Season
Affiliates
Number of injuries
Number of tendon injuries
2014–2015
151.263
25.730
73 (0.28%) tendon ruptures
781 (3.04%) tendinosis
Fig. 12.1
Upper extremity injuries. (a) Epicondylitis in the elbow with eco-Doppler study. (b) Supraspinatus rupture
The most common of the tendon injuries are:
The use of biologic therapies in tendon injuries is the present and the future in treating these injuries. The goal of these therapies is to restore the tissue with the same and indistinguishable properties from the original one. Likewise, the crux of the matter is not to repair but to regenerate, reconstruct and restore the functionality.
The use of biologic therapies in tendon injuries is the present and the future in treating these injuries. The goal of these therapies is to restore the tissue with the same and indistinguishable properties from the original one. Likewise, the crux of the matter is not to repair but to regenerate, reconstruct and restore the functionality.
12.1.1 Anatomy and Histology
Tendons are fibrous connective tissue composed of collagen fibre bundles that connect muscle to bone and act as contractile force transmitters enabling skeletal movement. All these are covered by the peritendon.
There are anatomical sites where the tendon slides can suffer a wear disease. These sites are the bony furrows, the landmarks, where the tendon frequently has a tendon sheath.
In the bone soil furrows, the roof consists of a fibrous sheath that converts the canal in a tunnel or fibro-osseous duct and the tendon slides protected by the synovial sheath that has a parietal membrane and other tendon membrane that are separated by a virtual synovial cavity with synovial fluid inside. In the parietal tendon membrane and tendon membrane reflection areas, a non-ended cavity is formed. All this can be surrounded by a fascia coating thickening that also protects the tendons and is called retinaculum.
The vascularity of the tendon almost always comes from its deep side, where the mesotendon is placed, or can also come through links or vessels that come from the bone insertion.
And the last anatomical detail of the tendons is the synovial bursa, which is in places where it can be rubbed with other muscles or osteoligamentous structures. The bursae contain synovial fluid as a cushion to facilitate the sliding (Llusá et al. 2006).
12.1.2 Biomechanics of the Tendon
Tendons have viscoelastic behaviour; they do not act as rigid links between muscles and bones. The viscoelasticity is given by the collagen and the water and by the interaction between the collagen and the proteoglycans (Wang et al. 2012).
The mechanical proprieties of the tendon have traditionally been studied stretching an isolated tendon to failure (Butler et al. 1978). There, a force-elongation curve is obtained with four different regions. Region I is associated with non-damaging forces; in region II, the already aligned forces are stretched and at the end point some fibres start to break. Further elongation brings into region III, where fibre failure occurs unpredictably; when further elongation occurs, it brings the tendon into region IV where there is a complete failure (Maganaris et al. 2008). Different types of tendons differ in their mechanical proprieties due to their different functions.
The key to tendons’ tensile strength is collagen. For about 70–80% of the dry weight, tendon is collagen type I, and in minor amounts there are collagen types III, V, IX, X, XI and XII, which also have important functions.
The tendon acts as a spring, stretching when there is a tensile force, accumulating part of this energy and liberating it when it regains its original shape. What makes it act in this way is the plasticity given by the periodic wave pattern of the collagen fibres, named the crimp pattern. When the tensile force is higher than 2%, the fibres lose its pattern, and until 4% the tendon can regain its periodic wave pattern. With a tensile force is from 4 to 8%, the fibres start to brake, and they are unable to regain completely their pattern (Maffulli 1999; Doral et al. 2010).
12.1.3 Aetiology
The tendon injuries are often chronic, and the causes are an overload, a degenerative process or a rupture, but also it could be acute injury.
Repetitive movements both in work activity (cleaning glass, craftwork cutting, etc.) and sports activity (swimming, launching, etc.) are the cause of many of these injuries.
12.1.4 Injury Classification (Fig. 12.3)
According to the anatomical location:
- 1.
Tendon insertion or tenoperiosteal area. These are tendinopathy insertion or enthesitis and avulsions.
- 2.
Tendinous body: swelling, tendinosis (degeneration) and partial or complete rupture.
- 3.
Musculotendinous junction: sprains.
- 4.
Paratenon: peritendinitis and tenosynovitis.
Fig. 12.3
Anatomical location of tendon injuries
12.1.5 Diagnosis
Diagnosis is performed by clinical examination and complementary studies.
Clinical Examination: Signs and Symptoms
Pain during sports activities and in normal life. More acute when doing forced movements.
Pain when palpating the insertion of the tendon or the tendinous body, when there is a tendinosis or an enthesitis.
Strength decreased with or without pain when doing contraction against resistance of the injury.
Pain when passive stretching of the injured tendon.
Crepitation in tenosynovitis.
“Hatchet strike defect” in complete ruptures (Cugat 1993).
Specific test: to evaluate the rupture or injury of some tendons, such as Thompson manoeuvre in Achilles tendon.
Complementary Studies
X-rays: Calcifications, bony protrusions and bone avulsion can be observed.
MRI
ULTRASOUND: Ultrasound is an imaging technique very useful to evaluate the tendons. It is a great complementary tool to the conventional radiography for an exhaustive diagnosis. Ultrasound is a non-invasive technique that allows us to use it as many as needed to do comparative and dynamic studies. The main uses are as follows: diagnosis, define the type of injury, locate and grade it, give a prognosis and suggest a treatment for the patient and also conduct the follow-up. The most frequent injuries of the tendons are tendinopathy, enteropathy, complete or partial ruptures, dislocations and partial dislocations. On the interventionist side, the ultrasounds are becoming more useful to conduct ultrasound-guided treatments. It provides precision to the treatments because it allows us to view the structure to intervene and have a precise control over the needle while doing the procedure.
12.1.6 Treatment
- 1.
Surgical: Only when conservative treatment does not get satisfactory evolution and in big ruptures.
- 2.
Conservative: Biologic therapy, physiotherapy and rehabilitation.
12.2 Biologic Therapy: Growth Factors
12.2.1 What Are Growth Factors?
Growth factors are substances, such as vitamins or hormones, which are required for the stimulation of growth in living cells and cellular differentiation. They are biochemical signals capable of modulating the cellular response, involved in a large number of biological functions among which cellular proliferation is important, though they also decisively affect cellular survival, migration, differentiation and even apoptosis.
Growth factors are synthetised as cellular mediators by a great amount of varied cell types, to diverse stimuli as an injury. It has been noticed that all types of connective tissues (bone, muscle, cartilage, synovial membrane, tendon, ligament, meniscus, skin, etc.) contain many of these signalling proteins which play a very important role in the remodelling and repair of the different types of connective tissue.
Growth factors carry out their function at very low concentration on body fluids and tissues, in the region of pico- or nanograms. Typically, they act by binding to a cellular receptor, which is specific for a second messenger where a tyrosine kinase protein acts. This causes a signalling cascade that ends up with a signal transduction inside the nucleus and the activation of one or more genes.
12.2.2 Mode of Action
The process of tissue regeneration includes a complex set of biological events controlled by the action and synergy of a cocktail of growth factors. There are three agents involved in tissue regeneration, the cellular component, a combination of multiple biological mediators that include growth factors and cytokines among others and a matrix or scaffold that gives support to the new tissue under construction.
The signalling pathways leading from the receptor binding to a biologic response are very complex.
Tyrosine kinase receptors are cell membrane molecules and have kinase activity, which means that they have the ability to phosphorylate or add phosphate groups on the cytoplasmic domain. A growth factor, the ligand, binds this receptor, which dimerises and activates the kinase activity (Hubbard 1999). After this activation, the receptor can add more phosphates to certain downstream targets or bring other molecules into the signalling complex by its phosphotyrosine residues (Lemmon and Schlessinger 2010). It could also be transmitted differently when the receptor does not have intrinsic tyrosine kinase activity. They instead recruit molecules, which have the ability to phosphorylate. These receptors have an intracellular domain with a protein kinase family (JAKs) which autophosphorylates and then recruits signal transducers and activators of transcription (STATs) (O’Shea et al. 2002) (Fig. 12.4).
