The effect of a Hill-Sachs defect on glenohumeral translations, in situ capsular forces, and bony contact forces.

BACKGROUND: Hill-Sachs defects have been associated with failed repairs for anterior shoulder instability. However, the biomechanical consequences of these defects are not well understood because of the complicated interaction between the passive soft tissue and bony stabilizers. HYPOTHESIS: The creation of a 25% Hill-Sachs defect would not significantly alter the glenohumeral translations but would increase the in situ forces in the glenohumeral capsule as well as the glenohumeral bony contact forces. STUDY
DESIGN: Controlled laboratory study.
METHODS: A robotic/universal force-moment sensor (UFS) testing system was used to apply joint compression (22 N) and an anterior or posterior load (44 N) to cadaveric shoulders (n = 9) with the skin and deltoid removed (intact) at 3 glenohumeral joint positions (abduction/external rotation): 0°/0°, 30°/30°, and 60°/60° (corresponds to 90°/90° of shoulder abduction/external rotation). A 25% bony defect on the posterolateral humeral head (defect) was then created in the most common position of anterior shoulder dislocation (90°/90°), and the loading protocol was repeated. A nonparametric repeated-measures Friedman test with a Wilcoxon signed-rank post hoc test was performed to compare translations, in situ forces in the capsule, and bony contact forces between each state (P < .05).
RESULTS: At 0°/0°, anterior translation significantly increased from 15.3 ± 8.2 mm to 16.6 ± 9.0 mm (P < .05) in response to an anterior load. At 30°/30°, anterior and posterior translations, respectively, significantly increased in response to both anterior (intact: 13.6 ± 7.1 mm vs defect: 14.2 ± 7 mm; P < .05) and posterior loads (intact: 15.7 ± 5.8 mm vs defect: 17.7 ± 5.1 mm; P < .05). In situ force in the capsule during anterior loading was increased in the defect state at both 60°/60° (intact: 38.9 ± 14.4 N vs defect: 43.2 ± 15.9 N; P < .05) and 30°/30° (intact: 39.6 ± 13.8 N vs defect: 45.6 ± 9.3 N; P < .05). The medial bony contact forces were also increased in the defect state at 30°/30° (intact: 25.0 ± 13.8 N vs defect: 28.9 ± 13.2 N; P < .05) during anterior loading.
CONCLUSION: We believe that the stabilizing function of the intact capsule was the primary contributor to the finding of only small increases of anterior translation, capsule forces, and bony contact forces observed with a 25% Hill-Sachs defect in response to an anterior load. CLINICAL RELEVANCE: These findings imply that a 25% Hill-Sachs defect in isolation may not be responsible for recurrent instability if the function of the capsule is restored to the intact state and that the presence of the Hill-Sachs defect may be a marker for significant concomitant injury to the anterior glenoid rim. However, the small changes in these parameters may have long-term implications for the development of osteoarthritis.