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. 2014 Dec;18(12):2340-50.
doi: 10.1111/jcmm.12378. Epub 2014 Oct 29.

Mesenchymal Stem-Cell Potential in Cartilage Repair: An Update

Free PMC article

Mesenchymal Stem-Cell Potential in Cartilage Repair: An Update

M Mazor et al. J Cell Mol Med. .
Free PMC article


Articular cartilage damage and subsequent degeneration are a frequent occurrence in synovial joints. Treatment of these lesions is a challenge because this tissue is incapable of quality repair and/or regeneration to its native state. Non-operative treatments endeavour to control symptoms and include anti-inflammatory medications, viscosupplementation, bracing, orthotics and activity modification. Classical surgical techniques for articular cartilage lesions are frequently insufficient in restoring normal anatomy and function and in many cases, it has not been possible to achieve the desired results. Consequently, researchers and clinicians are focusing on alternative methods for cartilage preservation and repair. Recently, cell-based therapy has become a key focus of tissue engineering research to achieve functional replacement of articular cartilage. The present manuscript is a brief review of stem cells and their potential in the treatment of early OA (i.e. articular cartilage pathology) and recent progress in the field.

Keywords: cartilage; growth factors; mesenchymal stem cell; osteoarthritis; repair.


Fig. 1
Fig. 1
Molecular changes in osteoarthritic (OA) cartilage. The main matrix-degrading enzymes are matrix metalloproteinases (MMPs). MMPs are up-regulated in OA and included in the over-degeneration of a main extracellular matrix components: types II, VI, XI collagens and proteoglycans. At early stages, the degradation of the predominant proteoglycan, aggrecan is mainly caused by aggrecanases, (ADAMTS). The expression of matrix-degrading enzymes is further fuelled by the appearance of inflammation. Once degraded, cartilage fragments fall into the joint and contact the synovium. In contact with foreign bodies, synovial cells react by producing inflammatory mediators (IL-1β and TNF-β), which leads to additional activation of MMPs, cytokines and further cartilage degradation. Yet, positive feedback such as the activation of the bone morphogenetic proteins (BMPs) and tumour growth factor-β (TGF-β) under the control of IL-1β and TNF-β contribution in maintaining matrix synthesis. It is well known that one of the key transcription factors (SOX9) indebted in expression of collagen type II and aggrecan is regulated by BMPs and TGF-β. On the other hand, negative regulator of SOX9 expression is NF-κ B and mainly regulated by TNF-α and IL-1β.
Fig. 2
Fig. 2
Cell-based repair of cartilage lesions. MSCs isolated from various tissues have the potential to undergo chondrogenesis and form hyaline cartilage. Furthermore, to form hyaline cartilage tissue, chondrocytes combine with appropriate scaffold matrix and bioactive factors to promote ECM formation. Constructed hyaline cartilage tissue is then implanted in the cartilage lesion site. BMCS, bone marrow-derived stem cells; ASC, adipose-derived stem cells; SSC, synovium-derived stem cells; HCSC, hyaline cartilage-derived stem cells.

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