Cartilage response to in vitro models of injury in combination with growth factor and antioxidant treatments

Approximately one in five Americans is affected by arthritis, making it one of the most prevalent diseases and the leading cause of disability in the United States. Post-traumatic arthritis occurs after joint injury (e.g., ACL rupture or intraarticular fracture) and makes up a substantial proportion of the population with arthritis. In previous clinical studies, patients suffering from a traumatic joint injury have shown an increased risk in osteoarthritis (OA), independent of surgical intervention to stabilize the joint. Thus, the early events post-injury have an important effect on tissue within the joint in the long term. To understand the processes involved in the onset of OA and factors leading to OA post-traumatic injury, in vitro models have been developed to isolate components of the complex processes occurring in vivo. While in vitro models do not mimic true physiologic conditions in vivo, by isolating the effects of mechanical compression, cytokine treatment, and cartilage co-cultured with adjacent tissue, in vitro models can give insight into key biological and mechanical pathways occurring in vivo. This study focuses on changes in cartilage gene and protein expression and associated cartilage matrix degradation in response to static or injurious compression of the tissue in the presence or absence of cytokines including TNF-a and IL-6. In addition, normal or injuriously compressed cartilage explants were co-cultured with injured (excised) joint capsule tissue, another in vitro model of post-traumatic cellular behavior. Both young bovine cartilage and human cartilage from a wide range of ages were used. The growth factors insulin-like growth factor-1 (IGF-1) and Osteogenic protein-i (OP-1), as well as the antioxidant, superoxide dismutase mimetic (SODm), were tested to examine if they had the capability to abrogate the negative effects of these injury models.

Department dc:contributor.department

Massachusetts Institute of Technology. Biological Engineering Division.

Grantor dc:publisher

Massachusetts Institute of Technology

Year dc:date.issued

2008

Author dc:creator

• Wheeler, Cameron, 1978-

Advisor dc:contributor.advisor

• Alan J. Grodzinsky.

• Biological Engineering Division.

Statement dc:rights

• MIT theses are protected by copyright. They may be viewed, downloaded, or printed from this source but further reproduction or distribution in any format is prohibited without written permission.

Licence dc:rights.uri

• http://dspace.mit.edu/handle/1721.1/7582

Language dc:language.iso

eng

Handle dc:identifier.uri

http://hdl.handle.net/1721.1/42385

OAI identifier oai:identifier

oai:dspace.mit.edu:1721.1/42385