The intrinsic pathogenetic mechanisms of tendinopathies are largely unknown and whether inflammation or degeneration has the prominent role is still a matter of debate. Assuming that there is a continuum from physiology to pathology, overuse may be considered as the initial disease factor; in this context, microruptures of tendon fibers occur and several molecules are expressed, some of which promote the healing process, while others, including inflammatory cytokines, act as disease mediators. Neural in-growth that accompanies the neovessels explains the occurrence of pain and triggers neurogenic-mediated inflammation. It is conceivable that inflammation and degeneration are not mutually exclusive, but work together in the pathogenesis of tendinopathies.

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Pathogenesis of tendinopathies: inflammation or degeneration?

The Olympic Games is the largest sport event in the world. In Beijing, 10 500 athletes competed, selected from a large group of elite athletes in 204 countries. Sports participation on the elite level, aside from winning medals, fame and other rewards, is also important from a health perspective. There is no longer any doubt that regular physical activity reduces the risk of premature mortality in general, and of coronary heart disease, hypertension, colon cancer, obesity and diabetes mellitus in particular. The question is whether the health benefits of sports participation outweigh the risk of injury and long-term disability, especially in high-level athletes. Sarna et al 1 have studied the incidence of chronic disease and life expectancy of former male world-class athletes from Finland in endurance sports, power sports and team sports. The overall life expectancy was longer in the high-level athlete compared with a reference group (75.6 vs 69.9 years). The same group also showed that the rate of hospitalisation later in life was lower for endurance sports and power sports compared with the reference group.2 This resulted from a lower rate of hospital care for heart disease, respiratory disease and cancer. However, the athletes were more likely to have been hospitalised for musculoskeletal disorders. Thus, the evidence suggests that although there is a general health benefit from sports participation, injuries represent a significant side effect.

One priority of the International Olympic Committee (IOC) is to protect the health of the athlete. During recent years, prevention of injuries and illnesses has been high on the IOC agenda. During the Athens Games, an injury surveillance system was applied for all team sports.3 During the Beijing Games, the IOC ran, for the first time, an injury surveillance system covering all the athletes, showing a 10% incidence of injuries.4 In …

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The International Olympic Committee (IOC) Consensus Statement on periodic health evaluation of elite athletes March 2009

BackgroundFew randomized controlled trials compare different methods of management in chronic tendinopathy of the main body of tendo Achillis.PurposeTo compare the effectiveness of 3 management strategies—group 1, eccentric loading; group 2, repetitive low-energy shock-wave therapy (SWT); and group 3, wait and see—in patients with chronic tendinopathy of the main body of tendo Achillis.Study DesignRandomized controlled trial; Level of evidence, 1.MethodsSeventy-five patients with a chronic recalcitrant (>6 months) noninsertional Achilles tendinopathy were enrolled in a randomized controlled study. All patients had received unsuccessful management for >3 months, including at least (1) peritendinous local injections, (2) nonsteroidal anti-inflammatory drugs, and (3) physiotherapy. A computerized random-number generator was used to draw up an allocation schedule. Analysis was on intention-to-treat basis.ResultsAt 4 months from baseline, the Victorian Institute of Sport Assessment (VISA)-A score increased in ...

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Eccentric Loading, Shock-Wave Treatment, or a Wait-and-See Policy for Tendinopathy of the Main Body of Tendo Achillis A Randomized Controlled Trial

Overuse disorders of tendons, or tendinopathies, present a challenge to sports physicians, surgeons, and other health care professionals dealing with athletes. The Achilles, patellar, and supraspinatus tendons are particularly vulnerable to injury and often difficult to manage successfully. Inflammation was believed central to the pathologic process, but histopathologic evidence has confirmed the failed healing response nature of these conditions. Excessive or inappropriate loading of the musculotendinous unit is believed to be central to the disease process, although the exact mechanism by which this occurs remains uncertain. Additionally, the location of the lesion (for example, the midtendon or osteotendinous junction) has become increasingly recognized as influencing both the pathologic process and subsequent management. The mechanical, vascular, neural, and other theories that seek to explain the pathologic process are explored in this article. Recent developments in the nonoperative management of chronic tendon disorders are reviewed, as is the rationale for surgical intervention. Recent surgical advances, including minimally invasive tendon surgery, are reviewed. Potential future management strategies, such as stem cell therapy, growth factor treatment, and gene transfer, are also discussed.

Management of Tendinopathy

Injury and degeneration of tendon, the soft tissue that mechanically links muscle and bone, can cause substantial pain and loss of function. This review discusses the composition and function of healthy tendon and describes the structural, biological, and mechanical changes initiated during the process of tendon healing. Biochemical pathways activated during repair, experimental injury models, and parallels between tendon healing and tendon development are emphasized, and cutting-edge strategies for the enhancement of tendon healing are discussed.

https://www.annualreviews.org/doi/pdf/10.1146/annurev-bioeng-071811-150122

Tendon Healing: Repair and Regeneration

Genetic aspects of tendinopathy

Tendinopathy, a broad term used to describe disorders in and around tendons, 1,2 is associated with repetitive tensile forces exerted on tendons. Rapid increases in the duration and intensity of these forces may cause tendon injuries, possibly the starting point in the pathogenesis of chronic tendinopathy. The exact incidence of chronic tendinopathy is unknown given the vast population of professional and recreational athletes suffering from this condition at different anatomic sites. Studies on incidence of tendinopathies are usually site or sport specific, and only provide an approximation of the magnitude of the problem faced by musculoskeletal and sports medicine clinicians in treating this disorder. In addition, a large number of sedentary subjects develop tendinopathy with no apparent history of increased physical activity. Disorganized, haphazard healing, with frayed, separated, and otherwise disrupted collagen fibrils, are features of tendinopathy. These lesions are characterized by the absence of inflammatory cells and a poor healing response. Age-related tendon changes, and not just mechanical overload, may thus play a role in the pathogenesis of tendinopathy, although the exact etiologic, pathophysiologic, and healing mechanisms are still unknown. Gene expression studies have shown an absence of any inflammatory process in chronic Achilles tendinopathy. Microdialysis experiments have shown no evidence of intratendinous chemical inflammation, with prostaglandin E2 (PGE2) levels being normal in chronic tendinopathies. Microdialysis has also shown higher levels of glutamate, an excitatory neurotransmitter and a potent modulator of pain in the central nervous system, in tendinopathic tendons compared with normal tendons. The same technique reveals that the local concentration of lactate in the tendinopathic Achilles tendon is almost twice that of the normal Achilles tendon. It is possible that there is an ischemic component in the pathogenesis of tendinopathy. Ischemia may precede the start of tendinopathy, but examination of tendinopathic lesions reveals neovascularization and increased blood flow in the affected area of the tendon. Neovascularization may be a response to a primary injury or may be the result of a metabolic disorder. It is possible that anaerobic conditions exist in areas of tendinopathy that have a poor blood supply, and are the primary cause of neovascularization. Neovessels and their accompanying nerves, may be responsible for the pain in the tendinopathic tendon, which would account for the success of local injection of sclerosants such as Polidocanol in the management tendinopathy. Chronic tendinopathy may well be the final manifestation of a long-standing metabolic process in which inflammation, although an initiator, does not participate in the final histopathologic and biochemical features of chronic tendinopathy. It is important in understanding this hypothesis to recall the mechanism of tendon healing. A tendon heals by undergoing inflammatory (1–7 days of injury), proliferative (7–21 days), and remodeling (3 weeks–1 year) phases. Despite collagen maturation and remodeling, tendons are biochemically and metabolically less active than bone and muscle. Type III collagen synthesized by fibroblasts in the proliferative phase is gradually replaced by type I collagen from days 12 to 14, with a progressive increase in tensile strength.

Nonsteroidal antiinflammatory drugs in tendinopathy: friend or foe

The elbow is a common site of orthopaedic injury in the paediatric population. The number of these injuries continues to rise following increased levels of participation in paediatric recreational and competitive sport. Injuries to the paediatric elbow can be classified as either overuse or acute. Delineating injury patterns to the elbow in children can be challenging, given the cartilaginous composition of the distal humerus and the multiple secondary ossification centres that appear and unite with the epiphysis at defined ages. Pitching in baseball, serving in tennis, spiking in volleyball, passing in American football and launching in javelin-throwing can all produce elbow pathology by forceful valgus stress, with medial stretching, lateral compression and posterior impingement. In children and adolescents, the epiphyseal plate is weaker than the surrounding ligaments, predisposing them to epiphyseal plate injuries. On the other hand, post-pubescent or skeletally mature athletes are more prone to tendinous or ligamentous injury. Injuries may cause significant impact on the athlete, parents and healthcare system. With the exception of baseball, there are few prospective cohort studies on the epidemiological trends of childhood elbow injuries in other sports. This paper aims to describe the epidemiological trends in paediatric elbow injuries related to sports, suggests prevention strategies and discusses the scope for further research. A web-based search of existing articles pertaining to paediatric elbow injuries in sports was performed. The implications of acute and overuse injuries and the possibility of permanent damage should be understood by parents, coaches and the athletes. Proper understanding of the intrinsic and extrinsic risk factors that could lead to elbow injuries is thus required. Measures to prevent elbow injuries should include proper coaching, warm-up, officiation, legislation, medical expertise and protective gear. There are still many opportunities for prospective studies and other research projects among young athletes in various sports. Current studies will serve as a baseline for future research to assess the success of specific interventions in reducing the incidence of elbow injury in the paediatric athlete. Further epidemiological studies in various sports will help expand our knowledge and prevent potential disability and deformity in the paediatric elbow.

A review of epidemiology of paediatric elbow injuries in sports.

Disorganized, haphazard ineffective healing is a constant feature of chronic tendinopathy. Normal tendon is composed mostly of type I collagen. Tendinopathic tendons, conversely, have a greater proportion of type III collagen, which is associated with tendon rupture. Matrix metalloproteinases (MMPs) are involved in remodelling of the extracellular matrix (ECM) of tendons, because they are either up- or down-regulated in tendinopathy. A balance between MMPs and tissue inhibitors of metalloproteinases is required to maintain tendon homeostasis. The mechanism of activation of MMPs is poorly understood, and their precise role in tendinopathy is unclear.

https://www.foot.theclinics.com/article/S1083-7515(05)00013-6/pdf

Molecular Events in Tendinopathy: A Role for Metalloproteases

INTRODUCTION Chronic tendinopathy is frequent in both elite and recreational athletes. Sedentary subjects may also develop tendinopathy in the absence of any history of increased physical activity. Most research on tendon injuries has focused on a description of the condition and its management, rather than on the underlying cellular and molecular mechanisms of causation. Although several such mechanisms have been implicated, the causes of tendon problems in athletes are poorly understood. ‘‘Differential strain,’’ ‘‘stress shielding,’’ joint position, and even underuse have all been advanced as alternative biomechanical explanations to the classical overuse model for the pathogenesis of tendinopathy.

Merzesh Magra

Papers

Genetic aspects of tendinopathy

Nonsteroidal antiinflammatory drugs in tendinopathy: friend or foe

A review of epidemiology of paediatric elbow injuries in sports.

Molecular Events in Tendinopathy: A Role for Metalloproteases

Genetics: does it play a role in tendinopathy?