건병증 치료를 위한 통증성 원심성 트레이닝 - 80페이지 논문 정리중...

[문형철]

건병증 치료 참 어렵다. 

특히 최적의 움직임 회복을 위한 performance training까지 가려면 정말 어렵고 힘든 과정이다.

아킬레스 건, 슬개건,극상근 건의 pathology와 원심성 트레이닝에 관한 논문이다.

참 재미있고, 꼭 필요한데.. 언제나 읽어볼까나!

After 12 weeks, 89% of the patients with pain from the mid-portion were satisfied and back in previous activities. In the group with insertional Achilles tendinopathy the results were poor. 

- 12주 트레이닝 후 89%의 아킬레스 중간부위 통증 환자에서 안전한 결과를 얻음.

- 그런데 아킬레스 부착부 건병증에서는 좋지 않은 결과를 얻음. 

A new model for eccentric training was designed for patients with insertional Achilles tendinopathy. The eccentric calf muscle training was done from tip-toe to floor level (study II). With this new regimen 67% of the patients were satisfied and back in previous activities. 

- 아킬레스 건부착부 건병증환자에게 새로운 원심성 트레이닝 모델을 디자인함. 

- 원심성 종아리근육 트레이닝을 tip-toe to floor level로 시행함. 

- 이 새로운 방법으로 67%환자가 만족한 결과를 얻음. 

panic bird...

Eccentric training in the treatment of tendinopathy.pdf

Abstract

Chronic painful tendinopathies are common, not only in sports and recreationally active people, but also among people with a sedentary lifestyle. Both the lower and upper limbs are affected. There is lack of knowledge about the etiology and pathogenesis to tendinopathy, and many different treatments options have been presented. Unfortunately, most treatments have not been tested in scientific studies.

- 만성적인 통증성 건병증은 스포츠와 레저활동뿐 아니라 좌식생활을 하는 일반사람들에게서도 흔함. 

- 상지, 하지 모두 흔히 존재함. 

- 건병증의 원인과 병리에 대한 지식이 부족한 것이 현실이고, 많은 치료적 선택이 제기되고 있음. 불행하게도 대부분의 치료법은 과학적으로 검증되지 못한 것임. 

Conservative (non-surgical) treatment has since long shown unsatisfactory results and surgical treatment is known to give unpredictable results. 

- 보존치료는 만족스럽지 못하고, 수술적 치료는 예측할수 없은 결과를 낳는 것으로 알려지고 있음. 

The aim of this thesis was to eval‎uate new models of painful eccentric training for the conservative treatment of different chronic tendinopathies. After promising results in a pilot study, using painful eccentric calf muscle training in patients with chronic mid-portion Achilles tendinopathy, we investigated if these results could be reproduced in a larger group of patients with both mid-portion and insertional Achilles tendinopathy (study I). 

- 이 논문의 목적은 많은 건병증의 보존치료를 위해 통증성 원심성 트레이닝의 새로운 모델을 평가하기 위한 것임. 

- 만성 중간부위 아킬레스 건병증 환자에서 통증성 원심성 종아리근육 트레이닝을 이용하여 통증이 재발되는지 알아봄. 

After 12 weeks, 89% of the patients with pain from the mid-portion were satisfied and back in previous activities. In the group with insertional Achilles tendinopathy the results were poor. 

- 12주 트레이닝 후 89%의 아킬레스 중간부위 통증 환자에서 안전한 결과를 얻음.

- 그런데 아킬레스 부착부 건병증에서는 좋지 않은 결과를 얻음. 

A new model for eccentric training was designed for patients with insertional Achilles tendinopathy. The eccentric calf muscle training was done from tip-toe to floor level (study II). With this new regimen 67% of the patients were satisfied and back in previous activities. 

- 아킬레스 건부착부 건병증환자에게 새로운 원심성 트레이닝 모델을 디자인함. 

- 원심성 종아리근육 트레이닝을 tip-toe to floor level로 시행함. 

- 이 새로운 방법으로 67%환자가 만족한 결과를 얻음. 

The next step was to investigate the effects of painful eccentric quadriceps training on patients with jumper´s knee/patellar tendinopathy (study III). 

- 다음 스텝은 슬개건 병증환자에게 통증성 원심성 대퇴사두근 트레이닝을 시행함. 

Two different training protocols were used. Eccentric training performed on a 250 decline board showed promising results with reduced pain and a return to previous activities, while eccentric training without the decline board had poor results. In a following prospective study, patients with jumper´s knee/patellar tendinopathy were randomised to either concentric or eccentric painful quadriceps training on a 250 decline board (study IV). After 12 weeks of training, there were significantly better results in the group that did eccentric training. 

In a pilot study (study V), we investigated painful eccentric deltoideus and supraspinatus muscle training on a small group of patients on the waiting list for surgical treatment of subacromial impingement syndrome. After 12 weeks of training, 5 out of 9 patients were satisfied with the results of treatment and withdrew from the waiting list for surgery. 

In conclusion, the present studies showed good clinical results with low risks of side effects and low costs. Thus, we suggest that painful eccentric training should be tried in patients with Achilles and patellar tendinopathy before intratendinous injections and surgery are considered. For patients with chronic painful impingement syndrome, the results of our small pilot study are interesting, and stimulates to randomised studies on larger materials.

Introduction/Background

Treatment of patients with chronic painful tendinopathies constitutes a

clinical challenge. Tendinopathy not only affects athletes and recreationally

active people, but also people with sedentary lifestyles. Tendon disorders are

common, and both lower and upper limbs are affected. Traditionally, it has

been suggested that the condition is inflammatory. Hence, treatment with

rest and immobilisation has been recommended in conjunction with

nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroid

injections (Andres, et al. 2008). However, research has shown that there is

an absence of a prostaglandin E2-mediated inflammation (PGE2) within the

tendon in chronic painful tendinopathies (Alfredson, et al. 1999;Alfredson, et

al. 2001;Alfredson, et al. 2003a). For a long time, conservative (nonsurgical)

treatment has been associated with relatively poor clinical results,

and surgical treatment has been associated with unpredictable results

(Maffulli, et al. 1999). In a long-term follow-up study, 53% of patients with

patellar tendinopathy had ended their sports career due to this painful

condition (Kettunen, et al. 2002). About 25–33% of athletes with lower

extremity tendinopathy demonstrated poor results following conservative

therapy, and required surgical treatment (Kvist 1994;Cook, et al. 1997). In

patients requiring surgery, only 46–64% recover sufficiently to return to

sports activities after a rehabilitation period of 6–12 months (Cook, et al.

1997;Coleman, et al. 2000;Chiara Vulpiani, et al. 2003). Many different

treatment options have been presented. Unfortunately, the majority of these

treatment modalities are not scientifically based, but instead empirically.

The aim of this thesis was to eval‎uate new models of painful eccentric

training for the conservative treatment of different chronic tendinopathies. 

The normal tendon Anatomy

Tendons are interposed between muscles and bones, and transmit the force

created in the muscle to the bone which, in turn, enables joint movement.

Basically, each muscle contains two tendons, one proximal and one distal.

The point where the tendon connects to a muscle is referred to as the

myotendinous junction (MTJ), and the point where it connects to bone is

referred to as the osteotendinous junction (OTJ) (Ippolito, et al.

1986;Kannus 2000). The place where a muscle’s proximal tendon attaches to

bone is referred to as the muscle origin, and the distal tendon attachment is

referred to as an insertion. Healthy tendons are brilliant white in colour and

fibroelastic in texture, and show great resistance to mechanical loads

(Kannus 2000).

The tendon is covered by the epitenon, a fine, loose connective tissue sheath

containing blood vessels, lymphatics, and nerves. The epitenon extends

deeper into the tendon between the tertiary bundles and the endotenon.

More superficially, the epitenon is surrounded by the paratenon, a loose

areolar connective tissue consisting essentially of type I and type lll collagen

fibrils (Kvist, et al. 1985). 

 Collagen fibre orientation

It is well documented that the collagen fibrils are oriented not only longitudinally, but also transversely and horisontally; the longitudinal fibrils also cross each other, thus forming spirals and plaits (Chansky, et al. 1991;Jozsa, et al. 1991) (Fig. 1). 

 This complex ultra-structure of the tendons provides good buffer capacity

against longitudinal, transversal, horisontal, as well as rotational forces

during movement and activity. There is great tendon-to-tendon variation,

and within a tendon site-to-site variation, as regards collagen content and

type distribution (Fan, et al. 1997).

Internal architecture

 The basic elements of a tendon are collagen bundles, cells, and ground

substance (a viscous substance rich in proteoglycans and

glycosaminoglycans-GAGs). Collagen provides the tendon with tensile

strength, whereas ground substance provides structural support for the

collagen fibres and regulates the extracellular assembly of procollagen into

mature collagen (Astrom 1997). These elements are produced by tenoblasts

and tenocytes, which are the elongated fibroblasts and fibrocytes that lie

between the collagen fibres (Hess, et al. 1989).

Collagen is hierarchically arranged in levels of increasing complexity,

beginning with tropocollagen (a triple-helix, polypeptide chain). Soluble

tropocollagen molecules form cross-links to create insoluble collagen

molecules, which then aggregate progressively into microfibrils and then into

electron microscopically clearly visible units, i.e. the collagen fibrils (Kannus

2000). A bunch of collagen fibrils forms a collagen fibre, which is the basic  unit of a tendon. Then fibres (primary bundles), fascicles (secondary

bundles), and tertiary bundles finally form the tendon itself (Jozsa, et al.

1997;Astrom 1997) (Fig. 2).

 General innervation

Inside a tendon, the nerves, which are relatively few in numbers, follow the vascular channels that run along the axis of the tendon, and anastomose with each other via obliquely and transversally oriented nerve endings. Most of the nerve fibres are sensory nerve endings on the surface of the tendon (Jozsa, et al. 1997).

Based on anatomical and functional differences, nerve endings in tendons, ligaments, and joint capsules can be classified into four categories: type l Ruffini corpuscles (pressure receptors that are sensitive to stretch); type ll Vater-Pacini corpuscles (activated by movement); type lll Golgi tendon organs (mechanoreceptors); and type lV receptors (free nerve endings functioning as pain receptors) (Jozsa, et al. 1993). 

General biomechanical forces in tendons

Tendons have a great capacity to withstand tensile and stretching forces, but are less tolerant to shearing and compressive forces transmitted by the muscles (Hess, et al. 1989). The stress-strain curve facilitates the understanding of the behaviour of the tendon during tensile load (Fig. 3).

 At rest, the tendon has a crimped or wavelike structure. When the tendon is

stretched, the tendon progresses through three regions (toe, linear and

partial failure). The first region is referred to as the toe region, and as the

tendon is progressively loaded the fibres begin to straighten until reaching a

2% strain. This is the first part of the stress-strain curve, occurring due to the

elastic properties of collagen. Beyond this point, tendons deform in a linear

fashion (linear region) as a result of intramolecular sliding of collagen triple

helices, and fibres become more parallel (O'Brien 1992). If strain does not

exceed 4%, the tendon will return to its original length when unloaded

(Loitz, et al. 1989). Microscopic failure of fibres occurs when the strain

exceeds 4–8%. However, recently, strain values of up to 6–8% was said to be

physiological (Magnusson, et al. 2003). The last region of the curve

illustrates macroscopic tensile and partial failure of collagen fibres. This

results in a complete tendon rupture when the strain has reached 8–10% of  its original length (O'Brien 1992). A healthy tendon is strong, its tensile strength being related to thickness and collagen content. A tendon with an area of 1 cm2  is capable of resisting a weight of 500–1,000 kg (Jozsa, et al.1997).

Metabolism

 It is well established that tendon cells are metabolically active, both in

energy production and in the biosynthesis of collagen and matrix

components. Energy is derived mainly from three different sources: the

Krebs cycle, the anaerobic glycolysis, and the pentose phosphate shunt. Over

a life span, the metabolic pathway changes towards anaerobic glycolysis

(Hess, et al. 1989;Kannus, et al. 1991;O'Brien 1997). Tendons have

approximately eight times lower oxygen consumption than skeletal muscle.

The low oxygen consumption makes it possible for a tendon to carry loads

and remain tensioned without risk of ischemia and injury.

One negative aspect of the low metabolic rate in tendons is the slow recovery

after activity, and healing after injury (Williams 1986).

Disuse/immobilisation

 Few studies have investigated the effects of immobilisation on collagen

synthesis rate in humans. One study showed decreased collagen synthesis in

the patellar tendon after 10–21 days of immobilisation. However, there were

no changes in the tendon cross-sectional area (CSA) (de Boer, et al. 2007). In

a study on Achilles tendons, no difference in Achilles CSA was found

following two weeks of immobilisation. The conclusion drawn was that the

Achilles tendon seems to be more resistant to short-term immobilisation

than muscle tissue (Christensen, et al. 2008). Animal studies have shown

decreased stiffness, GAGs and water content after immobilisation (Woo, et

al. 1982;Barnard, et al. 1987;Loitz, et al. 1989;Karpakka, et al. 1990).

Exercise/remobilisation

 Compared to muscle tissue, the metabolic turnover in tendon tissue is slower

due to poor circulation (Kannus, et al. 1997a). However, a study by Langberg

et al. found that exercise increased the formation of collagen type I in the

peritendinous tissue (Langberg, et al. 1999). The same research group later

demonstrated increased collagen turnover (both synthesis and degradation)

after four weeks of training (Langberg, et al. 2001), and they also presented a

study with increased collagen synthesis rate after 12 weeks of eccentric

training (Langberg, et al. 2007). Increasing age and disuse leads to a

decrease in tendon stiffness, which in turn can be mitigated by resistance  exercise (Magnusson, et al. 2008). Physical activity seems to improve the

tensile mechanical properties of tendons, in contrast to disuse. Effects like

increased GAGs content, and better alignment of collagen fibres have been

shown in animal studies (Woo, et al. 1982;Kellett 1986;Barnard, et al.

1987;Loitz, et al. 1989;Karpakka, et al. 1990).

The Achilles tendon

Anatomy

The triceps surae has two muscle bellies, the gastrocnemius and the soleus muscles. These are the strongest muscles of the calf, and they merge to form the Achilles tendon (O'Brien 1984) (Fig. 4). The Achilles tendon is the thickest and strongest tendon of the human body (O'Brien 1992). According to O'Brien, the CSA of the tendon is 0.8–1.4 cm2. The gastrocnemius tendon begins as a broad aponeurosis at the distal margin of the muscle bellies, whereas the soleus tendon begins as a band proximal to the posterior surface of the soleus muscle (O'Brien 1992). The tendon becomes narrower and more rounded distally. The tendon length of the gastrocnemius tendon is 11–26 cm, and the length of the soleus tendon portion is 3–11 cm. As the tendon descends, it may spiral up to 900 laterally, so that fibres that were originally posterior become lateral, lateral fibres become anterior, anterior fibres become medial, and medial fibres become posterior at the distal end (Jozsa, et al. 1997). In this way, elongation and elastic recoil within the tendon is possible, and stored energy can be released during locomotion (Alexander 1977). Another important factor of the rotation is that a region of concentrated stress may be produced where the two tendons meet. This is most prominent at 2–5 cm proximal to the calcaneus insertion, and corresponds well with the region of the tendon that according to some authors has the poorest vascular supply (Curwin 1984;Reynolds, et al. 1991).

 The myotendinous junction (MTJ)

The MTJ is a specialised anatomic region in the muscle-tendon unit. Morphological studies have shown that at the MTJ, the collagen fibrils insert into the deep recesses that are formed between the finger-like processes of the muscle cells (Kvist, et al. 1991) (Fig. 5). This structure and composition increase the contact area between muscle fibres and tendon collagen fibres 10- to 20-fold (Tidball 1991). Although the MTJ can sustain high forces, it still remains the weakest structure of the muscle-tendon unit (Garrett 1990;Jarvinen 1991).

 The osteotendinous junction (OTJ)

The OTJ consists of tendon, fibrocartilage, and bone (Milz, et al. 2002). The insertion of tendons into bone involves a gradual transition from tendon to fibrocartilage, to lamellar bone. The tissue changes from soft to hard. The tendon attachment to bone consists of four zones: pure fibrous tissue, unmineralised fibrocartilage, mineralised fibrocartilage and bone (Astrom, et al. 1995).

 The enthesis organ concept was presented by Benjamin and McGonagle, who

defined the enthesis organ as a collection of related tissues at and near the

enthesis, which serve a common function of stress dissipation (Benjamin, et

al. 2001). It is widely applicable at different entheses and is most clearly

recognised where the Achilles tendon attaches to the calcaneus. Immediately

above the Achilles insertion on the posterior surface of the calcaneus, in the

space between the tendon and bone, the retrocalcaneal bursa is located.

There is also a subcutaneous calcaneal bursa, between the skin and tendon.

The bursae both decrease the friction and compression on the tendon (Rufai,

et al. 1995). The concept of an enthesis organ is of particular significance for

clinicians, as it can help explain the injury pattern and why symptoms

associated with a particular enthesopathy are diffuse (Benjamin, et al. 2006).

Tendon structure

 Unlike other tendons around the ankle (tendons with a synovial sheath), the

Achilles tendon is enveloped by a paratenon, which is a membrane that

consists of two layers: a deeper layer surrounding, and in direct contact with,

the epitenon, and a superficial layer, the peritenon (Kvist, et al. 1980).

There are specific variations in proteoglycan content within the Achilles

tendon. At the insertion site there is an increased amount of aggrecan, which

protects the enthesis from compressive and shearing forces. In the midportion

of the Achilles tendon there is more versican, which provides the

tendon with tensile strength (Waggett, et al. 1998).

Circulation

 The blood supply to the Achilles tendon comes mainly from the muscle and

is usually divided into three regions: the musculotendinous junction, the

length of the tendon, and the tendon bone junction. The blood vessels

originate in vessels in the perimysium and periosteum, and run via the

paratenon and mesotenon. The main blood supply to the middle portion of

the tendon takes place through the paratenon (O'Brien 1997).

Innervation

 The nerve supply to the Achilles tendon originates mainly from the sural

nerve, via nerve fascicles that occur subcutaneously. The innervation within

the Achilles tendon has been sparsely studied. However, recently, Bjur et al.

defined the innervation pattern, and showed a general (PGP9.5), a sensory

(SP/CGRP), and an autonomic nervous system in the Achilles tendon (Bjur,

et al. 2005).

Biomechanics

It is difficult to determine the tendon tensile forces in vivo (Komi, et al.

1992;O'Brien 1992). Komi and co-workers used buckle transducers in the

tendon, and studied a wide range of activities such as walking, running,

jumping, and bicycling (Komi, et al. 1987;Komi 1990). The peak Achilles

tendon force during running at 6 m/sec was estimated to 9 kilo newton (kN),

corresponding to 12.5 times the bodyweight, (11.0 kN/cm2). Other studies

show that an athlete can generate forces in the Achilles tendon during

jumping and running activity of 6–14 times the bodyweight (Kader, et al.

2002;Paavola, et al. 2002).

Achilles tendinopathy

Definitions

The terminology relating to the chronic painful conditions in the Achilles

tendon is somewhat confusing. Different terms have been used in the past to

describe the conditions. Terms such as Achilles tendinitis and

tendonitis have been widely used, assuming that there is an inflammation

within the tendon. However, histopathological, biochemical, and molecular

studies have shown an absence of a true prostaglandin-mediated

inflammatory process inside the chronic painful tendon (Kannus, et al.

1991;Astrom, et al. 1995;Alfredson, et al. 1999;Alfredson, et al. 2003a).

Puddu et al. proposed the term tendinosis as a histological description of

degenerative pathology with an absence of inflammatory changes (Puddu, et

al. 1976). The term achillodynia has been used by Astrom, as a

symptomatic diagnosis (Astrom 1997). The authors recommend that the

terms tendinosis (tendon degeneration) and peritendinitis are reserved

for conditions where the pathology has been verified by surgical exploration,

imaging, histological analysis of biopsies, or a combination (Astrom 1997).

Maffulli et al. suggest that the combination of tendon pain, swelling, and

impaired performance should be clinically labelled as tendinopathy

(Maffulli, et al. 1998). This has been widely supported in the last decade

(Khan, et al. 2002). The terms insertional and non insertional Achilles

tendinopathy were proposed by Clain et al. (Clain, et al. 1992). Today,

tendinopathy is used to describe a condition with tendon pain, swelling,

and impaired function, and tendinosis is used when the pathology is

objectively verified by ultrasound (US), magnetic resonance imaging (MRI)

or examination of biopsies.

Achilles tendon injuries can be acute or chronic. The term chronic is widely

used when symptoms persist for longer than three months.

 Epidemiology

Tendinopathy is often seen in individuals in the age group of 30–60 years

(Kvist 1991a). They may participate in middle- or long-distance running,

badminton, or track and field activities (Kvist 1991b;Fahlstrom, et al. 2002).

However, inactive individuals can also suffer from mid-portion Achilles

tendinopathy (Kvist 1991a, 1994). In elite runners, the incidence of

tendinopathy has been reported to be 7–9% (Lysholm, et al. 1987). Kvist

showed that 66% of 698 competitive and recreationally active patients

suffered from Achilles tendinopathy (Kvist 1991b). In badminton players,

Achilles tendinopathy accounts for 10.5% of all overuse injuries (Jorgensen,

et al. 1990).

The incidence of insertional Achilles tendinopathy has not been well

established. In a surgical and histopathological survey of 163 patients with

chronic Achilles tendinopathy, the preval‎ence of insertional tendinopathy

was 20% (Astrom, et al. 1995). Insertional tendinopathy is often diagnosed

in older, non-active, and overweight individuals (Meyerson 1999).

 Aetiology

The aetiology to Achilles tendinopathy is still unclear. Many different

theories have been presented (Kvist 1991b;Astrom 1997). The aetiology is

believed to be multifactorial, involving intrinsic and extrinsic risk factors. In

acute tendon injuries, extrinsic risk factors are predominating, and in

chronic Achilles tendinopathy a combination of intrinsic and extrinsic

factors is often seen (Kannus, et al. 1997b;Khan, et al. 1998). It should be

stressed that scientific evidence of the role of intrinsic and extrinsic factors is

still lacking.

Intrinsic risk factors

Age is related to the development of tendinopathy in the Achilles tendon,

and an old tendon is more vulnerable than a young one (Kannus, et al.

1991;Kvist 1991a).

Anatomical factors like leg-length discrepancy and malalignment (genu

valgum, forefoot varus), have by some authors been suggested as causative in

the development of Achilles tendinopathy (Kvist 1991b, 1994). However, this

is controversial and has been questioned by other authors (Kannus, et al.

1997b). 

 Decreased joint flexibility of the ankle will increase ground reaction

force during landing. This finding has been linked to Achilles tendinopathy

(Kaufman, et al. 1999).

 Muscle weakness/imbalance of the gastrocnemius muscles could

disturb and change the coordinated movements of the kinetic chain through

the hip, knee, and ankle. This is a common finding in tendinopathy.

However, it is unclear whether this is the cause to, or a result of,

tendinopathy (Kountouris, et al. 2007).

 High bodyweight and adipose tissue levels seem to be associated with

tendinopathies in the lower limb (Gaida, et al. 2008).

 Gender. Some studies on women indicate that oestrogen protects from

tendinopathy (Cook, et al. 2007).

 Genetics. There are reports shoving a correlation between the incidence of

Achilles tendinopathy and blood group 0 (Jozsa, et al. 1989). Furthermore,

an association between the alpha 1 type V collagen (COL5A1) and Achilles

tendinopathy has been found (Collins 2003).

 Systemic diseases like Marfan’s and Ehlers-Danlos Syndrome, and

rheumatoid arthritis are well known to be associated with defects of the

collagen metabolism, causing weakness of the tendons (Jozsa, et al. 1997).

Extrinsic risk factors

 Training errors have been reported to be common among runners that

have Achilles tendinopathy (Kvist 1994). Training errors were identified as

primary aetiological factors in over 75% of the cases (Clement, et al. 1984).

 Poor technique,  improper footwear, and running on hard,

 slippery or uneven surfaces could be predisposing risk factors for

Achilles tendinopathy (James, et al. 1978).

 Overuse is believed to be the major cause to tendinopathy (Jozsa, et al.

1997). “Too much too soon” was stated by Brody (Brody 1987). However, it is

not clear if overuse is solely responsible. In a study of 58 patients with

Achilles tendinopathy, 31% were not active in sports or vigorous physical

activity (Rolf, et al. 1997). Around 50% of patients presenting with midportion

Achilles tendinosis at the Sports Medicine Unit in Umea, Sweden are

not active in any sports or recreational activity (Alfredson, personal

communication 2009). 

 Underuse. As with tendinopathy in general, overuse and poor training

habits are suggested to be the main aetiological causes of insertional Achilles

tendinopathy (Benjamin, et al. 2000). However, a new idea concerning the

aetiology of insertional Achilles tendinopathy has been presented

(Almekinders, et al. 2003;Maganaris, et al. 2004). When there is a lack of

tensile load on the ventral side of the Achilles tendon, there is a tendency to

develop cartilage-like or atrophic changes on the stress-shielded side of the

enthesis (Benjamin, et al. 1986;Rufai, et al. 1995). This may lead to disturbed

remodelling and primary degenerative lesions in that area. Since

tendinopathy is not always related to high loading activity, but is also agerelated,

the suggestion is that insertional tendinopathy results from

underuse and stress-shielding, rather than overuse.

Pathogenesis

The pathogenesis in the chronic painful Achilles tendon is unknown,

although several theories have been presented. Three theories dominate the

discussion. The primary inflammatory theory, where inflammation leads to a

degeneration, with at least six different states of collagen degeneration

(hypoxic, mucoid, hyaline, fibrocartilaginous metaplasia, tendon

calcification, and lipoid). Collagen degeneration is suggested to be

irreversible, and is seen as an end-stage of the pathology (Jozsa, et al. 1997).

The mechanical theory claiming that repeated load-bearing within the

normal physiological stress range of a tendon causes fatigue, and eventually

leads to tendon failure. Repeated and/or prolonged stress at higher levels of

strain could also lead to microscopic degeneration within the tendon. Later

the mechanical properties of the tendon can be altered and lead to a

symptomatic tendon due to micro trauma. Some authors have suggested that

the pathology is a state of failed healing, where the injured tendon is in a

healing phase, including active cells, increased protein production,

disorganisation of matrix, and neovascularisation (Clancy 1989;Khan, et al.

2002). The vascular theory, suggesting that as tendons are more

metabolically active than previously believed and require a vascular supply,

the compromise of such a vascular supply may cause degeneration. Some

tendons like the Achilles tendon and the supraspinatus tendon are at higher

risk than others. It has been suggested that there is a hypovascular region in

the mid-portion of the Achilles tendon 2–6 cm proximal to the calcaneal

insertion (Carr, et al. 1989), which makes this part of the tendon more prone

to injuries. This theory has been questioned by Astrom and Westlin, who

showed a uniform blood flow in the Achilles tendon, except at the insertion

where the flow was lower (Astrom, et al. 1994). A recently published study

supports the theory of a hypovascular weak area in the mid-portion (Chen, et

al. 2009) 

 Histology

Histological eval‎uation of the pathological Achilles tendon has demonstrated

that there is no evidence of an ongoing PGE2 mediated inflammatory

process inside the tendon. However, there could be a neurogenic

inflammation (Hart, et al. 1998;Alfredson, et al. 1999;Alfredson, et al.

2003a). The histological findings in tendinopathy show four distinct

structural changes within the tendon: increased cellularity, increased

production of ground substance, (especially GAGs), separation of collagen

bundles, and neovascularisation (Jozsa, et al. 1990). There are certain

differences in the morphology of mid-portion Achilles tendinopathy and

insertional Achilles tendinopathy. In the Achilles insertion there are several

structures, e.g. the superficial and retrocalcaneal bursa, Kager’s fat pad, and

sometimes a prominent upper calcaneus Haglund’s deformity, that all alone

or in combination could give rise to symptoms in this area. The

retrocalcaneal bursa and Kager´s fatpad has an important function to

promote free movement between tendon and bone. It is not uncommon with

an inflammation in the retrocalcaneal bursa due to increased compression

between tendon and bone (Canoso, et al. 1988;Theobald, et al. 2006).

According to Shaw et al., the bursa contains sensory nerve endings, and may

have a proprioceptive function in monitoring insertional angle changes

between bone and tendon during foot movements (Shaw, et al. 2007).

 Pain mechanisms

New methods like intratendinous microdialysis and molecular biology

techniques have shown that there is no inflammation inside the chronic

painful Achilles tendon (Alfredson, et al. 2001;Alfredson, et al. 2003a).

These new techniques together with ultrasound (US) in combination with

colour Doppler (CD), and immunohistochemical analyses of tendon tissue

biopsies, have facilitated a better understanding of the pain mechanisms. By

using US with CD, Ohberg et al. showed that neovascularisation is present in

pathological and symptomatic, but not in normal pain-free Achilles tendons

(Ohberg, et al. 2004a). Neovascularisation and accompanying nerves might

be important factors related to the pain mechanisms of tendinopathies

(Alfredson, et al. 2003b). It is worth noting that not all tendons with

neovascularisation are painful (Zanetti, et al. 2003). Bjur et al. found nerves

linked to the vascular structures in tendinosis tendons (Bjur, et al. 2005).

Furthermore, the neurokinin-1-receptor, associated with the neuropeptide

substance P (SP), has been found in the vascular wall (Forsgren, et al. 2005).

Follow-up studies of patients with Achilles tendinopathy who have become

pain-free after treatment with eccentric training have shown an absence of

neovessels (Ohberg, et al. 2004b). 

 Clinical symptoms

Patients with chronic Achilles tendinopathy most commonly have a history

of a gradual onset of tendon pain, often related to a change in activity level.

However, as stated previously, non-active individuals may also suffer from

Achilles tendinopathy. Initially, the patients often experience stiffness, pain

or discomfort at the beginning of activity, followed by less pain during

activity, and a return of the stiffness and pain afterwards (Rogers 1996).

Later on, pain increases during activity, and patients have to stop the

activity. The patients often complain about stiffness in the morning, and

together with pain during activity, this is a characteristic of chronic Achilles

tendinopathy. It is suggested that the amount of morning pain and stiffness a

patient suffers serves as a good indicator of the tendon condition, the more

symptoms, the poorer stage of the tendon condition (Cook, et al. 2002).

 Clinical examination

Examination should include the biomechanics of the lower extremity, i.e. leg,

ankle, and foot, during loading activity. Range of motion in the ankle joint

should also be noted. Inspection and palpation of the surrounding structures

must be included in a clinical examination, and tenderness and thickening of

the tendon should be noted. The examiner should be gentle during palpation

of the tendon, as there may be some pain during palpation even if there is no

injury (Cook, et al. 2001).

 Differential diagnoses

It is important to exclude total or partial ruptures (Maffulli, et al. 1998). If

plantar flexion tonus is poor or nonexistent, a rupture should be suspected.

Tonus of the muscle-tendon unit should be examined with the patient under

resting conditions in prone position. Partial ruptures are difficult to diagnose

clinically, and therefore the patient’s history is important in these cases.

Tenosynovitis of the medial flexor tendons, and dislocation of the lateral

peroneal tendons, also needs to be excluded. Other possible differential

diagnoses are os trigonum syndrome, tumours of the Achilles tendon

(xanthomas), neuroma of the sural nerve, and an accessory soleus muscle

(Cook, et al. 2002;Alfredson 2005;Alfredson, et al. 2007). Muscle strains in

the MTJ are not uncommon (Kvist 1991a). Partial muscle ruptures are most

common in the medial muscle belly, commonly referred to as tennis leg

(Millar 1979). At the insertion of the Achilles tendon, an inflamed superficial

and/or retrocalcaneal bursae could be co-existing as well as a Haglund

deformity of the upper calcaneus (Vega 1984). 

Treatment

The purpose of the treatment of patients suffering from Achilles

tendinopathy is to decrease pain and improve physical activity, thereby

making it possible for the patient to continue to participate in physical

activities. During the last decade, several different treatment options have

been presented. Unfortunately, many of these treatments lack scientific

evidence.

 Rest are often recommended, however rest is detrimental to the tendon

causing weakness and impaired tendon properties (Kannus, et al. 1997a)

 NSAIDs have not been shown to be efficient in the treatment of Achilles

tendinopathy (Astrom 1992). Interestingly, a study showed that NSAIDs

blocked protein synthesis in skeletal muscles after exercise (Trappe, et al.

2002).

 Corticosteriod injections have shown promising short-term pain relief

results, but poor long-term results (Kleinman, et al. 1983;Jones 1985;Gill, et

al. 2004). Also, there are reports of tendon ruptures following corticosteroid

injections (Kleinman, et al. 1983;Jones 1985).

 Extracorporeal shockwave therapy (ESWT). In patients with midportion

Achilles tendinopathy, Costa et al. did not find clinical improvement

after ESWT treatment (Costa, et al. 2005). These results were supported by

Rasmussen et al., who for some reason suggested that treatment with ESWT

anyhow should be used as a supplementary treatment (Rasmussen, et al.

2008). Rompe et al. demonstrated more pain reduction with ESWT

compared to the wait-and-see approach (Rompe, et al. 2007), but no benefit

compared to eccentric exercises (traditional method used by Alfredson et al)

(Alfredson, et al. 1998). The same authors compared eccentric exercise (as

above) with ESWT in patients with insertional Achilles tendinopathy, and

eccentric exercise showed inferior results compared to the group receiving

ESWT (Rompe, et al. 2008).

 Low-level laser treatment in patients with mid-portion Achilles

tendinopathy have shown better results in combination with eccentric

exercises than alone (Stergioulas, et al. 2008).

 Ultrasound is used to treat Achilles tendon pain, but there is no evidence of

beneficial effects in controlled trials (Robertson, et al. 2001). 

 Heel pads were eval‎uated by Lowdon et al. who found them ineffective.

This study did not separate insertional tendinopathy from mid-portion

tendinopathy, and the heel-pads were not custom-fit (Lowdon, et al. 1984).

 Topical glyceryl trinitrate patches treatment showed promising results

in a randomised double-blind study on patients with mid-portion Achilles

tendinopathy. One negative side effect was that 53% of patients reported

severe headaches during the treatment period (Paoloni, et al. 2004).

 Strength training. It appears that exercise is a positive stimulus to the

collagen alignment (Kannus, et al. 1997a). Eccentric contraction seems to be

more beneficial than concentric activation (Mafi, et al. 2001). In the mid

1980s, Curwin and Stanish presented the first eccentric exercise

intervention program for tendinopathy, using a program with progressively

increased moderate eccentric load, and changes in speed, where the patient’s

symptoms controlled the progression of load (Curwin 1984). The exercises

were performed without tendon pain. More than a decade later, in a pilot

study, Alfredson et al. used painful eccentric heel drops on a step as

treatment for patients with mid-portion Achilles tendinopathy (Alfredson, et

al. 1998). This study reported excellent results with a significant decrease in

pain and a return to previous activity level after 12 weeks of training. There

were some main differences between Curwin’s and Alfredson’s protocols

(Curwin 1984;Alfredson, et al. 1998). Alfredson used painful training,

heavier loads, and single leg exercises. The Alfredson protocol has been

widely used, and the good clinical results have been reproduced by other

groups (Roos, et al. 2004;de Vos, et al. 2007;Rompe, et al. 2007).

 Sclerosing injections of polidocanol outside of the tendon, where the

neovessels enter the tendon, have shown promising clinical results, including

decreased pain and improved physical activity (Alfredson, et al. 2005b).

 Traditional surgical treatment has consisted of a longitudinal tendon

incision and excision of abnormal tendon tissue, followed by a period of

immobilisation. A critical review by Tallon et al. on the outcome of surgery

for chronic Achilles tendinopathy, found successful results in 70% of the

cases. However, clinical results were better in studies with a poor scientific

design, and less good in studies with a good scientific design (Tallon, et al.

2001). In the past, patients suffering from pain in the insertion of the

Achilles tendon have generally been treated with surgery when conservative

(non-operative) treatment has failed. However, the clinical outcome

following surgery has shown great variations (35–59%) as regards the return

to unlimited activity (Maffulli, et al. 1999;McGarvey, et al. 2002). 

[professional Lee]

조직의 힐링이 먼저고 이 힐링이 원래 조직으로 재생되지 못하고 여러 다른 조직들 예를 들어 건조직에 섬유화가 되거나 지방이 끼거나 반흔조직이 생기거나 하면 원래의 장력이 생성되지 못하고 지속적으로 괴롭히는 것 같습니다. 우리들은 건이 회복되는데 오래 걸리는 줄 아는데 일반인들은 몇개월이면 끝난다고 생각하기도 하고요 그러다보니 적절한 스트레스가 가해지는 것이 아니라 오버스트레스가 가해지다보니 지속적으로 손상부위가 회복이 안되는 악순환 그러다 보니 통증 그러나 보니 근약화 정말 요세는 줄기세포 치료제를 만들어서 금방 회복되면 좋겠다는 생각이 많이 듭니다.

[문형철]

근육은 수축성 구조이고, 건은 장력을 인지하는 구조입니다. 줄기세포치료를 해도 해결되지 않을 것입니다. 건의 장력에 문제를 일으키는 근육, 근막, abnormal movement pattern을 해결해주지 못하면 호전되지 않기 때문입니다.