Abstract
Copyright: © 2012 Dealy CN. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. The challenge of injury to the articular cartilage of the joints is the inability of the tissue to effectively self-regenerate. Accordingly, most clinical cartilage repair strategies have focused on use of exogenous cells and/or materials to fill in localized acute defects. Problems still to be overcome using these approaches include attaining seamless integration of repair and host tissue, as well as faithful reproduction of true hyaline cartilage, without which permanent and durable repair is not achieved. A critical consideration in cartilage repair is the nature of the cells expected to do the job. Alternatives to the clinical paradigm of exogenous adult chondrocytes as repair cells need to be developed in order to achieve fully functional articular cartilage repair. Moreover, strategies must be devised to treat the widespread and chronic damage found in osteoarthritis, in which surgical intervention to achieve focal repair is not feasible.
Highlights
The existence of multiple endogenous chondrogenic progenitor cell populations in the joint and articular cartilage is exciting in terms of offering potential endogenous cell sources for cartilage repair
Strategies to augment the response of endogenous progenitor populations to cartilage injury may involve exogenous factors, and exogenous progenitor cells
A recent study examining articular cartilage repair by human embryonic stem cell-derived chondrocytes, which were implanted into full thickness focal defects in rat articular cartilage in vivo and monitored using a human-specific antibody, revealed gradual replacement of the human cells with rat cells during repair of the defect region [39]
Summary
The existence of multiple endogenous chondrogenic progenitor cell populations in the joint and articular cartilage is exciting in terms of offering potential endogenous cell sources for cartilage repair. Transient stimulation of β-catenin signaling, a signal typically associated with osteoarthritic progression [26], instead caused thickening of the articular cartilage in vivo [27] and increased proliferation of isolated superficial zone progenitors in vitro while promoting subsequent differentiation of the cells towards permanent articular cartilage in vivo [5]. In particular the potential use of mesenchymal stem cells for treatment of articular cartilage damage has been intensely investigated (reviewed in [28,29,30]).
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