Chronic SLAP tears from repetitive microtrauma are commonly seen in overhead sporting activities [6]. The pathophysiology of chronic SLAP tears has been much debated, and various mechanisms have been proposed. All these mechanisms are centered around a repetitive overhead motion of hyperabduction and external rotation, which produces large forces and increased shear and compression forces on the glenohumeral joint and strain on the rotator cuff and capsule-labral structures [5]. One of the suggested pathophysiology is alteration in the kinetic chain. Throwing requires a complex series of coordinated motions resulting in the transmission of large forces from the legs, the core, via the shoulder, onto the arm and hand. If such coordinated effort of the “kinetic chain” is altered, such alteration can lead to abnormal forces, leading to injury to the labrum or the rotator cuff [11]. An overhead athlete is particularly predisposed to such alterations due to the “thrower’s paradox,” i.e., a thrower must possess sufficient laxity to allow excessive external rotation, yet sufficient stability to prevent glenohumeral joint subluxation [15]. It is commonly noted in overhead athletes that the range of external rotation is increased and the internal rotation is correspondingly decreased [2]. This pattern is termed as glenohumeral internal rotation deficit or GIRD. Such changes, although advantageous to an elite training athlete, may predispose the athlete to labral injuries (Fig. 11.2).

Another patho-mechanical explanation of a chronic SLAP tear may well be as a result of contracture of the posterior shoulder capsule, resulting in a relative posterior superior migration of the humeral head [5]. Such a posterior contracture appears with repetitive overhead external rotation and can result in a secondary posterior superior position of the humeral head. This, in turn, increases the shear forces across the glenohumeral joint, leading to internal impingement. Burkhart et al. [5] also described the “peel-back” mechanism, which may potentially explain chronic SLAP tears. During the abduction and external rotation of the shoulder, torsional forces in the biceps and labrum increase as the arm moves to this extreme position, leading to a twist at the base of the biceps, which transmits such a force onto the labrum, resulting in a “peel back.” Furthermore, in athletes with such altered mechanics of posteroinferiorly contracted capsule, a “peel-back” mechanism is exacerbated if the position of the scapula is protracted and laterally rotated (Fig. 11.3).

It is likely that all the above mechanisms have a role to play in the pathophysiology of the chronic SLAP tear seen in an overhead athlete. Snyder et al. [14] developed an arthroscopic classification for SLAP tears, which is common to both acute traumatic SLAP tears and chronic SLAP tears caused by repetitive micromotion. Various modifications to the original SLAP classification by Snyder et al. [14] have been proposed, notably type 5, where a Bankart lesion extends into the superior labrum and biceps anchor, and type 8 with a posterior labral extension into a 6 o’clock position. Such type 5 and type 8 lesions are commonly seen in acute SLAP tears, resulting from a concomitant shoulder dislocation, as indeed the type 9 (more severe labral tears with circumferential involvement). SLAP tears, in contrast, as a result of chronic repetitive overhead motion, would classically lead to a type 2 SLAP tear. Such type 2 SLAP tears have been further classified into type 2A, B, and C [13]. The most frequent lesion seen in chronic SLAP tear is a type 2B SLAP tear.