A rotator cuff muscle without stimulation and with a torn tendon will undergo atrophy and retraction. Ruptures lead to severe changes in the muscle [8–10]. These changes are more accentuated in slow contracting type 1 muscle fibers when compared to fast contracting type 2A and 2B fibers [6, 11]. Fibrous tissue is stored intramuscularly [11], and a short time after the occurrence of the tear, the muscle starts to retract and loses its ability to build up tension [12]. In a supraspinatus tenotomy model in sheep, the muscle retracted 29 mm on average 16 weeks after tenotomy. This retraction corresponds with the physiological range of movement of the muscle. The pennation angle increased from 30° to 55°, and the cross-sectional area decreased by 57 % compared to the healthy opposite side [12]. This retraction leads to shortening of the muscle fibers by the breakdown of serially arranged sarcomeres up to 50 %. Due to this loss of sarcomeres, the muscle gets shorter instead of thinner.

Over the years, the cross-sectional area can decrease. With increasing retraction, the pennation angle of the muscle increases. As discussed above, this leads to the incorporation of fatty infiltration in between the muscle fibers. In this model, retraction and atrophy are therefore caused by shortening of “healthy” muscle tissue and not muscle degeneration in the proper sense [6]. Steinbacher et al. [13] confirmed this in a study where they reported that the cause for atrophy in rotator cuff tears greater than or equal to 3 cm (Bateman grade III and IV) is found in the decrease of the absolute myofibril volume and not in the death of fibers [13].

Deposition of fat into the muscle is termed fatty infiltration (Fig. 21.1). Fatty infiltration is a common finding not only in cuff tears but also in neurologic lesions of the rotator cuff. This infiltration can occur within different sites of the muscle, for example, in the interstitial space [13] where its accumulation leads to a limitation of its mechanics [6, 17]. Its accumulation not only occurs in between the muscle fibers but also in type I muscle fibers in the sarcoplasm [13]. On the other hand, fatty infiltration is also found in the extramuscular space (epimysium of the muscle belly) as well as in the torn tendon [10].

Over the years, different theories were established to explain the origin of the fatty infiltration.

Tendons of the rotator cuff are essentially made of two components: an extracellular matrix (ECM) and a cellular component. The extracellular matrix, which is the most important part of tendons in terms of mechanical properties, is made up of collagen (65–80 %), elastin (1–2 %), and a mixture of water, proteoglycans, glycosaminoglycans (GAGs), and glycoproteins. In rotator cuff tendons, there are more proteoglycans than in other purely tensional tendons. The most common proteoglycans are called decorin and biglycan (containing one or two GAG chains).

The cellular component of the tendon is divided into tenoblasts and tenocytes, representing 95 % of the whole amount of cells. Tenoblasts are precursors of tenocytes [26], while tenocytes are mature cells producing collagen and other components of the ECM.

The collagen fibers of the tendon are directly responsible for its mechanical properties. Lake et al. [27, 28] have extensively investigated the ultrastructure and mechanical properties of the rotator cuff tendons, especially of the supraspinatus tendon in recent works. The shoulder joint has a great range of motion and subsequently experiences multiaxial stresses. This is reflected in the collagen pattern having different distributions in tendon tissue. The stress-strain curve of the supraspinatus tendon, the most complex and commonly involved in damage, shows particular mechanical properties. These properties are different in the anterior, posterior, and bursal joint sides and can be attributed to the varying distribution of collagen. While axial loading shows higher stiffness in medial and anterolateral parts, resistance to transverse loading results in higher stiffness in posterolateral and anterolateral sides. This may be explained by the multidirectional complex loadings near the osteotendinous insertion.

The enthesis is the intermediary between the tendon and bone, and it has a remarkable difference in mechanical properties. The enthesis exists as a means of reducing the concentration of stress between the soft tendinous tissue and the hard bony tissue. As such, this site is most prone to rupture because of the great stresses it has to experience. The healthy enthesis employs different strategies to increase the strength of this crucial zone such as functional grading and change in microstructure through a transitional tissue, a reduced angle of fiber direction at the attachment, and interdigitation of tissue with bone [29].

According to literature, the enthesis is commonly described as consisting of four distinct zones (Fig. 21.3). More recent literature suggests that in reality these four zones are not distinctly segregated; rather, it exists as a fibrocartilaginous zone and has a graded transition from tendon to bone [30]. These four zones have been described as follows:

In fibrocartilaginous tissue, the main cell population is constituted by chondrocytes that are arranged in rows, which follow the tensile strains of the tendon [31, 32]. The mineral content gradient seems to be one of the main characteristics of the enthesis. It has been shown that mineral clusters and collagens fibrils seem to interdigitate until they reach the fully mineralized region.