Volume 3 • Issue 3 • 1000e112 J Tissue Sci Eng ISSN:2157-7552 JTSE an open access journal Editorial Open Access Pei, J Tissue Sci Eng 2012, 3:3 DOI: 10.4172/2157-7552.1000e112 Recent reviews of consecutive knee arthroscopies have demonstrated the occurrence of chondral defects ranging from 60% to 65%, irrespective of the surgical indication [1]. Osteoarthritis, trauma, and disorders of the subchondral bone – such as osteochondritis dissecans or osteonecrosis, which secondarily afect articular cartilage – may cause defects in cartilage. Based on current trends, osteoarthritis is predicted to be the fourth leading cause of disability worldwide by the year 2020 [2]. Articular cartilage is a unique, hypocellular, avascular tissue mostly made of extracellular collagens and proteoglycans; it has a limited ability to self heal afer trauma and degenerative disease [3]. Current clinical practice usually involves a bone marrow stimulation technique in which subchondral bone is broken to facilitate cartilage repair from bone marrow stromal cells (BMSCs) and cytokines. However, with this procedure, cartilage defects are most ofen repaired with fbrocartilage, which is known to be biochemically and biomechanically diferent from native hyaline cartilage; this tissue subsequently undergoes degeneration [4]. Autologous chondrocyte transplantation (ACT) is currently used clinically; however, it has not proven to be as successful as originally predicted [5]. Obtaining vital and diferentiated chondrocytes presents one of the major challenges for successful ACT. Each biopsy presents an additional trauma to already damaged joint cartilage and may cause postoperative pain and increase the long-term risk of developing osteoarthritis [4]. Furthermore, the expansion phase the chondrocytes have to undergo in vitro leads to rapid cell de-diferentiation with a loss of chondrogenic potential [6]. Additionally, isolation of cells from the cartilage matrix by enzymatic digestion diminishes cartilage-specifc mRNA levels and changes are exaggerated during expansion [7]. Te ex vivo expansion of articular chondrocytes leads to a telomere erosion comparable to 30 years of aging in vivo [8]. Although re-diferentiation of these cells has been shown in vitro [9], only partial gene expression was restored [7] and a progressive loss of cell ability to form stable ectopic cartilage in vivo became evident [10]. Tus, newly synthesized cartilage ofen consists of more fbrous tissue than hyaline cartilage [11]. It becomes important to fnd an alternative, easily obtainable cell source with stable chondrogenic potential [12]. Mesenchymal stem cells (MSCs) are a promising cell source for cartilage regeneration because, compared to articular chondrocytes, they are easily obtainable in high numbers, expand in vitro without losing their diferentiation potential [13], and have more pronounced expansion ability with no higher risk for replicative aging [14]. Due to an ‘age phenotype’ of chondrocytes but not MSCs from patients of advanced age, MSCs were found to be more attractive for cartilage repair in older individuals. One possible source of MSCs is adipose tissue, which is easily accessible in large quantities. Apart from a similar osteogenic and adipogenic diferentiation potential, however, adipose-derived MSCs showed a reduced chondrogenic diferentiation capacity under standard induction conditions [15]. In addition to adipose tissue, bone marrow is a particularly attractive source for MSCs. Some recent reports indicated that BMSC-based repairs perform better than chondrocyte-based ones [16,17], despite one report suggesting that BMSC transplantation showed comparable results with ACT in the repair of articular cartilage defects [18]. Compared to the ACT approach having a greater efect in younger patients, transplantation with BMSCs did not show any diference in ages older or younger than 45 [18]. A major hurdle in cartilage tissue engineering with BMSCs is their diferentiation toward endochondral ossifcation [19]. During in vitro chondrogenesis, BMSCs up-regulate not only hyaline cartilage- specifc markers such as collagen II and aggrecan, but also markers typical for hypertrophic chondrocytes such as collagen X and alkaline phosphatase (ALP) [20-22]. Collagen X makes up 45% of the collagen produced in hypertrophic chondrocytes and is therefore considered an important marker of enchondral ossifcation [23]. In contrast, collagen X is almost negligible in healthy mature chondrocytes and engineered cartilage [24,25]. One of the challenges that need to be solved for the advancement of regenerative cartilage medicine is to fnd a tissue-specifc stem cell that generates articular cartilage-like chondrocytes and does not undergo hypertrophy as a terminal diferentiation stage. Under chondrogenic induction, BMSCs showed a 5- to 10-fold increase in osteocalcin and ALP compared to synovium-derived stem cells (SDSCs) [26]; in contrast, SDSCs have fewer tendencies to become hypertrophic when incubated in a chondrogenic induction medium [27-33]. Figure 1 shows the diferent lineage tendencies of both human stem cells. Tere is increasing evidence demonstrating that SDSCs are a tissue-specifc stem cell for chondrogenesis [34]. Synovium is the closest tissue to articular cartilage, not only in development but also in function; synovial cells share properties with chondrocytes, such as cartilage oligomeric matrix, link protein, and sulfated glycosaminoglycans (GAGs). Synovium is also the only tissue that can produce hyaline cartilage in benign conditions; under appropriate stimulatory conditions, synovial cells are able to migrate into articular cartilage defects and subsequently undergo chondrogenic diferentiation. It was demonstrated that SDSCs match more closely with articular chondrocytes in gene profle than BMSCs and are better at chondrogenic diferentiation than stem cells from bone marrow, periosteum, adipose tissue, and muscle. Both chondrocytes and synovial cells bordering the joint cavity could also synthesize superfcial zone protein (SZP) that provides a protective microenvironment for cartilage progenitor cells at the surface of articular cartilage. *Corresponding author: Ming Pei, Stem Cell and Tissue Engineering Laboratory, Department of Orthopaedics, Exercise Physiology, and Mechanical and Aerospace Engineering, West Virginia University, One Medical Center Drive, Morgantown, PO Box 9196, WV 26506, USA, Tel: 304-293-1072; Fax: 304-293-7070; E-mail: mpei@hsc.wvu.edu Received September 04, 2012; Accepted September 05, 2012; Published September 07, 2012 Citation: Pei M (2012) Can Synovium-derived Stem Cells Deposit Matrix with Chondrogenic Lineage-specifc Determinants? J Tissue Sci Eng 3:e112. doi:10.4172/2157-7552.1000e112 Copyright: © 2012 Pei M. 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. Can Synovium-derived Stem Cells Deposit Matrix with Chondrogenic Lineage-specific Determinants? Ming Pei* Stem Cell and Tissue Engineering Laboratory, Department of Orthopaedics, Exercise Physiology, and Mechanical and Aerospace Engineering, West Virginia University, Morgantown, WV 26506, USA Journal of Tissue Science & Engineering J o u r n a l o f T i s s u e S c i e n c e & E n g i n e e r i n g ISSN: 2157-7552