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A Delayed Bone-Tendon Junction Healing Model Established for Potential Treatment of Related Sports Injuries
  1. Lin Wang
  1. Department of Orthopaedics and Traumatology, The Chinese University of Hong Kong, Hong Kong
    1. Ling Qin (lingqin{at}cuhk.edu.hk)
    1. Department of Orthopaedics and Traumatology, The Chinese University of Hong Kong, Hong Kong
      1. Wing-Hoi Cheung (louis{at}ort.cuhk.edu.hk)
      1. Department of Orthopaedics and Traumatology, The Chinese University of Hong Kong, Hong Kong
        1. Hong-Bin Lu
        1. Department of Orthopaedics and Traumatology, The Chinese University of Hong Kong, Hong Kong
          1. Xiao-Hong Yang
          1. Department of Orthopaedics and Traumatology, The Chinese University of Hong Kong, Hong Kong
            1. Kwok-Sui Leung
            1. Department of Orthopaedics and Traumatology, The Chinese University of Hong Kong, Hong Kong
              1. Kai-Ming Chan
              1. Department of Orthopaedics and Traumatology, The Chinese University of Hong Kong, Hong Kong

                Abstract

                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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