Achilles Tendon Disorders Etiology And Epidemiology Pdf

achilles tendon disorders etiology and epidemiology pdf

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Achilles tendinopathy is one of the most frequently ankle and foot overuse injuries, which is a clinical syndrome characterized by the combination of pain, swelling, and impaired performance. The two main categories of Achilles tendinopathy are classified according to anatomical location and broadly include insertional and noninsertional tendinopathy.

Metrics details. Achilles tendinopathy is the most prevalent tendon disorder in people engaged in running and jumping sports. Aetiology of Achilles tendinopathy is complex and requires comprehensive research of contributing risk factors. There is relatively little research focussing on potential biomedical risk factors for Achilles tendinopathy. The purpose of this systematic review is to identify studies and summarise current knowledge of biomedical risk factors of Achilles tendinopathy in physically active people.

Epidemiology of Tendon Problems in Sport

Rees, A. Wilson, R. Primary disorders of tendons are common and constitute a high proportion of referrals to rheumatologists. Certain tendons are particularly vulnerable to degenerative pathology; these include the Achilles, patella, elements of the rotator cuff, forearm extensors, biceps brachi and tibialis posterior tendons.

Disorders of these tendons are often chronic and can be difficult to manage successfully in the long term. Significant advances have been made in understanding the pathophysiology of these conditions. Histopathological evidence, together with advances in imaging techniques, has made us more appreciative of the degenerative rather that inflammatory nature of these conditions. Additionally the presence of neovascularization is now well-recognized in long-standing tendinopathy.

We review the mechanical, vascular and developing neural theories that attempt to explain the aetiology of degenerative tendinopathy. We also explore theories of why specific tendons such as the Achilles and supraspinatus tendons are particularly prone to degenerative pathology.

Traditionally, treatments have placed a heavy emphasis on anti-inflammatory strategies, which are often inappropriate. Recently, however, significant advances in the practical management of tendon disorders have been made.

This concept is currently being extended to include other commonly injured tendons. Other current treatments are reviewed, as are potential future treatments. Primary disorders of tendons tendinopathies are common. Rotator cuff disease was the most common cause of shoulder pain found in the latter two studies. However, they are by no means only linked to sport; in one series of 58 patients nearly one-third did not participate in vigorous activity [ 6 ].

Commonly involved tendons are detailed in Table 1. Common primary disorders of tendons classified by anatomical area and tendons most commonly affected. There is a combination of anti-gravity and non-anti-gravity tendons. Some tendons are high load such as the Achilles and patella whilst some are subject to smaller loads such as the forearm extensor and supraspinatus.

Historically the term tendinitis has been used to describe chronic pain relating to a symptomatic tendon. Its use is deeply ingrained in the literature and implies that inflammation is central to the pathological process. However, opinion has moved away from this theory. Histological studies of surgical specimens of chronic tendinopathy consistently show either absent or minimal inflammation.

The predominant lesion is one of degenerative change. This is seen in, for example, the Achilles [ 10 , 11 ], rotator cuff [ 12 ], patella [ 13 ] and extensor carpi radialis brevis tennis elbow [ 14 ].

Importantly tendinopathy is not necessarily symptomatic [ 15 ]. The macroscopic appearance is of a disorganized tissue, which is soft and yellow or brown in colour mucoid degeneration. There is loss of the tightly bundled collagen appearance [ 14 , 16 ]. Microscopically there is degenerative change to the collagen with accompanying fibrosis [ 17—19 ]. Typical histopathological changes are shown in Fig. Histopathological changes seen in tendinopathy demonstrating a lack of an inflammatory response.

A Normal tendon with scattered elongated cells. B Slightly pathological tendinous tissue with islands of high cellularity and initial disorganization. C Highly degenerated tendon with some chondroid cells; distinct lack of inflammatory infiltrate.

Hindfoot tendinopathies in athletes. Tendon injuries basic science and clinical medicine, Springer, London, , with kind permission of Springer Science and Business Media. This figure may be viewed in colour as supplementary data at Rheumatology Online. Additionally neovascularization is consistently identified both in histology [ 17 , 20 ] and with the use of powered Doppler ultrasound US in vivo [ 21 , 22 ]. This neovascularization is reminiscent of that seen in both rheumatoid arthritis and osteoarthritis [ 23—25 ].

More recent evidence from Alfredson et al. They performed microdialysis of chronically involved intact Achilles tendons and were unable to demonstrate the presence of the inflammatory mediator prostaglandin E2.

Alternatively, tendon degeneration may be secondary to failure of regulation of specific matrix metalloproteinase MMP activities in response to repeated injury [ 27 ]. However, most of the histopathological evidence is derived from samples at the point where surgical intervention is necessary, i.

It is therefore still possible that inflammation is involved at the initiation of the degenerative process. There is a lack of good quality histological data from symptomatic tendon disorders of short duration.

Two studies, one of the Achilles tendon and one of the patella tendon, included patients with symptoms of only 4 months' duration [ 28 , 29 ]. Both studies showed a lack of an inflammatory infiltrate but the number of patients with symptoms of such short duration was very small.

Certainly, in vitro studies have demonstrated that mechanical loading of human tendon fibroblasts increases production of both prostaglandin E2 PGE2 [ 30 , 31 ] and leucotriene B4 LTB4 [ 32 ] and that these mediators may contribute to degenerative tendon change [ 33 ].

However, the onset of symptoms does not necessarily coincide with onset of pathology. With advances in imaging these degenerative changes are being recognized in asymptomatic active populations [ 34 , 35 ]. It is therefore possible that in the early symptomatic cases the pathological process may have been present for much longer.

A schematic representation of the disease process is shown in Fig. Schematic representation of the process from initial injury to degenerative tendinopathy, highlighting the potential lack of either a significant inflammatory stage or discernible injury. One way around the lack of human histopathology in early tendon disease is to look at evidence from experimentally induced tendon damage.

The evidence from two different rat models [ 36 , 37 ] suggests a degenerative and not an inflammatory process. In rabbit models pathology appears to be related to experimental protocol. However, a more chronic loading programme over 11 weeks failed to show any detectable injury response [ 39 ].

The most detailed animal work on tendinopathy induced by overuse has probably been performed in horses, and on the equine superficial digital flexor tendon in particular.

Marr and co-workers describe an inflammatory reaction, but only within the first 2 weeks [ 40 ]. In an attempt to produce an animal model of tendinopathy, both collagenase and prostaglandin E1 have been injected into tendons [ 41—44 ]. Both substances produce a tendinopathy that is similar to the histopathological appearance in humans. Such models have, however, been criticized as they do not directly simulate the overuse process [ 45 ].

In summary the limited early human histology suggests no significant inflammatory role at 4 months. Animal models suggest that an inflammatory reaction is present in acute situations but that a degenerative process soon supersedes this. There is confusion within the literature. Numerous terms are used to describe the pathology of tendons, the most common of which are tendinitis implying inflammation , tendinosis a degenerative tendon condition without accompanying inflammation and tendinopathy no implication for pathology.

These terms are often used interchangeably and without precision [ 46 ]. Puddu et al. In the clinical setting, however, it may be more appropriate to refer to a symptomatic primary tendon disorder as a tendinopathy as this makes no assumption as to the underlying pathological process. Tendinitis, however, is not an appropriate term for such a condition.

Historically there have been two main theories on the causes of tendon degeneration and subsequent rupture, one a mechanical theory the other a vascular theory.

More recently a neural theory has begun to develop. In the mechanical theory it is argued that repeated loading within the normal physiological stress range of a tendon causes fatigue and eventually leads to tendon failure.

At rest a tendon has a crimped or wavelike structure. As the tendon is loaded it passes through two stretch regions. The first known as a toe stretch region is due to the stretching out of this crimped structure.

Only a small amount of force is required to straighten out the crimp [ 49 ]. If stretching is continued past the toe region then the tendon enters a linear relationship between load and strain Fig.

Here the load is directly taken up by the collagen fibrils and the stress—strain values are thus determined directly by the physiological properties of the collagen fibrils. Tendons divide into those that experience low strains and those that experience higher strains. The latter are usually loaded during locomotion and as part of their role function as significant elastic energy stores. Stress—strain relationship for progressive loading of a tendon showing three distinct regions toe, linear and partial failure prior to complete rupture.

This can eventually lead to a symptomatic tendon with altered mechanical properties as a result of repeated microtrauma [ 49 , 55—57 ]. This theory explains how chronic repetitive damage to tendons could accumulate over time and perhaps why tendinopathy would be degenerative rather than inflammatory in nature.

The increased incidence of tendinopathy with age and in the active population is consistent with this theory. However, this theory does not fully explain why certain areas of particular tendons are particularly prone to degenerative change, neither does it explain the pain sometimes associated with chronic tendinopathy.

Also it is somewhat counterintuitive that exercise well within a physiological range should actually harm that tendon. Perhaps, however, accumulated microdamage in a tendon is analogous to the same process that results in a stress fracture. A fracture, though, has the potential for a very good recovery as increased osteoblastic activity followed by osteoclastic remodelling can give an excellent result. A damaged tendon, however, is subject to fibroplasia, which will result in scar tissue formation and a weakened tendon.

Tendons are metabolically active tissues requiring a vascular supply. Compromise of this supply may cause degeneration. It is argued that certain tendons are susceptible to vascular compromise [ 58 ]; these include the supraspinatus [ 59 ], the Achilles [ 60 ] and the tibialis posterior [ 61 ].

This is the area most susceptible to both degenerative change and neovascularization. Additionally vascular compromise may be worse during exercise [ 63 ]. However, this theory remains controversial. Also why would a young athletic population be susceptible to vascular compromise?

Achilles Tendinopathy: Current Concepts about the Basic Science and Clinical Treatments

Achilles tendinopathy is one of the most frequently ankle and foot overuse injuries, which is a clinical syndrome characterized by the combination of pain, swelling, and impaired performance. The two main categories of Achilles tendinopathy are classified according to anatomical location and broadly include insertional and noninsertional tendinopathy. The etiology of Achilles tendinopathy is multifactorial including both intrinsic and extrinsic factors. Failed healing response and degenerative changes were found in the tendon. The failed healing response includes three different and continuous stages reactive tendinopathy, tendon disrepair, and degenerative tendinopathy. The histological studies have demonstrated an increased number of tenocytes and concentration of glycosaminoglycans in the ground substance, disorganization and fragmentation of the collagen, and neovascularization.

Achilles Tendon Disorders. J Am Osteopath Assoc ; 11 — Disorders of the Achilles tendon, the largest tendon in the human body, are common and occur in both active and sedentary persons. A thorough history and physical examination allow primary care physicians to make an accurate diagnosis and to initiate appropriate management. A growing body of related literature is the basis for current therapeutic regimens, which use a multimodal conservative approach, including osteopathic manipulative treatment. Although primary care physicians can manage most cases of Achilles tendon disorders, specialty care may be needed in certain instances. When appropriately managed, Achilles tendon disorders generally carry a favorable prognosis.

Achilles tendon AT ruptures are one of the most common tendon ruptures, but there have been no studies investigating these injuries in the United States US using data representative of the entire US population. The purpose of this study was to determine the incidence and risk factors for AT ruptures in the US. We hypothesized that male sex, older age, and sport participation would increase the risk for AT ruptures. Incidence was calculated for sex, race, and age. AT ruptures were characterized based on the mechanism of injury, with subanalyses performed on sport-related AT ruptures to examine sex-, race-, and age-related differences. From to , a significant increase in the incidence of AT ruptures was observed, from 1. The majority of AT ruptures occurred in male compared with female patients, with an incidence rate ratio of 3.

Achilles Tendon Disorders: Etiology and Epidemiology. Tero A.H. J7rvinen, MD, PhD a,b,c,*,. Pekka Kannus, MD, PhD a,b,d.,. Nicola Maffulli, MD, MS, PhD.

Epidemiology of Achilles tendon rupture in the US

Rees, A. Wilson, R. Primary disorders of tendons are common and constitute a high proportion of referrals to rheumatologists. Certain tendons are particularly vulnerable to degenerative pathology; these include the Achilles, patella, elements of the rotator cuff, forearm extensors, biceps brachi and tibialis posterior tendons.

The etiology of Achilles tendon rupture is multifactorial, but the injury occurs most frequently in the athletic population. The Achilles tendon is a conjoined tendon, derived from the gastrocnemius and soleus muscles, that inserts into the calcaneal tuberosity. It is the largest and strongest tendon in the human body and experiences the highest loads of any tendon in the body, with tensile loads reaching up to 10 times body weight during athletic activities. There is a hypovascular watershed area at the same level, and the result is that this point is the most common location of Achilles tendon ruptures.

Achilles Tendinopathy: Current Concepts about the Basic Science and Clinical Treatments


В обычных обстоятельствах это насторожило бы Стратмора, но ведь он прочитал электронную почту Танкадо, а там говорилось, что весь трюк и заключался в линейной мутации. Решив, что никакой опасности нет, Стратмор запустил файл, минуя фильтры программы Сквозь строй. Сьюзан едва могла говорить. - Никакой Цифровой крепости не существует, - еле слышно пробормотала она под завывание сирены и, обессилев, склонилась над своим компьютером. Танкадо использовал наживку для дурачков… и АНБ ее проглотило. Сверху раздался душераздирающий крик Стратмора.

Она не сразу поняла, что он пытается застегнуть верхнюю пуговицу ее блузки. - Сьюзан, - позвал он, задыхаясь.  - Ты должна помочь мне выбраться отсюда. Она ничего не понимала. Все это было лишено всякого смысла. - Сьюзан, ты должна мне помочь. Стратмор убил Чатрукьяна.

Во-вторых, Стратмор гораздо лучше меня знает, что происходит в шифровалке в данный момент. Почему бы тебе не позвонить. - Потому что дело именно в. Он что-то скрывает. Джабба вытаращил глаза: - Мидж, дорогая.

В данный момент мы ничего не знаем про Северную Дакоту, кроме анонимного адреса. - Возможно, это приманка, - предположила Сьюзан.


Doria M.


PDF | The Achilles tendon is the strongest tendon in the human body. Because most Achilles tendon injuries take place in sports and there has.



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