Chondrocyte response to in vitro mechanical injury and co-culture with joint capsule tissue

Acute traumatic joint injury in young adults leads to an increased risk for the development of osteoarthritis (OA) later in life irrespective of surgical intervention to stabilize the injured joint. Although the mechanism by which injury leads to joint degeneration remains to be elucidated, several injury-related factors may contribute to the development of OA. These factors include but are not limited to altered mechanical loading and initiation of a cellular response in cartilage or other joint tissues at the time of the injury. Three in vitro models of joint injury were investigated to separately evaluate the effects on cartilage of mechanical overloading and damage to joint capsule and synovial lining. Models of injury included (1) mechanical injury lto cartilage explants alone, (2) co-culture of normal cartilage explants with an excised specimen of joint capsule tissue, and (3) co-culture of mechanically injured cartilage explants with excised joint capsule tissue. These models have been shown previously to result in matrix damage and decreased biosynthesis by the chondrocytes. We measured gene expression levels of matrix molecules and matrix proteases and found them to be expressed in control cartilage at levels ranging over five orders of magnitude, and to be differentially regulated in these three models of joint injury.

Department dc:contributor.department

Massachusetts Institute of Technology. Biological Engineering Division.

Grantor dc:publisher

Massachusetts Institute of Technology

Year dc:date.issued

2005

Author dc:creator

• Lee, Jennifer H. (Jennifer Henrica)

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/1721.1/33866

OAI identifier oai:identifier

oai:dspace.mit.edu:1721.1/33866