Static anatomic variants of the scapula, including anatomy of the acromion and glenoid, and their association with rotator cuff pathology have long been studied in cadaveric experimental models. Bigliani et al. developed a classification system of acromial shape that included “flat” (Type 1), “curved” (Type 2), and “hooked” (Type 3) (Fig. 5.2) [21]. A correlation was observed between Type 3 acromion and the presence of rotator cuff tears in cadaver shoulders. In support of this work, Flatow et al. performed another cadaveric study which assessed excursion of the rotator cuff under the acromion through biomechanical testing, stereophotogrammetry, and radiographs [22]. The authors found an increase in subacromial contact with Type 3 acromions. Other features of the acromion associated with rotator cuff disease include anterior tilt of the acromion [23], lateral extension of the acromion [24], lateral tilt of the acromion [25], and the presence of an os acromiale [26]. Related to the acromion morphology is the finding that a narrow supraspinatus outlet is associated with rotator cuff tears [27].

Cadaveric studies have also demonstrated that glenoid orientation also plays an important role in rotator cuff pathology. Glenoid inclination, a measure of the angle of the glenoid in plane of the scapula, was examined in cadaveric shoulders with and without rotator cuff tears. A greater glenoid inclination angle, or a more upward-facing glenoid, was observed in shoulders with cuff tears [28]. Another cadaveric study observed an increased risk for superior humeral head migration with greater glenoid inclination, indicating that a more upward-facing glenoid could contribute to cuff pathology and impingement [11, 28]. In contrast, Kandemir et al. found no difference in glenoid version or inclination in cadavers with intact versus torn rotator cuffs [9]. Finally, there is a relationship between the lateral extension of the acromion and the glenoid inclination angle that produces the “critical shoulder angle” such that larger angles are associated with rotator cuff tears, and smaller angles are associated with glenohumeral osteoarthritis [10].

Biomechanical evaluation of cadaver shoulders has provided insight into the role of the scapula in glenohumeral joint mechanics and pathology. Impingement (including internal and external or subacromial) has been carefully investigated in cadaveric experimental models. Karduna et al. altered scapular orientation (including posterior tilt, upward rotation, and external rotation) and evaluated clearance in the subacromial space [12]. Results demonstrated a decrease in subacromial clearance with increased upward rotation of the scapula. This is contrary to what was expected given clinical data that has observed a decrease in upward rotation with impingement and may suggest a compensatory modification in joint kinematics [30].

The role of scapular orientation in internal impingement, classified as contact between the undersurfaces of the posterior cuff with the humerus, superior labrum, and glenoid rim, has also been studied through biomechanical evaluation. Mihata et al. modified scapular orientation and evaluated glenohumeral joint positioning and contact pressures and found that decreased upward rotation and increased internal rotation increased the glenohumeral contact pressure and impingement area in cadaver shoulders [13]. This is contrary to the subacromial impingement studies from Karduna et al. and suggests the role of scapular orientation in both forms of impingement is still controversial.

Despite our improved understanding of the role of the scapula in rotator cuff disease and impingement through clinical observations and cadaveric evaluation, evidence is still mixed regarding the cause and effect relationship between scapular dyskinesis and rotator cuff pathology. Recently, a new scapular dyskinesis rat model was developed to better understand this relationship from a basic science perspective [17, 18]. The rat model allows for controlled and repeatable induction of scapular dyskinesis and the opportunity for qualitative and quantitative evaluation of subsequent joint function (including spatial, temporal, and kinetic parameters and passive joint mechanics) and supraspinatus tendon properties (including mechanics, structure, and organization) in response to the prescribed alteration in scapular motion.

The objective of the rat model study was to evaluate the effect of scapular dyskinesis on glenohumeral joint function and tendon properties. In the scapular dyskinesis group, surgical transection of the accessory and long thoracic nerve was performed, and entire medial border prominence of the scapula was observed during ambulation, indicative of abnormal positioning of the scapula and acromion in these animals. The scapular dyskinesis group also demonstrated altered joint function in the form of increased propulsion force, decreased vertical force, and increased internal rotation range of motion. Propulsion force is required for forward locomotion in the rat, and an increase in this parameter may indicate greater stress being placed on the glenohumeral joint. A decrease in vertical force suggested a functional deficit and possible pain. The increased internal rotation range of motion suggested a loosening in the posterior structures of the shoulder do to the unstable scapula. The scapular dyskinesis group also had altered tendon properties (including mechanical, histological, and structural) (Fig. 5.3). There are two possible mechanical mechanisms for these alterations: (1) altered acromial position and reduced subacromial clearance led to tendon mechanical abrasion and wear and (2) increased demand was placed on the rotator cuff in the scapular dyskinesis group in an attempt to restore dynamic stability to the joint. This study was the first to directly identify scapular dyskinesis as a causative mechanism of altered glenohumeral function and rotator cuff tendon properties.

A follow-up study by Reuther et al. examined the impact of scapular dyskinesis in an overuse population [17, 18]. As expected, the combination of overuse and scapular dyskinesis had a greater effect on tendon properties than scapular dyskinesis alone. This study suggested that the risk for shoulder injury in patients with scapular dyskinesis might be higher in individuals who frequently perform overhead activities.

While there is an abundance of biomechanical and animal model research evaluating the relationship between scapular dyskinesis and rotator cuff disease, clinical evidence is also robust. Warner et al., using Moire topography, demonstrated abnormal scapular positions at rest in patients diagnosed with impingement syndrome [31]. Symptomatic patients with rotator cuff disease have abnormal scapular kinematics, and muscle activity ratios comparted to asymptomatic patients with disease and those with normal anatomy [32–36]. Shoulder pain related to impingement in swimmers is associated with abnormal recruitment patterns of the serratus and lower trapezius [37], and the pain associated with rotator cuff tears is linearly related to scapular dyskinesis [38].

Scapular rehabilitation may be helpful in treating rotator cuff-related shoulder pain and fatigue [39]. Two recent systematic reviews of the literature concluded the scapula-focused approach was significantly better at improving patient disability early [40], and scapular strength [41], but the effect did not seem as impressive for pain or range of motion. The limited number of trials in the literature (seven) made definitive conclusions difficult.

In summary, clinical evidence and cadaveric and experimental model systems have demonstrated both static and dynamic variants of the scapula can contribute to rotator cuff pathology. Abnormal position and motion of the scapula can increase stresses on the rotator cuff and lead to impingement and damage. Careful considerations should be given to these findings when managing these conditions and patient expectations clinically.