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Stem Cells International
Volume 2017, Article ID 2905104, 11 pages
https://doi.org/10.1155/2017/2905104
Research Article

Therapeutic Benefit for Late, but Not Early, Passage Mesenchymal Stem Cells on Pain Behaviour in an Animal Model of Osteoarthritis

1Arthritis Research UK Pain Centre and School of Life Sciences, University of Nottingham, Nottingham, UK
2Institute for Science and Technology in Medicine, Guy Hilton Research Centre, Keele University, Staffordshire, UK
3Institute for Science and Technology in Medicine, Keele University at RJAH Orthopaedic Hospital, Oswestry, UK
4School of Science and Technology, Nottingham Trent University, Nottingham, UK

Correspondence should be addressed to Alicia J. El Haj; ku.ca.eleek@jah.le.j.a

Received 26 May 2017; Accepted 7 September 2017; Published 24 December 2017

Academic Editor: Víctor Carriel

Copyright © 2017 Victoria Chapman 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.

Abstract

Background. Mesenchymal stem cells (MSCs) have a therapeutic potential for the treatment of osteoarthritic (OA) joint pathology and pain. The aims of this study were to determine the influence of a passage number on the effects of MSCs on pain behaviour and cartilage and bone features in a rodent model of OA. Methods. Rats underwent either medial meniscal transection (MNX) or sham surgery under anaesthesia. Rats received intra-articular injection of either 1.5 × 106 late passage MSCs labelled with 10 μg/ml SiMAG, 1.5 × 106 late passage mesenchymal stem cells, the steroid Kenalog (200 μg/20 μL), 1.5 × 106 early passage MSCs, or serum-free media (SFM). Sham-operated rats received intra-articular injection of SFM. Pain behaviour was quantified until day 42 postmodel induction. Magnetic resonance imaging (MRI) was used to localise the labelled cells within the knee joint. Results. Late passage MSCs and Kenalog attenuated established pain behaviour in MNX rats, but did not alter MNX-induced joint pathology at the end of the study period. Early passage MSCs exacerbated MNX-induced pain behaviour for up to one week postinjection and did not alter joint pathology. Conclusion. Our data demonstrate for the first time the role of a passage number in influencing the therapeutic effects of MSCs in a model of OA pain.