The in vivo stabilizing role of the long head of the biceps tendon (LHB) is poorly understood. However, its role as a pain generator in the shoulder was described in 1948 by Hitchcock and Bechtol,10 who were also among the first to advocate biceps tenodesis. Tenodesis or tenotomy of the LHB has been reported to be an effective pain-relieving treatment option for recalcitrant biceps tendinitis and tendinopathy with low complication rates. However, the LHB has been reported in several in vitro studies to have the mechanical ability to stabilize the glenohumeral joint. Therefore, tenodesis or tenotomy could theoretically alter glenohumeral joint kinematics, creating a subsequent concern for potential pathological changes in patients after these procedures. These concerns have sparked significant debate about the best indications for biceps tenodesis or tenotomy and for which patient populations the procedure is suitable. Moreover, the importance of investigating the stabilizing role of the LHB in vivo is emphasized by these debates.
Evidence of the ability of the LHB to constrain glenohumeral motion is based primarily on cadaveric studies, which reported that the LHB has stabilizing effects on the glenohumeral joint anteriorly, posteriorly, superiorly, and inferiorly, suggesting concavity compression as its primary mechanism for providing glenohumeral stability. Others have suggested a pivotal role of the LHB in preventing superior humeral head migration. In vitro biomechanical investigations have also reported that the LHB significantly constrains rotational range of motion. Overall, cadaveric models have suggested that without the stabilizing presence of the LHB, increased glenohumeral translations of between 5 and 25 mm can occur in the superior-inferior and anterior-posterior planes.
To date, however, translations of this magnitude have not been demonstrated in vivo. In the shoulders of patients with isolated ruptures of the LHB, when compared with their contralateral healthy shoulders, average superior position differences of the humeral head of 2.2 mm (maximum difference of 6 mm) at 45°, 90°, and 120° of abduction were measured by Warner and McMahon40 using serial, static radiographs. The authors theorized this amount of superior translation could contribute to an iatrogenic impingement syndrome. However, in the clinical literature, the stabilizing role of the LHB has not been as evident. For instance, the distance between the acromion and the humeral head in static radiographs was not altered after tenotomy. Similarly, Boileau et al4 have further questioned the stabilizing role of the LHB, showing no clinical evidence of instability or proximal humeral migration in patients who were treated with tenodesis compared with those treated by superior labral anterior posterior (SLAP) repair. Moreover, significantly more patients were able to return to their previous level of sports participation when compared with SLAP repair in this study.
Clearly, surgeons still face a confusing and contradictory body of evidence surrounding the biomechanical function of the LHB. While cadaveric studies show a stabilizing effect of the LHB, clinical data suggest that there is no clinically demonstrable increased humeral head motion after LHB tenodesis or tenotomy. Therefore, the purpose of this study was to investigate the effects of the LHB on glenohumeral kinematics in vivo using highly sensitive and accurate 3-dimensional imaging. To do this, we used a biplane fluoroscopy system to compare shoulders in patients who had undergone an isolated LHB tenodesis with their healthy contralateral shoulder during abduction, a simulated late cocking phase of a throw, and a simulated lifting task (loaded forward flexion). Our hypothesis was that there would be no differences in glenohumeral translations greater than 1.0 mm between the shoulders.