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 the B–T junction is difficult and sometimes delayed, establishing a delayed B–T healing experimental model is therefore essential to study the efficacy of potential biophysical and biological interventions for treatment of B–T junction healing.
Objective To test the hypothesis that a delay in B–T healing could be modelled 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) compared with controls (n = 10) were evaluated at 8 and 12 postoperative weeks.
Results Radiology showed consistent delay in osteogenesis at the healing interface in all samples in the delayed healing group; growth of new bone was only 25.8% and 50.1% of that in the control group at weeks 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 weeks 8 and 12, respectively. The healing quality was also reflected 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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Competing interests None.