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BioMed Research International
Volume 2015, Article ID 470934, 8 pages
Research Article

Influence of Intra-Articular Administration of Trichostatin A on Autologous Osteochondral Transplantation in a Rabbit Model

1Medical School of Nanjing University, Hankou Road, Nanjing, Jiangsu 210093, China
2The Center of Diagnosis and Treatment for Joint Disease, Nanjing Drum Tower Hospital Affiliated to Medical School of Nanjing University, Zhongshan Road, Nanjing, Jiangsu 210008, China
3Laboratory for Bone and Joint Disease, Center for Genomic Medicine, 4-6-1 Shirokane-dai, Minato-ku, Tokyo 108-8639, Japan
4Orthopaedic Surgery, Centre for Orthopaedic Research, The University of Western Australia (M508), Crawley, WA 6009, Australia
5Model Animal Research Center of Nanjing University, Xuefu Road, Nanjing, Jiangsu 210032, China

Received 10 January 2015; Revised 9 March 2015; Accepted 9 March 2015

Academic Editor: Magali Cucchiarini

Copyright © 2015 Huacheng Hou 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.


Autologous osteochondral transplantation (AOT) is a method for articular cartilage repair. However, several disadvantages of this method have been reported, such as transplanted cartilage degeneration and the lack of a connection between the grafted and adjacent cartilage tissues. To evaluate the effect of intra-articular administration of trichostatin A (TSA) on AOT, we conducted a case control study in a rabbit model. International Cartilage Repair Society (ICRS) macroscopic scores, the modified O’Driscoll histology scores, and real-time PCR were utilized to evaluate the results. At 4 weeks, both macroscopic and histological assessments showed that there was no significant difference between the TSA and control groups. However, the mean macroscopic and histological scores for the TSA-treated group were significantly higher than the scores for the control group at 12 weeks. TSA was shown to directly reduce collagen type II (COL2), aggrecan, matrix metalloproteinase (MMP), and a disintegrin and metalloproteinase domain with thrombospondin motifs 5 (ADAMTS-5) expression and to simultaneously repress the upregulation of MMP-3, MMP-9, and MMP-13 levels induced by interleukin 1β (IL-1β) in chondrocytes. In conclusion, TSA protects AOT grafts from degeneration, which may provide a benefit in the repair of articular cartilage injury.