Tendons are vital components of the musculoskeletal system as they serve to attach the contractile units of the body (muscles) to the levers (bones). They are thereby responsible for the transmission of the forces required to produce movement. The cross-sectional areas of tendons are small in relation to their attached muscles, and therefore, the stress (force per unit area) they are exposed to is substantial during activity. It is perhaps no surprise, therefore, that they are subject to inflammatory and degenerative pathology. Tendon injuries are reported to account for up to 30% of all running-related injuries and can result in considerable morbidity lasting several months despite appropriate management.
Macroscopically healthy tendons are white in color and are found in a variety of forms, from rounded cords to flattened ribbons, depending on their function and anatomical site. Normal adult tendon fibers are composed predominantly of large Type I collagen fibrils (6580% of the dry mass) arranged in a ropelike configuration with smaller amounts of Type III collagen, proteoglycans, and elastic fibers (2%). The predominant cells found within the tendon structure are tenocytes and tenoblasts (immature tenocytes), which account for 90% to 95% of the cell population. These cells lie between the collagen fibers along the long axis of the tendon. The remaining cells include chondrocytes at the tendon insertion sites, the synovial cells of the tendon sheath, and vascular cells. The endotenon, a thin retinacular structure, invests each tendon fiber. The epitenon surrounds the tendon and contains the vascular, lymphatic, and nerve supply and is in turn surrounded superficially by the paratenon. Synovial tendon sheaths, consisting of an outer fibrotic sheath and an inner synovial sheath, may be found in areas subject to increased mechanical stress, where efficient lubrication is required. The inner sheath produces synovial fluid by a process of ultrafiltration. At the myotendinous junction, the weakest point of the musculotendinous unit, collagen fibrils of the tendon insert into deep recesses formed by the myocytes of the associated muscle. The osteotendinous junction is composed of four zones (dense tendon zone, fibrocartilage, mineralized fibrocartilage, and bone). The blood supply of tendons originates from intrinsic systems at the myotendinous and osseotendinous junctions and an extrinsic system through the paratenon or synovial sheath.
Contrary to traditional beliefs, tendons are metabolically active. Tenocytes have a low metabolic rate and a well-developed anaerobic energy generation capacity that allows them to resist load and maintain tension for prolonged periods. Animal studies suggest that the physical properties of tendons (tensile strength, stiffness, collagen content, and cross-sectional area) are all enhanced with physical activity. Type I collagen synthesis in particular depends on overall protein synthesis and on tensile loading and is thought to occur in a nonuniform way throughout the tendon structure.
The relationship between tendinosis (degeneration without inflammation) and tendinitis (inflammation) is unclear. The terms are often used interchangeably, leading to confusion. The best generic descriptive term for clinical conditions arising in and around tendons is tendinopathy. The low metabolic rate that makes the cells of the tendon suitably adapted for their role in load bearing also, however, results in delayed healing following injury. Tendinopathies tend to occur with greater frequency in the older athlete, and it is perhaps not surprising that with increasing age the metabolic pathways of tenocytes shift from aerobic to more anaerobic energy production. In addition, tendon vascularity is compromised at the junctional zones between the intrinsic and extrinsic systems or where there is localized torsion, friction, or compression. A good example of this is seen in the Achilles tendon, where there is a zone of hypovascularity 2 to 7 centimeters (cm) proximal to the tendon insertion, a common site of rupture. It is important to note that tendon blood flow also decreases with increasing age and mechanical loading.
Despite the relative frequency of tendon overuse injuries in sports medicine practice, the etiology of tendinosis and tendinitis remain unclear. The processes are multifactorial but on a local level are thought to be one of accumulated trauma as a result of repetitive mechanical loading. Tenocyte damage may occur as a result of localized hypoxia or as a result of free radicals produced during reperfusion after relaxation, which may be compounded by hyperthermia within the tendon produced by repeated or prolonged bouts of exercise. On a macroscopic level, there may be a combination of intrinsic factors such as malalignment, inflexibility, and muscle weakness or imbalance. Biomechanical faults, in particular hyperpronation of the foot, are reported to play a causative role in two thirds of Achilles tendon disorders in athletes. These may be exacerbated by age-related degeneration and diminished vascular supply. Tendons loaded beyond their physiological threshold respond by inflammation of their sheath (synovitis/tendinitis), degeneration of their body (tendinosis), or a combination of the two processes. Macroscopically, the diseased tendons look gray-brown and amorphous, and they may be thickened. Histological examination of tendons in symptomatic patients reveals disordered healing and noninflammatory degeneration. The fibers are thin and disorganized with scattered vascular in-growth. Inflammatory lesions and granulation tissue are infrequent in the chronic situation. Pain may result from a number of mechanical and biomechanical factors. Chemical irritants implicated in the production of pain include glutamate and Substance P.
Common sites of tendinopathies include the ankle (Achilles tendon/tibialis posterior), knee (patellar tendon), shoulder (supraspinatus tendon/bicipital tendon), and elbow (“tennis” elbow/“golfer's” elbow).
The diagnosis of tendinopathy or tendinitis depends on the acquisition of a detailed history and a thorough examination. The patient generally complains of pain on loading the affected structure. There has often been a change in the frequency or intensity of activity prior to the onset of symptoms. Examination may reveal localized pain on deep palpation or thickening of the affected structure. Significant loss of function or the presence of a palpable defect should alert the examiner to the possibility of partial or complete tendon rupture. Magnetic resonance imaging (MRI) or ultrasound scanning with Doppler may be useful to identify changes within the tendon substance, including the increased blood flow associated with neovascularization.
It is important at the outset to identify whether the problem is an acute episode with an inflammatory component or a chronic condition. Tendinopathies may require lengthy multimodal management, and patients often respond poorly to treatment. The mainstay of treatment is generally conservative. As in most conditions, the keystone of successful treatment lies in the accurate assessment of the factors contributing to the problem. These must then be systematically addressed during the treatment phase. Training patterns and the equipment used by the athlete should be assessed, preferably in conjunction with the coaching staff. Poor technique and “training errors” should be avoided, and where possible, biomechanical factors should be corrected. There is little convincing evidence for the use of nonsteroidal anti-inflammatory drugs (NSAIDs) in chronic tendinopathy, although they may be useful in the acute situation. It is important to recognize that in many sites, there is little evidence of a lasting benefit from the peritendinous injection of corticosteroids. If there is an inflammatory component such as a tenosynovitis or bursitis, these agents may be used to address any associated inflammation, and cautious use of locally applied ice may be helpful in providing pain relief. The degree of tendon loading that should be applied to promote healing is a matter of debate. Prolonged immobilization of tendons is detrimental, leading to tendon atrophy and reduced tensile strength. Controlled stretching is likely to increase collagen synthesis and improve the quality of the regenerate tendon.
Many physical therapies have been proposed for the treatment of tendinopathies, with little good-quality evidence for their efficacy. There is evidence from animal models of the usefulness of extracorporeal shock wave therapy (ESWT) in improving experimentally produced tendinopathy, but the results of clinical trials in humans are conflicting. Other treatments have included the use of pulsed magnetic fields, laser therapy, and radiofrequency coblation, again with variable results. There is good support for the use of an eccentric training program in short-term symptom relief in Achilles and patella tendinopathies. Other modalities used with conflicting evidence include dry needling, the image-guided injection of sclerosants, and the use of glyceryl trinitrate (GTN) patches. Surgical debridement of the macroscopically unhealthy tissue can be considered in cases resistant to other treatment modalities.
Future therapies may involve the use of cytokines and growth factors, gene transfer, or the implantation of mesenchymal stem cells to modify the healing environment.
The assessment and management of tendinopathies is one of the key skills required in the sports medicine practitioner. Further research and scientific evaluation of the available literature are required before evidence-based management protocols can be instituted.
Achilles Tendinitis, Patellar Tendinitis, Peroneal Tendinitis, Tendinopathy
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