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1 Department of Orthopaedics and Traumatology, The Chinese University of Hong Kong, Hong Kong
* To whom correspondence should be addressed. E-mail: lingqin{at}cuhk.edu.hk.
Accepted 21 April 2008
| Abstract |
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Background: Animal models for the study of tendinopathy and bone-tendon (B-T) junction repair have been established in the past for sports medicine research. As healing at B-T junction is difficult and sometime with delay in healing, establishing a delayed B-T healing experimental model is therefore essential to study efficacy of potential biophysical and biological interventions for treatment of B-T junction healing.
Objective: We hypothesized that a delay in B-T healing could be modeled by shielding the B-T healing interface for the initial few weeks.
Methods: Using an established partial patellectomy model in rabbits, the B-T healing interface was shielded with a latex slice for the first 4 postoperative weeks in mature female rabbits. The characteristics of delay in B-T repair (n=10) were compared with controls (n=10) were evaluated at 8 and 12 postoperative weeks.
Results: Radiology showed consistent delay in osteogenesis at healing interface in all samples in the delayed healing group, with new bone size of only 25.8% and 50.1% of the control groups at week 8 and 12, respectively. Bone mineral density was 56.0% lower in the delayed healing group at week 8, but this difference diminished at week 12. The quality of B-T healing was poor in the delayed healing group, with 22.9% and 24.2% lower failure load than the control group at week 8 and week 12, respectively. The healing quality was also echoed by histological findings.
Conclusions: A delayed B-T healing experimental model was established for the first time for future sports medicine research.
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