At the terminal myotendinous junction, tendinous collagen fibrils are inserted into deep recesses formed by myocyte processes, allowing the tension generated by centrally located myofibrils to be transmitted to the collagen fibrils of the terminal myotendinous junction (Fig. 13.2). Sarcomeres attach to endomysium (the tendinous system) at every Z membrane level along the whole length of the myofiber—forming parietal myotendinous junctions (PMTJ) (Fig. 13.2). Human muscles have 500 PMTJ every 1 mm. It is the main force transmission device of the myofiber and of the muscle. At the beginning/end of a myofiber, its myofibrils are separated from each other by endomysium and form terminal myotendinous junction (TMTJ; Fig. 13.2). This is a very important proprioceptive zone as Golgi apparatus as well as Vatter-Paccini and Ruffini corpuscules are largely located here [3]. This complex architecture reduces the tensile stress exerted on the tendons during muscle contraction. It is wrongly understood that the terminal myotendinous junction is the weakest link of a muscle as a whole. In fact, it is supported by both superficial endomysium (Fig. 13.3) and, additionally, by tendinous fibers arising from the TMTJ (Fig. 13.4). What is thought to be a “myotendinous junction” tear is a tendinous tear with frequent involvement of endomysium and perimysium including the level of the TMTJ and PMTJ too. We must remember that 1 mm of the tendon myofiber has already attached to endomysium at 500 levels; close but quite away in terms of myofiber built. At the muscle belly level, tendons may distribute their fibers on one side—these are called semipennate (Fig. 13.1), or on all sides—pennate (Fig. 13.5). This means that semipennate tendon is located on the surface of the muscle and pennate tendon is located within a muscle belly. Many muscles have tendons which run superficially (semipennate) and at some level become pennate—“dive” inside the muscle belly (Fig. 13.5). This may be wrongly interpreted as a tendon end when, in fact, the tendon disappears from the muscle surface [2].

Tendons respond to repetitive overload beyond the physiological threshold with either inflammation of their sheath or tearing with possible degeneration of scars of their body or both. Tendon or ligament tears are followed by a repair process which may differ in quality and duration. However, tendon damage may even occur from stresses within the physiological limits as frequent cumulative microtrauma may not allow enough time for repair. Frank inflammatory lesions and granulation tissues are infrequent and are mostly associated with tendon ruptures or other associated chronic inflammatory conditions. The presence of inflamed synovial or fatty tissue (paratenon, bursas, sheaths, and their fatty tissues) may disturb the scar healing process.

Tendon healing occurs in three overlapping phases. Initially, in the inflammatory phase, the erythrocytes and inflammatory cells (particularly neutrophils) enter the site in the first 24 h. This is followed by the proliferative phase which begins after 5 days. Synthesis of type III collagen peaks during this stage and lasts for few weeks. After about 6 weeks, the remodeling phase starts with decreased cellularity as well as reduced collagen synthesis.

Classically, in many cases, tendons with intratendinous lesions detected on US or magnetic resonance imaging (MRI) are not painful. However, pain may be present in patients with tendinopathy, which is usually attributed to inflammation. Pain may originate from a composite of both mechanical and biochemical factors. Anti-inflammatory treatment is usually helpful in such cases and, clinically, it is justified by pain and edema.