The Journal of Bone & Joint Surgery

The Journal of Bone & Joint Surgery, Volume 84, Issue 11

Current Concepts Review | November 01, 2002

Achilles Tendinopathy

Mika Paavola, MD, PhD; Pekka Kannus, MD, PhD; Tero A.H. Järvinen, MD, PhD; Karim Khan, MD, PhD; Lászlo Józsa, MD, PhD; Markku Järvinen, MD, PhD

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Investigation performed at Tampere University Hospital and Medical School, University of Tampere, Tampere, Finland; Urho Kaleva Kekkonen Institute, Tampere, Finland; the University of British Columbia, Vancouver, British Columbia, Canada; and the National Institute of Traumatology, Budapest, Hungary

Mika Paavola, MD, PhD
Tero A.H. Järvinen, MD, PhD
Markku Järvinen, MD, PhD
Department of Surgery, Tampere University Hospital, P.O. Box 2000, FIN-33521, Tampere, Finland. E-mail address for M. Paavola: csmipa@uta.fi. E-mail address for T.A.H. Järvinen: blteja@uta.fi. E-mail address for M. Järvinen: llmaja@uta.fi

Pekka Kannus, MD, PhD
Accident and Trauma Research Center and the Tampere Research Center of Sports Medicine, Urho Kaleva Kekkonen Institute, Kaupinpuistonkatu 7, PL 30, 33501 Tampere, Finland. E-mail address: klpeka@uta.fi

Karim Khan, MD, PhD
Department of Family Practice (Sports Medicine) and School of Human Kinetics, University of British Columbia, 210 War Memorial Gym, 6081 University Boulevard, Vancouver, BC V6T 1Z1, Canada. E-mail address: kkhan@interchange.ubc.ca

Lászlo Józsa, MD, PhD
Department of Morphology, National Institute of Traumatology, P.O. Box 21, H-1430 Budapest, Hungary

In support of their research or preparation of this manuscript, one or more of the authors received grants or outside funding from the Sigrid Juselius Foundation, Helsinki, Finland; Tampere University Hospital Research Fund; and the Research Council for Physical Education and Sports Ministry of Education, Finland. None of the authors received payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, educational institution, or other charitable or nonprofit organization with which the authors are affiliated or associated.

J Bone Joint Surg Am, 2002 Nov 01;84(11):2062-2076

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Extract

• The combination of Achilles tendon pain, swelling, and impaired performance indicates the clinical diagnosis of Achilles tendinopathy.

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Introduction

• The combination of Achilles tendon pain, swelling, and impaired performance indicates the clinical diagnosis of Achilles tendinopathy.

• The chronic form of Achilles tendinopathy is not an inflammatory condition.

• In its early phases, Achilles tendinopathy often responds favorably to conservative treatment with rest or modified activity, cold, stretching, nonsteroidal anti-inflammatory medications, and correction of provoking factors.

• Surgery is considered an acceptable choice among patients who have failed to respond to conservative treatment.

• Operative management includes longitudinal division of the crural fascia, excision of the macroscopic adhesions, and excision of any intratendinous lesion that is identified on preoperative imaging examinations or intraoperatively.

Achilles tendon problems are very common among athletes as well as the general population ^1,2 . The terminology used to describe the painful condition of the Achilles tendon is superfluous, confusing, and most often does not reflect the underlying abnormality. Terms such as Achilles tendinitis and tendonitis have been widely used, even though inflammatory cell infiltration in the tendon is not seen in biopsy specimens from patients with chronic Achilles tendon problems and the biochemical mediators of inflammation, such as prostaglandin E2, are not found to be more abundant in patients with chronic Achilles tendon pain than in normal controls ^1,3-7 . In this context, it should be noted, however, that the absence of inflammatory cell infiltration in the chronic state does not exclude a prior inflammatory condition.

Additional terms such as Achilles tendinopathy, tenopathy, tendinosis, partial rupture, paratenonitis, tenosynovitis, tendovaginitis, peritendinitis, and achillodynia have been used to describe the problems of noninsertional pain associated with this tendon. Åström used the term achillodynia as a symptomatic diagnosis and recommended that tendinosis (tendon degeneration) and peritendinitis be reserved for patients in whom the pathological condition has been verified by surgical exploration, radiographic imaging, histological analysis of a biopsy specimen, or a combination of such studies ⁸ . Maffulli et al. suggested that the combination of tendon pain, swelling, and impaired performance should be given the clinical label of tendinopathy, and it should include the histopathological entities peritendinitis and tendinosis⁹ . This suggestion has a sound basis since the clinical rationale to differentiate the histopathologic entities of Achilles peritendinitis and tendinosis is an uncertain one, and there have been no randomized studies comparing the outcomes of treatment or the natural history of these two conditions. In this review, the painful condition of the Achilles tendon is called Achilles tendinopathy¹⁰ .

No specific time criteria are used to classify overuse injuries of the tendon as acute or chronic. El Hawary et al. suggested that symptoms are present for less than two weeks in acute tendinitis, for two to six weeks in subacute tendinitis, and for more than six weeks in chronic tendinitis ¹¹ . These somewhat arbitrary distinctions are not based on histopathologic or clinical criteria.

For the patient, the most common problem of Achilles tendinopathy is the pain-induced limitation in sports and sports-related activities, while the activities of daily living are only minimally affected. The goal of treatment is to return the patient to the desired level of physical activity without residual pain. In athletes, an additional demand is that the recovery time should be as short as possible.

The etiology, pathogenesis, and natural course of Achilles tendinopathy are largely unknown. Also, current conservative and operative treatment modalities vary considerably from clinic to clinic and country to country and often rely on empirical evidence without supporting scientific data. Most of the treatment studies have been retrospective, and only a few have included objective criteria to evaluate the outcome. Thus, there is a need to synthesize current knowledge relating to Achilles tendinopathy and to outline the strategies for future studies.

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Fig. 1:: Myofibroblast in the paratenon of the Achilles tendon. In the cytoplasm of the cell, microfilaments (asterisks) and dense material (arrows) can be seen (transmission electron microscope, ×21,000). M = mitochondrion, and E = cisternae of the endoplasmic reticulum.

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Fig. 2:: Lysis of the collagen fiber can be seen around degenerated tenocytes in Achilles tendinopathy (Masson trichrome staining, ×300).

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Fig. 3:: Only a few unconnected collagen fibers are visible in the mucoid degeneration (asterisks) located inside the Achilles tendon. Fibers also demonstrate unequal and irregular crimping of the collagen fibers (Masson trichrome staining, ×100).

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Fig. 4:: Calcium deposits (black) have been precipitated on the surface of the collagen fibers in the calcifying tendinopathy of the Achilles tendon (transmission electron microscope, ×6800).

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Fig. 5:: Tendolipomatosis in Achilles tendinopathy. Lipid cells (L) are located between the collagen fibers (C), which are atrophied in Achilles tendinopathy (scanning electron microscope, ×1200).

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Fig. 6:: Obliterative arteritis (thin arrows) and venous proliferation with periphlebitis (thick arrow) are visible in the paratenon of patients with chronic Achilles tendinopathy (hematoxylin and eosin, ×100).

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Fig. 7:: Longitudinal ultrasound image of an Achilles tendon with intratendinous changes. The tendon is thickened, and its regular echostructure is altered. A focal intratendinous degenerative lesion can be seen as a hypoechogenic area (X) inside the thickened tendon. Hyperechoic adhesions can be seen at the anterior border of the tendon.

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Figs. 8-A and 8-B:: Figs. 8-A and 8-B Longitudinal (Fig. 8-A) and transverse (Fig. 8-B) T2-weighted gradient echo magnetic resonance images of Achilles tendinopathy demonstrate thickening of the tendon and signal changes within the Achilles tendon.

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Fig. 9-A:: Photograph of a patient with chronic Achilles tendinopathy, demonstrating a tender, nodular swelling (arrows) that moved as the ankle was dorsiflexed and plantar flexed.

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Fig. 9-B:: This patient had an intratendinous necrotic focus, which was excised and sent for histopathologic analysis. (Reproduced, with modification, from: Józsa L, Kannus P. Human tendons: anatomy, physiology, and pathology. Champaign, IL: Human Kinetics; 1997. Reprinted with permission.)

Anatomy and Function of the Achilles Tendon

The substance of the Achilles tendon consists of collagen (about 95% is type-I collagen) and elastin embedded in a matrix consisting of proteoglycan and water ¹¹ , with type-I collagen accounting for approximately 70% and elastin accounting for 1% to 2% of the dry mass of the tendon ¹² . These protein and carbohydrate substances are produced by tenoblasts and tenocytes, which are elongated fibroblasts and fibrocytes and lie in rows between the collagen fibers.

At rest, the Achilles tendon fibers have a wavy configuration ¹³ . At the cellular level, the primary response to tendon and fiber elongation is straightening of the collagen fiber crimps ¹³ . In addition to collagen fiber crimps, elastin fibers as well as elastic extracellular matrix proteins, such as tenascin-C, provide additional elasticity to the Achilles tendon ^12-14 .

Macroscopically, the Achilles tendon constitutes the distal insertion of the gastrocnemius-soleus musculotendinous unit (i.e., the triceps surae muscle). The gastrocnemius muscle, with two bellies, originates from the posterior surface of the femoral condyles, and the soleus originates from the posterior surfaces of the proximal end of the tibia and fibula and the interposed tendinous arch. The tendon aponeuroses from the three muscle bellies join to form the Achilles tendon, which transmits loads generated by the gastrocnemius and soleus muscles to the calcaneus. The soleus is the prime mover in plantar flexion of the ankle, aided by the gastrocnemius. The gastrocnemius muscle also flexes the knee joint ¹⁵ .

The Achilles tendon is surrounded throughout its length by thin gliding membranes called paratenon . The paratenon functions as an elastic sleeve (although probably not so effectively as a true tendon sheath) and permits free movement of the tendon within the surrounding tissues ¹⁶ . The paratenon forms a thin space between the tendon and the crural fascia. The crural fascia is then covered by subcutaneous tissue and skin ¹⁷ . Under the paratenon, the entire Achilles tendon is surrounded by a fine, smooth connective tissue sheath called the epitenon . On its outer surface, the epitenon is in contact with the paratenon. The inner surface of the epitenon is continuous with the endotenon, which binds the collagen fibers and fiber bundles together and provides the neural, vascular, and lymphatic supply to the tendon.

The Achilles tendon receives its blood supply from three regions. It comes from the intrinsic vascular systems at (1) the musculotendinous junction and (2) the osteotendinous junction and from the extrinsic segmental vascular system through (3) the paratenon surrounding the tendon ^18,19 . At the myotendinous junction, a number of longitudinal vessels penetrate from the muscle to the interfascicular connective tissue of the tendon (endotendon), but only the vessels in the perimysium continue to the tendon ¹⁹ . Anteriorly, the tendon is attached to a richly vascularized tissue that supplies vessels to it. These vessels provide the most important blood supply ²⁰ . Studies performed with angiographic injection techniques have demonstrated a zone of relative avascularity between 2 and 6 cm proximal to the tendon insertion ^18,21 . Åström and Westlin evaluated microvascular perfusion in the human Achilles tendon by laser Doppler flowmetry ²² . Blood flow was substantially lower near the calcaneal insertion but otherwise was distributed evenly throughout the tendon.

The Achilles tendon is supplied by nerves from the attaching muscles and by small fasciculi from cutaneous nerves, in particular the sural nerve ²³ . The number of nerves and nerve endings are relatively low in large tendons such as the Achilles, and many nerve fibers terminate on the tendon surface or in the paratenon ¹ . This, however, does not mean that the sensory supply to the Achilles tendon is insufficient; on the contrary, the Achilles tendon contains numerous receptors relating to both pain and other neurotransmitter actions ²⁴ . These nerves follow the vascular channels within the long axis of the tendon, anastomose with each other via obliquely and transversely oriented fibers, and finally terminate in sensory nerve endings ¹ .

In vivo experiments have measured peak forces of up to 9.0 kN (corresponding to 12.5 times body weight) in the human Achilles tendon in response to running at full speed, whereas lower maximum forces (in the range of 1.0 to 4.0 kN) are applied to the Achilles tendon in activities such as jumping and cycling, in which most of the mechanical work is done by the ankle joint ^25-28 . During walking and running, force builds up within the tendon before the heel strikes the ground and is suddenly released during early impact ²⁷ . Thereafter, force builds up relatively quickly until peak values occur at the end of the push-off phase ²⁷ . In vivo measurements have also shown that the Achilles tendon can be subjected to uneven forces through modification of the contractile states of the individual muscles ²⁹ . Whether asynchronous contraction of the various muscles of the triceps surae or the uncoordinated agonist-antagonist muscle contractions contribute to the pathogenesis of Achilles tendinopathy remains to be established.

Epidemiology of Achilles Tendinopathy

The occurrence of Achilles tendinopathy is highest among individuals who participate in middle and long-distance running, orienteering, track and field, tennis, badminton, volleyball, and soccer ^30-37 . Johansson ³³ and Lysholm and Wiklander ³⁴ reported an annual incidence of Achilles disorders that was between 7% and 9% in top-level runners. In studies with an extensive number of patients, the most common clinical diagnosis of Achilles disorders was tendinopathy (55% to 66%) followed by insertional problems (retrocalcaneal bursitis and insertional tendinopathy) (20% to 25%) ^30,31,38,39 . In a cohort study with eleven years of follow-up, Kujala et al. reported that seventy-nine (29%) of 269 male orienteering runners and seven (4%) of 188 controls reported Achilles tendon overuse injury on a questionnaire; the age-adjusted odds ratio was 10.0 in runners compared with controls ³⁸ .

Kvist studied the epidemiologic factors of Achilles tendon disorders in a large group of competitive and recreational athletes with Achilles tendon problems ^30,39 . In those reports, which consisted of 698 patients, 66% had Achilles tendinopathy and 23% had Achilles tendon insertional problems. The injury was located at the myotendinous junction in 8% of the patients, and a complete tendon rupture had occurred in 3%. Eighty-nine percent of the patients were men. The main sports activity of the patients who had an Achilles tendon disorder was running (53%), and patients who participated in running sports represented 27% of all patients studied in this clinic. Malalignment of the lower extremity was found in 60% of the patients with an Achilles tendon disorder ^30,39 .

Achilles tendon disorders are more common in older athletes than in young athletes (teenage and child athletes) ⁴⁰ . In a report of 470 patients with Achilles tendinopathy and insertional symptoms, only 25% of the subjects were young athletes, 10% were younger than fourteen years, and most of the younger patients had been diagnosed with calcaneal apophysitis (Sever disease) ¹⁹ .

Etiology and Pathophysiology

Sports injuries can be caused by intrinsic or extrinsic factors, either alone or in combination ⁴¹ . In acute trauma, extrinsic factors predominate while overuse injuries are generally multifactorial in origin. In chronic tendon disorders, an interaction between these two types of factors is common ⁶ .

In the epidemiological studies, various alignment and biomechanical faults are claimed to play a causative role in two-thirds of the athletes with an Achilles tendon disorder ^30,31 . However, the mechanism by which this occurs remains in dispute ⁴² . The most common and perhaps most important malalignment in the ankle is caused by hyperpronation of the foot. Increased foot pronation has been proposed to be associated with Achilles tendinopathy ^42,43 . Kvist demonstrated that limited mobility of the subtalar joint and limited range of motion of the ankle joint were more frequent in athletes with Achilles tendinopathy than in those with other symptoms ³⁹ . In addition, varus deformity of the forefoot correlates with Achilles tendinopathy ^39,42-44 . Recently, Kaufman et al. observed that increased hindfoot inversion and decreased ankle dorsiflexion with the knee in extension is associated with Achilles tendinopathy ⁴⁵ .

In addition to hyperpronation and the other malalignments noted above, leg-length discrepancy is one of the more controversial potential contributing factors ⁴⁶ . The traditional orthopaedic view is that discrepancies of <20 mm are not clinically important ⁴¹ . In elite athletes, however, a discrepancy of >5 mm may be symptomatic and, consequently, for those who have a discrepancy of =10 mm, a built-up shoe or shoe insert has been recommended to prevent overuse symptoms. However, it must be recognized that the true occurrence of these proposed biomechanical alterations, their magnitude, and, above all, their clinical importance is not well known ⁴⁶ .

The importance of muscle weakness and imbalance as well as disturbed musculotendinous flexibility in the development of Achilles tendon disorders is also a matter of debate. However, muscular strength, power, endurance, and flexibility are an important part of physical performance and can thus be important in the prevention of certain sports injuries, particularly tendon injuries ⁴¹ . If the muscle is weak or fatigued, the energy-absorbing capacity of the whole muscle-tendon unit is reduced and the muscle no longer protects the tendon from strain injury and subsequent inflammation and pain ⁴⁶ . Recently, Alfredson et al. reported very good short-term improvements in patients with chronic Achilles tendinosis after heavy-load eccentric training, a rehabilitation program that is based on increasing the length, tensile strength, and force of the muscle-tendon unit ⁴⁷ . This concept is, however, open to speculation as the studies did not provide conclusive evidence on whether muscular weakness, imbalance, and musculotendinous tightness are the causes or the consequences of injuries.

By one definition, an overuse tendon injury is caused by repetitive strain of the affected tendon such that the tendon can no longer endure tensile stress. As a result, tendon fibers begin to disrupt microscopically, leading to inflammation and painv. Training errors have been reported to be involved in 60% to 80% of runners who have tendon overuse injuries. The most common errors include running a distance that is too long, running at an intensity that is too high, increasing distance too greatly or intensity too rapidly, and performing too much uphill or downhill work ^31,43,46 . Monotonous, asymmetric, and specialized training, such as running only (i.e., without cross-training), as well as poor technique and fatigue are additional risk factors for Achilles tendon overuse injuries. Poor environmental conditions have also been suggested to contribute to Achilles tendon problems ^1,46,49 . The lack of high-quality prospective studies limits the strength of the conclusions that can be drawn regarding these extrinsic risk factors. Also, the exact pathogenesis of Achilles tendinopathy and other disorders remains largely unknown ^1,2,50,51 , and no studies of randomized treatment interventions with long-term results (i.e., after more than twelve months of follow-up) have been published, to our knowledge.

The acute phase of Achilles tendinopathy is caused by acute overexertion, blunt trauma, or acute muscle fatigue and is characterized by inflammatory cell reaction, circulatory impairment, and edema formation ^{1,31,39,51-53} . Crepitus, which is due to the movement of the Achilles tendon within a paratenon filled with fibrin exudate, may be present. If the treatment of this acute condition fails, or has been overlooked, the fibrin may organize and form adhesions to the tendon, paratenon, and crural fascia ^16,31,39,51 . The pathways and cellular mechanism that lead to tendon degeneration (tendinosis) are not well understood ^49,51,54 . Frequently, tendon degeneration can be found in conjunction with peritendinous adhesions, although this does not indicate that either condition causes the other ¹ . In addition, decreased arterial blood flow, with local hypoxia and impaired metabolic activity and nutrition, and a persistent inflammatory reaction have been proposed as factors leading to chronic tendon overuse injury and degeneration ⁵⁵ . Also, free radicals and exercise-induced hyperthermia may contribute to the development of Achilles tendon degeneration ⁵⁵ . All of these factors, however, lack direct scientific evidence.

An old theory suggests that tendon degeneration may be preceded by acute and then chronic phases of inflammatory "tendinitis" ^3,52,56 . However, inflammatory cell infiltration has not been shown in biopsy specimens of Achilles tendons with a chronic disorder or tendinopathy or in ruptured tendons with degenerative changes ^54,57,58 . Conversely, there have been no studies involving biopsy specimens from Achilles tendons in the nonchronic stages of the disorder, as far as we know, and thus it is not known whether inflammation is present in these stages.

Leadbetter stated that one explanation for tendon degeneration is the failure of the cell matrix to adapt to excessive changes in load ⁵⁹ . He suggested that continued abusive load and irritation might stimulate the local release of cytokines, resulting in both autocrine and paracrine modulation of further cellular activity.

The mechanical theory of a so-called tendon overuse disorder, which was described above, proposes that, when a tendon has been strained repeatedly to 4% to 8% strain, it is unable to endure further tension, whereupon injury occurs. Accordingly, the tendon tissue becomes fatigued such that the ability of tendon cells to repair the fiber damage is overwhelmed by the repetitive microtraumatic process. The structure of the tendon is disrupted by this repetitive strain (often eccentric in nature), and collagen fibers begin to slide past one another, breaking their cross-links and causing tissue denaturation, leading to inflammation ^1,46 . This cumulative microtrauma is thought not only to weaken collagen cross-linking but also to affect the noncollagenous matrix as well as the vascular elements of the tendon, finally leading to tendinosis. Leadbetter named this the "tendinosis cycle." ⁵⁹

Pain is the most disconcerting and irritating symptom of Achilles tendon disorders. Traditionally, it has been proposed that the pain associated with chronic Achilles tendinopathy develops as a result of inflammation, separation of the collagen fibers, or tissue degeneration ^60,61 . However, none of these hypotheses pass scientific scrutiny; many chronically painful Achilles tendons have no evidence of inflammation, and, conversely, many degenerated tendons do not cause pain ^7,60,61 . On the basis of these observations, alternative explanations have been sought for the origin of pain in chronic tendon disorders. It has been speculated (and preliminary evidence has been presented) that as yet unidentified biochemical noxious compounds (candidates include chondroitin sulphate or nociceptive neurotransmitters, such as glutamate, substance P, or calcitonin gene-related peptide) or the neovascularization of the tendon could irritate pain receptors in the tendon ^22,60-64 .

Histopathology

On the basis of a histopathologic examination, the findings in Achilles tendinopathy can be divided into peritendinous changes and intratendinous degeneration; frequently, these entities coexist ⁶⁵ .

Peritendinous Changes

In chronic Achilles tendinopathy, the peritendinous tissue appears thickened on macroscopic examination, and fibrinous exudate, prominent and widespread proliferation of fibroblasts, and formation of new connective tissue and adhesions are evident on histological examination ^1,66-69 .

Two types of cells have been identified in the peritendinous tissue in the chronic phase of Achilles tendinopathy: fibroblasts and myofibroblasts ( Fig. 1 ) ⁶⁶ . During biological processes that include extensive tissue-remodeling, fibroblasts may acquire morphological and biochemical features of contractile cells and they have been named myofibroblasts ⁷⁰ . The myofibroblasts have stress fibers that are composed of a-smooth muscle actin in their cytoplasm, and thus they are capable of creating forces required for wound contraction ⁷⁰ . In Achilles tendinopathy, these cells are especially well established at the sites of scar formation ⁶⁶ , and it has been estimated that, in chronic tendinopathy, about 20% of the cells in the peritendinous tissue are myofibroblasts ⁶⁶ . The myofibroblasts synthesize abundant amounts of collagen and are believed to be responsible for the formation of permanent scarring and the shrinkage of peritendinous tissue around the tendon ^66,68 . These cells most likely also play an important role in the clinical symptoms of this disorder ^66,68 . They can induce and maintain a prolonged contracted state in the peritendinous adhesions around the tendon and thus influence the development of a contracture around the tendon ^66,68 . This, in turn, may lead to constriction of vascular channels and impaired circulation and may further contribute to the pathogenesis of Achilles tendinopathy. The proliferating connective tissue around the Achilles tendon causes increased intratendinous tension and pressure, resulting in increased friction between the tendon, paratenon, crural fascia, and the skin ⁶⁸ .

Intratendinous Degeneration

Puddu et al. proposed the term tendinosis, as substantial tissue degeneration can be seen inside the tendon ⁵² . In general, the macroscopic intratendinous changes in Achilles tendinopathy can be described as poorly demarcated intratendinous regions with a focal loss of tendon structure, although in some cases a discrete, palpable nodule can be found ⁵⁷ . Histologically, degenerative changes are found in 90% of the biopsy specimens taken from symptomatic parts of the tendon ⁵⁷ . These changes can be classified as: (1) hypoxic degeneration, (2) hyaline degeneration, (3) mucoid or myxoid degeneration, (4) fibrinoid degeneration, (5) fatty degeneration, (6) calcification, or (7) fibrocartilaginous or osseous metaplasia ^1,68 . Occasionally, these alterations can be found simultaneously, adjacent to each other in the tendon affected by tendinopathy. Hypoxic degenerative tendinopathy, alone or in combination with other forms of tendon degeneration, was shown to be associated with subcutaneous tendon rupture in >75% of 891 ruptured tendons ⁵⁴ .

There is a great variation in cellular density among different parts of the degenerated areas of the Achilles tendon. In some areas, an increased number of tenocytes can be seen and the metabolic activity of the cells is high, whereas, in other areas, tenocytes are totally lacking or only a few tenocytes with pyknotic nuclei can be seen ( Fig. 2 ) ¹ . Pathological changes are also frequently seen in the tendon matrix. Mucoid material with a simultaneous loss or separation of collagen fibers from each other is a common finding ( Fig. 3 ). The collagen fibers commonly show unequal and irregular crimping as well as loss of the transverse bands, separation and complete rupturing of the fibers, and increased crimping. The degenerated and degraded type-I collagen fibers are sometimes replaced by calcification ( Fig. 4 ) or by the accumulation of lipid cells (tendolipomatosis) ( Fig. 5 ) ^1,68 .

In Achilles tendinopathy, the degenerated tendon usually shows an irregular hypervascular pattern with proliferation of capillaries and arterioles in the peritendinous tissue ¹ . Narrowing or complete obliteration of newly formed arteries and arterioles is often seen ( Fig. 6 ). Occasionally, macrophages together with fibroblasts are seen in the hypervascular, degenerated regions. These features are presumed to be an indication of a healing process. However, healing does not usually result and, instead, loose granulation tissue is produced, ultimately leading to scar formation ¹ .

The prevalence and clinical relevance of these intratendinous degenerative changes in Achilles tendinopathy are largely unknown ⁷¹ . Tendinosis can frequently be found in patients with Achilles tendinopathy, but changes such as hypoxic degenerative tendinopathy, mucoid degeneration, tendolipomatosis, and calcifying tendinopathy, either alone or in combination, can be seen in about 30% of a healthy, asymptomatic urban population of individuals who are at least thirty-five years old ^54,57,71,72 .

The histological, histochemical, and fine structural alterations in chronic degenerative tendinopathy are generally similar to those found in acute spontaneous tendon ruptures ^{54,57,69,71,72} , whereas degenerative changes are more prominent in the ruptured tendons ^{54,57,69,71,72} .

Diagnosis

History and Clinical Examination

The patient's history should provide the majority of the information to make the diagnosis of Achilles tendinopathy ^1,73,74 . The time-interval between the onset of symptoms and the first visit to a physician, as well as the onset of the symptoms, the injury mechanism in patients with an acute case, and possible previous Achilles tendon problems and their treatment, must be recorded ^1,74 . The course of events since the onset of symptoms, with special emphasis on the activities that seem to make the pain worse and the interventions that seem to relieve the pain, provide valuable additional information ⁷⁵ .

Pain is the cardinal symptom of Achilles tendinopathy that leads a patient to seek medical help, and it is the most common measure used to classify the severity of the disorder ¹ . It has been suggested that the patient's symptoms can reflect the degree of the tendon abnormality. Patients in the early phase primarily report that they have pain following strenuous activities, whereas those in the later phase report that pain accompanies all activities and may even occur at rest. At this stage, the patient is usually unable to perform sports ^74-79 .

The physical examination should follow the classic orthopaedic scheme of "look, feel, and move." ¹ Inspection and palpation should provide a record of the contour of the muscle-tendon unit, possible areas of swelling and crepitation, increased erythema, local heat, and palpable tendon nodules or defects ^1,80 . In addition, patients with symptoms of Achilles tendinopathy should be examined for ankle instability and biomechanical faults ¹ .

In the acute phase of Achilles tendinopathy, the tendon is diffusely swollen and, on palpation, tenderness is usually greatest in its middle third. Sometimes, crepitation can be palpated ^1,30,32 . Typically, in patients with acute symptoms, the area of swelling and tenderness does not move when the ankle joint is dorsiflexed.

In the more chronic phase of Achilles tendinopathy, exercise-induced pain is still the cardinal symptom while crepitation and swelling diminish ¹ . In patients with a chronic case, a tender, nodular swelling is usually present and is believed to signify tendinosis ^32,79 . Particularly in patients with tendinosis, the focal tender nodules may move as the ankle is dorsiflexed and plantar flexed ⁸¹ .

Imaging Methods

Ultrasonography has been used increasingly to examine Achilles tendon injuries and other tendon disorders since it provides a readily available, quick, safe, and inexpensive method to verify the existence and location of intratendinous lesions ^1,82-89 . The primary disadvantages are that ultrasound is operator-dependent, provides somewhat limited soft-tissue contrast, and is not as sensitive as magnetic resonance imaging ⁷⁷ . The results of ultrasonography have been found to be reliable when they demonstrate adhesions around an Achilles tendon. However, this technique has been shown to be unreliable when it fails to detect adhesions, and patients with few adhesions may have a false-negative result on ultrasonography ⁸⁷ . On the other hand, abnormalities detected by ultrasonography in an asymptomatic Achilles tendon, in turn, can predict the development of Achilles tendinopathy very accurately in advance ⁹⁰ .

In the acute phase of Achilles tendinopathy, ultrasonography reveals fluid surrounding the tendon ⁸⁸ . In its more chronic form, peritendinous adhesions can be seen as thickening of the hypoechoic paratenon with poorly defined borders ( Fig. 7 ) ^1,91,92 . Discontinuity of tendon fibers, focal hypoechoic intratendinous areas, and localized tendon swelling and thickening are the most characteristic ultrasonographic findings in patients with a surgically verified intratendinous lesion (tendinosis) of the Achilles tendon ^1,87,93 .

Magnetic resonance imaging has been used extensively to visualize pathological conditions of the tendon, as it satisfies two fundamental principles of imaging. First, it provides high intrinsic tissue contrast, which allows normal tendons to be distinguished from abnormal tendons, and, second, it provides high spatial resolution that allows detailed anatomic structures to be identified ^77,94 . The ability of magnetic resonance imaging to acquire images from multiple planes (longitudinal, transverse, and oblique) is also a clear advance ( Figs. 8-A and 8-B ) ⁹⁵ . The disadvantages of magnetic resonance imaging are its relatively high cost, limited availability in some countries, time-consuming scanning, and slow and often incomplete resolution of signal changes after operative intervention ^1,77 . In addition, Soila et al. recently showed that the normal anatomy of an asymptomatic Achilles tendon varies, and this sometimes causes diagnostic misinterpretation ⁹⁶ .

In patients with chronic Achilles tendinopathy, magnetic resonance imaging frequently reveals tendon thickening on sagittal images and altered signal appearance within the tendon tissue ^51,97-102 . According to their study, Movin et al. suggested that the gadolinium-enhanced intratendinous signal abnormality in patients with chronic Achilles tendinopathy was related to an increased amount of interfibrillar noncollagenous extracellular matrix and altered fiber structure ⁵⁸ .

Treatment

Little reliable experimental or clinical scientific work has been done on the treatment of Achilles tendon disorders. Without scientific evidence and, thus, a firm understanding of the nature of this disorder, it is difficult to prescribe a proper treatment regimen for Achilles tendinopathy. Both conservative and operative treatments vary considerably among countries, clinics, and physicians. Most treatment regimens are based only on what empirically seems to work, without much scientific support ^1,77,103 . Thus, the therapies and treatment regimens reflect only current perceptions and therefore are likely to be replaced or modified in the coming years.

In the early phases of Achilles tendinopathy, various forms of conservative treatment are normally used ^{1,2,6,16,43,74,103-106} . Operative treatment is recommended for patients who do not respond adequately to a three to six-month trial of appropriate conservative treatment ^{4-6,17,31,37,107-109} . In a recent eight-year follow-up study, nonoperative treatment was unsuccessful in 29% of the eighty-three patients with acute to subacute Achilles tendinopathy ¹⁰⁶ .

Conservative Treatment

Initial conservative treatment should be directed toward relieving symptoms ¹⁰³ . This should consist of a combination of strategies aimed at controlling inflammation and correcting training errors, limb malalignment, decreased flexibility, muscle weakness, and the use of poor equipment during sports ¹⁰³ . In addition, injection of heparin (to prevent edema or fibrin exudate in the paratenon, i.e., prevention of the formation of adhesions between tendon and paratenon) and various modalities of physical therapy (heat, ultrasound, and electrical stimulation) are used in the treatment of some patients with Achilles tendinopathy ¹ .

The control of inflammation is recommended in the early phase of Achilles tendon overuse injury. This is accomplished by decreasing activity, the use of cold packs, and the administration of anti-inflammatory medication ^1,16 . Decreasing the intensity, frequency, and duration of the activity that caused the injury, or modification of that activity, may be the only action needed to control the inflammation and symptoms in the acute phase. Modified rest, which allows activity in the uninjured parts of the body such as the upper extremities, has been recommended ^1,103 . Cryotherapy has been regarded as the single most useful intervention for tendon inflammation in the acute phase of this disorder ^1,110 . Cold therapy is able to control pain and edema as well as to reduce regional blood flow and the metabolic demands of the tissue and thereby help to prevent further tissue damage at the site of the injury. It also delays inflammation by decreasing the effects of histamine on vascular membranes, neutrophil activation, and leukocytes ¹ . Cold therapy has beneficial effects during rehabilitation by decreasing pain and muscle spasm to allow better mobilization ^{16,79,111,112} .

Nonsteroidal anti-inflammatory drugs, in the form of pills or topical gels, are frequently used in the treatment of acute as well as chronic forms of Achilles tendinopathy. The benefit of these drugs is, however, controversial ^{6,77,79,110,113} . Healing of acute soft-tissue injury is slightly more rapid and inflammation is slightly better controlled with the use of nonsteroidal anti-inflammatory drugs than without them ¹¹⁴ . The effect of nonsteroidal anti-inflammatory drugs in chronic Achilles tendon problems is less clear. In patients with chronic Achilles tendinopathy, Åström and Westlin found no beneficial effect associated with oral administration of nonsteroidal anti-inflammatory drugs ¹¹⁵ . Recently, it has been claimed that anti-inflammatory medication (nonsteroidal anti-inflammatory drugs or corticosteroid injections) would not benefit patients in the advanced stage of tendinosis as it is not an inflammatory disorder ^60,116 . However, it is clear that nonsteroidal anti-inflammatory drugs do diminish pain and, thus, have been used for short periods to facilitate rehabilitation ^1,77 .

The role of corticosteroid injections in the treatment of Achilles tendinopathy is controversial as there are insufficient published data to determine the comparative benefits and risks ^{1,113,117-120} . Peritendinous injection of corticosteroids, which is used to treat tendinous or peritendinous inflammation, has been claimed to cause spontaneous rupture of the Achilles tendon. However, the proof of the deleterious effects of peritendinous injections of corticosteroids on human tendon properties is based solely on uncontrolled case studies, and there have been no well-controlled prospective clinical trials, to our knowledge ^118,120 . In some experimental studies, cortisone has been observed to inhibit the formation of granulation tissue and to delay tendon healing ^121,122 . On the other hand, other studies have shown no adverse effects of corticosteroids on tendon tissue ^123-125 . Oxlund observed increased tensile strength of the tendon with no change in collagen content after short-term local administration of cortisol around the peroneal tendons of rats ¹²⁶ . Intratendinous injections have always been contraindicated in clinical medicine because the pressure increase of such an injection alone may cause serious hypoxic degenerative changes of the tendon tissue ^1,120 . On the basis of these reports, the use of corticosteroid injections in the treatment of this condition remains unclear ^{1,118-120,127} .

Recently, promising results have been described in studies of patients with Achilles tendinopathy who were treated with ultrasound-guided injection of a sclerosing agent (polidocanol) to decrease the neovascularization detected in chronic midportion Achilles tendinosis ^62-64 . Because of the small number of patients as well as the short duration of clinical follow-up, these preliminary reports should not yet be used as the basis for recommendations for the treatment of patients with Achilles tendinopathy, although very effective relief of the symptoms of the Achilles tendinopathy was demonstrated ⁶³ .

Stretching and strengthening of the triceps surae muscle and the Achilles tendon have been advocated to preserve the function of the musculotendinous unit by restoring normal ankle joint mobility and decreasing the strain of the Achilles tendon with normal motion ⁷⁷ . Niesen-Vertommen et al. found eccentric training to be superior to concentric training in decreasing pain in chronic Achilles tendinopathy ¹²⁸ . In the prospective, uncontrolled follow-up study by Alfredson et al., promising preliminary results were obtained with use of a regimen of intensive heavy-load eccentric muscle training for the treatment of chronic Achilles tendinopathy and the results were reproduced in a short-term (three-month) multicenter study ^47,129 . Similar good results after eccentric calf muscle training were also reported by Silbernagel et al., who used a longer, twelve-month duration of follow-up ¹³⁰ . In addition to cryotherapy and a stretching-and-strengthening program, many other physical therapy modalities, such as heat, ultrasound, electrical stimulation, and laser photostimulation, are commonly employed in the treatment of Achilles tendinopathy. Again, scientific evidence on the effectiveness of these treatment modalities is sparse and controversial, especially with regard to the long-term clinical benefits ^{1,6,77,131,132} .

Surgical Treatment

Surgery has been considered an acceptable choice among patients with chronic Achilles tendinopathy after attemps at conservative treatment have failed ^{4,5,17,31,37,107-109} . However, no prospective randomized studies comparing operative and conservative treatment of Achilles tendinopathy have been published, as far as we know, and most of our knowledge on treatment efficacy is based on clinical experience and descriptive studies.

Recently, Tallon et al. reviewed studies that described outcomes after surgical treatment of chronic Achilles tendinopathy ¹³³ . In their review, the methodology scores with respect to the type of the study, the subject selection process, and the outcome measures were generally low, thus indicating that the studies had methodologic limitations. A negative correlation was found between the reported success rates and the overall methodology scores, but the positive correlation between the year of publication and the overall methodology score suggested that the quality of the studies was improving.

The relationship between operative treatment and healing of the tendon is still not well understood ^1,77 . Although the results of uncontrolled studies have generally been good, the results may not have been due to operative treatment alone as it was usually combined with a postoperative period of immobilization, rest, and a prolonged period of controlled rehabilitation ^68,134 .

Various surgical techniques have been used to treat Achilles tendinopathy. Many authors have recommended that, after the longitudinal division of the crural fascia, the paratenon should be incised and macroscopic adhesions excised ^{5,16,37,107,109} . In some studies, the adhesions have been reported to be found mainly between the Achilles tendon and the paratenon, whereas, in others, the paratenon has been noted to be adhered mainly to the crural fascia, or even to the skin ^{4,5,16,109,135,136} . When an intratendinous lesion is seen in a preoperative ultrasonogram or magnetic resonance imaging examination and a nodule or thickening is palpable within the tendon, many authors have recommended that a longitudinal incision be made over the thickened area and the necrotic area or granulation tissue excised ^{1,4-6,37,103,107,135,137-139} ( Figs. 9-A and 9-B ). The use of a side-to-side suture or turned-down tendon flap has been proposed to reinforce the tendon if there is a need for extensive débridement ^{5,37,53,108,140} . Alternatively, some authors have used open or percutaneous multiple longitudinal incisions of the tendon to treat this condition ^100,141,142 .

In most studies, operative treatment of Achilles tendinopathy has given satisfactory results in 75% to 100% of the patients ^{4,5,16,31,37,107,109,135,143-149} . However, most of these reports were retrospective, and only a few had results that were based on objective evaluations, such as range of motion of the ankle.

In a report by Paavola et al., operative treatment of Achilles tendinopathy was shown to result in good and acceptable short-term results with use of subjective, clinical, and functional tests as the outcome criteria ¹⁰⁹ . Patients with pure peritendinous adhesions had a somewhat lower rate of complications associated with the operative treatment and a trend toward better recovery than did those with peritendinous adhesions combined with an intratendinous lesion ¹⁰⁹ . Alfredson et al. prospectively evaluated the effect of operative treatment on isokinetic calf muscle strength in thirteen patients with various types of Achilles tendon overuse injuries ¹³⁸ . They found that management with six months of rehabilitation after operative treatment was not enough to return the concentric and eccentric plantar flexion strength in the involved limb to that of the noninjured side. However, in a more recent study involving eleven patients with chronic tendinosis, Alfredson et al. found no obvious advantages in the recovery of isokinetic concentric and eccentric plantar flexion strength after the use of a short duration of immobilization (two weeks) compared with use of a longer duration (six weeks) in a previous study with a more heterogeneous group of patients ¹⁵⁰ . In the study by Maffuli et al., acceptable results were achieved after percutaneous longitudinal tenotomies (which can also be done under ultrasound guidance ¹⁴³ ) were performed in fifty-two middle and long-distance runners with unilateral Achilles tendinopathy (peritendinitis and/or intratendinous lesion) ¹⁴² . The patients were evaluated by isometric strength and endurance measurements and subjective evaluation (six and eighteen months after the operation, respectively). The authors found that the presence of peritendinitis was a poor prognostic factor, since the patients with tendinopathy associated with peritendinitis were less satisfied and had less strength and endurance after the follow-up period compared with patients with isolated tendinopathy ¹⁴² .

Some studies have shown a relatively high rate of complications associated with operative treatment of Achilles tendinopathy ^16,31,37,136 . Recently, an overall complication rate of 11% was documented in a series of 432 consecutive patients ¹³⁶ . Most of the complications (54%) in that study involved compromised wound-healing, and the problem seemed to appear more frequently in patients who had operative treatment of a partial Achilles tendon rupture than in those who had operative treatment of Achilles tendinopathy only.

Postoperative Regimen

There is extensive variation in the descriptions of, and often sparse information on, the methods used for rehabilitation after operative treatment of chronic Achilles tendinopathy. Immobilization with use of a cast, walking boot, or walker splint for periods ranging from two to eight weeks has been recommended ^{4,5,57,135,137,138,140,149-151} . Immediate non-weight-bearing range-of-motion exercises have also been proposed ^{16,37,107,109,137,142,143} . Range-of-motion and stretching exercises, beginning one to two weeks postoperatively, have been recommended by most authors ^{4,5,135,138,149-151} . A gradual return to sports has been advised when the strength of the calf muscle has been regained ^{59,100,107,137,140,149,151} .

We recommend that ankle mobilization and partial weight-bearing with the aid of crutches be started in a gradual manner immediately after operative treatment. Stretching exercises of the Achilles tendon-gastrocnemius muscle complex should be initiated, and full weight-bearing allowed, whenever the patient is able to walk without limping, usually one to two weeks postoperatively. Light sports-specific training is allowed when there is no pain during walking and no limitation in the active range of motion of the ankle joint. This usually occurs four to six weeks after the operation. Full sports-specific training is allowed six to twelve weeks after the surgery.

Prognosis

Little is known about the natural course of Achilles tendinopathy. However, a recent eight-year follow-up study determined the long-term outcome of patients initially treated nonoperatively for acute or subacute Achilles tendinopathy ¹³⁶ . The long-term prognosis of these patients was generally good. Seventy (84%) of the eighty-three patients were able to return to full levels of physical activity, and, at eight years, seventy-eight patients (94%) were asymptomatic or had only mild pain on strenuous exercise. On the involved side, a delay of up to six months between the onset of symptoms and the initiation of conservative treatment did not compromise the long-term outcome. Nevertheless, twenty-four (29%) of the eighty-three patients failed to respond to conservative treatment and underwent operative treatment ¹³⁶ . Also, even at the eight-year follow-up, there was a clear side-to-side difference between the involved and the uninvolved side in the performance tests, clinical examination, and ultrasonography. Furthermore, some overuse symptoms (exertional pain with or without swelling and stiffness) developed in the initially uninvolved Achilles tendon as well in thirty-four (41%) of the eighty-three patients ¹³⁶ .

Future Studies of Achilles Tendinopathy

The etiology, pathogenesis, and natural course of Achilles tendinopathy are largely unknown. Histopathological studies have been limited to its chronic phase, and thus it is not clear whether the degenerative features are preceded by an inflammatory phase. In the absence of inflammation, at least in the chronic stage, other factors such as irritation of mechanoreceptors or triggering of nociceptive receptors may cause pain in this condition. In future studies, histopathological description of acute and subacute Achilles tendinopathy is needed, and accurate description of the mechanisms of pain in Achilles tendinopathy will be important.

Current conservative and surgical treatment modalities of Achilles tendinopathy vary considerably and rely mainly on empirical evidence without convincing scientific support. In the near future, randomized, controlled trials on the role of corticosteroid injections, different strengthening modalities, and growth factors and gene therapy in the treatment of Achilles tendinopathy will be needed ^120,152-158 .

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Topics

achilles tendon ; tendon ; achilles tendonitis

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Mika Paavola, Pekka Kannus, Tero A.H. Järvinen, Karim Khan, Lászlo Józsa, Markku Järvinen; Achilles Tendinopathy. The Journal of Bone & Joint Surgery. 2002 Nov;84(11):2062-2076.

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