The mechanism of creation of superior labrum, anterior, and posterior lesions in a dynamic biomechanical model of the shoulder: the role of inferior subluxation.

Lesions of the superior glenoid labrum are a source of shoulder disease. However, the mechanisms of injury to this region are unknown, and controversy exists regarding the role of shoulder instability in creation of this lesion. With a cadaver model that simulates physiologic rotator cuff forces and produces traction on the biceps tendon, the creation of type II superior labrum, anterior, and posterior (SLAP) lesions and the role of glenohumeral subluxation were investigated: Left and right shoulders from each of 8 paired cadavers (age 62 +/- 7.2 years, 5 male and 3 female) were randomized to be tested in either a 20 mm inferiorly subluxed position or in a reduced position. The long head of the biceps tendon was held near the musculotendinous junction with a novel cryogenic clamp. Traction on the long head of the biceps tendon was applied at a fast rate of 12.7 cm/sec with a servohydraulic testing machine. A load cell was used to monitor the biceps tendon load. After testing to failure, the presence or absence of a type II SLAP lesion was determined by 2 experienced shoulder surgeons masked to the test group. The production of type II SLAP lesions differed significantly (P = .03) between reduced shoulders (2 SLAP lesions out of 8 tests) and the shoulders with inferior subluxation (7 SLAP lesions out of 8 tests). This experiment has shown that traction on the biceps tendon in this biomechanical model can reproducibly create type II SLAP lesions, and inferior subluxation facilitates the generation of such lesions.