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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)
▼ Articular
cartilage is an avascular, aneural tissue that covers the ends of diarthroidal joints. Once damaged by disease or injury,
cartilage lacks the ability to self-repair. Generating tissue engineered
cartilage is an exciting field that may provide a possible solution to this problem. The purpose of this study is to determine the efficacy of a through-thickness perfusion bioreactor to generate scaffold-free tissue engineered
cartilage.
The results of the study show that allowing long-term static culture to cell constructs before perfusion increases the efficacy of the bioreactor. Immediate perfusion of cell constructs in the bioreactor is shown to decrease the efficacy to produce scaffold-free constructs with desirable biomechanical and biochemical properties. The results of the study also show possible options in future works that could increase the efficacy of the bioreactor.
Advisors/Committee Members: Steve Elder (chair), Jun Liao (committee member), Raj Prahbu (committee member), James Cooley (committee member).
Subjects/Keywords: neonatal porcine cartilage; cartilage bioreactor
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APA (6th 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 (16th 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 (7th 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)
▼ 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 associated with joint injury would stimulate menisci to increase production of matrix-degrading enzymes, cytokines and chemokines, which could contribute to joint tissue destruction and subsequent development of osteoarthritis. We examined meniscus pathology in established osteoarthritis, characterized the alterations in meniscus cell processes between normal and osteoarthritic menisci, and explored potential pathways involved in osteoarthritis pathogenesis including a novel pathway proposed to mediate osteoarthritis development.
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…
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APA (6th 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 (16th 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 (7th 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 ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
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APA (6th 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 (16th 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 (7th 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 ·
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MLA ·
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APA (6th 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 (16th 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 (7th 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)
▼ 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 of an appropriate weight-bearing surface, so a need exists for a joint ‘resurfacing’ material which can integrate into the joint. Recent studies have shown that injured tendon develops some chondroid features, suggesting potential as a cartilage resurfacing material. Our initial study utilized a surgical model of tendinopathy in sheep to investigate the features of tendon healing over time, and to identify the time point at which the injured tendon has the most chondroid features. The second study used pathological chondroid tendon harvested at 8 weeks, and implanted this material into acute lesions of the ovine trochlear groove. Pathological tendon implants were compared to normal tendon implants, untreated lesions and non-operated subjects. Joints were evaluated using radiographic and gross evaluation, gene expression analysis, and histology 6 months after graft implantation. Gross, radiographic, gene expression and histological analyses demonstrating a degenerative response to grafting of pathological tendon. In contrast, on gross evaluation, normal tendon appeared to provide a suitable cartilaginous surface in some subjects, although gene expression and histological data did not indicate any improvement in contrast to ungrafted sheep with untreated lesions. This pilot study suggests that normal tendon may be a valuable source of graft material for acute cartilage lesions, and may be a useful ‘scaffold’ for resurfacing. Overall this pilot study indicates that normal tendon, as a freely available autogenous tissue with multiple dispensable sources within the body, presents an intriguing option as a scaffold for future cartilage repair and warrants further attention.
Subjects/Keywords: Cartilage;
tendon;
tendinopathy;
osteoarthritis;
cartilage resurfacing
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th 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 (7th 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)
▼ 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 population. The disease erodes and disrupts the articular surface, which when healthy provides a low-friction, load-bearing, wearresistant surface for articulation in joints. Osteoarthritis is most frequently idiopathic, but also results from traumatic joint injury. An understanding of the link between joint injury and the degeneration of articular
cartilage and potential for protecting the articular surface depends on an understanding of both the biological and mechanical responsiveness of articular
cartilage to injury. This thesis investigates this link, exploring the frictional behavior of articular
cartilage and how it responds to mechanical and biochemical damage.
Advisors/Committee Members: Bonassar, Lawrence (chair), Maher, Suzanne A. (committee member), Estroff, Lara A. (committee member).
Subjects/Keywords: cartilage; friction; osteoarthritis
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th 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 (7th 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 ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th 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 (7th 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 ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th 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 (7th 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)
▼ 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 instability, but also complex age related changes and obesity. Lesions often start as a focal defect, and due to changes in homeostasis and the progressive degradation of
cartilage matrix often progresses into OA.
Cartilage damage causes changes in chondrocyte expression pattern that lead to increased catabolic- and decreased anabolic-processes. A lot is known about disease pathogenesis, but this has not yet resulted in an effective clinical therapy to halt OA progression and induce regeneration. Over the last years,
cartilage regeneration has gained increasing attention and this has led to the identification of soluble mediators and CPCs with chondrogenic capacities in native
cartilage. The combination of anabolic growth factors and stem cells has demonstrated great regenerative potential in vivo and in vitro. These observations might prove crucial in the development of new, improved OA therapies. Several challenges however remain to be solved. The underlying cause of OA can be one of many and disease progression is also dependent on many different factors including the patient’s age and lifestyle. An effective therapy will have to take into account patient specific expression profiles (‘OA phenotype’) of affected joints like e.g. relevant receptors and other anabolic and anti-catabolic factors. Based on these results, a therapy can be designed for specific subgroups or individual patients. A regenerative response to OA damage is closer than ever in this era of tissue engineering and rapid technological innovations. However, further understanding of the complex pathways that initiate and lead to progression of OA, separated by spatial and temporal expression, is necessary to improve clinically relevant OA models.
Advisors/Committee Members: Creemers, L.B..
Subjects/Keywords: Articular cartilage; Osteoarthritis; Regeneration; Cartilage repair; Cartilage biology; Soluble mediators; Stem cells
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
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APA (6th 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 (16th 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 (7th 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 ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th 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 (7th 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)
▼ 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 lubrication of joints. Treatments to repair
cartilage defects mainly consist of cell therapies, which do not yield biomechanically sound tissue. Therefore tissue engineering has been proposed as a viable alternative. In order to meet biomechanical demands tissue engineered constructs require specific architecture, which could be accomplished by 3D deposition of hydrogels. Unfortunately, hydrogels are not mechanically compatible with native articular
cartilage. The use of reinforced hydrogels in biofabrication allows tailoring of mechanical properties with a retained biocompatibility. Mechanical loading in a bioreactor can contribute to the improvement of tissue engineered constructs by mimicking in vivo conditions. Mechanical tuning in biofabrication as well as mechanical training could contribute to a clinically applicable tissue.
Advisors/Committee Members: Malda, J.
Subjects/Keywords: Cartilage; tissue engineering; mechanics; biofabrication
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th 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 (7th 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 ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th 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 (7th 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 ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th 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 (7th 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 ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th 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 (7th 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 ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th 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 (7th 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 (6th 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 (16th 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 (7th 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)
▼ 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 to prevent joint disease have not been investigated at length, and very little emphasis has been placed on the effects of trace mineral supplementation on joint health. To test the hypothesis that complexed trace minerals (CTM; Zn, Mn, Cu amino acid complexes and Co glucoheptonate) would benefit articular
cartilage, sixteen Quarter Horse yearlings (9.1±0.17 mo) entering a submaximal exercise training program were balanced by age, sex, BW, and farm of origin, and randomly assigned to either CTM (n = 8) or inorganic (n = 8) dietary Cu, Zn, Mn, and Co for 12 wk. Horses had received their respective diets for 12 wk prior to trial initiation. Synovial fluid samples were collected at wk 0, 8, and 12 of exercise, and analyzed for concentrations of carboxypropeptide of type II collagen (CPII), and collagenase cleavage neoepitope of type II collagen (C2C), and chondroitin sulfate-846 (CS-846). Treatment differences were detected using PROC MIXED in SAS (v9.4) with diet, time, and diet × time interaction included as fixed effects and horse (diet) as a random effect. At wk 12, CPII was higher (P ≤ 0.0001), and C2C (P < 0.0001) and CS-846 (P = 0.005) were lower than at wk 0, but none were affected by diet in this study. The ratio of CPII:C2C, or synthesis to degradation, increased from wk 0 to 8 (P < 0.0001) in all horses but continued increasing to wk 12 (P = 0.015) in CTM horses. Dietary Cu, Zn, Mn, and Co source appears to enhance
cartilage synthesis relative to degradation during low-intensity exercise training in young horses. Dietary CTM may lead to improved joint
cartilage maintenance as the horse progresses through its performance career.
Advisors/Committee Members: White, Sarah H (advisor), Leatherwood, Jessica L (committee member), Fluckey, James (committee member).
Subjects/Keywords: Equine; Trace minerals; Cartilage
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APA (6th 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 (16th 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 (7th 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 ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th 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 (7th 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 ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th 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 (7th 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)
▼ 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 ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th 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 (7th 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)
▼ 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 ghrelin axis in cells of human and mouse fetal cartilage. This thesis highlights for the first time the physiological role of the ghrelin axis in the bone microenvironment of aged mice. Furthermore it improves our understanding of the complex expression patterns of the ghrelin axis in cartilage cells of human and mouse fetal skeletons.
Subjects/Keywords: ghrelin; bone; cartilage; chondrocytes; mice
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MLA ·
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Export
to Zotero / EndNote / Reference
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APA (6th 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 (16th 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 (7th 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 ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
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APA (6th 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 (16th 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 (7th 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 ·
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CSE |
Export
to Zotero / EndNote / Reference
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APA (6th 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 (16th 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 (7th 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 (6th 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 (16th 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 (7th 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 ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th 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 (7th 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 ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th 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 (7th 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)
▼ 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 the joints of the body (e.g. the knee, hip, etc...) articular
cartilage serves as a low friction, load bearing material and is subjected to near-constant mechanical loading. Through excessive loading of the joint, usually caused by obesity or injury, the protective articular
cartilage begins to diminish, leading to the progression of osteoarthritis (OA). Osteoarthritis is the most common joint disorder in the world and is characterized by the deterioration of articular
cartilage. Determining the link between
cartilage deterioration and mechanical loading is one motivation that drove this research. Articular
cartilage is composed of a dense extracellular matrix (ECM), a less-stiff pericelluar matrix (PCM), and highly specialized cells called chondrocytes. As the sole cell type in
cartilage, chondrocytes are responsible for the healthy turnover of the ECM by creating, maintaining, and repairing the matrix. Multiple lines of evidence suggest chondrocytes can transduce mechanical stimuli into biological signals. The hypothesis for this research is that physiologically pertinent loading of chondrocytes results in a specific set of bio-signals resulting in matrix synthesis. To test this hypothesis, two unbiased, large-scale metabolomic and phosphoproteomic datasets were generated by modeling physiological compressive loading on 3D-embedded chondrocytes. To assess loading-induced changes in metabolites (e.g. small molecules representing the functional state of the cell) and proteome-wide patterns of post-translational modifications (i.e. phosphorylation), chondrocytes were encapsulated in physiologically stiff agarose, compressively loaded in tissue culture, and analyzed via liquid chromatography – mass spectrometry (LC-MS). The results helped identify global and local biological patterns in the chondrocytes which are a direct result from mechanical loading. In addition, a novel mouse model that expresses
cartilage specific bioluminescence was used to assess loading induced changes in vivo. The results from the mouse model allowed for in vivo validation and integration of the in vitro results from the metabolomic and phosphoproteomic results. To my knowledge, such research has never been done, and considerably expands the scientific knowledge of chondrocyte mechanotransduction.
Advisors/Committee Members: Chairperson, Graduate Committee: Ronald K. June II (advisor), Aaron A. Jutila, Martin K. Gelbke and Daniel M. Gannon were co-authors, and Ronald K. June was a corresponding author of the article, 'The mechanical microenviroment of high concentration agarose for applying deformation to primary chondrocytes' in the journal 'Journal of biomechanics' which is contained within this thesis. (other), Aaron A. Jutila was a main author, Bradley K. Hwang, Jonathan K. Hilmer, Timothy Hamerly, Cody A. Minor and Seth T. Walk were co-authors, and Ronald K. June was a corresponding author of the article, 'Candidate mediators of chondrocyte mechanotransduction via targeted and untargeted metabolomic measurements' in the journal 'Archives of biochemistry and biophysics' which is contained within this thesis. (other), Carley N. McCutchen, Jonathan K. Hilmer were co-authors, and Ronald K. June was a corresponding author of the article, 'Mechanotransduction in primary human osteoarthritic chondrocytes is mediated by metabolism of energy, lipids, and amino acids' submitted to the journal 'Arthritis and rheumatology' which is contained within this thesis. (other), Jonathan K. Hilmer was a co-author, and Ronald K. June was a corresponding author of the article, 'Shotgun phosphoproteomics identifies activation of vimentin, ankyrin, vam6/vpS39-like protein in primary human osteoarthritic chondrocytes after mechanical stimulation' submitted to the journal 'eLife' which is contained within this thesis. (other), Sarah E. Mailhiot, Timothy Hamerly, Edward E. Schmidt were co-authors, and Ronald K. June was a corresponding author of the article, 'Alterations in joint metabolomics following surgical destabilization and exercise in a novel cartilage reporter mouse model' submitted to the journal 'Annals of biomedical engineering' which is contained within this thesis. (other).
Subjects/Keywords: Osteoarthritis.; Loads (Mechanics).; Cartilage.
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th 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 (16th 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 (7th 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)
▼ 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 (6th 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 (16th 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 (7th 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 (6th 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 (16th 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 (7th 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 (6th 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 (16th 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 (7th 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
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