Jonathan B. Shook
Guido Marra
Overview
In 1906 Perthes first described the capsulolabral defect that, >30 years later, Bankart went on to coin the “essential lesion.” Since then, a plethora of anatomic and biomechanical studies have helped to clarify the elements that contribute to anterior glenohumeral instability (AGI). We now know that the shoulder joint is the most frequently dislocated joint and that >90% of these dislocations are anterior. The innate bony anatomy of the glenohumeral joint makes it particularly prone to instability. It has been likened to a golf ball on a tee. A small glenoid matched to a large humeral head allows the joint to be very mobile. The joint is thus quite dependent on the surrounding soft tissues for stability. When the bony anatomy is disrupted, or when the soft tissues fail, instability is the result. The specific pathoanatomy related to AGI is discussed below under two general categories: static stabilizers and dynamic stabilizers (Table 32-1).
Static Stabilizers
Capsule and Ligaments
More time and effort has probably been spent trying to elucidate the structures of the capsule and ligaments of the glenohumeral joint than any other aspect of the shoulder. It has been >150 years since investigators first described distinct ligaments that contributed to the shoulder joint's stability. Since then, many others have collaborated in their efforts to arrive at a generally accepted model of the capsuloligamentous complex. We consider three major ligaments when discussing anterior glenohumeral instability: the inferior, middle, and superior (Fig. 32-1).
These ligaments act as checkreins and countervail forces on the humeral head at the extremes of range of motion. When they become lax or disrupted, the humeral head translates beyond its normal boundaries of the glenoid.
The inferior glenohumeral ligament complex (IGHLC) is universally accepted as the primary static restraint to AGI. Investigators have conducted cadaveric dissections, histologic analysis, and biomechanical studies to delineate the individual components of the complex. The most popular model describes the complex with an anterior and posterior band with an interposed axillary pouch. It functions as a sling, or hammock, that changes position and undergoes reciprocal tightening and loosening with arm rotation. The anterior band is particularly important at limiting anterior translation when the arm is externally rotated and abducted to 90 degrees. Injury to this band of the complex is one of the most significant factors leading to AGI.
The IGHLC can rupture as the result of a traumatic anterior dislocation. Traumatic failure of the IGHLC most frequently occurs when it is avulsed with the anterior labrum, forming a Bankart lesion. Additionally, it may become stretched out over time by repetitive microtrauma. Overhead athletes are especially prone to this type of injury. With either type of injury, the anterior capsule can undergo plastic deformity as a result of trauma. The capsule becomes more and more voluminous, causing increased glenohumeral translation.
The middle glenohumeral ligament (MGHL) appears to function as the primary restraint to anterior translation when the arm is externally rotated and abducted from 60 to 90 degrees. The MGHL can be absent in ≤30% of individuals, and some feel that this predisposes to AGI. Additionally, the MGHL can be avulsed along with the IGHLC with a Bankart lesion.
The superior glenohumeral ligament (SGHL) has little to do with limiting pure anterior translation. But more recently it has been implicated for its role in the rotator interval laxity. Some believe that a widened rotator interval as a result of a deficient SGHL may be implicated in recurrent AGI. Table 32-2 summarizes each of these ligaments' roles in preventing AGI.
A less common and often overlooked cause of AGI is the humeral avulsion of the glenohumeral ligament (HAGL) lesion. Unlike the more commonly seen avulsion of the ligaments from the glenoid/labrum side, it is possible to detach the ligaments from the humeral side. This may be caused by either an anterior shoulder dislocation or hyperabduction.
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The HAGL lesion must be identified and anatomically repaired to restore stability to the shoulder.
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Figure 32-1 Glenohumeral capsuloligamentous complex. (From O'Brien SJ, Neves MC, Amoczky SP, et al. The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med. 1990;18:449–456 , with permission.) |
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Figure 32-2 Arthroscopic picture of a Bankart injury viewed from the posterior portal (humeral head on the left and glenoid on theright). |
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TABLE 32-1 Static and Dynamic Stabilizers |
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TABLE 32-2 Glenohumeral Ligaments |
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Glenoid Labrum
Few structures are as important when considering AGI as is the glenoid labrum. It serves as the anterior anchor point for the capsuloligamentous complex, as well as a chock block during anterior translation of the humeral head. Additionally, it deepens the glenoid and increases the surface area contact of the humeral head.
When this structure becomes detached from the glenoid rim and scapular neck, it is called a Bankart lesion (Fig. 32-2). Whether this is truly the “essential lesion,” as Bankart proposed, remains a topic of debate. Cadaveric studies have shown that simply detaching the labrum is not sufficient to cause AGI. In contrast, multiple authors have observed intraoperatively that detachment of the labrum is quite common after traumatic anterior instability episodes. One study has demonstrated detachment of the labrum in ≤97% of first time anterior dislocators without evidence of associated intracapsular injury. It has also been observed that recurrent anterior subluxers and dislocators have a fraying of the labrum. The severity of the deleterious effect on the labrum appears to be additive based on the number of instability episodes.
Another variety of labral injury, an anterior labral periosteal sleeve avulsion, or ALPSA, can result in AGI. This injury differs from the classic Bankart lesion in that the labrum is incompletely dissociated from the glenoid. A periosteal sleeve remains attached to the labrum that allows it to displace medially and rotate inferiorly. The lesions heal but will lead to recurrent AGI owing to excessive anterior capsular laxity. The sleeve must be detached, creating a full Bankart lesion, and then anatomically reattached to restore the labrum and capsule to proper function.
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Figure 32-3 Anteroposterior radiograph demonstrating a bony Bankart injury (black arrow) and Hill-Sachs lesion (white arrow). |
Humeral and Glenoid Bone Loss
When the humeral head dislocates anteriorly, its posterolateral margin comes into contact with the anterior glenoid rim. In the process of dislocating, the portion of the humeral head in contact with the glenoid can sustain an impression fracture. This fracture and bone loss is termed a Hill-Sachs lesion (Fig. 32-3). It can occur in ≤80% of anterior dislocations and may be present in an even higher percent of recurrent dislocators. Small lesions usually do not affect stability of the joint, but those >30% of the articular surface deserve attention. These larger lesions can predispose one to recurrent AGI, and they require reconstruction to restore stability to the glenohumeral joint. Despite capsular and labral repairs, large Hill-Sachs lesion can render the joint unstable.
Bone loss can take place on the glenoid side of the joint, and most frequently occurs as a bony Bankart (Fig. 32-3). This arises when a portion of the anteroinferior rim of the glenoid is fractured off with the capsulolabral attachments as the humeral head dislocates anteriorly (Fig. 32-4). When the fractured piece contains >20% to 25% of the glenoid surface area, it should be repaired back to the remaining glenoid.
Glenoid bone loss may also occur as a result of chronic wear. Recurrent anterior subluxation of the humeral head can cause gradual deterioration of the glenoid rim. When this defect becomes large enough, instability may result even after capsulolabral repair. As with traumatic bone loss, large defects require bone grafting. Many procedures have been described to augment glenoid bone stock including the transfer of the coracoid process (Bristow procedure or Latarjet procedure) and the use of autograft bone block.
Humeral and Glenoid Version
Although humeral and glenoid version appears to have some influence on posterior glenohumeral instability, it most likely has little or no effect on anterior instability. Clinical studies and sophisticated CT analyses have failed to show any significant relationship between version and AGI. However, one must be sure that apparent changes in glenoid version are not the result of glenoid bone loss.
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Figure 32-4 Coronal plane MRI demonstrating fracture of the anteroinferior glenoid (black arrow) and maintenance of the labral attachment to the glenoid rim (gray arrow). |
Rotator Cuff
The rotator cuff is generally viewed as a dynamic rather than static stabilizer, but passive tension within the cuff appears to play some role in preventing AGI. Specifically, the subscapularis has been shown to limit anterior translation of the humeral head at low ranges of shoulder abduction. When the subscapularis becomes injured or ruptured, as such is the case particularly in older individuals who suffer traumatic anterior dislocations, its static block to anterior translation is lost.
Negative Intra-Articular Pressure
Negative intra-articular pressure develops within the shoulder joint because of the relatively higher osmotic pressure in the surrounding interstitial tissue that causes water to be drawn out of the joint. This effect appears to be important when dynamic stabilizers are not functioning properly. A defect in the capsule or labrum, or degenerative changes in the glenohumeral joint, eliminate the effect. The importance of this negative pressure is probably negligible, though, when dynamic stabilizers are functioning properly.
Dynamic Stabilizers
Traditionally, the dynamic stabilizers of the shoulder have received less attention than static stabilizers. Most early stabilization procedures were nonanatomic reconstructions,
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which resulted in altered biomechanics of the joint. This subsequently led to secondary problems, such as decreased range of motion and glenohumeral arthritis. But with advancements in laboratory and surgical techniques, we have been able to understand better the dynamic factors that affect shoulder stability.
Rotator Cuff and Surrounding Musculature
We are increasingly recognizing the importance of the rotator cuff as a dynamic stabilizer of the shoulder. The coordinated contracture of the rotator cuff causes a force coupling of the muscles and a joint reaction force vector toward the center of the glenoid. The net result is a joint compression force that keeps the humeral head located within the glenoid fossa. Dysfunction of the rotator cuff muscles owing to poor neuromuscular control, injury, atrophy, contracture, or tendon deficiency can result in uncoupling of the muscles and a net force vector directed away from the center of the glenoid. Consequently, excessive translation of the humerus occurs and undue strain is placed on the capsuloligamentous structures and the labrum. The net result of rotator cuff dysfunction is instability.
Scapulothoracic Motion
Motion in the scapulothoracic plane is also a very important factor in glenohumeral joint stability. Dysfunction of the coordinated timing and positioning of the glenoid and humeral head can be caused by dyskinesis of the scapular rotators. Most often, this is caused by fatigue of the serratus anterior and trapezius muscles. Less commonly, dysfunction may be caused by long thoracic nerve palsy.
Long Head of the Biceps
It appears that the long head of the biceps brachii serves an important function in dynamic shoulder stabilization, especially when the rotator cuff or capsuloligamentous structures are overwhelmed. It serves its greatest role in preventing anterior displacement when the arm is in internal rotation at the middle and lower levels of elevation. When there is a Bankart lesion, the function of the biceps in preventing humeral head displacement may be even more important than the rotator cuff muscles. Indeed, in patients with rotator cuff weakness, the biceps tendon may become hypertrophied.
Proprioception
Multiple investigators have found mechanoreceptors in the shoulder capsule and ligaments. These receptors are thought to provide feedback information about the joint position and motion. This enables a coordinated interaction of the dynamic shoulder stabilizers. Individuals with a history of AGI appear to have a higher threshold for detecting passive motion of their shoulder. Whether or not these feedback loops function at speeds fast enough to prevent instability episodes remains a topic of debate.
Suggested Readings
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Bankart ASB. The pathology and treatment of recurrent dislocation of the shoulder joint. Br J Surg. 1938;26:23–29.
Bigliani LU, Kelkar R, Flatow EL, et al. Glenohumeral stability. Biomechanical properties of passive and active stabilizers. Clin Orthop Relat Res. 1996;330:13–30.
Iannoti JP, Williams GR, eds. Disorders of the Shoulder: Diagnosis and Management. Philadelphia: Lippincott Williams & Wilkins; 1999.
Lippitt S, Matsen F. Mechanisms of glenohumeral joint instability. Clin Orthop. 1993;291:20–28.
O'Brien SJ, Neves MC, Arnoczky SP, et al. The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med. 1990;18:449–456.
O'Brien SJ, Schwartz RS, Warren RF, et al. Capsular restraints to anterior-posterior motion of the abducted shoulder: a biomechanical study. J Shoulder Elbow Surg. 1995;4:298–308.
Taylor DC, Arciero RA. Pathologic changes associated with shoulder dislocations. Arthroscopic and physical examination findings in first-time traumatic anterior dislocations. Am J Sports Med. 1997;25:306–311.
Turkel SJ, Ithaca MW, Panio MW, et al. Stabilizing mechanism preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg Am. 1981;63-A:1208–1217.