骨移植治疗大关节盂缺损的稳定机制。
Stabilizing mechanism in bone-grafting of a large glenoid defect.
机构信息
Biomechanics Laboratory, Division of Orthopedic Research, Mayo Clinic, 200 First Street S.W., Rochester, MN 55905, USA.
出版信息
J Bone Joint Surg Am. 2010 Sep 1;92(11):2059-66. doi: 10.2106/JBJS.I.00261.
BACKGROUND
Conventional wisdom suggests that the glenoid defect after a shoulder dislocation is anteroinferior. However, recent studies have found that the defect is located anteriorly. The purposes of this study were (1) to clarify the critical size of the anterior defect and (2) to demonstrate the stabilizing mechanism of bone-grafting.
METHODS
Thirteen cadaver shoulders were investigated. With use of a custom testing machine with a 50-N compression force, the peak translational force that was needed to move the humeral head and lateral humeral displacement were measured. The force was used to evaluate the joint stability. An osseous defect was created stepwise in 2-mm increments of the defect width. The bone graft was harvested from the coracoid process. The defect size was expressed as the estimated defect size divided by the measured glenoid length. Testing was performed with (1) the glenoid intact, (2) a simulated Bankart lesion, (3) the Bankart lesion repaired, (4) a 2-mm defect, (5) the Bankart lesion repaired, (6) the defect bone-grafted, (7) a 4-mm defect, (8) the Bankart lesion repaired, (9) the defect bone-grafted, (10) a 6-mm defect, (11) the Bankart lesion repaired, (12) the defect bone-grafted, (13) an 8-mm defect, (14) the Bankart lesion repaired, and (15) the defect bone-grafted.
RESULTS
Force and displacement decreased as the size of the osseous defect increased. The mean force after the formation of a defect of > or =6 mm (19% of the glenoid length) with the Bankart lesion repaired (22 +/- 7 N) was significantly decreased compared with the baseline force (52 +/- 11 N). Both the mean force (and standard deviation) and displacement returned to the levels of the intact condition (68 +/- 3 N and 2.6 +/- 0.4 mm, respectively) after bone-grafting (72 +/- 12 N and 2.7 +/- 0.3 mm, respectively).
CONCLUSIONS
An osseous defect with a width that is > or =19% of the glenoid length remains unstable even after Bankart lesion repair. The stabilizing mechanism of bone-grafting was the restoration of the glenoid concavity.
背景
传统观点认为，肩关节脱位后的盂唇缺损位于前下。然而，最近的研究发现，缺损位于前方。本研究的目的是：（1）明确前侧缺损的临界尺寸，（2）展示植骨的稳定机制。
方法
对 13 具尸体肩关节进行了研究。使用带有 50N 压缩力的定制测试机，测量移动肱骨头所需的峰值平移力和外侧肱骨头位移。使用该力来评估关节稳定性。骨缺损宽度以 2mm 为增量逐步形成。骨移植物取自喙突。将缺损大小表示为估计的缺损大小除以测量的盂唇长度。测试分别在以下情况下进行：（1）盂唇完整，（2）模拟 Bankart 损伤，（3）Bankart 损伤修复，（4）2mm 缺损，（5）Bankart 损伤修复，（6）缺损植骨，（7）4mm 缺损，（8）Bankart 损伤修复，（9）缺损植骨，（10）6mm 缺损，（11）Bankart 损伤修复，（12）缺损植骨，（13）8mm 缺损，（14）Bankart 损伤修复，（15）缺损植骨。
结果
随着骨缺损的增大，力和位移减小。与基线力（52 ± 11N）相比，形成> =6mm（盂唇长度的 19%）骨缺损并修复 Bankart 损伤后，平均力（22 ± 7N）显著降低。植骨后，平均力（和标准差）和位移均恢复至正常状态（分别为 68 ± 3N 和 2.6 ± 0.4mm）（分别为 72 ± 12N 和 2.7 ± 0.3mm）。
结论
即使 Bankart 损伤修复后，宽度> =19%盂唇长度的骨缺损仍不稳定。植骨的稳定机制是恢复盂唇凹度。
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