SAGE-Hindawi Access to Research Journal of Tissue Engineering Volume 2011, Article ID 587547, 10 pages doi:10.4061/2011/587547 Research Article The Constitutive Expression of Type X Collagen in Mesenchymal Stem Cells from Osteoarthritis Patients Is Reproduced in a Rabbit Model of Osteoarthritis Fackson Mwale, 1, 2 Sonia Rampersad, 2 H´ el` ene Richard, 3 Yao Guoying, 2 Sora Al Rowas, 2 Padma Madiraju, 2 John Antoniou, 1, 2 and Sheila Laverty 3 1 Division of Orthopaedic Surgery, McGill University, Montreal, Quebec, Canada H3H 2P2 2 Lady Davis Institute for Medical Research, SMBD—Jewish General Hospital, 3755 Chemin de la Cˆ ote Ste-Catherine, Montreal, Quebec, Canada H3T 1E2 3 Comparative Orthopaedic Research Laboratory, Faculty of Veterinary Medicine, University of Montreal, Saint Hyacinthe, Quebec, Canada J2S 7C6 Correspondence should be addressed to Fackson Mwale, fmwale@ldi.jgh.mcgill.ca Received 21 April 2011; Accepted 18 June 2011 Academic Editor: Alastair J. Sloan Copyright © 2011 Fackson Mwale et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The expression of type X collagen (COL X), a late-stage chondrocyte hypertrophy marker in human mesenchymal stem cells (MSCs) from osteoarthritis (OA) patients poses a major setback to current cartilage and intervertebral disc tissue engineering efforts. However, it is not yet clear whether COL X is expressed by all human bone marrow stem cells or if it is related to age, gender, site, disease status, or drug therapy. In the current study, we report that COL X expression is upregulated in MSCs from rabbits in a surgical instability model of OA (anterior cruciate ligament transection (ACLT)) when compared to control rabbit MSCs. Thus COL X expression in OA is a common phenomenon that is due to the disease process itself and not to other environmental factors. It is, therefore, critical to understand MSC phenotype in OA patients, as these cells are essential clinically for biological repair of cartilage lesions using autologous stem cells. 1. Introduction Osteoarthritis (OA) is characterized by a slow degeneration of articular cartilage and subchondral bone [1, 2]. At the molecular level, degradation of type II collagen (COL II) and proteoglycan components of the extracellular matrix occurs resulting in a loss of both the tensile and compressive strength of articular cartilage [1, 3, 4]. The incidence of OA increases progressively with age [5] and is viewed as an age- related dynamic reaction pattern of a joint in response to insult or injury. Many authors have reported evidence for chondrocyte differentiation in OA including proliferation, cell cloning, expression of type X collagen (COL X) [6],an- nexins and alkaline phosphatase, parathyroid-hormone-re- lated peptide, matrix calcification, and apoptotic cell death of the terminally differentiated chondrocytes. These cellular changes are also observed in the growth platewhenthegrowth cartilage is converted intobone(endochondralossification) [7]. In line with these findings, we recently identified calcium deposits and COL X in degenerative and scoliotic interverte- bral discs (IVD), but not in control discs, and the level of the indicators of calcification potential was consistently higher in degenerative and scoliotic discs than in control discs [8]. If the biological repair of cartilage and IVD is to become a real- ity, calcification or subsequent bone formation of engineered tissues has to be avoided. COL X, a short-chain collagen was first isolated from chick hypertrophic chondrocytes and is a specific marker for hypertrophic chondrocytes of the growth plate, the final stage before cartilage is converted to bone [9]. It is synthe- sized and secreted prior to calcification and interacts with fibrils of COL II throughout the cartilage matrix [10]. It was