Mechanism and patterns of bone loss in patients with anterior shoulder dislocation

Bony defects are common injuries associated with anterior shoulder dislocation. It is generally thought that these bony defects are created at the time of dislocation. However, there have been no biomechanical reports demonstrating the exact time point when these lesions occur. The purpose of this study was to clarify when, how, and which types of bony defects were created during experimental dislocation in cadaveric shoulders.

Fifteen fresh-frozen cadaveric shoulders (mean age at the time of death, 79 years) were fixed in a custom testing machine. First, the glenohumeral joint was inspected by arthroscopy. Then, the arm was held at 60° of abduction and maximum external rotation and was manually extended horizontally under fluoroscopy until an anterior dislocation occurred. Next, a force of 800 N was applied to a Kirschner wire inserted in the humeral head in the direction of the pectoralis major with use of an air cylinder. We waited until the arm came to equilibrium under this condition. Finally, the glenohumeral joint was arthroscopically examined. We further performed x-ray micro-computed tomography and histologic examination in 1 shoulder with a bipolar lesion.

After the anterior dislocation, a Bankart lesion was created in 9 of 15 shoulders and a fragment-type glenoid defect (avulsion fracture) was created in 4. A Hill-Sachs lesion, on the other hand, was not observed after the dislocation. The equilibrium arm position was 40° ± 17° in flexion, 45° ± 22° in abduction, and 27° ± 19° in external rotation. In this arm position, newly created lesions were Hill-Sachs lesions in 6 shoulders and erosion-type glenoid defects (compression fracture) in 7. Micro-computed tomography, performed in a single specimen, showed a flattened anterior glenoid rim with collapse of trabecular bone. Histologic analysis of nondecalcified sections using hematoxylin-eosin staining indicated that the anterior rim of the glenoid was compressed and flattened. The cortex of the anterior glenoid rim could be clearly observed.

The fragment-type glenoid defect (avulsion fracture) was observed at the time of dislocation, whereas the erosion-type defect (compression fracture) was observed when the arm came to equilibrium in the midrange of motion. Hill-Sachs lesions were created not at the time of dislocation but after the arm came to equilibrium.