Anatomy and Biomechanics of the Sporting Shoulder

Fig. 1.1

Bony geometry of the scapula and glenoid (courtesy of Lennard Funk, http://www.shoulderdoc.co.uk)

The glenoid is a shallow socket that holds humeral head; its mean depth is 2.5 mm on anteroposterior direction and 9 mm in superior inferior direction. It is retroverted on average 1.2° (range 9.5° of anteversion to 10.5° of retroversion) and inclined superiorly on average 5° (range 7° of inferior inclination to 15.8° of superior inclination) [3]. Friedman et al. [4] reported that its bending radius is larger than humeral head radius in 93% of examined joints; the remainder have glenoid and humeral head with the same bending radius.

Only a maximum of 30% of the humeral articular surface articulates with glenoid articular surface at any time [5]; bearing in mind the importance of soft tissue static and dynamic restrains in shoulder stability. The glenohumeral ratio shows a dimensional relationship between humeral head and glenoid: it’s the result of the division between the maximum diameter of the glenoid and the maximum diameter of the humeral head. It’s different according to different planes: 0.75 in the sagittal plane and 0.6 in the coronal plane [6].

All the bony characteristics influence stability, therefore changes in bony anatomy could result in shoulder instability. An excessive retroversion of the glenoid could be a rare cause of posterior instability, but more frequently it is only a contributory factor.

Most important bony lesions that result in instability occur after traumatic events and involve the anterior-inferior glenoid rim and the posterolateral aspect of the humeral head, called a bony Bankart lesion and a Hill–Sachs lesion, respectively (Fig. 1.2).

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Bony Bankart lesion (courtesy of Lennard Funk, http://www.shoulderdoc.co.uk)

Bony Bankart lesions become significant when they involve more than 20% of the length of the glenoid and are predisposed to recurrence despite correct soft tissues repair; if the bony Bankart lesion involves more than 50% of the length of the glenoid, shoulder stability is reduced by more than 30% [7]. Bony Bankart lesions are classified as described by Bigliani et al. [8]: type I, a displaced avulsion fracture with attached capsule; type II, a medially displaced fragment malunited to the glenoid rim; type III, an erosion of the glenoid rim lower than 25% (III A) and more than 25% (III B). If a bone fragment is present it will be reabsorbed within a year [9]. The PICO method, suggested by Baudi et al. [10], could be used to calculate bone deficiency produced by a bony Bankart lesion: it needs Computed Tomography Multiplanar Reconstruction of both shoulder and defects and is calculated as a ratio between the surface of the damaged glenoid and the surface of not damaged glenoid.

A Hill–Sachs lesion is an impact fracture occurring after one or more traumatic anterior shoulder dislocations and involves the posterior-lateral articular surface of the humeral head (Fig. 1.3). Smaller Hill–Sachs lesions don’t influence stability; the level of influence on shoulder instability depends on the size of lesion and its location. According to their size, Hill–Sachs lesions are classified as mild (2 × 0.3 cm), moderately severe (4 × 0.5 cm) and severe (>4 × 0.5 cm) [11]. In addition, Burkhart and De Beer [12] classified them according to their orientation as engaging or not engaging (the impact fractures that extend to the area of contact between articular surfaces of the glenohumeral joint during abduction, external rotation and extension have a higher risk of engagement). Naturally, risk of engagement is higher if the glenoid surface is reduced. An arthroscopic classification of Hill–Sachs lesions by Calandra et al. [13] can be used to identify 3 types of defects: Grade I, that doesn’t involve subchondral bone; Grade II, that involves subchondral bone; Grade III, that involves subchondral bone widely. Similar but specular lesions occur in posterior traumatic instability: the posterior glenoid rim could be fractured after acute traumatic dislocation or eroded after repeated subluxations (reverse bony Bankart lesion) [14] and the humeral head could be fractured in its anterior articular surface (reverse Hill–Sachs lesion or McLaughlin lesion) [15]. Reverse Hill–Sachs lesions could be engaging during adduction, flexion and internal rotation if they extend into the zone of contact between articular surfaces during that motion [16].

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Hill-Sachs lesion of the posterior humeral head (courtesy of Lennard Funk, http://www.shoulderdoc.co.uk)

Considering bony stabilisers, it’s important to underline the glenoid track concept, defined as a contact area between glenoid and humeral head, created by shifting of the glenoid from the inferomedial to the posterolateral portion of the posterior articular surface of the humeral head when the arm moves in maximum external rotation, extension and abduction. This area’s width is 84% of the glenoid width, therefore, any glenoid articular surface loss (as in bony Bankart lesions) greatly influences the width of the glenoid track. The glenoid track influences the risk of engagement of a Hill–Sachs lesion: if the bony loss in the humeral head remains within the glenoid track there is no possibility that the Hill–Sachs lesion overrides the glenoid rim. On the contrary, if a Hill–Sachs lesion extends over the medial margin of the glenoid track, risk of engagement rises according to the lesion’s position [17, 18].

1.2.2 Soft Tissue Static Stabilisers

Soft tissue static stabilisers include glenoid labrum, glenohumeral capsule, glenohumeral ligaments, rotator interval, negative intracapsular pressure and the adhesion-cohesion mechanism.

The glenoid labrum is a triangular section ring around the glenoid rim to which it’s connected by fibrocartilage and fibrous bone. The superior half of glenoid labrum is more movable than the inferior half that is tenaciously connected to the glenoid rim. Its superior border blends with the origin of the long head of the biceps. Its jobs are to make the glenoid socket deeper, to increase contacting area and congruity, to generate a suction effect, to function as an insertion area for capsular-ligamentous structures and to help muscles to compress the humeral head within the glenoid. The glenoid labrum acts on the humeral head like a plunger: loss of the glenoid labrum reduces depth of the glenoid socket more than 50%, reducing stability [19].

There are different kinds of labrum lesions and it’s very important not to confuse tears with anatomical variants that don’t require surgical repair, like sublabral foramen associated with cord-like middle glenohumeral ligament or meniscoid labrum [20] (Fig. 1.4).

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Labral tears occur in the antero-inferior labrum, posterior labrum and superior labrum (SLAP) (courtesy of Lennard Funk, http://www.shoulderdoc.co.uk)

The most common injury to the labrum, found in more than 90% of traumatic anterior instability [21], is a Bankart lesion. It is defined as a detachment of the anteroinferior aspect of the labrum and its attached portion of the inferior glenohumeral ligament. Despite its frequency, it cannot be considered a cause of instability in isolation, seeing that a concomitant plastic deformation needs to produce certain instability [22]. Green and Christensen [23] classified Bankart lesions in 5 arthroscopic types: type 1 refers to an entire labrum; type 2 is a simple detachment of labrum with no other significant lesions; type 3 is an intraparenchymal tear of labrum; type 4 and 5 are complex tears with a significant or complete degeneration of the inferior glenohumeral ligament, respectively. This classification has a prognostic value: type 4 and 5 has a good chance (87%) of recurrent instability after arthroscopic Bankart procedure.

Another lesion that involves anteroinferior aspect of the labrum is the anterior labro-ligamentous periosteal sleeve avulsion (ALPSA) lesion: the anterior labro-ligamentous complex rolls up in a sleeve-like fashion and becomes displaced medially and inferiorly on the glenoid neck [24]. ALPSA lesions probably have a higher risk of redislocation than undisplaced Bankart tears, as the normal bumper and capsule that stabilise the front of the shoulder are displaced and the anterior glenoid is deficient of a capsule and labrum.

Specular lesions can be described for the posterior aspect of the labrum: a reverse Bankart lesion involves the posterior labrum and the posterior band of inferior glenohumeral ligament [25]; a POLPSA is a posterior labroligamentous sleeve avulsion, that if chronic could become a Bennett lesion (an extraarticular calcification along the posteroinferior glenoid neck close to the posterior band of the glenohumeral ligament) [26]. Reverse Bankart lesions are quite frequent in athletes, in particular contact athletes such as rugby players, being reported with a 20% incidence in a study of 142 elite rugby player shoulder arthroscopies [27]. The mechanism of injury could trace back to a direct blow to the anterior and lateral aspect of the shoulder, while the arm is adducted; a rare mechanism of injury is a posterior blow to the arm, while holding a tackle shield [28].

As far as the superior labrum is concerned, a very common lesion in throwing overhead athletes is the SLAP (superior labrum anterior and posterior) tear. Described for the first time by Snyder et al. [29], SLAP lesions occur during the ending deceleration phase of throwing, because of a traction force wielded by the long head of biceps on the glenoid labrum. Snyder has classified SLAP tear in 4 different types: type II and IV are the most significant in determining instability because they involve both labrum and long head of the biceps, so resulting in an increased total range of motion, particularly in antero posterior and superior inferior translation. Moreover, SLAP lesions are common in contact athletes: Funk and Snow [30] reported a 35% incidence of SLAP tears, arthroscopically diagnosed, in 51 rugby players’ shoulders.

Capsuloligamentous structures include the joint capsule, whose mean thickness is 5 mm, and glenohumeral ligaments (superior, middle and inferior), described as located at the thickening of the capsule (Fig. 1.5). These structures have received great attention and many cadaveric and clinic studies have tried to clarify their anatomical and biomechanical characteristics and their relationship with dynamic stabilisers.

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The anterior glenohumeral joint ligaments: Superior (SGHL), Middle (MGHL) and anterior band of the Inferior (IGHL) (courtesy of Lennard Funk, http://www.shoulderdoc.co.uk)

The constitutional trait of laxity facilitates extensive motion in multiple planes and may be essential to athletic performance. On the other hand, capsular stretching is noted along with a Bankart lesion and it’s present in up to 28% of patients with recurrent anterior instability [31].

Glenohumeral ligaments act at maximum degrees of range of motion, when they appear in tension; at middle degrees of motion, when they are slack, stability depends on rotator cuff and long head biceps activities, those compress the humeral head inside the glenoid concavity.

Superior and middle glenohumeral ligaments, together with the coracohumeral ligament, long head of the biceps and a thin layer of capsule, help to form rotator interval and they will be discussed in detail later.

The inferior glenohumeral ligament, better-called the inferior glenohumeral ligament complex (IGHLC), is formed by 3 parts: two thicker bands on the anterior and posterior and an axillary thinner recess, assuming a sling-like structure. During abduction, external rotation and extension the IGHLC moves anteriorly, forming a restraint to anterior translation of the humeral head (Fig. 1.6).

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The effect of internal and external rotation on the IGHLC (courtesy of Lennard Funk, http://www.shoulderdoc.co.uk)

On the other hand, during adduction, flexion and internal rotation, the IGHLC moves posteriorly, forming a restraint to posterior translation. The IGHLC suffers an initial plastic deformation during initial dislocation, but the damage becomes more critical after several episodes [32]. It could be damaged more frequently at the glenoid insertion (anteroinferior glenoid rim), but also in the middle part or at the humeral insertion [33]. The incidence of humeral avulsion of the glenohumeral ligament (HAGL) has been reported as high as 10%, but they are often unrecognised [34].

Usually capsular stretching is noted along with a Bankart lesion and it’s present in up to 28% of patients with recurrent anterior instability [31]. The posterior capsular also can be damaged, seeing that recurrent posterior subluxations or luxations produce capsular redundancy and increase joint volume, resulting in posterior instability. Capsular redundancy, both anterior and inferior and posterior, is a very common find in atraumatic multidirectional instability.

The rotator interval is a triangular space, with medial base and lateral apex, limits of which are the coracoid medially, the long head of biceps and its groove laterally, the superior fibres of subscapularis inferiorly and the anterior fibres of supraspinatus superiorly. The rotator interval is composed of the coracohumeral ligament (CHL) and superior and middle glenohumeral ligaments deeper, even if the middle glenohumeral ligament contribution is relatively variable (different studies has reported its absence, from 10 to 40% of cases). Usually, it is larger in males than in females and becomes smaller with internal rotation. It is an important inferior stabiliser and its insufficiency could be clinically appreciated with sulcus sign examination. A rotator interval defect could be a little foramen or could reach larger size, influencing significantly inferior stability [35].

Negative intracapsular pressure plays a role in shoulder stability. Intracapsular pressure is about −42 mmHg H₂O and it acts especially when rotator cuff muscles are not contracted and glenohumeral ligaments and capsular structure are not in tension. Loss of intracapsular negative pressure manifests itself as augmented anterior translation; this factor could be marginal when muscles are contracted and capsuloligamentous structures are in tension, especially in athletes [36].

Furthermore, synovial fluid generates the adhesion-cohesion mechanism: when two articular cartilage wet surfaces, such as the humeral head and glenoid, come into contact with each other this creates an adhesion-cohesion bond that provides stability to the glenohumeral articulation [37]. The suction effect of the glenoid labrum, the negative intracapsular pressure and the adhesion-cohesion mechanism are the three mechanisms providing the vacuum effect.

The acromioclavicular system (ACS) is formed by a complex of ligaments (conoid, trapezoid and acromioclavicular capsular ligaments) that stabilize the acromioclavicular joint (Fig. 1.7). The conoid and the trapezoid are attached from the distal clavicle to the coracoid. The ACS helps to prevent excessive superior translation of the shoulder. An acromion-clavicular dislocation up to Rockwood type 3 could require surgical repair as these cause pain and functional restrictions [38], with good results even in athletes [39].