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Effect of suprascapular nerve injury on muscle and regenerated enthesis in a rat rotator cuff tear model

  • Kenichiro Eshima (Department of Orthopedic Surgery, Kurume University Hospital) ;
  • Hiroki Ohzono (Department of Orthopedic Surgery, Kurume University Medical Center) ;
  • Masafumi Gotoh (Department of Orthopedic Surgery, Kurume University Medical Center) ;
  • Hisao Shimokobe (Department of Orthopedic Surgery, Kurume University Hospital) ;
  • Koji Tanaka (Department of Orthopedic Surgery, Kurume University Hospital) ;
  • Hidehiro Nakamura (Department of Orthopedic Surgery, Kurume University Medical Center) ;
  • Tomonoshin Kanazawa (Department of Orthopedic Surgery, Kurume University Hospital) ;
  • Takahiro Okawa (Department of Orthopedic Surgery, Kurume University Medical Center) ;
  • Naoto Shiba (Department of Orthopedic Surgery, Kurume University Hospital)
  • Received : 2022.08.17
  • Accepted : 2022.12.08
  • Published : 2023.06.01

Abstract

Background: Massive rotator cuff tears (RCTs) are complicated by muscle atrophy, fibrosis, and intramuscular fatty degeneration, which are associated with postoperative tendon-to-bone healing failure and poor clinical outcomes. We evaluated muscle and enthesis changes in large tears with or without suprascapular nerve (SN) injury in a rat model. Methods: Sixty-two adult Sprague-Dawley rats were divided into SN injury (+) and SN injury (-) groups (n=31 each), comprising tendon (supraspinatus [SSP]/infraspinatus [ISP]) and nerve resection and tendon resection only cases, respectively. Muscle weight measurement, histological evaluation, and biomechanical testing were performed 4, 8, and 12 weeks postoperatively. Ultrastructural analysis with block face imaging was performed 8 weeks postoperatively. Results: SSP/ISP muscles in the SN injury (+) group appeared atrophic, with increased fatty tissue and decreased muscle weight, compared to those in the control and SN injury (-) groups. Immunoreactivity was only positive in the SN injury (+) group. Myofibril arrangement irregularity and mitochondrial swelling severity, along with number of fatty cells, were higher in the SN injury (+) group than in the SN injury (-) group. The bone-tendon junction enthesis was firm in the SN injury (-) group; this was atrophic and thinner in the SN injury (+) group, with decreased cell density and immature fibrocartilage. Mechanically, the tendon-bone insertion was significantly weaker in the SN injury (+) group than in the control and SN injury (+) groups. Conclusions: In clinical settings, SN injury may cause severe fatty changes and inhibition of postoperative tendon healing in large RCTs. Level of evidence: Level Basic research, controlled laboratory study.

Keywords

References

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