Deformation and strain characteristics along the length of the anterior band of the inferior glenohumeral ligament.

Efficacious surgical treatment of anterior glenohumeral instability often requires repair of the anteroinferior capsulolabral structures, including the glenoid origin of the anterior band of the inferior glenohumeral ligament. Rupture in this location, the Bankart lesion, may be accompanied by nonrecoverable stretching of the anterior band. The purpose of this study was to evaluate the amount and location of nonrecoverable stretching with tensile testing. Twelve glenoid-soft tissue-humerus complexes from fresh-frozen glenohumeral joints were studied by means of a custom jig, an Instron machine, and a video digitizing system. The joints were positioned to simulate that known to cause apprehension for anterior instability. Nonrecoverable deformation differed along the length of the anterior band but was slight in all locations. For those that failed at the glenoid insertion region, the mean nonrecoverable deformation was 0.10 +/- 0.16 mm (mean +/- SEM) at the bone-labral junction of the glenoid insertion region and 0.38 +/- 0.23 mm at the labral-ligament junction of the glenoid insertion region. It was 0.53 +/- 0.23 mm at the ligament midsubstance and 0.04 +/- 0.10 mm at the humeral insertion region. For those that failed at the glenoid insertion region, the nonrecoverable stretching was 1.4% +/- 1.9% at the bone-labral junction of the glenoid insertion region and 3.5% +/- 2.0% at the labral-ligament junction of the glenoid insertion region. It was 2.3% +/- 1.1% at the ligament midsubstance and 0.0% +/- 1.4% at the humeral insertion region. Rupture of the anterior band resulted in little nonrecoverable stretching at both the site of failure and elsewhere along the length, remote from the failure site. Surgical repairs after initial dislocation may restore the length of the anterior band of the inferior glenohumeral ligament with little shortening.

The cyclops lesion: a cause of diminished knee extension after rupture of the anterior cruciate ligament.

Four patients presented with persistent diminution of knee motion after rupture of the anterior cruciate ligament with a novel lesion as the cause. Each had participated in an aggressive rehabilitation program for a minimum of 2 months with emphasis on regaining full range of knee motion. Because chronic impairment of knee extension can be disabling, in those who did not regain full range of motion, arthroscopy of the knee ensued. All had a lesion in the intercondylar notch near the tibial insertion of the anterior cruciate ligament that acted as a mechanical obstruction to full knee extension. Grossly and histologically, these were similar to the cyclops lesion that also has been shown to cause loss of knee extension after anterior cruciate ligament reconstruction. Arthroscopic debridement of the cyclops lesion and manual manipulation of the knee under anesthesia lead to restoration of full knee extension in all knees. In 1 other knee with chronic instability after anterior cruciate ligament rupture, the cyclops lesion was present but was very small and was not associated with diminished knee extension. When loss of full extension persists for 2 months after anterior cruciate ligament disruption despite aggressive rehabilitation, the presence of a cyclops lesion should be considered.