MedSport, Department of Orthopaedic Surgery, University of Michigan Medical Center, Ann Arbor, 48106-0391, USA.
Am J Sports Med. 2012 Feb;40(2):388-94. doi: 10.1177/0363546511425018. Epub 2011 Nov 3.
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.
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.
Controlled laboratory study.
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).
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.
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.
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.
Hill-Sachs 缺陷与前肩不稳定的修复失败有关。然而，由于被动软组织和骨性稳定器之间的复杂相互作用，这些缺陷的生物力学后果尚不清楚。
创建 25%的 Hill-Sachs 缺陷不会显著改变盂肱关节的平移，但会增加关节囊的原位力以及盂肱骨性接触力。
对照实验室研究。
使用机器人/通用力-力矩传感器（UFS）测试系统在去除皮肤和三角肌的情况下向尸体肩部施加关节压缩（22 N）和前或后负荷（44 N）（n = 9）（在 3 个盂肱关节位置下：外展/外旋 0°/0°、30°/30°和 60°/60°（对应于 90°/90°的肩外展/外旋）。然后在前肩脱位最常见的位置（90°/90°）上创建后外侧肱骨头上的 25%骨缺陷（缺陷），并重复加载方案。使用非参数重复测量 Friedman 检验和 Wilcoxon 符号秩检验进行后验检验，以比较每个状态下的平移、关节囊的原位力和骨性接触力（P <.05）。
在 0°/0°时，在前负荷作用下，前向平移从 15.3 ± 8.2 毫米显著增加至 16.6 ± 9.0 毫米（P <.05）。在 30°/30°时，在前向和后向负荷作用下，前向和后向平移分别显著增加（完整：13.6 ± 7.1 毫米对缺陷：14.2 ± 7 毫米；P <.05）。在 60°/60°（完整：38.9 ± 14.4 N 对缺陷：43.2 ± 15.9 N；P <.05）和 30°/30°（完整：39.6 ± 13.8 N 对缺陷：45.6 ± 9.3 N；P <.05）时，前负荷期间关节囊的原位力在缺陷状态下也增加。在 30°/30°时，前向负荷时骨性接触力也增加（完整：25.0 ± 13.8 N 对缺陷：28.9 ± 13.2 N；P <.05）。
我们认为，在存在前负荷时，完整关节囊的稳定功能是导致观察到的 25%Hill-Sachs 缺陷仅导致前向平移、囊内力和骨性接触力小幅度增加的主要原因。
这些发现表明，如果恢复关节囊的完整功能，孤立的 25%Hill-Sachs 缺陷可能不会导致复发性不稳定，并且 Hill-Sachs 缺陷的存在可能是前肩胛盂缘明显伴随损伤的标志物。然而，这些参数的微小变化可能对骨关节炎的发展产生长期影响。
