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.

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.

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.

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.

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.

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.