Unstable Joints: Cartilage Stress Anomaly and OA
Sponsor: Centers for Disease Control and Prevention
Assistant
Professor, Department of Orthopaedic Surgery
The University of Iowa
Iowa City, IA 52242
e-mail: Todd-McKinley@uiowa.edu
|
Name |
Organization |
Role on Project |
|
M. James Rudert, Ph.D. |
University of Iowa
|
Co-Investigator |
|
Nicole M. Grosland, Ph.D. |
University of Iowa |
Co-Investigator |
|
Thomas D. Brown, Ph.D. |
University of Iowa |
Co-Investigator |
Successful orthopaedic management of displaced intra-articular fractures, to forestall post-traumatic osteoarthritis (OA), depends on avoidance of a mechanical environment that is deleterious to articular cartilage. To date, almost no attention has been directed to the causative mechanisms by which instability induces post-traumatic osteoarthritis. Many confounding factors, especially heterogeneity of injury, preclude systematic human clinical study of the relative importance of instability versus incongruency as causes of osteoarthritis secondary to intra-articular fractures. We propose laboratory studies, to investigate mechanisms of how global joint instability manifests itself in terms of mechanical anomaly at the tissue and cellular level, where osteoarthritis metabolically originates.
1. In an established rabbit knee defect model, we
modulate instability by means of partial sectioning of the anterior cruciate
ligament, and document the speed/severity of the resulting secondary
degenerative changes.
If dynamic instability can be shown to be a potent determinant of post-traumatic osteoarthritis, this would strongly argue that orthopaedic management of these difficult injuries ought to prioritize attaining suitable thresholds of joint stability, rather than the presently dominant strategy of aggressive interventions to attain precise congruency in order to minimize contact stress elevations.