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Permanent link (DOI): https://doi.org/10.7939/R3P64N

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The role of cultured chondrocytes and mesenchymal stem cells in the repair of acute articular cartilage injuries Open Access

Descriptions

Other title
Subject/Keyword
joint injury
articular cartilage
cultured chondrocytes
mesenchymal stem cells
Type of item
Thesis
Degree grantor
University of Alberta
Author or creator
Secretan, Charles Coleman
Supervisor and department
Jomha, Nadr (Department of Surgery)
Bagnall, Keith (Department of Surgery)
Simmonds, Andrew (Department of Cell Biology)
Examining committee member and department
Churchill, Thomas (Department of Surgery)
Simmonds, Andrew (Department of Cell Biology)
Bagnall, Keith (Department of Surgery)
Jomha, Nadr (Department of Surgery)
Raso, Jim (Department of Surgery)
Matyas, John (Department of Veterinary Medicine, University of Calgary)
Department
Department of Surgery
Specialization

Date accepted
2010-04-14T20:24:42Z
Graduation date
2010-06
Degree
Doctor of Philosophy
Degree level
Doctoral
Abstract
Osteoarthritis (OA) is a disease that has significant individual, social, and economic impact worldwide. Although many etiologies lead to the eventual development of OA, one potentially treatable cause is the acute articular cartilage (AC) injury. These injuries are common and have a poor inherent healing capacity, leading to the formation of OA. In an effort to repair AC injuries several treatment strategies have been developed but none have proven completely successful. Studies examining AC tissue-engineering strategies have suggested that those with the most potential for success involve the introduction of autogenous or allogenous cells to the site of injury. These strategies are designed to encourage creation of a matrix with the appropriate characteristics of normal AC. However, development of a completely successful repair method has proven difficult because the biomechanical properties of normal AC are not easy to replicate, a cell source with the appropriate functional characteristics has not been optimized, and the problem of effective incorporation of a repair construct into the host tissue remains unresolved. In an effort to more fully understand the cartilage repair process, this work first focused on the development and utilization of an in vitro human explant model of AC to study the ability of seeded human chondrocytes to integrate into an AC defect. Further work elucidated the gene expression patterns of cultured adult human chondrocytes and human mesenchymal stem cell (MSC)-derived chondrocytes. Results from this work determined that cultured human chondrocytes were able to adhere to articular cartilage defects in a viable in vitro explant model and produce a matrix containing collagen type II. However, further work with the in vitro expanded chondrocytes revealed that these cells have increased expression of collagen type I which promotes the formation of a less durable fibrocartilagenous tissue. This unfavorable expression persisted despite placing the chondrocytes in an environment favoring a chondrocytic phenotype. Further work with MSC-derived chondrocytes demonstrated a similar and unfavorable production of collagen type I. This work represented an important first step towards a treatment for acute AC lesions but it is clear that further work to optimize the culture microenvironment is still required.
Language
English
DOI
doi:10.7939/R3P64N
Rights
License granted by Charlie Secretan (secretan@ualberta.ca) on 2010-04-14T18:03:32Z (GMT): Permission is hereby granted to the University of Alberta Libraries to reproduce single copies of this thesis and to lend or sell such copies for private, scholarly or scientific research purposes only. Where the thesis is converted to, or otherwise made available in digital form, the University of Alberta will advise potential users of the thesis of the above terms. The author reserves all other publication and other rights in association with the copyright in the thesis, and except as herein provided, neither the thesis nor any substantial portion thereof may be printed or otherwise reproduced in any material form whatsoever without the author's prior written permission.
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