yogabook / movement physiology / tendon

Tendon

A tendon (lat. tendinum) is a connective tissue, non-contractile part of a muscle that connects the contractile part (muscle belly) to a bone. In some cases, muscles also attach to other tendons, fascia or directly to bones. It is not uncommon for tendons of several muscles or muscle bellies to confluence into one. Near joints, tendons often run in a connective tissue sheath, the tendon sheath. They are often padded with bursae to protect them from bone pressure, particularly when they are located in areas subject to high mechanical stress, such as the hand and wrist, the foot, ankle and lower leg.

The typical dimensions of tendons are as follows:

1. Tendon: 500–2000 µm
2. Fasicle diameter: 50–400 µm
3. Fibre sizes: 10–50 µm
4. Fibrils: 50–500 nm
5. Tropocollagen: 1–5 nm

In the tendon, interfascicular tenocytes are situated between the individual fascicles, whilst within the fascicles themselves, normal tenocytes are situated between the fibres. The fibrils are crimped and contain many individual tropocollagen structures.

The basic structure of tendons is somewhat similar to that of a muscle, consisting of a structured arrangement of different fibres. Several collagen fibrils form a collagen fibre. Collagen fibre bundles are grouped around lateral extensions of a tendinocyte, the lateral extensions of which contain wing cells. These collagen fibre bundles are called primary bundles. Several primary fibre bundles form secondary fibre bundles, which are delimited by perimysium internum. Several secondary fibre bundles in turn form a tertiary fibre bundle, also surrounded by perimysium internum. All tertiary fibre bundles are enclosed by peritendineum externum (epitendineum). Vessels and nerves for the extrinsic neurovascular supply of the tendon enter through this.

Tendons consist of parallel, firmly connected fibers and are round or flat, depending on the shape of the muscle. Tendons are generally weakly vascularized and therefore belong to the bradytrophic tissues, which increases their regeneration time or turn over. They therefore belong to the bradytrophic tissues. They are supplied approximately one third each by their muscle, by the periosteum of the bony insertion site and by the lymph flow. The sensitive innervation is also rather low. The Golgi tendon organ, which measures tendon strength, is one of the most important proprioceptive receptors in the transition from the contractile to the tendinous area of the muscle. The elasticity of tendons is up to about 15%.

Cellularly, tendons consist of 90-59% tenocytes and tenoblasts, with the remainder consisting of vascular cells, chondrocytes, synovial cells and smooth muscle cells. The extracellular matrix consists mainly of collagen (95% type 1) and elastin. Tendons are categorised into gliding tendons, which change direction along their course, and traction tendons, which connect the insertion and origin in a largely straight line. Sliding tendons are most strongly compressed in the area of contact with their redirection, while the tension is greatest diametrically opposite. They are therefore exposed to shear forces. In the case of the Achilles tendon, which is biomechanically a tensile tendon, the fibres of the soleus twist from anterior and medial with those of the gastrocnemius from posterior and lateral. This effect is most pronounced in the area around 2-7 cm proximal to the insertion on the calcaneus (the Achilles waist) and leads to hypovascularisation there, resulting in reduced metabolism and increased susceptibility.

Close to the insertion of the tendon on the bone (enthesis), cartilage cells lie between the fibres of the tendon, which push the fibres apart. As the tension on the tendon increases, the cartilage cells are compressed, and their compressibility thus limits the elasticity of the tendon. Damage to tendons can occur from 4% (depending on the literature, the physiological elasticity is given as 3-5%) elongation, at more than 8-12% it is likely (tears). Healing takes place (except in the case of a total tear) in three overlapping phases, the first of which is the 3-7 day inflammatory phase. The prodelivery phase lasts from the 5th to the 21st day, followed by the maturation and restructuring phase lasting up to one year.
The tensile strength of a tendon without the use of unphysiological elastic elongation is approximately 6 kg/mm².

1. https://www.researchgate.net/publication/291421060_The_Achilles_Tendinopathy_Pathogenesis_Review
2. https://europepmc.org/article/pmc/6737558

Tendon elasticity

The elasticity of tendons is about 15%. According to recent research, an ion channel protein in the tendons acts as a force sensor that detects the longitudinal displacement of collagen fibres against each other. When larger shear forces are measured, the force sensor emits calcium ions into the interior of the tendon cells, which promotes the production of enzymes that bind the fibres together, increasing stiffness and resilience at the expense of elasticity. There are several genetic variants of this ion channel protein. The E756del variant, which originated in West Africa and is the result of a counter-reaction to malaria plasmodia, causes an excessive release of calcium, which results in firmer tendons. Carriers of this variant have an advantage in sports where the condition of the tendons is important (high-speed sports such as sprinting, fast jumping disciplines).

Tendon force

The force with which a muscle pulls on its attachment and origin. In the simplified model, a muscle attaches to a bone with a tendon at both the origin and the attachment. If you were to cut a tendon and insert an element to measure the traction force, you would obtain the tendon force of the muscle. The actual tendon force depends on the resting tone, the positions of the covered joints and, of course, the innervation to a high degree. Even without voluntary innervation, a muscle has a certain resting tone, so the tendon force is different from zero even in the most favorable joint positions. If the tendon were to be severed on one side, the head of the muscle would contract.

Tendon damage

According to all currently available findings, tendon damage is usually caused by repeated overuse (overuse). In particular, this means repeated strain on tendon elasticity beyond the physiological range of 3% to 5% at best. Among asymptomatic patients, there is a rate of 10% to 20% with demonstrable tendon damage, which leads to the assumption that the connection between the tendon disorder and the symptoms must be rather loose . Pathologically altered tenocytes are no longer long and slender between the collagen fibrils, but become rounder, as do their nuclei; the cytoplasm proliferates and the cells become more similar to hyaline cartilage cells. At the same time, metabolic activity increases, as does the production of matrix proteins. Dying and aboptotic tenocytes are rather rare. The collagen in diseased tendons also changes and loses its structure, individual bundles separate and the basic substance increases. Thinner and less resilient type 3 collagen is increasingly formed. Collagen fibrils also bend more frequently, which suggests an underlying lack of tensile strength. The composition of the proteoglycans also changes in the direction of large proteoglycans. The glucosamine glycan side chains increase massively and, due to their hydrophilic properties, lead to increased water retention, which is the reason for the detectable tendon oedema. The disruption in the tendon favours a vascularisation process of the tendon that is not detectable in areas with a preserved fibre structure. As most studies have been carried out on tendons that are already clearly degenerated, there is a lack of fundamental knowledge about the onset of the disorder, which is why there are currently three hypotheses: the collagen hypothesis, the inflammation hypothesis and the cell-based hypothesis. Although all three hypotheses contain interesting aspects, none seems to be valid on its own and further research is needed. The cell-based theory led to the description of three states, the first of which are physiological or reversible: reactive, dysrepair and degenerative.

1. As described above, short-term destruction leads to oedema due to the increased production of proteins. No collagen change takes place here. Once the overloading stimuli have ceased and the reaction to them has subsided, the tendon returns to its physiological state.
2. If overload persists, the increased production of proteins leads to impairment of the collagen structure. This phase is known as dysrepair. The disorders here are focal rather than diffuse and disseminated as in the reactive disorder. The proportion of collagen type 3, which is less resilient, increases, which reduces the tensile strength. This disorder is also still reversible, but healing takes longer.
3. Degenerative stage 3 shows extensive changes in the collagen, marked changes in the extracellular matrix and neovascularisation. The neovascularisation appears to mainly affect areas with a severely disrupted collagen structure, which suggests that the formation of new vessels does not serve tendon healing. Tenocytes die off here and it must be assumed that there is defective healing. In a study with a 16-week eccentric training programme, which was expected to have a positive influence on the tendon tissue, the degenerative tendon tissue appeared unchanged, as if it did not react at all to the training stimuli, in contrast to tissues in the other two stages. However, the clinical symptoms improved. The lack of a positive reaction to the training stimulus is explained by an inability to detect it due to lost tenocytes. In studies of the
4. Achilles tendon and patellar tendon, it was shown that the risk of this disorder becoming symptomatic is 3 to 15 times higher than with unchanged tendons. The local pain receptors appear to be relevant for the perception of pain. The loss of physiological tendon architecture can lead to certain areas of the tendon no longer receiving sufficient maintenance stimuli to stimulate them to remodel. These degenerated areas, known as mechanically silent areas, therefore do not respond with healing and leave the transmission of tensile force to neighbouring areas, which then grow with sufficient training stimuli and can fully compensate for the failure. The tendon thickens overall to such an extent that the average functional cross-section is the same size again.

Several studies show the positive influence of eccentric and isometric exercise programmes on tendon function and symptoms.

There are a number of known factors that affect the elasticity of tendons and their health:

The typical dimensions of average tendons are as follows:

1. Tendon: 500–2000 µm
2. Fibre diameter: 50–400 µm
3. Particle sizes: 10–50 µm
4. Fibrils: 50–500 nm
5. Tropocollagen: 1–5 nm

In the tendon, interfascicular tenocytes are situated between the individual fascicles, whilst within the fascicles themselves, normal tenocytes are situated between the fibres. The fibrils are crimped and contain many individual tropocollagen structures.

The basic structure of tendons is somewhat similar to that of a muscle; they consist of a structured arrangement of various fibres. Several collagen fibrils form a collagen fibre. Bundles of collagen fibres group around the lateral processes of a tendinocyte, whose lateral extensions contain wing cells. These collagen fibre bundles are referred to as primary bundles. Several primary fibre bundles form secondary fibre bundles, which are bounded by the perimysium internum. Several secondary fibre bundles, in turn, form a tertiary fibre bundle, which is also bounded by the perimysium internum. All tertiary fibre bundles are enclosed by the external peritendinous sheath (epitendinous sheath). Blood vessels and nerves pass through this sheath to provide the extrinsic neurovascular supply to the tendon.

To protect against pressure from bones, they are often cushioned by bursae. Tendons consist of parallel fibres that are firmly bound together and, depending on the shape of the muscle, are roundish or flat. In general, tendons are poorly vascularised and therefore belong to the bradytrophic tissues, which increases their regeneration time or turnover rate. They are thus classified as bradytrophic tissues. They are supplied, in roughly equal thirds, by the muscle to which they are attached, by the periosteum at the bony insertion site and by the lymphatic system. The nerve supply is also rather limited. The Golgi tendon organ, which measures tendon tension, is one of the most important receptors for proprioception and is situated at the transition from the contractile to the tendinous region of the muscle. The elasticity of tendons is up to about 15 per cent; however, only 3–5 per cent of this can be utilised without causing damage.

In terms of cell composition, tendons consist of 90–59 per cent tenocytes and tenoblasts, with the remainder comprising vascular cells, chondrocytes, synovial cells and smooth muscle cells. The extracellular matrix consists mainly of collagen (95% of which is type 1) and elastin. Tendons are classified as gliding tendons, which change direction along their course, and tensile tendons, which connect the insertion and origin in a largely straight line. Gliding tendons are most strongly compressed at the point of contact with their deflection, whilst the tensile force is greatest directly diametrically opposite. They are therefore subjected to shear forces. In the case of the Achilles tendon, which is biomechanically a tensile tendon, the fibres of the soleus from the anterior and medial sides twist with those of the gastrocnemius from the posterior and lateral sides. This effect is most pronounced in the region approximately 2–7 cm proximal to the insertion on the calcaneus (the Achilles tendon), where it leads to hypovascularisation, resulting in reduced metabolism and increased vulnerability.

Near the insertion of the tendon onto the bone (enthesis), cartilage cells are situated between the tendon fibres, pushing the fibres apart. As tension on the tendon increases, the cartilage cells are compressed; their compressibility thus accounts for the tendon’s limited elasticity. From 4% elongation (depending on the literature, physiological elasticity is given as 3–5%), damage (tears) to tendons can occur; at more than 8%, they are highly likely; and from 12%, they affect the entire cross-section of the tendon, i.e. all the bundles. Healing takes place (except in the case of a complete rupture) in three overlapping phases, the first of which is the 3–7-day inflammatory phase. The proliferation phase lasts from the 5th to the 21st day, followed by the maturation and restructuring phase, which can last up to one year. See also Tendon elasticity and Tendon healing.
The tensile strength of a tendon, without being subjected to unphysiological elastic stretching, is approximately 6 kg/mm².

In the 48 hours following a training session, there is an increase in metabolic activity within the tendon: matrix metalloproteinases (MMPs) trigger the breakdown of the matrix, whilst growth factors such as TGF or IGF activate its synthesis. Furthermore, various inflammatory mediators and enzymes are involved. One-off loads or those occurring at irregular intervals with long gaps in between do not result in the anabolic processes predominating; only prolonged, regular training leads to an increase in cross-sectional area – in other words, a form of tendon hypertrophy – with the insertion adapting better than the rest of the tendon. Thus, not all areas adapt to the same extent. The Achilles tendon generally adapts less than the ligamentum patellae, as an increased turnover of the Achilles tendon would imply a phase of increased vulnerability. In the event of immobilisation, the turnover is altered after just three days; however, there is initially no reduction in the tendon’s cross-sectional area, as the loss of functional fibre mass is compensated for by increased water retention; thus, at the outset, no quantitative change is detectable in the tendon, only a qualitative one. When tendon-strengthening loads are applied, the proportion of more resilient type 1 collagen in the tendon increases at the expense of type 3 collagen; furthermore, the stiffness of the tendon increases, leading to faster force transmission; the hysteresis rate also decreases, meaning less energy is lost, which makes movements more efficient. Traction tendons adapt primarily in response to sufficiently intense tension; however, they react to compression by releasing catabolic transmitters. Gliding tendons cover joints and are protected by embedded fibrocartilage, which is maintained by the compression that occurs. Tension on the tendon also generates contact pressure against the surrounding bone and provides a maintenance stimulus.

In general, the tendons of the postural muscles – which maintain the body’s position against gravity in everyday life – are in better condition than those of the phasic muscles. Tendon-strengthening exercises must be carried out regularly. Meaningful results can be expected after three to six months at the earliest, by which time improvements should be evident both morphologically and functionally. Tendinosis refers to degenerative tendinopathies. The terms tendinitis and paratendinitis, which are frequently found in the literature, are often used incorrectly, as there is little or no inflammatory process present. There are a number of risk factors for
tendinosis: Overuse, too rapid a progression in training or an excessive training volume, inadequate equipment (e.g. footwear), technical flaws, muscular imbalances, lack of flexibility, axial deviations and misalignments, age and being overweight. Tendinosis predominantly occurs in gliding tendons that are routed via a hypomochlion. In these areas, cartilage is embedded with ground substance and type 2 fibres. However, these areas are also hypovascularised, such as the tendon of the tibialis posterior below the medial malleolus or the supraspinatus on the head of the humerus. Whilst the cartilaginous adaptation in the area where the tendon changes direction is a sensible adaptation, hypovascularisation comes to the fore as a fundamental risk factor. In cases of tendinosis, there is increased expression of angiogenic substances such as VEGF and endostatin, which is generally reduced in the cartilaginous support areas. The chemical balance is therefore disrupted, leading to neovascularisation and, in addition, the ingrowth of free nerve endings. To enable this invasion, matrix material must be broken down, a process initiated by MMPs. One of the effects of MMPs is the conversion of tenocytes into a type of progenitor cell, which can, however, differentiate into cartilage cells as well as bone cells or fat cells, and then produce the corresponding matrix components. This process disrupts the alignment of the collagenous fibres, leading to altered cross-linking, a reduced cross-sectional area and a lower proportion of high-strength collagen type 1. Consequently, mechanical strength decreases whilst the cross-sectional area increases. The reduced load-bearing capacity, in turn, predisposes the tissue to further microtrauma, which in turn further reduces the load-bearing capacity, thus creating a vicious circle.

From a therapeutic perspective, there is a solid body of research on eccentric training, which also demonstrates positive physiological effects, such as reduced proliferation of endothelial cells, increased release of vasodilatory substances and, where applicable, the destruction of existing blood vessels and nerves. At the same time, the alignment of the fibres improves and the pathologically increased cross-sectional area returns to near-normal levels. In some cases where patients experienced little or no clinical improvement, it was found that the chaotic fibre alignment had not improved or that vascularisation persisted. However, the link between pain perception and neovascularisation has not yet been sufficiently clarified; there are well-founded doubts that neovascularisation alone is responsible for pain perception. It is noteworthy that insertion tenopathies or paratenonitis occasionally result in an exacerbation of pain rather than an improvement. In rehabilitation training programmes, analogue pain of up to NRS 5 is permitted. Should the prescribed load exceed this pain intensity, it must be reduced and a higher load gradually introduced at a later stage. During the first two weeks of rehabilitation training, a worsening of pain symptoms is permitted, including in the form of post-exercise pain, but it is expected that the pain will have subsided by the morning following the training session. Explosive movements present a particular challenge here, as not only must the intensity of the load be increased gradually, but the speed of execution must also be gradually increased. However, the movement should be pain-free. The final stage of training is then plyometric.

1. https://www.researchgate.net/publication/291421060_The_Achilles_Tendinopathy_Pathogenesis_Review
2. https://europepmc.org/article/pmc/6737558

Tendon elasticity

Tendons have an elasticity of up to around 15 per cent , although only a small proportion of these can be used without causing damage, see above. According to recent research, an ion channel protein in the tendons acts as a force sensor that detects the longitudinal displacement of collagen fibres relative to one another. When higher shear forces are measured, the force sensor releases calcium ions into the tendon cells, which stimulates the production of enzymes that bind the fibres together, thereby increasing stiffness and load-bearing capacity at the expense of elasticity. There are several genetic variants of this ion channel protein. The E756del variant, which originated in West Africa as a response to malaria plasmodia, causes an excessive release of calcium, resulting in stronger tendons. Carriers of this variant have an advantage in sports where tendon properties are crucial (power sports such as sprinting and fast-paced jumping disciplines).

Tendon elasticity and ligament elasticity

There are sometimes misleading statements about the elasticity of tendons and ligaments. It is particularly important to distinguish whether the material property in question is per unit diameter and length, or whether absolute elasticity is being referred to. When measuring the elasticity of tendons and ligaments, the slack effect is not taken into account: when a ligament is relaxed, it can rest on adjacent structures, thereby significantly altering its straight course from origin to insertion. A good example of this is the Lig. patellae, which, when the patella is pointing upwards, the knee joint is extended and the quadriceps is relaxed, can rest on Hoffa’s fat pad. In the case of the tendon, there is hardly any slack effect, as, being the effector organ of a muscle, it is always under the muscle’s in vivo resting tension; the higher the muscle’s tension, the higher the basal tension, and this also depends heavily on the position of the joints it traverses. The tensile force acting on the tendon is that measured by the Golgi tendon organ.

Although, from a material science perspective, ligaments have a higher specific elasticity than tendons, in vivo ligaments are usually wider, sometimes thicker, but above all considerably shorter than tendons. The stiffness k = E * A / L – which is relevant in practice, with E being the modulus of elasticity, A the area and L the length – clearly illustrates why this is the case. For example, whilst the ACL is relatively long for a ligament, it also has a comparatively even greater diameter. The ACL consists of an anteromedial and a posterolateral bundle, which are slightly twisted in a spiral fashion relative to one another; in every joint position, at least one of these bundles is always under sufficient pre-strain. The elongation of the ACL is therefore, in vivo, only a few millimetres in all load-bearing situations. The ligaments of the foot, which are usually very short, are under tension when the foot is loaded, so that no slack effect can occur here either. By comparison, some tendons are very long: plantaris (30–45 cm), flexors of the toes (20–30 cm), Achilles tendon (approx. 10–15 cm). At the other end, the tendon of the stapedius muscle in the inner ear measures approximately 1–2 mm. In contrast, there are very few long ligaments, the most notable being the longitudinal ligament of the spine, which is approximately 40–50 cm long. Some way behind this is the MCL of the knee joint, measuring 8–11 cm. The ACL is only 3.5–4 cm long, but has a diameter of approximately 10 mm. The anterior talofibular ligament of the foot is approximately 1.5–2 cm long, but many other ligaments merely span the joint space between two adjacent bones and are therefore only a few millimetres long; for example, the ligaments between the carpal and tarsal bones. In the carpal region, the dorsal ligaments are slightly longer (often 5–6 mm) than the palmar ligaments, which are approximately 2–3 mm long, so that a hollow palm can be formed. Even the important and relatively long Lisfranc ligament (Lig. cuneometatarsale interosseum) of the foot is only 8–10 mm long. The following table provides an overview of these characteristics.

	Tendon	Band
Maximum elongation up to the plastic range	~4 %	~5–7 per cent or more
Modulus of elasticity (slope \(E\))	very high (steep)	lower (flatter)
Fibre structure	aligned strictly parallel	slightly tousled/wavy
Elastin content	extremely low: < 1–2 %	higher: up to 10 per cent or more

Tendon injury

According to all currently available evidence, tendon damage is usually caused by repeated overloading (overuse). In particular, this means repeatedly stretching the tendon beyond its physiological elasticity range of 3 per cent to, at best, 5 per cent. Among asymptomatic patients, 10% to 20% are found to have detectable tendon damage, which suggests that the link between the tendon disorder and the symptoms must be rather tenuous . Pathologically altered tenocytes are no longer arranged in a long, slender manner between the collagen fibrils, but become rounder, as do their nuclei; the cytoplasm increases in volume, and the cells become more similar to hyaline chondrocytes. At the same time, metabolic activity increases, as does the production of matrix proteins. Dying and apoptotic tenocytes are relatively rare. The collagen in diseased tendons also changes and loses its structure; individual bundles separate and the ground substance increases. There is increased formation of thinner and less resilient collagen type 3. Collagen fibrils also bend off more frequently, suggesting an underlying deficiency in the tensile strength required to maintain the structure. The composition of the proteoglycans also shifts towards larger proteoglycans. The glucosamine glycan side chains increase massively and, due to their hydrophilic properties, lead to increased water retention, which accounts for the detectable tendon oedema. The disturbance in the tendon promotes a process of vascularisation of the tendon, which is not detectable in areas with an intact fibre structure. As most studies have been conducted on tendons that were already significantly degenerated, fundamental insights into the onset of the disturbance are lacking; consequently, there are currently three hypotheses: the collagen hypothesis, the inflammatory hypothesis and the cell-based hypothesis. Although all three hypotheses contain interesting aspects, none appears to be valid on its own, and further research is required. The cell-based theory has led to the description of three states, the first two of which are physiological and reversible: reactive, dysrepair and degenerative.

Cook-Grade

1. As described above, short-term damage leads to oedema due to increased protein production. At this stage, there is no change in the collagen. Once the excessive stress has ceased and the resulting reaction has subsided, the tendon returns to its physiological state.
2. In the event of persistent overload, the increased production of proteins leads to impairment of the collagen structure. This phase is referred to as ‘dysrepair’. The abnormalities here are more focal than diffuse and disseminated, as is the case with the reactive disorder. The proportion of less resilient collagen type 3 increases, which reduces tensile strength. This disorder is also still reversible, although healing takes longer.
3. Degenerative stage 3 is characterised by extensive changes to collagen, marked changes to the extracellular matrix and neovascularisation. Neovascularisation appears to affect primarily areas with a severely disrupted collagen structure, suggesting that the formation of new blood vessels does not serve the purpose of tendon healing. Here, tenocytes die off, and it must be assumed that the defect is not healing properly.

In another paper, he describes a four-stage damage mechanism:

1. Overload associated with cell activation and hyperplasia
2. The newly produced cells produce proteins and proteoglycans that bind excessive amounts of water
3. The significant expansion of proteoglycans causes cracks in the collagen due to the space they occupy
4. Neovascularisation (blood vessels and lymphatic vessels) and the sprouting of free nerve endings

In a study involving a 16-week eccentric training programme, which was expected to have a positive effect on tendon tissue, the degenerative tendon tissue remained unchanged, as if it were not responding at all to the training stimuli, in contrast to tissue in the other two stages. The clinical symptoms, however, improved. The lack of a positive response to the training stimulus is explained by an inability to detect it due to the loss of tenocytes. Studies of the Achilles tendon and patellar tendon have shown that the risk of this condition becoming symptomatic is 3 to 15 times higher than in unaffected tendons. Local pain receptors appear to play a role in pain perception. The loss of the tendon’s physiological architecture can result in certain areas of the tendon no longer receiving sufficient maintenance stimuli to stimulate remodelling. These degenerated areas, described as ‘mechanically silent’, therefore do not respond by healing and leave the transmission of tensile force to neighbouring areas, which subsequently grow in response to sufficient training stimuli and are able to fully compensate for the loss of function. In the process, the tendon thickens overall to such an extent that the average functional cross-sectional area returns to its original size.

Several studies demonstrate the positive impact of eccentric and isometric exercise programmes on tendon function and symptoms.

There are a number of known factors that affect the elasticity of tendons and their health:

1. Age: as we get older, advanced glycation end-products (AGEs) accumulate in the tendon, causing it to ‘glycate’, which dramatically shortens the toe region. The linear range becomes steeper, but some of the plastic elasticity is lost. Consequently, the overall elasticity is reduced and the tear occurs sooner and more abruptly.
2. Cholesterol, particularly LDL cholesterol, is deposited in the tendon (lipid infiltrations), which triggers a local inflammation inflammatory cascade involving the activation of matrix metalloproteinases (MMPs). This results in a reduction in the modulus of elasticity. The tendon loses its stiffness and becomes prone to tendopathies and ruptures.
3. Cortisone severely inhibits protein synthesis in fibroblasts and tenocytes, so that the formation of new type I collagen and matrix is virtually blocked. As a result, both the modulus of elasticity (stiffness) and the maximum tensile strength decrease rapidly.
4. Fluoroquinolones such as ciprofloxacin and levofloxacin induce apoptosis in tenocytes; they therefore have a direct cytotoxic effect by chelating magnesium and iron ions. There is increased expression of matrix metalloproteinases (MMP-1, MMP-2 and MMP-13), and the synthesis of type 1 collagen collapses. This leads to a massive reduction in elasticity and a massive reduction in tear resistance.
5. In rheumatic diseases, the overall increase in levels of pro-inflammatory cytokines (particularly TNF-alpha, IL-1 and IL-6) in the tendon leads to a permanent upregulation of catabolic enzymes such as MMP-1, MMP-3 and MMP-9, which destroy the collagen matrix, particularly at the entheses. Here, too, the elasticity curve drops dramatically, with tensile strength reduced to 30–50 per cent.
6. In the case of IBD, activated T-cells and inflammatory mediators migrate from the gut to the periphery (‘gut-joint axis’). This impairs collagen hydroxylation and synthesis, causing the plastic region to shift significantly to the left. The chances of recovery are dramatically reduced in this case.

Tendon healing

Tendon healing takes place in three phases, of which phase 1 in particular gradually merges into phase 2 towards the end:

1. Inflammatory phase, up to approx. 7 days after trigger: platelet accumulation; fibrinous cross-linking of collagen fibres; increase in permeability due to mediators such as bradykinin and histamine
2. Prodelivery phase, 2-3 weeks: the fibrin construct is replaced by granulation tissue, prodelivery of myofibroblasts and fibroblasts, the latter form uncrosslinked collagen III
3. Maturation and remodelling phase, from 3 weeks to approx. 6 months: successive replacement of collagen III by collagen I. After 6 months, the tendon is fully resilient, but the healing is not a restitutio ad integrum, the resilience of the repaired tendon is reduced.

Tendon sheath / vagina synovialis tendinis

The tendon sheath is the double-walled connective tissue covering of the tendon in which it glides. It is directly enveloped by a two-leaf stratum (inner and outer leaflet). The inner leaflet is fused with the tendon, the outer leaflet with the stratum fibrosum, the outer part of the tendon sheath. Between these two strata lies a buffer of synovia, which produces the synovial layer of the joint capsule, to which the inside of the tendon sheath is connected.

Tendon sheaths are formed where tendons run over joints or bony protrusions, where tendons are exposed to high tension and friction, and where low-friction sliding of the tendon in the tissue is mechanically essential (e.g. in areas with highly repetitive movements). Here, the tendon sheaths protect the tendon from abrasion and mechanical overloading.

Tendon sheaths are found, for example, on the fingers and toes (long tendons of the hand/foot muscles over the finger/toe joints), around the wrist and ankle, on the carpal bones (e.g. thumb canal), on the sole of the foot, heel and lower leg (e.g. Achilles tendon area), and also partly on the shoulder, knee and lower abdomen (e.g. on the rectus abdominis).

Ehthesis

The attachment of the tendon of a muscle to the bone is called an enthesis. There are two types of entheses: fibrous entheses and fibrocatilaginous entheses. Fibrous entheses typically occur on tendons that attach to metaphyses and diaphyses of the long tubular bones. They consist of dense connective tissue and contain Sharpey fibres, mineralised collagen fibres that radiate into the periosteum in order to strengthen the enthesis. The adductors of the hip joint are a good example of this. Fibrocartilaginous entheses are the attachments to apophyses and epiphyses of the long tubular bones. They consist of four zones: the tendon, a zone of non-calcified fibrocartilage, a zone of calcified fibrocartilage and finally the bone. This structure is better able to withstand shear forces and compressive stresses. In the case of the achilles tendon, a layer of fibrocartilage lies on top of the calcaneus and the fibrocartilage zone of the tendon. In a certain sense, the bursa subachillea and the subachillary fat body there can also be counted as an enthesis. Tendons of polyarticular muscles are usually surrounded by tendon sheaths in the area of the covered joints. A distinction is made between traction tendons, whose course is not deflected for enthesis, and gliding tendons, which are deflected, often via a bone, which can take on a hypomochlion function. Physiologically, tendons consist mainly of fibre-rich connective tissue, and this in turn consists mainly of collagen, which makes up 80% of the dry mass of the tendon. Tendon cells (tenocytes/wing cells) are located between the collagen fibres in an elongated arrangement. The wing cells communicate by exchanging ions and molecules by diffusion through the gap junctions that connect them. The extracellular matrix surrounding this structure consists of around 70% water and just under 30% type 1 collagen, as well as elastin and the so-called ground substance, which consists of highly cross-linked proteoglycans. At 200 mPa, the modulus of elasticity of tendons is one power of ten lower than that of bone. The non-straight course of the collagen fibres in a relaxed tendon allows physiological longitudinal elongation of 3%, up to a maximum of 5%, by straightening the course before the first damage to the tendon occurs, which is to be expected at 8% and occurs transmurally at 12%. Up to one per cent elongation, the collagen fibres lose their undulating course, after which linear elongation occurs up to around 3% elongation. The tensile strength of tendons lies in the range between 34 N and 46 N per square millimetre for the fibrocartilaginous part of the tendon and 60 to 120 minutes per square millimetre for the parallel-fibre area. A good 90% of the elastic energy stored in a tendon through stretching can be recovered, i.e. less than 10% goes into plastic deformation. The tendon can react and adapt to semi-regularly recurring stresses by increasing its metabolism. For example, an increased uptake of oxygen and glucose in the tendon under mechanical stress can be demonstrated. If a tendon is repeatedly exposed to high-threshold tensile loads over a period of 12 weeks with sufficient frequency, it adapts sustainably. The form of loading, whether eccentric, concentric or isometric, is of secondary importance.

Gliding tendon

A gliding tendon is a tendon that changes direction along its course. It is diverted over a bony protrusion with a hypomochlion function and has a cartilage reinforcement in the part of its course that can come into contact with the bone. Gliding tendons are most compressed in the area of contact with their diversion, while the pull is greatest at the exact opposite end. They are therefore exposed to shear forces.

Traction tendon

A traction tendon is a tendon that runs largely in a straight line without being deflected. Tension tendons are not exposed to compression or shear forces, but only to tensile forces.

Tendinitis

Inflammation of a tendon. This can occur together with or without inflammation of its tendon sheath (tendovaginitis) and is then also referred to as tendosynovitis. The cause is usually overuse.

Tendopathy / Tendinopathy

Tendon disorders with no specified etiology, but usually of an inflammatory or degenerative nature. Overuse is a common cause, with ergonomic or material deficiencies being a risk factor, as is a lack of regeneration.