Critical Shoulder Angle and Rotator Cuff Repair: Preclinical Findings

In a rat rotator cuff repair model, experimentally increasing the critical shoulder angle (CSA) through acromion lateralization was reported alongside less favorable healing-associated signals on imaging, mechanical testing, gait assessment, and local biology at the tendon–bone interface.

Using a within-animal comparison, investigators contrasted the acromion-lateralized shoulder with the contralateral RCR-only control side. Across modalities, the report described converging differences linking increased CSA with changes in rotator cuff biomechanics, functional readouts, and mechanobiological markers at the repair site. Overall, the findings framed CSA as a variable connected to both mechanical performance and local biologic signaling in this preclinical setting.

Methods were described in a bilateral chronic rotator cuff tear rat model in which 48 Sprague-Dawley rats underwent creation of chronic tears in both shoulders, with acromion lateralization performed on one side (the “Acr” side) to increase CSA. Four weeks later, both shoulders underwent rotator cuff repair (RCR), allowing each animal to serve as its own control for systemic factors. Micro-computed tomography confirmed that the geometric manipulation increased mean CSA from approximately 29.7° to 37.2° (p < 0.001), establishing a measurable side-to-side difference before post-repair assessments. In this design, the manipulated variable was acromion lateralization to increase CSA.

After repair, the increased-CSA shoulders were described as having worse MRI findings, including a higher signal-to-noise quotient at 6 and 9 weeks postoperatively, which the authors reported as reflecting poorer healing-related outcomes. Biomechanical testing was similarly reported as demonstrating lower ultimate failure load and lower stiffness on the acromion-lateralized side (p < 0.05), aligning structural performance with the imaging findings. Gait parameters were also significantly poorer in the increased-CSA condition compared with the RCR-only side at the same time points (p < 0.05). Across imaging, mechanics, and gait, outcomes were described as directionally consistent in the increased-CSA shoulders.

At the tissue level, histological analysis at the tendon–bone interface in increased-CSA shoulders showed inferior integration (p < 0.01), including reduced fibrocartilage formation, disorganized collagen fibers, and a lower collagen I/III ratio.

Immunohistochemistry demonstrated significantly higher Piezo1 expression in the Acr group (p < 0.001), which the authors described as suggesting a mechanobiological response to increased mechanical stress. Because these findings derive from a rat model with an experimentally created increase in CSA, they were presented as preclinical evidence rather than human outcome data. The authors concluded that an increased CSA impaired tendon–bone interface healing following RCR in this model and suggested that these findings support consideration of CSA modification (e.g., with acromioplasty) in selected high-risk patients, while acknowledging the preclinical nature of the evidence.

Key Takeaways:

• The report used a within-animal rat model with acromial lateralization on one side to widen CSA and compare against a contralateral control repair.
• Across MRI, mechanical testing, and gait analysis, outcomes were reported as less favorable in the widened-geometry shoulders than in the control side.
• Histology suggested altered enthesis microstructure, and higher Piezo1 expression was reported as a mechanosensitive biologic signal in the increased-CSA condition.