How much force is acting on the shoulder joint to create a Hill-Sachs Lesion or reverse Hill-Sachs Lesion?

BACKGROUND: It has not been clarified yet how much force is acting on the shoulder joint to create Hill-Sachs/reverse Hill-Sachs lesions which are commonly observed in patients with anterior or posterior shoulder instability. The purpose of this study was to determine the magnitude of force to create these bony lesions using cadaveric shoulders. METHODS: Fourteen fresh-frozen cadaveric shoulders were used. Compression tests were performed using the universal testing machine. The specimens were randomly divided into two groups. In group A, the posterior humeral head (the bare area and articular cartilage) was first compressed against the anterior glenoid rim to simulate a Hill-Sachs lesion, followed by the anterior humeral head being compressed against the posterior glenoid rim. In group B, the same procedure was repeated in the reverse order. X-ray microcomputed tomography (microCT) was also performed. RESULTS: The maximum compression force to create a Hill-Sachs lesion was 771 ± 214 N (mean ± SD) on the articular cartilage of the posterior humeral head, which was significantly greater than the force of 447 ± 215 N to create it on the bare area (P = 0.0086). Regarding the reverse Hill-Sachs lesions, the maximum compression force was 840 ± 198 N when it was created on the articular cartilage of the anterior humeral head, which was significantly greater than the force of 471 ± 100 N when it was created at the footprint of the subscapularis tendon (P = 0.0238). MicroCT showed multiple breakage of the trabecular bone. CONCLUSION: A force to create a Hill-Sachs lesion or a reverse Hill-Sachs lesion was significantly greater when it was created on the humeral articular cartilage than at the non-cartilage area. Also, the force to create a reverse Hill-Sachs lesion was significantly greater than the one to create a Hill-Sachs lesion.

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

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.

In Vivo Glenoid Track Width Can Be Better Predicted With the Use of Shoulder Horizontal Extension Angle.

BACKGROUND: The glenoid track concept has been widely used to assess the risk of instability caused by a bipolar lesion. The mean glenoid track width is reported to be 83% of the glenoid width. However, this width seems to be affected by the range of motion of the shoulder. By clarifying the relationship between the range of shoulder motion and the glenoid track width, a more precise determination of the glenoid track width for each individual could be possible. PURPOSE: To determine the relationship between the glenoid track width and the range of motion of healthy volunteers. STUDY DESIGN: Descriptive laboratory study. METHODS: Magnetic resonance imaging was taken in 41 shoulders of 21 healthy volunteers (mean age, 32 years) with the arm in maximum horizontal extension, with the arm kept in 90° of abduction and 90° of external rotation. Three-dimensional surface bone models of the glenoid and the humerus were created with image analysis software. The distance from the anterior rim of the glenoid to the medial margin of the footprint of the rotator cuff tendon was defined as the glenoid track width. Active and passive ranges of shoulder motion were measured in the supine and sitting positions. The correlations between the glenoid track width and the ranges of shoulder motion were investigated with Pearson correlation coefficients. Intra- and interobserver reliabilities based on the intraclass correlation coefficient were also analyzed to assess the reliability of the glenoid track measurement. RESULTS: The intra- and interobserver reliabilities for the glenoid track measurement were excellent (0.988 and 0.988, respectively). Among all the measurements, the glenoid track width and the active range of motion in horizontal extension in the sitting position showed the greatest correlation coefficient ( r = -0.623, P < .0001). A correlation between the glenoid track width and this angle was expressed as Y = -0.49 X + 90, where X is the horizontal extension angle (degrees) and Y is the glenoid track width (percentage of glenoid width). CONCLUSION: The present data demonstrate that the greater the horizontal extension angle in abduction and external rotation, the smaller the glenoid track width. An individualized glenoid track width can be obtained by measuring the active horizontal extension angle with the arm in abduction and external rotation in the sitting position. CLINICAL RELEVANCE: An individualized glenoid track width enables selection of a more precise surgical option by the on-track/off-track concept.