**3. Etiology of rotator cuff tears**

model of rotator cuff tears using 20 cadaver shoulders, where the rotator cable acts as a stress shield for the crescent, and the two structures form a "suspension bridge." According to this model, tears in the crescent have minimal effects on shoulder function, while those that involve the cable impair its ability to distribute the load and tension between the anterior and posterior rotator cuff and therefore its role as a dynamic stabilizer of the humeral head [9]. This concept has clinical implications as it helps guide decision making in identifying tears that can be man-

While the rotator cuff is the main dynamic stabilizer of the glenohumeral joint, the glenohumeral joint capsule acts as a static stabilizer. It is a thin membranous structure located deep to the rotator cuff; it originates medially from the glenoid neck and inserts laterally to the

The capsule is thicker anteriorly than posteriorly. The anterior capsule contains focal thickened bundles, which are called superior, middle, and anterior-inferior glenohumeral ligaments (GHL). The posterior capsule has an inferior thickening called the posterior-inferior GHL, but does not have separate ligaments further superiorly. Directly inferiorly, between the anterior-inferior and posterior-inferior glenohumeral ligaments, the capsule forms the axillary pouch, which tightens in abduction, and relaxes in adduction [3–5, 10]. Contracture and loss of normal axillary pouch volume is frequently seen in adhesive capsulitis, whereas a patulous capsule with an enlarged pouch is often seen in multi-directional shoulder instability. The superior capsule is thin and was previously less well-studied. It originates from the glenoid neck along with its anterior-posterior counterparts, courses directly underneath the SS and anterior part of the IS, and attaches to 30–61% of surface area of the greater tuberosity (GT) [5, 10]. Nimura et al. measured superior capsule attachments in cadaveric shoulders. They reported thicker footprint at the anterior edge of SS and posterior edge of IS (5.6 ± 1.6 mm and 9.1 ± 1.7 mm, respectively), whereas the attachment was thinner at the middle area of the rotator cuff, near the posterior margin of SS (4.4 ± 1.2 mm). The authors concluded that the thinnest point of the capsule could contribute to the etiology of the initiation of degenerative rotator cuff tears [5]. The superior capsule is closely associated with the SS and IS, and typi-

The muscles of the rotator cuff help initiate movement of the shoulder joint, and also serve as the main dynamic stabilizer of this joint. Supraspinatus aids in abduction of the humerus, particularly in the scapular plane; external rotation is provided by infraspinatus (more active in adduction), and teres minor (more active in abduction); and internal rotation is the function of subscapularis. Furthermore, SS prevents abnormal inferior-superior translation of the humeral head, particularly during active arm elevation, by compressing the head into the glenoid fossa. The balancing forces between SSC anteriorly and IS and TM posteriorly provide stability in the sagittal plane, and the upward force of the deltoid is balanced by that of IS, TM,

aged non-operatively, versus those that require surgical fixation.

cally tears together with complete tears of these tendons [1–4].

*2.1.2. Shoulder capsule*

130 Advances in Shoulder Surgery

**2.2. Function**

and SSC in the coronal plane [11, 12].

anatomical neck of humerus.

While a significant number of rotator cuff tear cases present to the physician after a traumatic episode, most tears do not occur in a setting of a normal tendon. Preexisting degenerative changes are usually found in the torn tendons, and the injury that leads to clinical presentation is likely the "straw that breaks the camel's back." A number of both intrinsic and extrinsic pathways and risk factors are thought to contribute to chronic degeneration and weakening of the cuff tendons, as described below (**Table 1**).

The main intrinsic mechanism pathway is thought to be tenocyte apoptosis and inflammation resulting from chronic microtrauma to the rotator cuff tendons. Advancing age is the most common reason for this mechanism, and age has been found to be the strongest risk factor for rotator cuff disease. This is thought to be due to the combination of age-related degenerative changes and accumulation of microtrauma and macrotrauma over the course of an individual's lifetime [3, 4]. Older patients are also more likely to develop larger tears; Gumina et al.


**4. Outcomes of rotator cuff repair**

Rotator cuff repair was originally performed with open, and subsequently mini-open, techniques, which have produces good results, including restoration of shoulder strength and function. Advent and popularization of arthroscopy have allowed for a less invasive method of rotator cuff repair, contributing to decreased postoperative pain and more rapid return of motion. Other modern advancements, such as improved instrumentation, as well as stronger and more biocompatible suture and anchor materials, have led to new surgical techniques, such as a double-row rotator repair, which may contribute to better healing and possibly improved outcomes, especially for larger tears. Multiple clinical studies of arthroscopic repair have shown good to excellent results in as many as 90% of patients postoperatively, even including those with large and massive tears [20–23]. A recent systemic review and metaanalysis by McElvany et al. [24] included 108 clinical studies and showed postoperative clinical outcomes scores improved by an average of 103% of the preoperative scores. However, despite the overall good results, this same study found that 26.6% of the repairs failed to heal. Failure to heal may not (and often does not) affect short-term results, but may lead to deterioration of shoulder function after 2 years post-repair. Risk factors for failure of the rotator cuff tear to heal after surgery include preoperative fatty infiltration of the muscle, older age, and increased tear size. As many as 50% of larger (≥3 cm) tears may fail to heal after repair. One of the most important predictors for failure of rotator cuff repair, along with tear size, is muscle atrophy and fatty infiltration (**Figure 3**). Most common system used to classify fatty degeneration of rotator cuff muscles was described by Goutallier et al. [25]. Even small and medium tears are at risk for failure after repair with as little as grade 2 muscle degeneration [26]. Shoulders with more severe (grade 3 or 4) degeneration, where more than 50% of muscle volume is replaced by fat, are at a very high risk of poor outcomes, since, even if tendon repair and healing to bone is achieved, dynamic function of the rotator cuff muscle-tendon unit remains compromised.

Superior Capsule Reconstruction: Review of a Novel Operative Technique for Management...

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**Figure 3.** Fatty atrophy of the superior rotator cuff. (A) Sagittal MRI view of a right shoulder showing severe fatty degeneration (more than 50% of muscle volume replaced by fat) of the supraspinatus (SS), infraspinatus (IS), and subscapularis (SSC) muscles. (B) Arthroscopic view of the supraspinatus (SS), demonstrating severe muscle atrophy

(view from a posterolateral subacromial portal in the right shoulder).

**Table 1.** Risk factors for rotator cuff pathology.

reported a mean age of 59 years in a group of 586 patients undergoing arthroscopic tear repair, with those older than 60 being twice as likely to develop large and massive tears [13].

Tendon degeneration and poor healing potential are exacerbated by hypovascularity, which is worsened not only with advancing age, but also with smoking, and certain other conditions [4]. Smoking has a strong dose and time-dependent association with both the prevalence and size of tears; it negatively affects the vascularity of tendons, thereby predisposing them to tears and preventing healing [3, 4]. Similarly, hypercholesterolemia has been implicated in rotator cuff disease. The mechanism here is thought to be deposition of cholesterol by-products within the rotator cuff tendons, leading to worsening of biomechanical properties of the tendon and increasing the risk of tearing [14].

Genetic predisposition may also play a role. Patients diagnosed relatively early in life (before age 40) often have a family history of rotator cuff disease [3]. Particularly in irreparable tears, studies have shown expression of genes that favor fatty atrophy and fibrosis and inhibit myogenesis [15].

The most commonly accepted extrinsic mechanism for rotator cuff disease was originally described by Neer in his classic article from 1972, *Anterior Acromioplasty for the Chronic Impingement Syndrome in the Shoulder: a Preliminary Report*, and has guided clinical approach to management of impingement and rotator cuff tears ever since, although validity of some of these concepts has been challenged in the recent years. Neer suggested that repetitive contact between the rotator cuff tendons and the underside of the coracoacromial arch (which includes the anterolateral acromion, coracoacromial ligament, and the coracoid) results in trauma to the tendon, which produces the clinical entities of subacromial or subcoracoid impingement, and, in its more advanced stages, tendon tears [16]. Acromial morphology (hooked versus flat) and presence of subacromial enthesophytes have also been proposed to be contributing factors to symptomatic cuff disease, and surgical approach directed at increasing the space under coracoacromial arch by way of acromioplasty and coracoacromial ligament release has been advocated [17]. However, recent studies have questioned the benefit of these procedures [18], and attention has been directed to position and dynamic function of the scapula, as a contributor to rotator cuff impingement and tears [19]. Therefore, postural abnormalities and peri-scapular muscle strength have received greater recent attention as potentially contributing risk factor that can and should be addressed in management of rotator cuff disease.
