Tendons can be classified through multiple schema, according to anatomic considerations: specifically, shape (round or flat), anatomic location (intra-articular or extra-articular; intra-articular soft-tissue injuries have a lower likelihood of healing),² or the surrounding layer of connective tissue (paratenon or synovium, which acts to reduce friction and allows for tendon gliding).

The connection of the tendon between muscle and its point of origin or insertion at the bone requires several complex anatomic and morphologic characteristics that are continued through the microscopic and molecular level. Primarily, this
connection allows for the transfer of force from muscle to bone and enables highly specific motion by the musculoskeletal system. Not all muscles have a tendon; those that do primarily provide motion at a joint or need to provide force either over a distance or in a tightly confined space. Tendons provide a mechanical advantage for muscle by focusing or redirecting force, lengthening a lever arm, or acting around a pulley (such as in the flexor hallucis longus tendon).

The round or flat shape of the tendon is associated with specific functional consequences. Classic examples of round tendons include the flexor digitorum tendons of both the upper and lower extremities; flat tendons include the rotator cuff tendons and the Achilles tendon. Most round tendons behave similarly and are biomechanically subjected to a consistent environment. They are accustomed to high tensile loads and are capable of a high degree of motion, or gliding. The flat tendons are less easily categorized. They are generally subject to less glide but are capable of bearing high tensile loads (as in the quadriceps tendon) in addition to more complex loads such as compression and shear. Consequently, these different functions are represented in the structure of these tendons.

Further investigation of tendons reveals a complex composition with more functional implications. At the most basic level, tendon composition is organized consistently throughout the body, despite its often-differing superstructure. Like most connective tissue, the main functional components of tendon are water and collagen. Water is the primary constituent, comprising approximately 50% to 60% of tendon weight. Collagen makes up approximately 75% of the dry weight with 95% type I collagen and a small amount of type III and other collagens. Tendon is also composed of tendon cells, referred to as tenocytes, and proteoglycans. Proteoglycans are composed of a core protein covalently bound to one or more glycosaminoglycan (GAG) chains. GAGs are thought to play an important role in mechanics, specifically viscoelastic properties, through their association with water. The major subcategory of proteoglycans in tendon is the small leucine-rich proteoglycans (SLRPs). The most abundant SLRPs in tendon are decorin and biclycan, also known as class I SLRPs. Other SLRPs, though not as common, are also well described, such as fibromudulin and lumican (class II). Both classes have been found to play significant roles in tendon growth, regulation, and homeostasis. These molecules have been shown to bind to collagen and have significant impact on the hierarchical organization of tendon and its mechanical properties.³ Several investigators have suggested a role for these proteins in tendinopathy, although the specific mechanisms of this relation remain unclear.

At the molecular level, tendons are arranged in a hierarchy starting with the triple helix of collagen, then microfibrils, fibrils, fascicles, and ultimately the tendon itself (Figure 1). The mediated assembly and cross-linking of collagen into these microfibrils is critical for the mechanical strength of the tissue. This process is largely dependent on the family of extracellular SLRPs, which can dictate the overall thickness and quality of fibril assembly.⁴ Another important element of collagen assembly and structure is crimp. Crimp is evident ultrastructurally and appears as “crimped” lines in the tendon when viewed at the microscopic level. This crimping results from the specific orientation of the microfibrils in the tendon and contributes important mechanical properties that are discussed later in this chapter.

The superstructure of tendons is the progressive organization of fibrils into larger fascicles that group to yield a functional tendon, as well as supporting connective tissue that preserves local anatomic and physiologic relationships. These groups of fascicles are separated and bound together by a thin connective tissue layer known as the endotenon. Contiguous with the endotenon is the epitenon, which envelops the entire tendon. Some tendons are then wrapped with a paratenon
(eg, Achilles tendon), and some are covered with synovium (eg, flexor tendons), depending on the degree of gliding required. The endotenon and epitenon serve to permeate the tendon with vasculature, lymphatics, and nerves.

Another aspect of tendon’s morphology and functional relationships are its origin and insertion (its junctions). As the tissue that bridges muscle to bone, tendon has two junction regions: the myotendinous junction, where the muscle transitions to tendon, and the bone-tendon junction, where the tendon transitions to bone. Each is differentially organized and contributes to the varying properties along the length of the muscle-tendon-bone unit. The myotendinous junction is composed of the interdigitations of end sarcomeres and connective tissue elements. An end portion of the sarcomere, known as the z-line, which is arranged in a staggered organization with the next sarcomere, splits and gives rise to myofilament bundles that insert directly onto collagen fibrils. This arrangement minimizes stress to the myotendinous junction with forceful contractions.

At the bone-tendon junction, known as the enthesis, there are two typical arrangements with different biomechanical roles: direct or indirect insertions. Direct, or fibrocartilaginous, insertions have been classically characterized by a four-layer transition from tendon to bone: tendon, fibrocartilage, mineralized fibrocartilage, and bone (Figure 2). These insertions are typical in regions where the tendon-bone unit is subject to high tensile loads (such as the rotator cuff).^5,6 In an indirect insertion, which is less common than the direct insertion, the tendon fibers insert directly into the periosteum. The fibers that interdigitate with the periosteal tissue have commonly been referred to as Sharpey fibers. These transitions are more common in areas where tensile loading at the tendinous insertion does not predominate (such as the distal head of the rectus femoris).

At the cellular level there are also considerations that have implications for structure and function. Tendon is often classified as relatively hypocellular, yet recent evidence connects tenocytes with a highly defined role in maintenance of tendon structure.⁷ Tenocytes maintain the extracellular milieu that allows the normal function of tendon by secreting the extracellular matrix, synthesizing collagen and the proteoglycans. They possess long cellular processes that envelop and interdigitate with the collagen fibrils and other tenocyte processes and cell bodies. They are responsive to mechanical loading and can communicate with adjacent tenocytes through gap junctions at their interface as well as by production of inflammatory mediators under stress.⁷

Although tendon is considered largely hypovascular, blood flow has important consequences for tendon in health and disease. The blood supply and innervation of tendon, as mentioned previously, is primarily through the endotenon and epitenon. The tendon is fed primarily through vasculature that enters through the paratenon or at the bony insertions and continues to travel throughout the endotenon. The situation is more complex in sheathed tendons, in which blood supply must enter the tendon through mesotenon in vincula, defined as redundancies of the synovium that tether the tendon to its sheath in certain locations, analogous to the mesentery of the peritoneum (Figure 3). Sheathed tendon is also thought to receive some nutrition through diffusion via the synovial fluid. In addition to tendon’s hypovascularity, there are specific regions of relative avascularity between vascular zones, which are thought to be at particular risk for rupture. These hypovascular areas have been identified in the supraspinatus tendon, long head of the biceps tendon, Achilles tendon, and patellar tendon, all of which are prone to rupture.⁸

Innervation in tendon includes several types of nerve endings with different functions. Tendon is typically innervated by the same nerve as its muscle. The various special organs include Golgi organs, which provide steady-state information when undergoing large stimulations for prolonged periods; Pacinian corpuscles, which are considered sensitive, fast-adapting mechanoreceptors; and Ruffini endings, which are also very sensitive but can relay information for prolonged periods similar to Golgi organs. These end-organs are typically localized to the myotendinous region. Free nerve endings, responsible for nociception, on the other hand, tend to be clustered at the enthesis.

Tendon serves the primary purpose of allowing the transmission of force from muscle to bone, providing the capacity for locomotion, as well as allowing dynamic joint stability in concert with ligament, which provides more static restraint to joint translation. This is accomplished through an intricately designed and executed structure that enables these certain biomechanical properties. The relationship between structure and function is paramount.

Tendon injuries are an important aspect of musculoskeletal medical conditions. There are several types of tendon injury, ranging from overuse injuries (such as tendinosis) to rupture, with different clinical consequences. Tendon ruptures are classified into direct and indirect ruptures based on mechanism: direct injuries involve direct trauma to the tendon causing a tear, whereas indirect injuries result from forceful loading of the muscle-tendon-bone unit to the point of tendon failure.

Tendinopathy is an umbrella term for a group of syndromes on the same spectrum, considered to be overuse injuries, resulting in pain and varying degrees of loss of function of the tendon. Tendinosis has largely replaced the term tendinitis in the orthopaedic literature to describe the chronic overuse injury to tendon, as true inflammation is generally absent in these patients. These injuries are characterized by persistent pain and radiographic evidence of intrasubstance tendon degeneration.¹⁴ Upon histologic examination, the hallmarks of tendinosis include disrupted and disorganized collagen, increased extracellular matrix, increased tenocyte population, and neovascularization. Tendinosis, in addition to being a clinical problem itself, can lead to more severe injury, such as complete tendon rupture. Direct and indirect ruptures of tendons remain an important orthopaedic problem, with ongoing management challenges. Injury to the flexor tendons of the upper extremity is the most common and highly characterized of the direct tendon injuries. Penetrating trauma is usually responsible, with stab wounds making up a large portion of these injuries. These tendons typically have no preexisting condition that predisposes them to injury. The tendon is lacerated and retracts because of its muscular attachment. Additionally, the tendon sheath is violated, introducing the risk of infection into a hypovascular space and depriving the tendon of the normal synovial fluid, through which it obtains a portion of its nutrition.¹⁵