Authors
Michael J. Mienaltowski, Andrew A. Dunkman, Mark R. Buckley, David P. Beason, Sheila M. Adams, David E. Birk and Louis J. Soslowsky
Abstract
Injury adversely impacts the structure and mechanical properties of a tendon, thus causing pain and disability. Previously, we demonstrated that patellar tendons in mature (P150) and aged (P300) mice do not recover original functionality, even 6 weeks after injury, and that uninjured geriatric tendons (P570) are functionally inferior to uninjured mature tendons. In this study, we hypothesized that the repair response in injured geriatric mice would be further compromised, thus undermining patellar tendon function post-injury. Patellar tendons from wild-type mice were injured at 540 days. At 3 and 6 weeks post-surgery, structural, mechanical, and biochemical analyses were performed and compared to uninjured controls. Mechanical properties of geriatric tendons failed to improve after injury. When compared to mature and aged tendons post-injury, it was determined that at no age was there a suitable repair response. In previous studies, we were able to associate the absence of SLRPs with phenotypic changes both early and late in repair. Here we found that SLRPs were significantly decreased after injury, thus offering a possible explanation for why geriatric tendons were unable to mount an adequate repair response. Thus, we conclude that regardless of age after maturity, tendon healing ultimately results in a substandard outcome.