The labrum has several functions and three in particular: it increases the contact area between the humeral head and scapula, by 2 mm anteroposteriorly and 4.5 mm supero-inferiorly; it contributes to the “viscoelastic piston” effect, maintaining −32 mmHg intra-articular negative pressure; this is especially effective against traction stress and, to a lesser extent, against shear stress; it provides the insertion for stabilizing structures (capsule and glenohumeral ligaments), as a fibrous “crossroad” [15]. Labrum and ligaments are in synergy in a genuine complex, each structure’s contribution varying with the position of the limb: in abduction and external rotation (ABER), the inferior glenohumeral ligament (IGHL) absorbs 51% of the stress, the superior glenohumeral ligament (SGHL) 22%, and the MGHL 9% [16].

Biomechanical studies have sought to elucidate the function of an intact superior labrum/biceps complex and confirm the pathogenesis of injuries [17]. The function of the biceps is controversial and many authors have looked at this. The long head of the biceps tendon (LHBT) is felt to act as a humeral head depressor, aiding in glenohumeral compression and anterior and posterior glenohumeral stabilization and can limit external rotation [18, 19]. Giphart et al., however, found that there was no significant effect of the LHBT on glenohumeral kinematics [20].

A variety of mechanisms of injury are proposed in the pathogenesis of SLAP lesions, especially traction tension loads on the arm, compressive forces, and repeated microtrauma in throwing athletes. During the overhead throwing motion in the baseball pitch, SLAP lesions are often seen in the late and deceleration phase [21]. The increased lateral rotation in this late stage creates an increase in torsional stress in the insertion of the biceps, resulting in the dynamic peel-back mechanism and injury to the posterosuperior labrum [22]. In the last decade, understanding of the biomechanics and pathophysiology of the athletic shoulder has significantly improved. Especially in overhead athletes and throwers, several pathologic mechanisms have been identified which could not be explained by the traditional concepts of instability and impingement. Glenohumeral instability and posterior capsule contracture are believed to play a crucial role in the etiology of the painful athletic shoulder. Instability and contractures related to sports are frequently underappreciated. These may initiate a vicious cycle of secondary internal impingement, muscular dysfunction, and damage to intra-articular structures. The results can be devastating and may even end the athlete’s career [23].

The term “instability” constitutes a spectrum of disorders, which includes hyperlaxity, subluxation, and dislocation. Principally, glenohumeral instability can be classified according to its etiology, degree, frequency, and direction. The classic categorization of affected individuals into two groups with traumatic and atraumatic instability represented by the mnemonics TUBS (traumatic, unidirectional, Bankart lesion, surgical treatment) and AMBRII (atraumatic, multidirectional, bilateral, rehabilitation, inferior capsular shift, rotator interval closure) has been supplemented by a further grouping that is mainly comprised of overhead athletes with so-called micro-instability (microtraumatic instability) and that has been labeled with the acronym AIOS (acquired instability in overstressed shoulder). However, it should be emphasized that congenital or acquired hyperlaxity, micro-instability, and traumatic instability can overlap particularly in athletes engaged in overhead sports [24, 25].

Snyder et al. [6] described the most common mechanisms of SLAP lesions as compression injuries of the upper limb and traction injuries of the superior labrum biceps tendon complex with the shoulder in hyperextension. A three-part series of articles by Burkhart and colleagues looked at the association of kinetic chain disorders and scapular dyskinesia on SLAP injuries. The peel-back mechanism is associated with SLAP tears, with associated posteroinferior contraction and migration of rotation from the center toward the posterosuperior portion of the glenohumeral joint. With associated anteroinferior relaxation, there is a change in the biceps vector and elevated shearing in peel-back forces during the throwing cycle [21, 22, 26, 27].

Traumatic glenohumeral instability is also implicated as an associated etiology. It is typically initiated by a specific traumatic event, followed by other episodes of dislocation or subluxation usually in an anteroinferior direction when a sudden force overwhelms the anterior capsular structures. This occurs while the athlete’s arm is in an abducted, externally rotated, and extended position. The resulting combination of injuries represents the source of chronic instability, particularly those involving the inferior glenohumeral ligament (IGHL). Most studies agree that the IGHL is the most important passive stabilizer of the shoulder joint [28, 29]. The IGHL is formed by an anterior and a posterior band, which represents a thickening of the capsule connecting the inferior labrum to the glenoid and the humeral neck. The anteroinferior labrum and the anterior band of the IGHL together form the anteroinferior labro-ligamentous complex. The labrum is thought to serve as an insertion site for the IGHL and to provide stability to the glenohumeral joint by deepening the glenoid fossa [30]. Although generally common in contact collision sports, this type of instability is rarely observed in throwers or overhead athletes. When present, however, this type of instability can cause secondary damage to the rotator cuff and the superior and posterior labrum [31].

According to Soslowsky et al., inferior subluxation of the shoulder resulted in type II SLAP lesions [32]. Lo and Burkhart concluded that anterior lesions led to injuries of the superior and posterior labrum, because a history of trauma was observed in shoulders when they were positioned in abduction and external rotation [33]. They believe that recurrent anteroinferior instability is mainly responsible for the SLAP lesions.

These authors also suggest that more extensive lesions are a result of an increased number of dislocations, secondary to progression of a simple injury. However, this is not always the case, since extensive lesions have also been noted with low numbers of dislocations in the presence of high-energy trauma [34]. Durban et al. suggest that the severity of the lesions is a result of the initial high-energy trauma leading to the anterior shoulder instability with SLAP lesions [35]. Therefore, primary lesions of complex labral tears, such as type V SLAP lesions, should be examined thoroughly.

In 1985, Andrews postulated that a SLAP lesion, an anteroposterior tear of the superior labrum, was caused by overloading and traction of the long head of the biceps tendon during the follow-through phase of throwing [1]. Snyder categorized SLAP lesions into four types and suggested that type II SLAP lesions were the most common injuries and were primarily responsible for pain and restricted mobility of the shoulder joint in overhead athletes [6]. Maffet then added more types to this classification, because 38% of the SLAP lesion patients did not fall into the classification by Snyder. The authors use the Morgan and Maffet modifications [7] (Figs. 22.4, 22.5, 22.6, 22.7, and 22.8):

A complete clinical history with detailed mechanism of trauma description is essential. Symptoms associated with Bankart lesions typically do not include chronic pain but rather functional limitations that arise from symptoms of instability. In contrast, SLAP lesions frequently present with pain. We believe the combination of both lesions involves a great degree of energy with the arm in abduction and external rotation, where simultaneously the biceps labral complex is subjected to shear and torsional forces.

There are many tests that have been described in the literature. These include O’Brien’s test, Speed’s test, Yergason’s test, pain provocation test, biceps load test, biceps load test type II, crank test, and many more. Recent literature [36] has looked at a combination of tests to get the optimal sensitivity and specificity. And these often involve the combination of O’Brien’s, Hawkin’s, Speed’s, Neer’s, and Jobe’s test. High specificity tests include pain provocation and Yergason’s test. The authors feel that a combination of several tests is optimal for an accurate diagnosis.

The use of SLAP tests and assessments for traumatic anterior instability in combination with radiologic imaging can improve accuracy, but arthroscopy is the gold standard for both diagnosis and treatment of SLAP tears [37].

The high diagnostic accuracy of magnetic resonance (MR) arthrography in the detection of labro-ligamentous lesions has been demonstrated in several studies with a sensitivity of 88–96% and a specificity of 91–98% [38]. For the detection of lesions of the superior, middle, and inferior glenohumeral ligaments, Chandnani and coworkers reported sensitivities and specificities of 88–100% [39]. The sensitivities and specificities of unenhanced MR imaging for the diagnosis of labro-ligamentous injuries vary widely in the literature. A direct comparison with MR arthrography has not yet been performed in a larger series. The role of standard MR imaging in the diagnostic work-up of shoulder instability is questionable, particularly in regard to chronic cases and the identification of associated pathology. The advantages of MR arthrography result from capsular distension with separation of anatomic structures and improved delineation of tears following introduction of contrast media. MR arthrography thereby allows a more confident identification of pathology from the common anatomic variations of labral morphology, as well as the congenital variants of the glenohumeral ligaments and the labro-ligamentous unit, such as the Buford complex. MR arthrography (MRA) is the current gold standard imaging method to detect SLAP tears [39, 40].

We can clearly see a SLAP type II lesion in association with a Bankart lesion using MR arthrography (Fig. 22.9).