Tendon anatomy

Tendons provide tensile force transmission as well as storage and release of elastic energy with locomotion (Witvrouw, 2007). Tendons are composed of dense parallel collagen fibers, which are oriented in the direction of force and can withstand the greatest tensile forces developed within the body (Gelberman, 1983). Tendons do not have elastic fibers which limit their extensibility, so the muscle bellies provide the tissue elasticity and allow for the absorption and release of elastic energy (Witvrouw, 2007). The fibroelastic sleeve known as a paratenon permits free movement of tendons within tissue structures. Few tendons possess a paratenon, which surrounds but is separate from the tendon.  It is most commonly associated with the Achilles tendon, but the term is used inconsistently leading to confusion (Benjamin, 2008). The epitenon lies beneath the paratenon and is continuous with the endotenon. The endotenon is made of thin, loose connective tissue that facilitates the movement of adjacent fascicles and creates a conduit for blood vessels (Benjamin, 2008).


Tenocytes are specialized fibroblast cells which secrete the components of the extracellular matrix and are arranged in longitudinal rows with finger-like projections that allow for intracellular communication. With aging tenocytes decrease in number (Benjamin, 2008). Glucocorticoids can suppress collagen synthesis and tenocyte proliferation, but nitric oxide enhances collagen synthesis (Benjamin, 2008). Oral contraceptives have also been found to inhibit collagen synthesis due to a lower bioavailability of IGF-1 (Hansen, 2009).

Tendon blood flow

The collagen fibers are closely packed leaving little room for cells and vascular components, so the cells and the vascular supply are found in the epitenon or surface of the tendon and the endotenon or razor thin tissue between the collagen bundles (Gelberman, 1983). The blood supply to tendons originates from the perimysium at the musculotendinous junction, the vessels of the paratenon and the periosteal vessels at the tendon-bone junction. For example, contractions of the calf muscle quadruples the blood flow of the Achilles tendon (Langberg, 1998). The tendon vascular supply also forms a vasculature network that acts to regulate the metabolism of resting muscle and acts as a secondary conduit of blood flow during exercise (Clark, 2000). The peritendinous tissue of the Achilles tendon demonstrates increased blood flow during exercise, increased tissue metabolic activity, and an increased synthesis of type I collagen (Kjaer, 2000).

Tendon biomechanics

Tendons attach just beyond the joint they act on to increase the speed of action (Benjamin, 2008). Some tendons can return more than 90% of their stored energy due to the presence of a unique tendon characteristic called crimp (Benjamin, 2008). Tendon fibers fuse together with the fibers of the joint capsule. The deeper tendon fibers tense or retract the joint capsule for stability while the superficial tendon fibers move the joint (Benjamin, 2008). Most tendons also attach to the dense fibrous connective tissue surrounding the joint to dissipate stress at the enthesis to reduce the risk of tendon rupture as well as to transmit additional force through the adjacent fascia (Benjamin, 2008). The enthesis (osteotendinous and osteoligamentous structures) also dissipate forces into adjacent structures such as ligaments and fascia (Benjamin, 2006). Tendon entheses demonstrate similar stratification or zonular zones as found within ligament anchor sites with progressively increasing calcification.

Tendon anchoring systems

There are several types of muscle anchoring systems that efficiently distribute the force of muscle contraction. Fascia is also thought to form an outside-in anchorage system called an ectoskeleton within the limbs allowing for force transduction beyond the enthesis. This is best exemplified by the tensor fascia lata muscle in the hip region that attaches to the iliotibial tract (Wood Jones, 1944). The musculotendinous junction is the transition from the flexible intracellular contractile proteins to stiffer extracellular connective tissue causing it to be susceptible to injury. The teno-osseous junction or enthesis is the region where the tendon inserts into bone; it also transitions from a flexible viscoelastic tendon, and progressively stiffens through fibrocartilage, followed by mineralized fibrocartilage and finally to solid bone. The aponeurosis or flattened tendons are flat bundles of collagen fibers found at different angles and in different layers. They attach muscle directly to bone or increase the distribution of the tendinous attachment to bone. They may form fibrous sheets on the surface or within muscle such as in the soleus or gluteus minimus muscles. The aponeurosis acts to distribute muscle and tendon forces such as in the palmer or plantar aponeuroses (Benjamin, 2008). The perimysium forms the mechanical link between the muscle and tendon fibers. Extensor tendons tend to be flatter to reduce the risk of subluxation than the more circular flexor tendons (Benjamin, 2008).

Tendon calcification

Bony nodules can exist within some tendinous structures such as the sesamoid bones within the foot (Dennis, 1990) and fibrocartilaginous tendon attachment sites (Benjamin, 2002). Tendinous calcification can also occur at any site via the action of extracellular organelles called matrix vesicles. These are small bodies within the pre-mineralized matrix of cartilage and bone which are often associated with calcium phosphate crystals.  Proteoglycans typically inhibit calcification, but this changes with aging and diabetes (Gohr, 2007), causing a downregulation of a specific transcription factor called Msx2 (Yoshizawa, 2004). The Msx2 transcription factor causes the matrix vesicles to bud from the plasma membranes of mineral forming cells such as osteoblasts and chondrocytes. The acidic phospholipids of the cell matrix vesicle membrane then act as nucleation sites for hydroxyapatite crystal formation (Golub, 2009). The collagen fibrils form the scaffolding, and the matrix vesicle hydroxyapatite crystal complexes enter the collagen fibrils through the hole zones in the collagen structure, eventually filling all the available space. When all the available space has been filled, the collagen fibers become flexed away from the line of force resulting in weakening of the collagen fiber (Golub, 2009). The bone spurs at the entheses and joint margin are considered signs of fibrocartilage degenerative changes. They are more common in males, and also more widespread with increased physical activity and age (Benjamin, 2006).

Tendon injury

Following injury, neovascularization occurs which describes the growth of nerves and blood vessels into damaged or ruptured tendons and local area. The location of these growing nerves also corresponds to the region of pain. Neovascularization has been found to be modulated by physical activity, and subtle changes in sensory neuropeptides can allow recovery to progress faster (Benjamin, 2008). Free nerve fibers containing substance P and calcitonin gene-related peptide (CGRP) are found in the paratenon and between the tendon fascicles (Benjamin, 2008) as well as close to the vascular structures suggesting a potential for further neurogenic inflammation in addition to inflammation due to the injury itself (Alfredson, 2005).

Effects of physical training

The renewal of adult tendon tissue has been found in some studies to be extremely limited (Heinemeier, 2013). However, other studies have suggested that tendons possess circulatory responses and collagen turnover with physical activity and are more metabolically active than previously thought (Langberg, 2001). Physical activity is known to influence the turnover of the extracellular matrix. A small number of fibroblasts are found within the tendon and sheath and form a network with the extracellular matrix. Increased collagen synthesis within a tendon increases within one hour and can last at least three days. There may be a period during physical training where there is collagen turnover that restructures the tendon to allow for increased loading but no collagen enlargement. With longer periods of training new collagen is created, but with short-term training, the tendon size can decrease (Kjaer, 2006). Signaling pathways within the extracellular matrix convert mechanical stimulus to gene expression and collagen synthesis (Kjaer, 2005). Type I collagen formation peaks 48-72 hours after exercise (Langberg, 2000). Exercised tendons undergo constant turnover. Overuse injuries occur due to disruption of connective tissue homeostasis. Eccentric strengthening has been found to stimulate type I collagen synthesis in injured tendons but not in healthy tendons where the additional load does not require increased collagen synthesis (Langberg, 2007). Collagen fibrils tend to be small, and uniform in size in childhood then grow and become variable in adolescence. Collagen fibrils reach peak diameter between 20 and 29 years of age. With continued aging, lack of training or injury, the diameter of the fibrils decreases resulting in an increase of local fatty tissue and autonomic nerves which increase the risk of tendinosis and pain (Benjamin, 2006, Benjamin, 2008). In adults, tendon flexibility increases with training (Benjamin, 2008), hence the need for continual exercise with aging.



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Andre Panagos, MD

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