary among joints, but typically results from work performed within a single joint are applied to other joints. The results from the second study showed that some joints have more cellular death and/or decrease anabolic gene expression than other joints after receiving the same injury, which suggests the need for joint specific treatments. The third study examined the role of oxygen in the development of PTOA. Cartilage is avascular and has limited oxygen supply. Oxygen tension may be increased in arthritic joints, yet short exposure to high oxygen tension is beneficial to uninjured cartilage. In this final study, the effect of increased oxygen tension on cartilage viability after injury was evaluated. The immediate application of hyperoxic treatment minimized cell death after injury, suggesting that the immediate application of high oxygen following injury may be chondroprotective. These findings have implications in future treatments that could minimize the effect of cartilage injury and development of PTOA. Advisors/Committee Members: Fortier, Lisa Ann (chair), Williams, Rebecca M. (committee member), Farnum, Cornelia E (committee member), Rodeo, Scott Alan (committee member), Jin, Moonsoo (committee member).

Subjects/Keywords: cartilage injury; osteoarthritis; imaging

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APA (6^th Edition):

Novakofski, K. (2014). High Resolution Imaging Of Early, Subclinical Cartilage Injuries: Implications For The Diagnosis And Treatment Of Post-Traumatic Osteoarthritis. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/36101

Chicago Manual of Style (16^th Edition):

Novakofski, Kira. “High Resolution Imaging Of Early, Subclinical Cartilage Injuries: Implications For The Diagnosis And Treatment Of Post-Traumatic Osteoarthritis.” 2014. Doctoral Dissertation, Cornell University. Accessed March 07, 2021. http://hdl.handle.net/1813/36101.

MLA Handbook (7^th Edition):

Novakofski, Kira. “High Resolution Imaging Of Early, Subclinical Cartilage Injuries: Implications For The Diagnosis And Treatment Of Post-Traumatic Osteoarthritis.” 2014. Web. 07 Mar 2021.

Vancouver:

Novakofski K. High Resolution Imaging Of Early, Subclinical Cartilage Injuries: Implications For The Diagnosis And Treatment Of Post-Traumatic Osteoarthritis. [Internet] [Doctoral dissertation]. Cornell University; 2014. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/1813/36101.

Council of Science Editors:

Novakofski K. High Resolution Imaging Of Early, Subclinical Cartilage Injuries: Implications For The Diagnosis And Treatment Of Post-Traumatic Osteoarthritis. [Doctoral Dissertation]. Cornell University; 2014. Available from: http://hdl.handle.net/1813/36101

Texas A&M University

17. Dickson, Emily Claire. Effect of Complexed Trace Mineral Supplementation on Joint Health in Young, Exercising Horses.

Degree: MS, Animal Science, 2018, Texas A&M University

URL: http://hdl.handle.net/1969.1/173410

► Osteoarthritis has been named one of the major causes of lameness in horses, and remains one of the main reasons for performance loss. Nutritional interventions… (more)

Subjects/Keywords: Equine; Trace minerals; Cartilage

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APA (6^th Edition):

Dickson, E. C. (2018). Effect of Complexed Trace Mineral Supplementation on Joint Health in Young, Exercising Horses. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/173410

Chicago Manual of Style (16^th Edition):

Dickson, Emily Claire. “Effect of Complexed Trace Mineral Supplementation on Joint Health in Young, Exercising Horses.” 2018. Masters Thesis, Texas A&M University. Accessed March 07, 2021. http://hdl.handle.net/1969.1/173410.

MLA Handbook (7^th Edition):

Dickson, Emily Claire. “Effect of Complexed Trace Mineral Supplementation on Joint Health in Young, Exercising Horses.” 2018. Web. 07 Mar 2021.

Vancouver:

Dickson EC. Effect of Complexed Trace Mineral Supplementation on Joint Health in Young, Exercising Horses. [Internet] [Masters thesis]. Texas A&M University; 2018. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/1969.1/173410.

Council of Science Editors:

Dickson EC. Effect of Complexed Trace Mineral Supplementation on Joint Health in Young, Exercising Horses. [Masters Thesis]. Texas A&M University; 2018. Available from: http://hdl.handle.net/1969.1/173410

Texas A&M University

18. Kahn, Meredith K. Age-Related Effects on Markers of Inflammation and Cartilage Metabolism in Response to an Intra-Articular Lipopolysaccharide Challenge.

Degree: MS, Animal Science, 2014, Texas A&M University

URL: http://hdl.handle.net/1969.1/154113

► Eighteen Quarter Horses were utilized in a randomized complete design for a 28 d experiment to evaluate age-related effects on inflammation and cartilage turnover after… (more)

▼ Eighteen Quarter Horses were utilized in a randomized complete design for a 28 d experiment to evaluate age-related effects on inflammation and cartilage turnover after induction of a single inflammatory insult using lipopolysaccharide (LPS). Horses were grouped by age, with yearlings (yearling; n = 3 males, n = 3 females), 2 to 3 yr olds (2/3; n = 2 males, n = 4 females), and mature 5 to 8 yr olds (mature; n = 2 males, n = 4 females). On d 0, all horses were housed individually and fed diets that met or exceeded NRC (2007) requirements. On d 14, horses were challenged with an intra-articular injection of LPS. Carpal joints were randomly assigned to receive 0.5 ng LPS solution obtained from E. coli O55:B5, or 0.8mL sterile lactated Ringer’s solution as a contralateral control. Synovial fluid was collected prior to LPS injection at pre-injection h 0 (PIH 0) and 6, 12, 24, 168, and 336 h post-injection. Samples were later analyzed using commercial ELISA kits for prostaglandin E2 (PGE2), collagenase cleavage neoepitope (C2C), and carboxypropeptide of type II collagen (CPII). Heart rate (HR), respiratory rate (RR), and rectal temperature (RT) were monitored over the first 24 h and carpal circumference and surface temperature were recorded with additional measurements at 168 and 336 h. Data were analyzed using PROC MIXED procedure of SAS. Values for RT, HR, and RR were within normal range. HR and RT were influenced by age (P < 0.01), while RR was unaffected by age (P ≤ 0.21). Joint circumference was not influenced by age (P = 0.84), but circumference and surface temperature increased (P < 0.01) over time across all age groups. Synovial PGE2 concentrations tended (P = 0.09) to be influenced by age with yearlings having lower (P = 0.03) concentrations than mature horses. Synovial C2C concentrations were affected by age with yearlings and 2/3 yr olds having lower (P < 0.01) concentrations than mature horses. Concentrations of synovial CPII were influenced by age with yearlings and 2/3 yr old having lower (P ≤ 0.02) concentrations than mature horses. Ratios of CPII:C2C were influenced by age with mature and 2/3 yr old horses having increased (P < 0.01) values compared to yearlings. These results indicate that inflammation and corresponding cartilage turnover in response to LPS administration vary with age. Advisors/Committee Members: Coverdale, Josie A (advisor), Lucia, Jessica L. (committee member), Welsh, Thomas H. (committee member), Wickersham, Tryon A. (committee member).

Subjects/Keywords: Age; Horse; Lipopolysaccharide; Inflammation; Cartilage

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APA (6^th Edition):

Kahn, M. K. (2014). Age-Related Effects on Markers of Inflammation and Cartilage Metabolism in Response to an Intra-Articular Lipopolysaccharide Challenge. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/154113

Chicago Manual of Style (16^th Edition):

Kahn, Meredith K. “Age-Related Effects on Markers of Inflammation and Cartilage Metabolism in Response to an Intra-Articular Lipopolysaccharide Challenge.” 2014. Masters Thesis, Texas A&M University. Accessed March 07, 2021. http://hdl.handle.net/1969.1/154113.

MLA Handbook (7^th Edition):

Kahn, Meredith K. “Age-Related Effects on Markers of Inflammation and Cartilage Metabolism in Response to an Intra-Articular Lipopolysaccharide Challenge.” 2014. Web. 07 Mar 2021.

Vancouver:

Kahn MK. Age-Related Effects on Markers of Inflammation and Cartilage Metabolism in Response to an Intra-Articular Lipopolysaccharide Challenge. [Internet] [Masters thesis]. Texas A&M University; 2014. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/1969.1/154113.

Council of Science Editors:

Kahn MK. Age-Related Effects on Markers of Inflammation and Cartilage Metabolism in Response to an Intra-Articular Lipopolysaccharide Challenge. [Masters Thesis]. Texas A&M University; 2014. Available from: http://hdl.handle.net/1969.1/154113

Texas A&M University

19. Lucia, Jessica Lauren. Influence of an Intra-articular Lipopolysaccharide Challenge on Markers of Inflammation and Cartilage Metabolism and the Ability of Oral Glucosamine to Mitigate these Alterations in Young Horses.

Degree: PhD, Animal Science, 2013, Texas A&M University

URL: http://hdl.handle.net/1969.1/149284

► This project established an in vivo method to identify and manipulate expression of markers of osteoarthritis (OA). Specifically, strategies that predictably induce joint inflammation to… (more)

▼ This project established an in vivo method to identify and manipulate expression of markers of osteoarthritis (OA). Specifically, strategies that predictably induce joint inflammation to evaluate dietary methods of OA prevention in young horses have yet to be accomplished. Therefore, the 3 studies described herein were conducted to determine effectiveness of an intra-articular lipopolysaccharide (LPS) challenge on markers of inflammation and cartilage metabolism in young horses and potential of dietary glucosamine hydrochloride (HCl) to mitigate these alterations. In the first study, horses were challenged with 0.25 ng or 0.50 ng of intra-articular LPS solution or lactated ringer’s solution (control). Injection of LPS increased inflammation based on synovial prostaglandin E2 (PGE2) concentrations. Carboxypeptide of type II collagen (CPII), a maker of type II collagen synthesis, also increased in a dose-dependent manner. However, clinical parameters of health were not influenced and remained within normal ranges. Carpal circumference increased in response to repeated arthrocentesis. Lameness scores increased with LPS injection when compared to controls. This model of joint inflammation (0.5 ng LPS) was used in the second study to evaluate potential chondroprotective effects of oral glucosamine HCl supplementation in yearling horses. Specifically, the oral absorption of glucosamine HCl versus saline was determined by nasogastric dosing and incorporation of dietary glucosamine HCl into plasma and synovial fluid over time. Plasma and synovial fluid concentrations of glucosamine tended to increase over the 98-d period. In the third study, yearlings were challenged with intra-articular LPS to determine the potential of glucosamine HCl to mitigate inflammation when compared to contralateral joints. Injection of LPS increased synovial PGE2 and cartilage biomarkers CPII and collagenase cleavage neopeptide (C2C), a marker of type II collagen degradation. Oral glucosamine HCl decreased PGE2 and C2C concentrations, but increased levels of CPII. Results of these 3 studies provide a clearer understanding of joint inflammation and cartilage turnover in young horses and demonstrated a potential role of oral glucosamine to mitigate these effects and possibly prevent OA in horses. Advisors/Committee Members: Coverdale, Josie A (advisor), Welsh, Thomas H (committee member), Arnold, Carolyn E (committee member), Heird, James C (committee member).

Subjects/Keywords: lipopolysaccharide; cartilage; inflammation; horse

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APA (6^th Edition):

Lucia, J. L. (2013). Influence of an Intra-articular Lipopolysaccharide Challenge on Markers of Inflammation and Cartilage Metabolism and the Ability of Oral Glucosamine to Mitigate these Alterations in Young Horses. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/149284

Chicago Manual of Style (16^th Edition):

Lucia, Jessica Lauren. “Influence of an Intra-articular Lipopolysaccharide Challenge on Markers of Inflammation and Cartilage Metabolism and the Ability of Oral Glucosamine to Mitigate these Alterations in Young Horses.” 2013. Doctoral Dissertation, Texas A&M University. Accessed March 07, 2021. http://hdl.handle.net/1969.1/149284.

MLA Handbook (7^th Edition):

Lucia, Jessica Lauren. “Influence of an Intra-articular Lipopolysaccharide Challenge on Markers of Inflammation and Cartilage Metabolism and the Ability of Oral Glucosamine to Mitigate these Alterations in Young Horses.” 2013. Web. 07 Mar 2021.

Vancouver:

Lucia JL. Influence of an Intra-articular Lipopolysaccharide Challenge on Markers of Inflammation and Cartilage Metabolism and the Ability of Oral Glucosamine to Mitigate these Alterations in Young Horses. [Internet] [Doctoral dissertation]. Texas A&M University; 2013. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/1969.1/149284.

Council of Science Editors:

Lucia JL. Influence of an Intra-articular Lipopolysaccharide Challenge on Markers of Inflammation and Cartilage Metabolism and the Ability of Oral Glucosamine to Mitigate these Alterations in Young Horses. [Doctoral Dissertation]. Texas A&M University; 2013. Available from: http://hdl.handle.net/1969.1/149284

Harvard University

20. Chen, Peter Hao. Attenuation of Articular Cartilage Degeneration by the Genetic Deletion of HtrA1 in Mice.

Degree: DMSc, 2017, Harvard University

URL: http://nrs.harvard.edu/urn-3:HUL.InstRepos:42080110

►

Objective To investigate whether the genetic deletion of the serine protease, high temperature requirement protein A1 (HtrA1), will attenuate the progression of articular cartilage degeneration… (more)

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Objective To investigate whether the genetic deletion of the serine protease, high temperature requirement protein A1 (HtrA1), will attenuate the progression of articular cartilage degeneration in mouse osteoarthritis (OA) models. Methods We used two mouse models for our study. The first is a genetic model of OA and includes two strains of mice. The first strain is a heterozygous genetic deletion of type-XI collagen that results in OA in mice (Col11a1+/-). The second strain is a homozygous HtrA1 knockout (HtrA1-/-). By crossing the two strains, we can analyze a possible chondral-protective effect of HtrA1-deficiency on the progression of OA. The second model is a surgical/injury model of OA, in which we performed microsurgery on the knee joints of HtrA1-/- mice to destabilize the medial meniscus (DMM). This technique undermines the joint, and rapidly induces OA in the mice. By surgically inducing osteoarthritis in HtrA1-/- knockout mice, we can simulate the effect of HtrA1-deficiency on the progression of OA due to surgery or injury. Conditions of the articular cartilage from the knee joints of the Col11a1+/-;HtrA1-/- mice, Col11a1+/- mice, HtrA1-/- mice, and the surgical mice were then examined by histology, graded on a standard scoring system, and characterized by immunohistochemistry. Results We examined the HtrA1-/- knockout mice and found no overt phenotype abnormalities. We also found that the deletion of HtrA1 delays the progressive process of articular cartilage degeneration in Col11a1+/- mice. In our surgical model, the degenerative progression towards OA was dramatically delayed in HtrA1-/- mice when compared to the controls. Conclusion Deletion of HtrA1 delays the progression of articular cartilage degeneration in OA models induced either by collagen type-XI haploinsufficiency or by DMM surgery. Therefore, the development of antagonistic drugs that specifically target HTRA1 may be an effective method to treat OA in the future.

Orthodontics

Advisors/Committee Members: Han, Xiaozhe (committee member), Gori, Francesca (committee member), Nagai, Shigemi (committee member).

Subjects/Keywords: Osteoarthritis; Articular Cartilage; HTRA1

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APA (6^th Edition):

Chen, P. H. (2017). Attenuation of Articular Cartilage Degeneration by the Genetic Deletion of HtrA1 in Mice. (Doctoral Dissertation). Harvard University. Retrieved from http://nrs.harvard.edu/urn-3:HUL.InstRepos:42080110

Chicago Manual of Style (16^th Edition):

Chen, Peter Hao. “Attenuation of Articular Cartilage Degeneration by the Genetic Deletion of HtrA1 in Mice.” 2017. Doctoral Dissertation, Harvard University. Accessed March 07, 2021. http://nrs.harvard.edu/urn-3:HUL.InstRepos:42080110.

MLA Handbook (7^th Edition):

Chen, Peter Hao. “Attenuation of Articular Cartilage Degeneration by the Genetic Deletion of HtrA1 in Mice.” 2017. Web. 07 Mar 2021.

Vancouver:

Chen PH. Attenuation of Articular Cartilage Degeneration by the Genetic Deletion of HtrA1 in Mice. [Internet] [Doctoral dissertation]. Harvard University; 2017. [cited 2021 Mar 07]. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:42080110.

Council of Science Editors:

Chen PH. Attenuation of Articular Cartilage Degeneration by the Genetic Deletion of HtrA1 in Mice. [Doctoral Dissertation]. Harvard University; 2017. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:42080110

Queensland University of Technology

21. Mohamed Omer, Safraz. The ghrelin axis in the skeletal microenvironment.

Degree: 2014, Queensland University of Technology

URL: https://eprints.qut.edu.au/75528/

► This project characterised the bone microarchitecture of adult mice lacking the hormone, acyl ghrelin, by high resolution micro-computed tomography; and investigated the expression of the… (more)

Subjects/Keywords: ghrelin; bone; cartilage; chondrocytes; mice

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APA (6^th Edition):

Mohamed Omer, S. (2014). The ghrelin axis in the skeletal microenvironment. (Thesis). Queensland University of Technology. Retrieved from https://eprints.qut.edu.au/75528/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Mohamed Omer, Safraz. “The ghrelin axis in the skeletal microenvironment.” 2014. Thesis, Queensland University of Technology. Accessed March 07, 2021. https://eprints.qut.edu.au/75528/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Mohamed Omer, Safraz. “The ghrelin axis in the skeletal microenvironment.” 2014. Web. 07 Mar 2021.

Vancouver:

Mohamed Omer S. The ghrelin axis in the skeletal microenvironment. [Internet] [Thesis]. Queensland University of Technology; 2014. [cited 2021 Mar 07]. Available from: https://eprints.qut.edu.au/75528/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Mohamed Omer S. The ghrelin axis in the skeletal microenvironment. [Thesis]. Queensland University of Technology; 2014. Available from: https://eprints.qut.edu.au/75528/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Queen Mary, University of London

22. Thompson, Clare. Interactions between primary cilia length and hedgehog signalling in response to mechanical and thermal stress.

Degree: PhD, 2013, Queen Mary, University of London

URL: http://qmro.qmul.ac.uk/xmlui/handle/123456789/8720 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.664900

► The primary cilium is a microtubule-based organelle present on the majority of interphase cells where it functions as a hub for numerous signalling pathways including… (more)

▼ The primary cilium is a microtubule-based organelle present on the majority of interphase cells where it functions as a hub for numerous signalling pathways including hedgehog signalling. Chondrocytes, the unique cellular component of articular cartilage, possess primary cilia which are required for mechanotransduction and maintenance of a healthy extracellular matrix. However in osteoarthritis there is an increase in primary cilia length and prevalence associated with aberrant activation of hedgehog signalling which promotes cartilage degradation. The aim of this thesis was therefore to examine the influence of biophysical stimuli on chondrocyte primary cilia structure and function, relating changes in ciliary length to perturbations in hedgehog signalling. An in vitro mechanical loading model was established to study the influence of cyclic tensile strain on chondrocyte primary cilia. Loading at 10% strain activated hedgehog signalling measured by expression of Gli1 and Ptch1. Cilia progressively disassembled in response to increasing levels of mechanical strain in a manner dependent upon tubulin deacetylation. Cilia disassembly at 20% strain was associated with the loss of mechanosensitive hedgehog signalling despite continued expression of hedgehog ligand (Ihh). Therefore this behaviour may function as a protective mechanism limiting hedgehog-mediated cartilage degradation in response to high levels of mechanical strain. To further understand the influence the extracellular environment exerts over ciliary function, a second in vitro model was developed investigating the effects of thermal stress. In chondrocytes and fibroblasts, primary cilia underwent rapid resorption in response to elevated temperature and ligand mediated hedgehog signalling was inhibited. These studies demonstrate that regulated disassembly of the cilium in response to physical stress modulates both cilia size and function. In particular, the findings suggest that changes in the chondrocyte physical environment affect cilia structure and function and may therefore be an important factor in the aetiology of cartilage disease.

Subjects/Keywords: 616.7; Medicine; Cartilage disease

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APA (6^th Edition):

Thompson, C. (2013). Interactions between primary cilia length and hedgehog signalling in response to mechanical and thermal stress. (Doctoral Dissertation). Queen Mary, University of London. Retrieved from http://qmro.qmul.ac.uk/xmlui/handle/123456789/8720 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.664900

Chicago Manual of Style (16^th Edition):

Thompson, Clare. “Interactions between primary cilia length and hedgehog signalling in response to mechanical and thermal stress.” 2013. Doctoral Dissertation, Queen Mary, University of London. Accessed March 07, 2021. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8720 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.664900.

MLA Handbook (7^th Edition):

Thompson, Clare. “Interactions between primary cilia length and hedgehog signalling in response to mechanical and thermal stress.” 2013. Web. 07 Mar 2021.

Vancouver:

Thompson C. Interactions between primary cilia length and hedgehog signalling in response to mechanical and thermal stress. [Internet] [Doctoral dissertation]. Queen Mary, University of London; 2013. [cited 2021 Mar 07]. Available from: http://qmro.qmul.ac.uk/xmlui/handle/123456789/8720 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.664900.

Council of Science Editors:

Thompson C. Interactions between primary cilia length and hedgehog signalling in response to mechanical and thermal stress. [Doctoral Dissertation]. Queen Mary, University of London; 2013. Available from: http://qmro.qmul.ac.uk/xmlui/handle/123456789/8720 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.664900

University of Edinburgh

23. Paterson, Scott Ian. Chondrocyte death during articular cartilage drying : an investigation of its effect, mechanism, and prevention.

Degree: PhD, 2016, University of Edinburgh

URL: http://hdl.handle.net/1842/23386

► During open orthopaedic surgical procedures, the articular cartilage covering the exposed joint surfaces can be exposed to air for prolonged periods. This exposure facilitates cartilage… (more)

▼ During open orthopaedic surgical procedures, the articular cartilage covering the exposed joint surfaces can be exposed to air for prolonged periods. This exposure facilitates cartilage drying, characterised by changes to the extracellular matrix and chondrocyte death. Due to cartilage’s limited capacity for regeneration, it has been proposed that this may lead to post-operative joint degeneration. It has been proposed that chondrocyte death occurs as a result of both drying and nutritional deficiency. It is known that death during drying correlates with the drying interval and is initiated in the superficial chondrocytes, progressing to deeper layers at higher intervals. Additionally, it is well established that periodic rewetting (e.g. using 0.9% saline solution) can reduce chondrocyte death. The work presented in this thesis aimed to characterise chondrocyte death during drying, with particular reference to the chondrotoxic/protective effect of environmental variables (airflow) and surgical interventions (irrigation solutions), mechanism of injury and cell death, and the effect of in vivo drying on joint health. An ex vivo model of cartilage drying was developed and carried out on bovine and human intact cartilage and osteochondral explants, while varying environmental factors (drying interval, airflow velocity, oxygen concentration) and interventions (irrigation solutions and protective coverings. Throughout the study, cartilage drying was assessed in terms of 1) cartilage macroscopic appearance, 2) percent chondrocyte death (PCD), 3) cartilage water content, and 4) chondrocyte morphology. Histologically and fluorescently labelled samples were imaged using light and confocal laser scanning microscopy respectively, which formed the basis of the qualitative and quantitative assessments. Experimental drying at high airflow velocities had a more severe effect on cartilage appearance, PCD, and water content than in static air. This relationship was apparent in dried intact joints and osteochondral explants and in bovine and human samples. This suggests that the effects of surgical drying (where ventilation systems and airflow are routine) may be more pronounced than previously suggested and demonstrates a correlation between PCD and water-loss. Irrigation solutions supplemented with glucose (25-100 mM) had no significant effect on the PCD or water content in dried samples. Additionally, PCD was minimal in osteochondral explants cultured in the absence of glucose, even after 24 hr. This suggests that nutritional deficiency is unlikely to contribute to PCD during drying. However, chondrocyte death (in intact bovine cartilage) was reduced when drying was carried out at an oxygen concentration more reflective of the in vivo environment (5 %), which suggests that cell death during drying may be facilitated by a hyperoxic shock. Finally, in vivo cartilage drying was carried out on murine cartilage. Compared to sham operated controls, dried cartilage demonstrated a loss of surface integrity (4 weeks post-surgery) and…

Subjects/Keywords: 616.7; cartilage; drying; cell death

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Paterson, S. I. (2016). Chondrocyte death during articular cartilage drying : an investigation of its effect, mechanism, and prevention. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/23386

Chicago Manual of Style (16^th Edition):

Paterson, Scott Ian. “Chondrocyte death during articular cartilage drying : an investigation of its effect, mechanism, and prevention.” 2016. Doctoral Dissertation, University of Edinburgh. Accessed March 07, 2021. http://hdl.handle.net/1842/23386.

MLA Handbook (7^th Edition):

Paterson, Scott Ian. “Chondrocyte death during articular cartilage drying : an investigation of its effect, mechanism, and prevention.” 2016. Web. 07 Mar 2021.

Vancouver:

Paterson SI. Chondrocyte death during articular cartilage drying : an investigation of its effect, mechanism, and prevention. [Internet] [Doctoral dissertation]. University of Edinburgh; 2016. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/1842/23386.

Council of Science Editors:

Paterson SI. Chondrocyte death during articular cartilage drying : an investigation of its effect, mechanism, and prevention. [Doctoral Dissertation]. University of Edinburgh; 2016. Available from: http://hdl.handle.net/1842/23386

University of Gothenburg / Göteborgs Universitet

24. Carlson, Håkan, 1914-. Reactions of rabbit patellary cartilage following operative defects : a morphological and autoradiographic study : a morphological and autoradiographic study.

Degree: 1957, University of Gothenburg / Göteborgs Universitet

URL: http://hdl.handle.net/2077/17326

Subjects/Keywords: Cartilage; Patella

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APA (6^th Edition):

Carlson, Håkan, 1. (1957). Reactions of rabbit patellary cartilage following operative defects : a morphological and autoradiographic study : a morphological and autoradiographic study. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/17326

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Carlson, Håkan, 1914-. “Reactions of rabbit patellary cartilage following operative defects : a morphological and autoradiographic study : a morphological and autoradiographic study.” 1957. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed March 07, 2021. http://hdl.handle.net/2077/17326.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Carlson, Håkan, 1914-. “Reactions of rabbit patellary cartilage following operative defects : a morphological and autoradiographic study : a morphological and autoradiographic study.” 1957. Web. 07 Mar 2021.

Vancouver:

Carlson, Håkan 1. Reactions of rabbit patellary cartilage following operative defects : a morphological and autoradiographic study : a morphological and autoradiographic study. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 1957. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2077/17326.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Carlson, Håkan 1. Reactions of rabbit patellary cartilage following operative defects : a morphological and autoradiographic study : a morphological and autoradiographic study. [Thesis]. University of Gothenburg / Göteborgs Universitet; 1957. Available from: http://hdl.handle.net/2077/17326

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

National University of Ireland – Galway

25. Browe, David. Hypoxia activates the PTHrP – Zfp521 – MEF2C pathway to attenuate hypertrophy in mesenchymal stem cell derived cartilage .

Degree: 2016, National University of Ireland – Galway

URL: http://hdl.handle.net/10379/5719

► The treatment of cartilage defects remains an unmet medical need as the current treatment options are currently sub-optimal as the most common treatment options; microfracture… (more)

▼ The treatment of cartilage defects remains an unmet medical need as the current treatment options are currently sub-optimal as the most common treatment options; microfracture and autologous chondrocyte implantation (ACI) result in repair tissue consisting of predominantly fibro-cartilage rather than hyaline cartilage. Due to the ability of mesenchymal stem cells (MSCs) to differentiate along the cartilage lineage, MSCs have been touted as a cellular source to regenerate damaged cartilage. However, a number of prevailing concerns for such a treatment remain. Generally, administration of MSCs into a cartilage defect results in poor regeneration of the damaged cartilage, with most clinical trials reporting that as with microfracture and ACI, the repaired cartilage consists of fibro-cartilage rather than hyaline cartilage. Methods that improve the chondrogenic potential of transplanted MSCs in vivo may be advantageous. In addition, the proclivity of MSC-derived cartilage to undergo hypertrophic differentiation or form bone in vivo also remains a clinical concern. Hypertrophic differentiation of MSC-derived cartilage can be said to closely mimic the endochondral ossification observed in the skeletal development of the long bones of the body. If MSC-derived cartilage was to undergo hypertrophic differentiation in vivo this would result in the failure of the cartilage graft as the newly formed tissue would resemble bone which would lack the ability to absorb and transfer biomechanical loads to the same extent as hyaline cartilage. Physiological hypoxia has previously been shown to improve chondrogenesis of MSC-derived cartilage through upregulation of the chondrogenic transcription factor SRY sex determining region-box 9 (SOX9) and to reduce hypertrophy markers. This study focuses on establishing a mechanism of action by which hypoxia or low oxygen tension can be used to attenuate or limit hypertrophic differentiation of MSC-derived cartilage. Having established a mechanism of action, the subsequent goals of this study were to develop an in vitro culture regime to mimic the beneficial effects of physiological low oxygen tension in a normoxic environment. This was achieved using the pharmacological compound FG-4592, which is currently undergoing clinical trials for the treatment of chronic kidney disease. In conclusion, this study demonstrates that hypoxic differentiation of MSC-derived cartilage has beneficial effects in terms of improved chondrogenesis and attenuated hypertrophy. This study identifies PTHrP, Zfp521 and MEF2C as key factors that regulate hypertrophic differentiation of MSC-derived cartilage in response to physiological hypoxia, genetic activation of the HIF pathway and the hypoxia mimetic compound FG-4592. Advisors/Committee Members: Barry, Frank (advisor), Elliman, Stephen (advisor).

Subjects/Keywords: Cartilage; Hypertrophy; Hypoxia; Medicine

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APA (6^th Edition):

Browe, D. (2016). Hypoxia activates the PTHrP – Zfp521 – MEF2C pathway to attenuate hypertrophy in mesenchymal stem cell derived cartilage . (Thesis). National University of Ireland – Galway. Retrieved from http://hdl.handle.net/10379/5719

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Browe, David. “Hypoxia activates the PTHrP – Zfp521 – MEF2C pathway to attenuate hypertrophy in mesenchymal stem cell derived cartilage .” 2016. Thesis, National University of Ireland – Galway. Accessed March 07, 2021. http://hdl.handle.net/10379/5719.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Browe, David. “Hypoxia activates the PTHrP – Zfp521 – MEF2C pathway to attenuate hypertrophy in mesenchymal stem cell derived cartilage .” 2016. Web. 07 Mar 2021.

Vancouver:

Browe D. Hypoxia activates the PTHrP – Zfp521 – MEF2C pathway to attenuate hypertrophy in mesenchymal stem cell derived cartilage . [Internet] [Thesis]. National University of Ireland – Galway; 2016. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/10379/5719.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Browe D. Hypoxia activates the PTHrP – Zfp521 – MEF2C pathway to attenuate hypertrophy in mesenchymal stem cell derived cartilage . [Thesis]. National University of Ireland – Galway; 2016. Available from: http://hdl.handle.net/10379/5719

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

26. CRITCHLEY, SUSAN. Towards 3D bioprinting of anatomically accurate, mechanically reinforced cartilage templates for biological joint resurfacing.

Degree: School of Engineering. Discipline of Mechanical & Manuf. Eng, 2018, Trinity College Dublin

URL: http://hdl.handle.net/2262/82805

► Osteoarthritis (OA) is a pervasive disease worldwide which affects the articular cartilage and the underlying bone in synovial joints such as the knee. Currently, the… (more)

▼ Osteoarthritis (OA) is a pervasive disease worldwide which affects the articular cartilage and the underlying bone in synovial joints such as the knee. Currently, the only treatment for a severely degenerated knee joint is a total or partial joint replacement with a metal and polymer prosthesis. Whilst these procedures are well established, failures are not uncommon resulting in a more complicated revision surgery. The aging worldwide population and the increase in the instances of younger patients being diagnosed with OA are primary motivations behind the pursuit of new treatment options. Tissue engineering approaches have been gaining traction in recent years, having being successfully translated to the clinic to treat small focal defects. These therapies combine cells, scaffolds and signalling molecules to drive tissue formation and maturation to regenerate damaged tissues. 3D printing technology can be used in tandem with tissue engineering strategies to fabricate constructs that mimic the shape and function of a joint and to accurately position cells and biological cues within such biological implants. The overall objective of this thesis is to tissue engineer an anatomically accurate, mechanically reinforced biological implant for total joint regeneration. To this end, this thesis set out to investigate the following; 1) whether a developmentally inspired cartilage template formed through in vitro priming of bone marrow derived stem/stromal cells (BMSCs) in an alginate hydrogel can be used to regenerate a critically sized osteochondral defect; 2) to identify suitable cell sources derived from OA joints for hyaline cartilage tissue engineering; 3) to identify a suitable thermopolymer that can be 3D printed to mechanically reinforce cartilage templates and subsequently engineer bi-layered cartilage templates with a top chondral layer containing a co-culture of mesenchymal stromal/stem cells (MSCs) and chondrocytes and a bottom endochondral layer of BMSCs, and to then evaluate these constructs in vivo subcutaneously in nude mice and within caprine osteochondral defetcs; 4) to develop a technique to biofabricate an anatomically accurate, mechanically reinforced, bi-layered cartilage template for whole joint resurfacing. The thesis began by investigating if a tissue engineered cartilage template could undergo spatially defined differentiation to form bone and cartilage in a critical sized osteochondral defect in a rabbit model. The osteochondral unit develops postnatally from a cartilaginous precursor that undergoes endochondral ossification during skeletal maturation. Evaluation after 3 months demonstrated that the engineered cartilage template can enhance osteochondral repair, although consistent hyaline cartilage regeneration was not observed, suggesting room for further improvement. Co-cultures of chondrocytes and MSCs are commonly used to enhance chondrogenesis. Recognising that the proposed biological implant is targeted toward patients with OA, the next part of the thesis examined the potential to use… Advisors/Committee Members: Kelly, Daniel.

Subjects/Keywords: 3D bioprinting; cartilage tissue engineering

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APA (6^th Edition):

CRITCHLEY, S. (2018). Towards 3D bioprinting of anatomically accurate, mechanically reinforced cartilage templates for biological joint resurfacing. (Thesis). Trinity College Dublin. Retrieved from http://hdl.handle.net/2262/82805

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

CRITCHLEY, SUSAN. “Towards 3D bioprinting of anatomically accurate, mechanically reinforced cartilage templates for biological joint resurfacing.” 2018. Thesis, Trinity College Dublin. Accessed March 07, 2021. http://hdl.handle.net/2262/82805.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

CRITCHLEY, SUSAN. “Towards 3D bioprinting of anatomically accurate, mechanically reinforced cartilage templates for biological joint resurfacing.” 2018. Web. 07 Mar 2021.

Vancouver:

CRITCHLEY S. Towards 3D bioprinting of anatomically accurate, mechanically reinforced cartilage templates for biological joint resurfacing. [Internet] [Thesis]. Trinity College Dublin; 2018. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2262/82805.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

CRITCHLEY S. Towards 3D bioprinting of anatomically accurate, mechanically reinforced cartilage templates for biological joint resurfacing. [Thesis]. Trinity College Dublin; 2018. Available from: http://hdl.handle.net/2262/82805

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Montana State University

27. Zignego, Donald Lee. In vitro and in vivo systems mechanobiology of osteoarthritic chondrocytes.

Degree: PhD, College of Engineering, 2015, Montana State University

URL: https://scholarworks.montana.edu/xmlui/handle/1/10165

► All cells are subjected to and respond to mechanical forces, but the underlying processes linking the mechanical stimuli to biological responses are poorly understood. In… (more)

Subjects/Keywords: Osteoarthritis.; Loads (Mechanics).; Cartilage.

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APA (6^th Edition):

Zignego, D. L. (2015). In vitro and in vivo systems mechanobiology of osteoarthritic chondrocytes. (Doctoral Dissertation). Montana State University. Retrieved from https://scholarworks.montana.edu/xmlui/handle/1/10165

Chicago Manual of Style (16^th Edition):

Zignego, Donald Lee. “In vitro and in vivo systems mechanobiology of osteoarthritic chondrocytes.” 2015. Doctoral Dissertation, Montana State University. Accessed March 07, 2021. https://scholarworks.montana.edu/xmlui/handle/1/10165.

MLA Handbook (7^th Edition):

Zignego, Donald Lee. “In vitro and in vivo systems mechanobiology of osteoarthritic chondrocytes.” 2015. Web. 07 Mar 2021.

Vancouver:

Zignego DL. In vitro and in vivo systems mechanobiology of osteoarthritic chondrocytes. [Internet] [Doctoral dissertation]. Montana State University; 2015. [cited 2021 Mar 07]. Available from: https://scholarworks.montana.edu/xmlui/handle/1/10165.

Council of Science Editors:

Zignego DL. In vitro and in vivo systems mechanobiology of osteoarthritic chondrocytes. [Doctoral Dissertation]. Montana State University; 2015. Available from: https://scholarworks.montana.edu/xmlui/handle/1/10165

28. Allas, Lyess. Méthylation de H3K27 : régulation et rôle dans le cartilage articulaire : H3K27 methylation : regulation and role in articular cartilage.

Degree: Docteur es, Aspects moléculaires et cellulaires de la biologie, 2019, Normandie

URL: http://www.theses.fr/2019NORMC426

►

L’arthrose est la maladie rhumatologique la plus répandue et une des causes majeures de douleur et de handicap. Au cours de ce travail nous avons… (more)

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L’arthrose est la maladie rhumatologique la plus répandue et une des causes majeures de douleur et de handicap. Au cours de ce travail nous avons étudié le rôle et la régulation de la tri-méthylation de la lysine 27 de l’histone H3 (H3K27me3) dans l’arthrose et la chondrogenèse.Dans une première partie, nous avons montré que l’inhibition de la méthylase EZH2 par l’EPZ-6438 atténue l’inflammation et la libération de métalloprotéases par les chondrocytes traités à l’IL-1β. L’inhibition d’EZH2 réduit également l’hypertrophie des chondrocytes induite par le TGF-β1. L’EZP-6438 attenue aussi la dégradation du cartilage in vivo dans un modèle d’arthrose murin. De plus, l’inhibition d’EZH2 diminue le handicap locomoteur chez la souris et réduit l’expression du NGF dans les chondrocytes.Dans une deuxième partie, nous avons mis en évidence que les déméthylases JMJD3 et UTX favorisent la différenciation chondrogénique des cellules souches mésenchymateuses. D’autre part, la surexpression de JMJD3 et UTX favorise la formation de cartilage et la production de collagène de type II des cellules souches mésenchymateuses après différenciation et implantation in vivo.Notre étude a montré l’importance de la marque H3K27me3 dans le cartilage. Alors qu’EZH2 est impliquée dans l’inflammation, l’hypertrophie des chondrocytes et la destruction du cartilage, JMJD3 et UTX favorisent la chondrogenèse, la formation du cartilage et la production de collagène.

Osteoarthritis is the most widespread rheumatological disease and one of the main causes of pain and disability. This work aimed to study the role and regulation of the lysine 27 histone H3 tri-methylation (H3K27me3) during osteoarthritis and chondrogenesis.In the first part of the study, we showed that EZH2 inhibition by EPZ-6438 attenuates inflammation and metalloproteases release induced by IL-1β. EZH2 inhibition also reduces TGF-β1-mediated chondrocytes hypertrophy. EPZ-6438 attenuates in vivo cartilage degradation in osteoarthritis mice model. Furthermore, EZH2 inhibition ameliorates locomotor disability in mice and reduces NGF expression in chondrocytes.In the second part of the study, we highlighted that JMJD3 and UTX enhance mesenchymal stem cell chondrogenic differentiation. In addition, JMJD3 and UTX overexpression promotes cartilage formation and type II collagen production of mesenchymal stem cells after in vivo implantation.Our study demonstrated the importance of H3K27me3 in cartilage. While EZH2 is involved in inflammation, chondrocyte hypertrophy and cartilage degradation, JMJD3 and UTX enhance chondrogenesis, cartilage formation, and collagen production.

Advisors/Committee Members: Baugé, Catherine (thesis director).

Subjects/Keywords: H3K27me3; Osteoarthritis; Chondrogenesis; Epigenetic; Cartilage

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Allas, L. (2019). Méthylation de H3K27 : régulation et rôle dans le cartilage articulaire : H3K27 methylation : regulation and role in articular cartilage. (Doctoral Dissertation). Normandie. Retrieved from http://www.theses.fr/2019NORMC426

Chicago Manual of Style (16^th Edition):

Allas, Lyess. “Méthylation de H3K27 : régulation et rôle dans le cartilage articulaire : H3K27 methylation : regulation and role in articular cartilage.” 2019. Doctoral Dissertation, Normandie. Accessed March 07, 2021. http://www.theses.fr/2019NORMC426.

MLA Handbook (7^th Edition):

Allas, Lyess. “Méthylation de H3K27 : régulation et rôle dans le cartilage articulaire : H3K27 methylation : regulation and role in articular cartilage.” 2019. Web. 07 Mar 2021.

Vancouver:

Allas L. Méthylation de H3K27 : régulation et rôle dans le cartilage articulaire : H3K27 methylation : regulation and role in articular cartilage. [Internet] [Doctoral dissertation]. Normandie; 2019. [cited 2021 Mar 07]. Available from: http://www.theses.fr/2019NORMC426.

Council of Science Editors:

Allas L. Méthylation de H3K27 : régulation et rôle dans le cartilage articulaire : H3K27 methylation : regulation and role in articular cartilage. [Doctoral Dissertation]. Normandie; 2019. Available from: http://www.theses.fr/2019NORMC426

University of Melbourne

29. Liu, Xiao. The role of suppressor of cytokine signalling-3 in chondrocytes during skeletal development and in inflammatory arthritis.

Degree: 2013, University of Melbourne

URL: http://hdl.handle.net/11343/38641

► Interleukin-6 (IL-6) family cytokines, including IL-6, oncostatin M (OSM), interleukin- 11 (IL-11) and Leukemia Inhibitory Factor (LIF), are pivotal modulators of numerous cellular processes such… (more)

▼ Interleukin-6 (IL-6) family cytokines, including IL-6, oncostatin M (OSM), interleukin- 11 (IL-11) and Leukemia Inhibitory Factor (LIF), are pivotal modulators of numerous cellular processes such as acute phase and immune responses, cellular activation, differentiation, proliferation and survival. Binding of these cytokines to their receptors and the common gp130 subunit activates the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway. Suppressor of cytokine signalling-3 (SOCS3) is a major regulator of the JAK/STAT pathway. This thesis examines the impact of the IL-6 cytokine family (gp130 cytokines) on cartilage and the potential regulatory role for SOCS3 in chondrocytes. For this purpose, we generated a transgenic mouse line expressing Cre recombinase under the control of the mouse type II collagen promoter (Col2a1). Tissue-specific recombination of genes using the loxP-Col2a1-Cre mouse provides a means to investigate the deletion of a gene of interest in chondrocytes. This thesis begins by characterising the expression of Cre recombinase in organs and tissues of the SOCS3 conditional knockout mouse (Socs3Δ/Δcol2). Col2a1-Cre expression was found in both articular chondrocytes and cartilage explants, resulting in the excision of Socs3. However, some Col2a1-Cre expression was also observed in the eye, kidney, liver, heart and a small population of neutrophils. Because previous studies have also demonstrated Col2a1-Cre expression in synovial fibroblasts using a similar model, Col2a1-Cre expression and potential SOCS3 deletion was evaluated in these cells. I demonstrated that synovial fibroblasts from Socs3Δ/Δcol2 mice stimulated with gp130 cytokines failed to show any reduction in Socs3 mRNA expression, or differences in cytokine production. The consequences of Cre recombinase expression and Socs3 deletion in a proportion of synovial fibroblasts therefore appear to be minimal. Chondrocytes are not only responsible for maintaining cartilage homeostasis, but also play a critical role in skeletal development. Having characterised the specificity of SOCS3 deletion in Socs3Δ/Δcol2 mice, I proceeded to investigate the consequences of SOCS3-deficiency in chondrocytes during skeletal development. In an ageing cohort study, I found consistently reduced total body weight in Socs3Δ/Δcol2 mice compared to controls. Further examination showed retardation of longitudinal bone growth in Socs3Δ/Δcol2 mice. Immunohistochemistry showed reduced proliferation of SOCS3-deficient growth plate chondrocytes. These results suggest a key regulatory role for SOCS3 in growth plate chondrocytes during bone growth. I next examined the specific contribution of chondrocytes to joint inflammation and cartilage degradation in response to gp130 cytokines. Stimulation of primary chondrocytes with gp130 cytokines activated the JAK/STAT signalling cascade. SOCS3 deletion in chondrocytes…

Subjects/Keywords: chondrocytes; cartilage; arthritis; inflammation; cytokine

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Liu, X. (2013). The role of suppressor of cytokine signalling-3 in chondrocytes during skeletal development and in inflammatory arthritis. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/38641

Chicago Manual of Style (16^th Edition):

Liu, Xiao. “The role of suppressor of cytokine signalling-3 in chondrocytes during skeletal development and in inflammatory arthritis.” 2013. Doctoral Dissertation, University of Melbourne. Accessed March 07, 2021. http://hdl.handle.net/11343/38641.

MLA Handbook (7^th Edition):

Liu, Xiao. “The role of suppressor of cytokine signalling-3 in chondrocytes during skeletal development and in inflammatory arthritis.” 2013. Web. 07 Mar 2021.

Vancouver:

Liu X. The role of suppressor of cytokine signalling-3 in chondrocytes during skeletal development and in inflammatory arthritis. [Internet] [Doctoral dissertation]. University of Melbourne; 2013. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/11343/38641.

Council of Science Editors:

Liu X. The role of suppressor of cytokine signalling-3 in chondrocytes during skeletal development and in inflammatory arthritis. [Doctoral Dissertation]. University of Melbourne; 2013. Available from: http://hdl.handle.net/11343/38641

Clemson University

30. Cash, Hannah. The Mechanical and Functional Effects of Ionizing Radiation on Articular Cartilage.

Degree: PhD, Bioengineering, 2019, Clemson University

URL: https://tigerprints.clemson.edu/all_dissertations/2340

► Articular cartilage is a specialized connective tissue, predominately composed of water, collagen, and proteoglycans, that provides a smooth, lubricated surface for articulation in joints.… (more)

▼ Articular cartilage is a specialized connective tissue, predominately composed of water, collagen, and proteoglycans, that provides a smooth, lubricated surface for articulation in joints. It has long been considered radioinsensitive and therefore unaffected by exposure to radiation in medical settings. Due to the increased amount of yearly radiation exposure through radiotherapy and ionizing radiation diagnostic procedures, there has been a renewed interest in how radioinsensitive articular cartilage actually is. Despite this renewed interest, the majority of studies do not focus on articular cartilage as their primary goal, but rather, have observed the effects of total body irradiation. These studies have drawn different conclusions on the effects of ionizing radiation on articular cartilage, but they have each drawn the same overall conclusion that this research needs to be continued and broadened in order to make a consistent conclusion on the radioinsensitivity of articular cartilage. The purpose of this research was to investigate the mechanical and functional effects of low doses of Gamma radiation and X-ray radiation as well as the mechanical and functional effects of repeated exposures of low doses of Gamma radiation. This was accomplished by (1) analyzing the mechanical and functional effects of Gamma radiation at doses of 2Gy, 2.5Gy, and 3Gy, (2) analyzing the mechanical and functional effects of three repeated Gamma radiation exposures of 1Gy, 1.5Gy, and 2Gy as well as the mechanical and functional effects of three X-ray radiation doses of 1.5mGy, 25mGy, and 4000mGy, and (3) exploring two possible mechanisms for the mechanical changes seen in the irradiated articular cartilage. Results showed that there were differences in the mechanics of the irradiated plugs over a seven-day period after exposure. The irradiated plugs demonstrated a significantly lower modulus seven days after exposure. When analyzing the release of proteoglycans from the single dose Gamma irradiated plugs there was an acute and persistent release, which may be a contributor in the modulus decrease. However, for the repeated doses of Gamma irradiation, the plugs showed a lower amount of proteoglycans released, indicating that fractionation of Gamma irradiation may allow the plugs to recover from the exposures. There was also little difference between the amount of proteoglycans remaining in the X-ray irradiated plugs when compared to the control plugs, potentially indicating that low doses of X-ray radiation does not lead to significant changes in the proteoglycan structure within articular cartilage. Finally, senescent staining indicated no senescence in the chondrocytes exposed to 1.5mGy and 25mGy of X-ray radiation, but there was an indication of the presence of ADAMTS5, an enzyme that degrades the proteoglycan aggrecan, in 25mGy and 4000mGy plugs on day 1 after X-ray exposure. Advisors/Committee Members: Delphine Dean, Jeremy Mercuri, Endre Takacs, Jeffrey Willey.

Subjects/Keywords: Articular Cartilage; Ionizing Radiation; Mechanics

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Cash, H. (2019). The Mechanical and Functional Effects of Ionizing Radiation on Articular Cartilage. (Doctoral Dissertation). Clemson University. Retrieved from https://tigerprints.clemson.edu/all_dissertations/2340

Chicago Manual of Style (16^th Edition):

Cash, Hannah. “The Mechanical and Functional Effects of Ionizing Radiation on Articular Cartilage.” 2019. Doctoral Dissertation, Clemson University. Accessed March 07, 2021. https://tigerprints.clemson.edu/all_dissertations/2340.

MLA Handbook (7^th Edition):

Cash, Hannah. “The Mechanical and Functional Effects of Ionizing Radiation on Articular Cartilage.” 2019. Web. 07 Mar 2021.

Vancouver:

Cash H. The Mechanical and Functional Effects of Ionizing Radiation on Articular Cartilage. [Internet] [Doctoral dissertation]. Clemson University; 2019. [cited 2021 Mar 07]. Available from: https://tigerprints.clemson.edu/all_dissertations/2340.

Council of Science Editors:

Cash H. The Mechanical and Functional Effects of Ionizing Radiation on Articular Cartilage. [Doctoral Dissertation]. Clemson University; 2019. Available from: https://tigerprints.clemson.edu/all_dissertations/2340

Open Access Theses and Dissertations