Achilles Tendinopathy

Abstract

Achilles tendinopathy is a common cause of disability. Despite the economic and social relevance of the problem, the causes and mechanisms of Achilles tendinopathy remain unclear. Tendon vascularity, gastrocnemius-soleus dysfunction, age, sex, body weight and height, pes cavus, and lateral ankle instability are considered common intrinsic factors. The essence of Achilles tendinopathy is a failed healing response, with haphazard proliferation of tenocytes, some evidence of degeneration in tendon cells and disruption of collagen fibers, and subsequent increase in noncollagenous matrix. Tendinopathic tendons have an increased rate of matrix remodeling, leading to a mechanically less stable tendon which is more susceptible to damage. The diagnosis of Achilles tendinopathy is mainly based on a careful history and detailed clinical examination. The latter remains the best diagnostic tool. Over the past few years, various new therapeutic options have been proposed for the management of Achilles tendinopathy. Despite the morbidity associated with Achilles tendinopathy, many of the therapeutic options described and in common use are far from scientifically based. New minimally invasive techniques of stripping of neovessels from the Kager's triangle of the tendo Achillis have been described, and seem to allow faster recovery and accelerated return to sports, rather than open surgery. A genetic component has been implicated in tendinopathies of the Achilles tendon, but these studies are still at their infancy.

Full text

Achilles Tendinopathy
Umile Giuseppe Longo, MD,* Mario Ronga, MD,
w
and Nicola Maffulli, MD, MS, PhD, FRCS(Orth)
z
Abstract: Achilles tendinopathy is a common cause of disability.
Despite the economic and social relevance of the problem, the
causes and mechanisms of Achilles tendinopathy remain unclear.
Tendon vascularity, gastrocnemius-soleus dysfunction, age, sex,
body weight and height, pes cavus, and lateral ankle instability
are considered common intrinsic factors. The essence of Achilles
tendinopathy is a failed healing response, with haphazard
proliferation of tenocytes, some evidence of degeneration in tendon
cells and disruption of collagen fibers, and subsequent increase in
noncollagenous matrix. Tendinopathic tendons have an increased
rate of matrix remodeling, leading to a mechanically less stable
tendon which is more susceptible to damage. The diagnosis of
Achilles tendinopathy is mainly based on a careful history and
detailed clinical examination. The latter remains the best diagnostic
tool. Over the past few years, various new therapeutic options have
been proposed for the management of Achilles tendinopathy.
Despite the morbidity associated with Achilles tendinopathy, many
of the therapeutic options described and in common use are far
from scientifically based. New minimally invasive techniques of
stripping of neovessels from the Kager’s triangle of the tendo
Achillis have been described, and seem to allow faster recovery and
accelerated return to sports, rather than open surgery. A genetic
component has been implicated in tendinopathies of the Achilles
tendon, but these studies are still at their infancy.
Key Words: Achilles tendon, tendinopathy, sports, main body,
athletes
(Sports Med Arthrosc Rev 2009;17:112–126)
Achilles tendinopathy is a clinical condition characterized
by pain and swelling in and around the tendon, mainly
arising from overuse, but often presenting in middle aged
overweight patients with no history of increased physical
activity.
1
Achilles tendinopathy is a common cause of
disability in many athletes because of continuous prolonged
intense functional demands imposed on the Achilles tendon
(AT). In the past 3 decades, the incidence of Achilles
tendinopathy has risen as a result of greater participation in
recreational and competitive sports. A 10-fold increase in
AT injuries has been reported in runners compared with
age matched controls.
2
The lifetime incidence of Achilles
tendinopathy in top-level runners has been estimated at
around 7% to 9%. Achilles tendinopathy is also common
among athletes participating in racquet sports, track and
field, volleyball, and soccer.
3–7
Achilles tendinopathy is not only restricted to athletes:
up to one third of people affected are nonathletes who may
lose significant numbers of working days, with a marked
financial impact on society.
8
The management of Achilles
tendinopathy lacks evidence-based support, and tendino-
pathy sufferers are at risk for long-term morbidity with
unpredictable clinical outcome.
9
ANATOMY
The confluence of the gastrocnemius and soleus
muscles forms the AT. The gastrocnemius is more super-
ficial and originates from 2 heads above the knee. The
soleus is anterior to the gastrocnemius and originates below
the knee.
10
The plantaris muscle, present in approximately
90% of the population, has a short muscle belly of 7 to
10 cm, arises just below the lateral head of gastrocnemius,
and has a long slender tendon that runs medial to the AT.
11
There are 2 bursae at the calcaneal insertion of the AT.
A subcutaneous bursa lies superficial to the tendon and the
skin, and a retrocalcaneal bursa lies between tendon and
the calcaneum.
12
The AT derives its sensory nerve supply from the
nerves of the attaching muscles and cutaneous nerves, in
particular the sural nerve.
9,13,14
HISTOLOGY
The cells in a normal AT are well organized. Tenocytes
and tenoblasts form up to 95% of the cellular element of
the tendon.
15
Specialized fibroblasts, the tenocytes, appear
in transverse sections as stellate cells, possibly owing to the
uniform centrifugal secretion of collagen. Tenoblasts have
variable shapes and sizes, and are arranged in long parallel
chains.
15
Collagen constitutes about 90% of tendons protein, or
approximately 70% of the dry weight of a tendon.
14
The
collagen fibers are tightly packed in parallel bundles.
16
Type
I collagen is the commonest; it forms 95% of tendon
collagen, and is held in parallel bundles by small
proteoglycan molecules.
4
Elastin accounts for only about
2% of the dry mass of tendon
14
and can undergo up to
200% strain before failure.
Aging significantly decreases tendon glycosaminogly-
cans and increases collagen concentration.
17
Acute exercise
increases type I collagen formation in peritendinous tissue.
18
The essence of tendinopathy is a failed healing
response, with haphazard proliferation of tenocytes, some
evidence of degeneration in tendon cells and disruption of
collagen fibers, and subsequent increase in noncollagenous
matrix.
1,14,19–21
Tendinopathic lesions affect both collagen
matrix and tenocytes.
20,22
The parallel orientation of
collagen fibers is lost, there is a decrease in collagen fiber
diameter and in the overall density of collagen. Collagen
microtears may also occur, and may be surrounded by
erythrocytes, fibrin, and fibronectin deposits. Normally,
collagen fibers in tendons are tightly bundled in a parallel
Copyright r2009 by Lippincott Williams & Wilkins
From the *Department of Orthopaedic and Trauma Surgery, Campus
Biomedico University, Rome; wDepartment of Orthopaedics and
Traumatology, University of Insubria Ospedale di Circolo, Varese,
Italy; and zCentre for Sports and Exercise Medicine, Queen Mary
University of London, Barts and The London School of Medicine
and Dentistry, Mile End Hospital, London, England.
Reprints: Nicola Maffulli, MD, MS, PhD, FRCS(Orth), Centre for
Sports and Exercise Medicine, Queen Mary University of London,
Barts and The London School of Medicine and Dentistry, Mile End
Hospital, 275 Bancroft Road, London E1 4DG England (e-mail:
n.maffulli@qmul.ac.uk).
REVIEW ARTICLE
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fashion. In tendinopathic samples, there is unequal and
irregular crimping, loosening and increased waviness of
collagen fibers, with an increase in type III (reparative)
collagen.
22–26
At electron microscopy, various types of degeneration
have been described, namely (a) hypoxic degeneration, (b)
hyaline degeneration, (c) mucoid or myxoid degeneration,
(d) fibrinoid degeneration, (e) lipoid degeneration, (f)
calcification, and (g) fibrocartilaginous and bony metapla-
sia.
27–29
All can coexist, depending on the anatomic site and
the nature of their causal insult. Therefore, tendinopathy
can be considered the end result of a number of etiologic
processes with a relatively narrow spectrum of histopatho-
logic features.
1,30,31
In tendinopathic tendons, tenocytes are abnormally
plentiful in some areas.
32–34
They have rounded nuclei, and
there is an ultrastructural evidence of increased production
of proteoglycan and protein, which gives them a chondroid
appearance. Other areas may contain fewer tenocytes than
normal with small, pyknotic nuclei,
22
with occasional
infiltration of lymphocytes and macrophage type cells,
possibly part of a healing process
22
associated with
proliferation of capillaries and arterioles. Degeneration of
the AT is usually either ‘‘mucoid’’ or ‘‘lipoid’’.
27
Collagen
fibers that are thinner than normal, and large interfibrillar
mucoid patches and vacuoles are seen.
35
There is an
increase in the Alcian-blue-staining ground substance.
The characteristic hierarchical structure is also lost.
36–39
Vascularity is typically increased, and blood vessels are
randomly oriented, sometimes perpendicular to collagen
fibers.
40,41
Inflammatory lesions
40–43
and granulation tis-
sue
42,43
are infrequent, and, when found, are associated
with partial ruptures. Inflammatory cells and acellular
necrotic areas are exceptional, and probably not typical
of the degenerative process.
35,44–46
In contrast, mucoid
degeneration, fibrosis, and vascular proliferation with an
inflammatory infiltrate may be found in the parate-
non.
37,39–41,47,48
Using common staining techniques, light
microscopic degeneration was not a feature of tendons
from healthy, older persons. Type I collagen is the main
collagen in tendons; type III collagen is present in small
amounts.
We used an in vitro model to determine whether
tenocytes from ATs that were ruptured, nonruptured,
tendinopathic, and fetal show different behavior.
49
In
cultures from ruptured and tendinopathic tendons, there
was increased production of type III collagen. Athletic
participation places excess stress on the AT, which could
potentially lead to areas of microtrauma within the tendon.
These areas may heal by the production of type III
collagen, which is an abnormal healing response. Accumu-
lation of such episodes of microtrauma could result in a
critical point where the resistance of the tissue to tensile
forces is compromised and tendon rupture occurs.
ETIOLOGY
The etiology of Achilles tendinopathy remains unclear,
and many factors have been implicated. Tendon vascular-
ity, gastrocnemius-soleus dysfunction, age, sex, body
weight and height, pes cavus, and lateral ankle instability
are common intrinsic factors.
50
Excessive motion of the
hindfoot in the frontal plane, especially a lateral heel strike
with excessive compensatory pronation, is thought to cause
a ‘‘whipping action’’ on the AT, and predispose it to
tendinopathy. Also, forefoot varus is frequent in patients
with Achilles tendinopathy. Changes in training pattern,
poor technique, previous injuries, footwear, and environ-
mental factors such as training on hard, slippery or slanting
surfaces are extrinsic factors, which may predispose the
athlete to Achilles tendinopathy. Excessive loading of
tendons during vigorous physical training is regarded as
the main pathologic stimulus for tendinopathy,
51
possibly
as a result of imbalance between muscle power and tendon
elasticity. The AT may respond to repetitive supra-
physiologic overload by either inflammation of its sheath,
or degeneration of its body, or a combination of both.
52,53
It remains unclear whether different stresses induce
different responses. Active repair of fatigue damage must
occur, or tendons would weaken and eventually rupture.
The repair mechanism is probably mediated by resident
tenocytes, which continually monitor the extracellular
matrix (ECM). Failure to adapt to recurrent excessive
loads results in the release of cytokines leading to further
modulation of cell activity.
51
Tendon damage may even
occur from stresses within physiologic limits, as frequent
cumulative microtrauma may not allow enough time for
repair.
54
Microtrauma can also result from nonuniform
stress within tendons, producing abnormal load concentra-
tions and frictional forces between the fibrils, with localized
fiber damage.
51
Free radical damage occurring on reperfusion after
ischemia, hypoxia, hyperthermia, and impaired tenocyte
apoptosis have been linked with tendinopathy.
55
In animal
studies, local administration of cytokines and inflammatory
agents such as prostaglandins has resulted in tendino-
pathy.
56
Fluoroquinolones have also been implicated in the
pathogenesis of tendinopathy. Ciprofloxacin causes en-
hanced interleukin-1b-mediated matrix metalloproteinase 3
(MMP3) release, inhibits tenocyte proliferation and reduces
the collagen and matrix synthesis.
Degenerative tendinopathy is the most common
histologic finding in spontaneous tendon ruptures. Tendon
degeneration may lead to reduced tensile strength and a
predisposition to rupture. Indeed, ruptured ATs have more
advanced intratendinous changes than tendinopathic ten-
dons.
57
In Achilles tendinopathy, changes in the expression
of genes regulating cell-cell and cell-matrix interactions
have been reported, with down-regulation of MMP3
mRNA.
58
Significantly higher levels of type I and type III
collagen mRNAs have been reported in tendinopathic
samples compared with normal samples. Imbalance in
MMP activity in response to repeated injury or mechanical
strain may result in tendinopathy.
46,59–62
Pain is the main symptom of Achilles tendinopathy,
but the underlying mechanism causing pain is not fully
understood. Traditionally, pain has been thought to arise
through inflammation, or via collagen fiber separation or
disruption.
31
However, chronically painful ATs have no
evidence of inflammation.
48
As tendinopathies are not
inflammatory conditions, pain may originate from a
combination of mechanical and biochemical causes.
63
METALLOPROTEASES IN TENDINOPATHY OF
TENDO ACHILLIS
Tendon matrix constantly remodels, with higher rates
of turnover at sites exposed to high levels of strain. Matrix
metalloproteases (MMPS), a family of zinc and calcium
dependent endopeptidases active at a neutral pH, are
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involved in the remodel ling of ECM through their broad
proteolytic capability.
64
Degradation of collagen in tendon
ECM is initiated by MMPs. Twenty-three human MMPs
have been identified, with a wide range of extracellular
substrates.
65
MMPs can be subdivided into 4 main groups:
collagenases, which cleave native collagen types I, II, and
III; gelatinases, which cleave denatured collagens and type
IV collage; stromelysins, which degrade proteoglycans,
fibronectin, casein, collagen types III, IV, and V; and
membrane type MMPs. The activity of MMPs is inhibited
reversibly by tissue inhibitory of metalloproteinases
(TIMPs) in a noncovalent fashion in a 1:1 stoichiometry.
There are 4 types of TIMP: TIMP1, TIMP2, TIMP3, and
TIMP4. The balance between the activities of MMPs and
TIMPs regulates tendon remodeling, and an imbalance
produces collagen disturbances in tendons.
MMP3 may play a major role in regulation of tendon
ECM degradation and tissue remodeling. An increased
expression of MMP3 may be necessary for appropriate
tissue remodeling and prevention of tendinopathic
changes.
58
The timing of MMP3 production is probably
also critical in this process. MMP3 and TIMP1, TIMP2,
TIMP3, and TIMP4 are down-regulated in tendinopathic
tendons.
66
Decreased MMP3 expression may therefore lead
to tendinopathic changes in tendons. The expression of
MMP2 can be up-regulated in Achilles tendinopathy.
Physical exercise can influence local MMP and TIMP
activities in human tendo Achillis with a pronounced
increase in local levels of pro-MMP9 after exercise.
58
MMP9 may well have a role in a potential inflammation
reaction in human tendo Achillis-induced by intensive
exercise. Also, exercise causes a rapid increase in serum
MMP9, a probable result of increased leukocytes in the
circulation.
58
MMPs and their inhibitors are crucial to ECM
remodeling, and a balance exists between them in normal
tendons. Alteration of MMP and TIMP expression from
basal levels leads to alteration of tendon homeostasis.
Tendinopathic tendons have an increased rate of matrix
remodeling, leading to a mechanically less stable tendon
which is more susceptible to damage.
9,31,46,59–62,67–69
CLINICAL ASPECTS
Pain is the cardinal symptom of Achilles tendinopathy.
However, it should be understood that, even though
patients may present acutely, it is likely that the histo-
pathology, even in these instances, is already of a failed
healing response nature, bearing witness to the long
standing process which eventually causes clinically relevant
symptoms. Generally, pain occurs at the beginning and
end of a training session, with a period of diminished
discomfort in between. As the pathologic process pro-
gresses, pain may occur during exercise, and, in severe
cases, it may interfere with activities of daily living. In the
acute phase, the tendon is diffusely swollen and edematous,
and on palpation tenderness is usually greatest from 2 to
6 cm proximal to the tendon insertion. Sometimes, fibrin
precipitated from the fibrinogen-rich fluid around the
tendon can cause palpable crepitation. In chronic cases,
exercise-induced pain is still the cardinal symptom, but
crepitation and effusion diminish. A tender, nodular
swelling is usually present in chronic cases, and is believed
to signify tendinopathy.
The diagnosis of Achilles tendinopathy is mainly based
on a careful history and detailed clinical examination.
Diagnostic imaging may be required to verify a clinical
suspicion or to exclude other musculoskeletal disorders,
such as os trigonum syndrome, tenosynovitis or dislocation
of the peroneal tendons, tenosynovitis of the plantar
flexors, an accessory soleus muscle, tumors of the AT
(xanthomas), and neuroma of the sural nerve.
70
Clinical examination is the best diagnostic tool. Both
legs are exposed from above the knees and the patient was
examined during standing and prone. The foot and the heel
should be inspected for any malalignment, deformity,
obvious asymmetry in the tendons size, localized thicken-
ing, Haglund heel and any previous scars. The AT should
be palpated for tenderness, heat, thickening, nodule, and
crepitation.
6
The tendons excursion is estimated to deter-
mine any tightness. The ‘‘painful arc’’ sign helps to
distinguish between tendon and paratenon lesions. In
paratendinopathy, the area of maximum thickening and
tenderness remains fixed in relation to the malleoli from full
dorsiflexion to plantarflexion, whereas lesions within the
tendon move with ankle motion. There is often a discrete
nodule, whose tenderness significantly decreases or dis-
appears when the tendon is put under tension.
71
ROYAL LONDON HOSPITAL TEST
Once the tester has elicited local tenderness by
palpating the tendon with the ankle in neutral position
(Fig. 1A) or slightly plantarflexed, the patient is asked to
FIGURE 1. Royal London Hospital Test: Once the tester has elicited local tenderness by palpating the tendon with the ankle in neutral
position (Fig. 1A), the patient is asked to actively dorsiflex the ankle and to actively plantarflex it. With the ankle in maximum
dorsiflexion and in maximum plantarflexion, the portion of the tendon originally found to be tender is palpated again (Fig. 1B).
Longo et al Sports Med Arthrosc Rev Volume 17, Number 2, June 2009
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actively dorsiflex the ankle and to actively plantarflex it.
With the ankle in maximum dorsiflexion and in maximum
plantarflexion, the portion of the tendon originally found
to be tender is palpated again (Fig. 1B). Results are
classified as tenderness present on dorsiflexion or absent. In
asymptomatic tendons, the test is performed selecting an
area in the tendon 3 cm proximal to its calcaneal insertion
when the ankle is held in neutral.
We evaluated the sensitivity, specificity, reproducibil-
ity, and predictive value of palpation, of the painful arc sign
and of the Royal London Hospital test.
26
In patients with
tendinopathy of the AT with a tender area of intratendi-
nous swelling that moves with the tendon and whose
tenderness significantly decreases or disappears when the
tendon is put under tension, a clinical diagnosis of
tendinopathy can be formulated, with a high positive
predictive chance that the tendon will show ultrasono-
graphic and histologic features of tendinopathy.
IMAGING
Although plain soft tissue radiography is no longer the
imaging modality of choice in tendon disorders, it still has a
role in diagnosing associated or incidental bony abnorm-
alities. Magnetic resonance imaging (MRI) provides
extensive information about the internal morphology of
tendon and the external anatomy (Fig. 2). It is a useful tool
to evaluate the various stages of chronic degeneration and
differentiation between paratendinopathy and tendinopa-
thy of the main body of the tendon. Areas of mucoid
degeneration in the AT are shown at MRI as high signal
intensity zone on T1 and T2 weighted images.
MRI is superior to ultrasound (US) in detecting
incomplete tendon rupture. However, owing to the high
sensitivity of MRI, the data should be interpreted with
caution and correlated to the patient symptoms before
making any recommendations.
51
Ultrasonography is con-
sidered to be operator-dependent, but it correlates well with
histopathologic finding,
72
and especially in Europe, it is
regarded as a primary imaging method (Fig. 3). Thickening
of the AT is easily detected with both methods. Only if US
remain unclear, an additional magnetic resonance study
should be performed and, together with the clinical
diagnosis, indications for surgery can be made more
efficiently.
73
One of the main advantages of US over other
imaging modalities is the interactive facility, which helps
reproducing symptom by transducers compression and
concentrate on the pathologic area.
74
Although US can
demonstrate alterations in the AT with high specificity and
sensitivity it has, like MRI, a relatively high incidence of
false positive findings.
75
In a cross-sectional study on badminton players,
76
doppler flow was not associated with AT pain but with an
increased anteroposterior tendon diameter (an indicator of
tendinopathy). Athletes who had been playing badminton
for longer were more likely to have Doppler flow, and there
was a trend toward an association between a greater
number of badminton playing hours per week and Doppler
flow. The authors concluded that AT Doppler flow seemed
to be a sign of asymptomatic tendinopathy rather than pain
among active athletes. The association between weekly
badminton hours and badminton years and Doppler flow
suggested that Doppler flow may be a response to
mechanical load.
Victorian Institute of Sports Assessment-Achilles
To be in a position to practice evidence-based
medicine, the sports medicine community must conduct
studies with objective outcome measures. We developed
and tested the Victorian Institute of Sports Assessment-
Achilles (VISA-A), a questionnaire-based instrument to
measure the severity of Achilles tendinopathy.
77
To develop
the questionnaire, we performed item generation, item
reduction, item scaling, and pretesting. We then tested its
validity and reliability in clinical and control populations.
The VISA-A questionnaire contained 8 questions that
covered the 3 domains of pain (questions 1 to 3), function
(questions 4 to 6), and activity (questions 7 and 8.)
FIGURE 2. Magnetic resonance imaging showing tendinopathy
of the main body of the Achilles tendon.
FIGURE 3. Ultrasound view showing thickening of the Achilles
tendon.
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Questions 1 to 7 are scored out of 10, and question 8 carries
a maximum of 30. Scores are summed to give a total out
of 100. An asymptomatic person would score 100. For
question 8, participants must answer only part A, B, or C.
If the participant has pain when undertaking sport, he or
she automatically loses at least 10, and possibly 20, points.
The VISA-A questionnaire provides a valid, reliable,
and user-friendly index of the severity of Achilles tendino-
pathy. Although the limited time for consultation in routine
clinical practice means that the main role of this tool is
likely to be as an outcome measure in treatment studies, the
VISA-A scale can be easily administered in clinical practice.
The VISA-A has been cross-cultural adapted to Swedish
78
and Italian.
79
MANAGEMENT
Conservative Management of Tendinopathy
of the Main Body of Tendo Achillis
Over the past few years, various new therapeutic
options have been proposed for the management of Achilles
tendinopathy. Despite the morbidity associated with Achilles
tendinopathy in athletes, management is far from scienti-
fically based, and many of the therapeutic options described
and in common use are lacking a hard scientific back-
ground.
32,80
Physical therapy, rest, training modification, splintage,
taping, cryotherapy, electrotherapy, shock wave therapy,
hyperthermia, pharmaceutical agents such as nonsteroidal
anti-inflammatory drugs (NSAIDs) and various peritendi-
nous injections have been proposed. Most essentially follow
the same principles. Managements that have been investi-
gated with randomized controlled trials include non-
steroidal anti-inflammatory medication, eccentric exercise,
glyceryl trinitrate patches, electrotherapy (microcurrent
and microwave), sclerosing injections, and shock wave
treatment. Surgery should be reserved to patients in whom
conservative management has proved ineffective for at least
6 months.
Despite this abundance of therapeutic options, very
few randomized prospective, placebo, controlled trials exist
to assist in choosing the best evidence-based management.
81
There are no randomized or prospective studies that
compare different conservative and surgical management
regimens.
NSAIDs
Pharmacologic management strategies are essentially
based on empirical evidence. Even though tendon biopsies
show an absence of inflammatory cell infiltration,
19,20
anti-
inflammatory agents (NSAIDs and corticosteroids) are
commonly used. What may seem clinically as an ‘‘acute
tendinopathy’’ is actually a well-advanced failure of a
chronic healing response in which there is neither histologic
nor biochemical evidence of inflammation.
NSAIDs inhibit tissue inflammation by repressing
cyclooxygenase (COX) activity; with a reduction in the
synthesis of proinflammatory prostaglandins.
82
Manage-
ment of an anatomically defined medical condition is
ideally based on an understanding of its pathophysiology.
Although, as noted earlier, tendinopathy has a noninflam-
matory basis, NSAIDs are widely used in attempts as a
treatment.
83
Ironically, the analgesic effect of NSAIDs
84
allows patients to ignore early symptoms, possibly impos-
ing further damage on the affected tendon and delaying
definitive healing.
Topical naproxen gel produced a marginal advantage
in relieving symptoms after 3 and 7 days in patients with
acute tendinopathies who had symptoms for less than 48
hours.
85
Although NSAIDs may provide some pain relief in
such patients, they do not actually result in sustained
improvement in the healing process.
86
It is still not known
whether NSAIDs actually change the natural history of
Achilles tendinopathy or whether they merely exert an
analgesic action.
86
Recent studies on rats with acute tendon
injuries show that NSAID administration does not prevent
collagen degradation and loss of tensile force in tendons.
87
It is therefore questionable whether NSAIDs should be
used to alleviate pain in so-called acute tendinopathy.
87
NSAIDs are not effective in athletes with Achilles
tendinopathy.
88
Most studies of NSAID treatment of
tendinopathy have a short follow-up.
86
Double blind,
randomized, placebo-controlled clinical trials of NSAIDs
used in the management of tendinopathies based on clinical
symptoms and signs only have shown no beneficial effects.
89
Even these placebo-controlled clinical studies are difficult to
interpret because of the inability to control for the severity
of the lesion, level of athletic participation, and other
variables. NSAIDs could theoretically benefit patients with
tendinopathy by increasing the tensile strength of tendons
via accelerated formation of cross-linkages between col-
lagen fibers.
88,90
In animal models, COX inhibitors do show
a beneficial effect on tendon regeneration after transection,
in exactly this fashion.
91
However, these studies were
conducted on rats with tendo Achillis that had been
surgically divided, a situation that does not reflect the
conditions encountered in chronic tendinopathy. Another
study using a rat model showed that, in the first few days
after tendo Achillis transection, the inflammatory response
was necessary for normal repair, and should not be
inhibited.
92
Early NSAID administration led to a reduction
in the amount of force and stress required for the tendon to
fail.
92
During remodeling, on the other hand, inflammation
has a negative influence, and NSAIDs such as COX-2
inhibitors might be valuable for the final outcome.
92
Indeed, late treatment with COX-2 inhibitors leads to
increased tensile strength, although they do not change the
histopathologic picture.
92
COX-2 inhibitors should there-
fore be avoided in the early period after tendon injury,
given their deleterious effect on tensile strength.
Although in vitro studies on human tendon fibroblasts
treated with NSAIDs have shown a decreased expression of
prostaglandin E
2
, they also show an increased expression of
leukotriene B4.
93
The reduction in prostaglandin E
2
may
give patients some pain relief; increased leukotriene B4,
however, could potentially exacerbate the situation via
increased neutrophilic infiltration and lymphocyte activa-
tion,
94
paradoxically causing inflammatory and degenera-
tive changes in the tendon. Thus, in tendinopathy,
leukotriene pathway activation occurs after cyclical strain
on tendons, and administration of NSAIDs may actually
worsen the condition.
Evidence for the effectiveness of any available drug
management regimen is at best controversial when tested in
randomized controlled trials.
46
Pharmacologic manage-
ment strategies for tendinopathies vary considerably, and
are frequently based on empirical evidence. The continued
use of NSAIDs for the treatment of tendinopathies is
hardly justified. The available literature suggests that, in the
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absence of an overt inflammatory process, there is no
rational basis for the use of NSAIDs in chronic tendino-
pathy: they are unlikely to change its still ill defined natural
history.
95
Despite this reality, many clinicians still antici-
pate a quicker and better recovery using these agents. There
is no biologic basis for NSAID effectiveness in treating this
condition, and no evidence of any benefit. NSAIDs seem to
be effective, to some extent, for pain control. Early NSAIDs
administration after an injury may have a deleterious effect
on long-term tendon healing. It would thus seem reasonable
to shift our research efforts to other forms of conservative
management. Examining strategies that promote the mig-
ration and activation of tenocytes to influence tendon
healing and function might be an appropriate first step. It is
equally appropriate to limit our use of NSAIDs in the
management of tendinopathy. What may seem clinically as
an ‘‘acute tendinopathy’’ is actually a well-advanced failure
of a chronic healing response in which there is neither
histologic nor biochemical evidence of inflammation.
Clearly there is a controversy on whether NSAIDs
help or hinder the healing process. However, most
commonly they do provide pain relief, the one thing the
patient consults a physician for. Therefore a careful balance
between the underlying pathophysiologic condition being
managed and the patient’s subjective concerns for pain
relief should be considered.
Cryotherapy
Cryotherapy has been regarded as a useful interven-
tion in the acute phase of Achilles tendinopathy, as it has an
analgesic effect, reduces the metabolic rate of the tendon,
and decreases the extravasation of blood and protein from
new capillaries found in tendon injuries.
96
However, recent
evidence in upper limb tendinopathy indicates that the
addition of ice did not offer any advantage over an exercise
program consisting of eccentric and static stretching
exercises.
97
Eccentric Exercise
Scandinavian authors have shown that, in their hands,
a program of eccentric exercise is effective in the
nonoperative management of tendinopathy.
98
A program
of eccentric exercise has been proposed to counteract the
failed healing response which apparently underlies tendino-
pathy, by promoting collagen fiber cross-linkage formation
within the tendon, thereby facilitating tendon remodeling.
95
Although evidence of actual histologic adaptations after an
adapted program of eccentric exercise are lacking, and the
mechanisms by which a program of eccentric exercise may
help to resolve the pain of tendinopathy remain unclear,
clinical results after such exercise program seem promis-
ing.
95,99
Though effective in Scandinavian population,
99,100
the results of eccentric exercises observed from other study
groups
101,102
are less convincing than those reported from
Scandinavia, with a 50% to 60% of good outcome after a
regime of eccentric training both in athletic and sedentary
patients. In general, the overall trend suggested a positive
effect of an exercise program, with no study reporting
adverse effects. In a longitudinal study of 34 sedentary
patients (18 males, average age 44 y, range: 23 to 67; 16
females, average age 51 y, range: 20 to 76; average BMI:
28.6 ± 4.7, range: 22.1 to 35.4) with a clinical diagnosis of
unilateral tendinopathy of the main body of the AT, the
patients underwent a graded progressive eccentric calf
strengthening exercises program for 12 weeks. Fifteen
patients (44%) did not improve with eccentric exercise
regimen. Three patients improved after perintendinous
injections of aprotinin and local anesthetic. Surgery was
performed in 7 patients as 6 months of conservative
management failed to produce improvements. The overall
average VISA-A scores at latest follow-up was 50 (SD
26.5). Eccentric exercises, though effective in nearly 60% of
our patients, may not benefit sedentary patients to the same
extent reported in athletes. A further study in 45 athletic
patients (29 men, average age 26 y ± 12.8, range: 18 to 42;
16 women, average age 28 y ± 13.1, range: 20 to 46; average
height: 173 ± 16.8, range: 158 to 191; average weight
70.8 kg ± 15.3, range: 51.4 to 100.5) showed that only 27
of the 45 patients responded to the eccentric exercises. Of
the 18 patients who did not improve with eccentric
exercises, 5 (mean age 33 y) improved with 2 peritendinous
aprotinin and local anesthetic injections. Ten of the 18
patients (9 men, mean age 35 y; 1 woman aged 40 y) who
did not improve with eccentric exercises and aprotinin
injections proceeded to have surgery. The remaining 3
patients (3 women, mean age 59.6 y; 2 men, mean age 63 y)
of the 18 nonresponders to eccentric exercises and aprotinin
injections declined surgical intervention.
Owing to the lack of high-quality studies with
clinically significant results, no strong conclusions can be
made regarding the effectiveness of eccentric training
(compared with control interventions) in relieving pain,
improving function or achieving patient satisfaction.
Treatment effects are found to be overestimated in low
quality systematic reviews where nonrandomized studies
such as prospective cohorts are included. This may be due
to nonrandomization and inadequate allocation conceal-
ment methods contained within these prospective studies.
The treatment regime most commonly used is derived
from an initial study of Achilles tendinopathy. This
comprised 3 sets of 15 repetitions, carried out twice daily,
7 days a week for 12 weeks. It was found that the regime
was based on clinical experience, rather than derived from
any empirical evidence; for example, data from ‘‘dose
response’’-type studies
103
(Figs. 4A–H).
However, the lack of understanding about the basic
pathophysiology of tendinopathy makes determining the
optimal dosage of intervention difficult. Because the studies
in this area have not used an underlying rationale to
determine loading parameters, progressions and frequency
of treatment, further research needs to be undertaken
before an optimal dosage can be determined.
104,105
We performed a randomized controlled trial in whom
we compared the efficacy of 3 protocols—a wait-and-see’
approach, repetitive low-energy shock wave therapy, and
eccentric calf strengthening—for the management of
chronic tendinopathy of the main body of the tendo
Achillis. We concluded that spontaneous recovery after
more than 6 months of symptoms of tendinopathy of the
main body of the tendo Achillis is unlikely in the majority
of patients. The likelihood of recovery after 4 months was
comparable after both eccentric loading and shock wave
therapy, as applied. Success rates were in the region of 60%
with either of these management modalities. Eccentric
training or shock wave therapy should be offered to
patients with chronic recalcitrant tendinopathy of the main
body of tendo Achillis as an alternative to surgery.
Combined management strategies (eccentric training
and shock wave therapy) resulted in even higher success
rates compared to eccentric loading alone or shock wave
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therapy alone in a recent randomized controlled trial.
106
Eccentric training plus shock wave therapy should be
offered to patients with chronic recalcitrant tendinopathy of
the main body of the AT.
106
Nitric Oxide
Nitric oxide is a small-free radical generated by a
family of enzymes, the nitric oxide synthases. In a series of
experiments performed over the last 15 years, nitric oxide
played a crucial beneficial role in restoring tendon
function.
107
Free radicals are atoms or molecules with an
unpaired electron. The absence of an electron makes them
highly unstable and highly reactive. In biology, in large
doses, oxygen free radicals are toxic. Oxygen free radicals,
for instance, are responsible in large part for the catabolic
effects of ischemia-reperfusion injury, for radiation da-
mage, and for the toxic effects of ultraviolet light. All
organisms, including human beings, have developed me-
chanisms including enzymatic scavengers to protect against
free radical damage. Perhaps because free radicals have
been present for so long, many organisms have adapted
these for other purposes, and, in lower physiologic doses,
free radicals can be very effective messenger molecules.
108
Oxygen free radicals, in the correct dose, stimulated
fibroblast proliferation. Nitric oxide can enhance tendon
healing. Nitric oxide is 1 of the 10 smallest molecules. Its
size and its high reactivity allow it to travel across nearly
all biologic structures and to readily react with other atoms
or molecules to effect a change. Recently, a prospective,
randomized, double-blinded, placebo-controlled clinical
trial was performed in patients with tendinopathy of the
main body of the Achilles to evaluate the efficacy of nitric
oxide administration via an adhesive patch.
109
Topical
glyceryl trinitrate was demonstrated efficacy in treating
chronic noninsertional Achilles tendinopathy, and the
treatment benefits continue at 3 years.
108
Significant
differences in asymptomatic patient outcomes for the
glyceryl trinitrate group continue at 3 years, and this is
confirmed by the effect size estimate. This suggests that the
mechanism of action of topical glyceryl trinitrate on
chronic tendinopathies is more than an analgesic effect.
108
However, a recent study
110
failed to support the
clinical benefit of topical glyceryl trinitrate patches. There
did not seem to be any histologic or immunohistochemical
change in Achilles tendinopathy treated with topical
glyceryl trinitrate compared with those undergoing stan-
dard nonoperative therapy.
Intratendinous Injection
Sonographically guided intratendinous injection
of hyperosmolar dextrose yielded a good clinical response
in patients with chronic tendinopathy of the tendo
Achillis.
111,112
Sclerosing Injections and Neovascularization
In patients with chronic painful tendinopathy of tendo
Achillis, but not in normal pain-free tendons, there is
neovascularization outside and inside the ventral part of the
tendinopathic area. During eccentric calf muscle contrac-
tion, the flow in the neovessels disappears on ankle
dorsiflexion.
113,114
The good clinical effects with eccentric
training may be due to action on the neovessels and
accompanying nerves. Also, local anesthetic injected in the
area of neovascularization outside the tendon resulted in a
pain-free tendon, indicating that this area is involved in
pain generation. The above findings are the bases for a
novel management modality whereby the sclerosing sub-
stance polidocanol under US and color Doppler-guidance
is injected targeting the area with neovessels and nerves
outside the tendon. Rehabilitation after sclerosing
FIGURE 4. Figures from A to H show the sequence of the eccentric training.
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injections includes a short period of rest (1 to 3 d), followed
by gradual increase of tendon loading activities, but no
maximum loading (jumping, fast runs, heavy strength
training) for the 2 weeks. After this period, normal tendon
loading is allowed.
High Volume US-Guided Injections
The etiology of pain in tendinopathy is widely
debated, with recent evidence that neovascularization and
neo-innervation may be responsible.
115
Neovascularization
is mainly present in patients with tendinopathy, and the
area in which patients perceive most pain correlates with
the area where most neovascularization occurs on power
Doppler US.
115
We conducted a pilot study in patients with tendino-
pathy of the main body of tendo Achillis.
116
A high volume
image guided tendo Achillis injection of normal saline in
patients with resistant Achilles tendinopathy decreased the
amount of pain perceived by patients, whereas at the same
time by improving daily functional ankle and Achilles
movements in the short-term and long-term.
Physical Modalities
The role of physical modalities in the management
of tendinopathies remains unclear, and it is not possible
to draw firm, evidence-based conclusions on their
effectiveness.
Low-energy shock wave therapy to address the failed
healing response of a tendon is not widely known among
the medical community. A shock wave is defined as an
acoustic wave at the front of which pressure rises from the
ambient value to its maximum within a few nanoseconds.
117
Typical characteristics are high peak-pressure amplitudes
(500 bar) with rise times of < 10 ns, a short lifecycle (10 ms)
and a frequency spectrum (from 16 Hz to 20 MHz) ranging
from the audible to the far ultrasonic level.
118
This rapid
rise is followed by periods of pressure dissipation and
negative pressure before gradually returning to the ambient
pressure. The shock wave entering the tissue may be
reflected or dissipated, depending on the properties of the
tissue. The energy of the shock wave may act through
mechanical forces generated directly or indirectly via
cavitation.
118
The rationale for its clinical use being
stimulation of soft tissue healing and inhibition of pain
receptors, and hence, shock wave therapy has been
thoroughly investigated experimentally during the past
decade.
There is no consensus on the use of repetitive low-
energy shock wave therapy, which does not require local
anesthesia, and on the use of high-energy shock wave
therapy, which requires local or regional anesthesia.
101
Low-energy shock wave therapy has been used in patients
with chronic tendinopathy. The randomized controlled
trials on this subject are statistically and clinically hetero-
geneous, thus making conclusions from pooled meta-
analyses difficult to interpret. We have tested low energy
shock wave therapy for chronic tendinopathy of the main
body of the tendon Achillis using a randomized controlled
trial design.
119
Low energy shock wave therapy and
eccentric training produced comparable results, and both
management modalities showed outcomes superior to the
wait-and-see policy. The likelihood of recovery after 4
months was comparable after both eccentric loading
and shock wave therapy, but success rates were from
50% to 60%.
Hyperthermia induced by microwave diathermy raises
the temperature of deep tissues from 41 to 451C using
electromagnetic power.
119
Microwave diathermy has been
used physical medicine and sports traumatology in Central
and Southern Europe. Hyperthermia induced into tissue by
microwave diathermy can stimulate repair processes,
increase drug activity, allow more efficient relief from pain,
help removal toxic wastes, increase tendon extensibility and
reduce muscle and joint stiffness.
119
The biologic mechan-
isms that regulate the relationship between the thermal dose
and the healing process of soft tissues with low or high
water content or with low or high blood perfusion are
unknown. A recent randomized controlled trial in athletes
showed that hyperthermia is effective in the management of
established supraspinatus tendinopathy.
120
This modality
warrants further studies with a greater number of patients
and a longer-term follow-up to confirm its therapeutic
effectiveness. Nevertheless, adequately designed prospec-
tive-controlled clinical studies need to be completed to
confirm the therapeutic effectiveness of hyperthermia with
large number of patients, longer-term follow-up and mixed
populations. It is possible that it only exerts a relatively
short lived, but nevertheless useful, analgesic effect.
Ultrasound therapy is a widely available and fre-
quently used electrophysical agent in sports medicine.
However, systematic reviews and meta-analyses have
repeatedly concluded that there is insufficient evidence to
support a beneficial effect of US at dosages currently being
introduced clinically. A new direction for US therapy in
sports medicine has been proposed by research demonstrat-
ing that US can have clinically significant beneficial effects
on injured tissue when low-intensity pulsed US is used.
120
Low-intensity pulsed US refers to pulsed-wave US with a
spatial-averaged, temporal-averaged intensity equal to or
lower than 100 mW/cm
2
. This intensity is categorized as low
relative to the range that is commonly used in physical
therapy (from 0.5 to 2 W/cm
2
).
120
Low-intensity pulsed US
has been shown to be beneficial in accelerating fracture
healing in clinical studies and to stimulate union in 86% of
fractures displaying nonunion.
120
Although established in
the intervention of bone injuries, recent efforts have been
directed toward the effect of low-intensity pulsed US on
injuries to other connective tissues.
121
Low-intensity pulsed
US therapy has been tested in a randomized, double-blind,
placebo-controlled trial in patients with chronic lateral
epicondylitis.
45
It was no more effective for a large
treatment effect than placebo for recalcitrant lateral epico-
ndylitis.
Summary of Nonoperative Management of
Achilles Tendinopathy
Pharmacologic management strategies are essentially
based on empirical evidence. Even though they are not
proved for the management of Achilles tendinopathy, their
use is controversy, because they do provide pain relief, the
one thing the patient consults a physician for. In our clinical
practice commonly we do not prescribe NSAIDs. Cryother-
apy has been regarded as a useful intervention in the acute
phase of Achilles tendinopathy, as it has an analgesic effect.
A program of eccentric exercise can improve patient’s
symptoms in nearly 60% of the patients. In general, the
overall trend suggested a positive effect of an exercise
program, with no study reporting adverse effects. No
definitive evidences have been reached for the use of nitric
oxide to enhance tendon healing. Sclerosing injections can be
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an option, but contrasting results have been reported. High
volume US-guided injections are a new option of manage-
ment, and in our clinical practice this is the modality of
choice when a program of eccentric training fails to improve
patient’s symptoms. The role of physical modalities in the
management of tendinopathies remains unclear, and it is not
possible to draw firm evidence-based conclusions on their
effectiveness. There is some evidence that low-energy shock
wave therapy is useful to address the failed healing response
of a tendon. We also demonstrated a synergistic effect of
eccentric training and shock wave therapy.
Surgical Management of Tendinopathy of the
Main Body of Tendo Achillis
In 24% to 45.5% of patients with Achilles tendino-
pathy, conservative management is unsuccessful, and
surgery is recommended after exhausting conservative
methods of management, often tried for at least 6
months.
25,122
However, long-standing Achilles tendinopa-
thy is associated with poor postoperative results, with a
greater rate of reoperation before reaching an acceptable
outcome.
123
The objective of surgery is to excise fibrotic adhesions,
remove areas of failed healing and make multiple long-
itudinal incisions in the tendon to detect intratendinous
lesions and to restore vascularity and possibly stimulate the
remaining viable cells to initiate cell-matrix response and
healing.
96
Recent studies show that multiple longitudinal
tenotomies trigger neoangiogenesis at the tendo Achillis,
with increased blood flow.
124
This would result in improved
nutrition and a more favorable environment for healing.
Patients are encouraged to weight bear as soon as possible
after surgery.
Most authors report excellent or good results in up to
85% of cases, although this is not always observed in
routine nonspecialized clinical practice. It is difficult to
compare the results of studies, as most investigations do not
report their assessment procedure. Also, no prospective
randomized studies comparing operative and conservative
treatment of Achilles tendinopathy have been published,
thus most of our knowledge on treatment efficacy is on the
basis of clinical experience and descriptive studies.
It is still debatable why tendinopathic tendons respond
to surgery. For example, we do not know whether surgery
induces long-term revascularization, denervation or both,
resulting in pain reduction. It is also unclear exactly how
longitudinal tenotomy improves vascularization. Proximal
to its calcaneal insertion, the AT lies immediately super-
ficial to the pre-Achilles fat pad, a triangular area of
adipose tissue known as Kager’s triangle.
We introduced a new minimally invasive stripping of
neovessels from the Kager’s triangle of the tendo Achillis
for patients with Achilles tendinopathy.
125
This achieves a
safe and secure breaking of neovessels and the accompany-
ing nerve supply.
MINIMALLY INVASIVE STRIPPING
In chronic painful tendinopathy of tendo Achillis,
but not in normal pain-free tendons, there is neovascular-
ization outside and inside the ventral part of the tendino-
pathic area.
31,35,126–128
During eccentric calf muscle
contraction, the flow in the neovessels disappears on ankle
dorsiflexion. The good clinical effects with eccentric
training may be due to action on the neovessels and
accompanying nerves.
31,35,126,127
Classically, open surgery
for tendinopathy of the main body of the AT has provided
good results.
31
However, wound complications can occur
with these procedures, and recovery is prolonged.
25
We have developed a novel management modality
whereby a minimal invasive technique of stripping of neo-
vessels from the Kager’s triangle of the AT is performed.
This achieves a safe and secure breaking of neovessels and
the accompanying nerve supply.
The patient undergoes local or general anesthesia,
according to surgeon’s or patient’s preferences. The patient
is positioned prone with a calf tourniquet that is inflated to
250 mm Hg after exsanguination. Four skin incisions are
made. The first 2 incisions are 0.5 cm longitudinal incisions
at the proximal origin of the AT, just medial and lateral to
the origin of the tendon. The other 2 incisions are also
0.5 cm long and longitudinal, at the level of the tendon
insertion on the calcaneus.
Mosquito forceps or a tendon passer is inserted in the
proximal incisions (Fig. 5A), and the AT is freed of the
peritendinous adhesions. A number 1 unmounted Ethibond
(Ethicon, Somerville, NJ) suture thread is inserted proxi-
mally, passing through the 2 proximal incision. The
Ethibond is retrieved from the distal incisions (Fig. 5B),
over the posterior aspect of the AT. Using a gentle see-saw
motion, similar to using a Gigli saw, the Ethibond suture
thread is made to slide posterior to the tendon (Fig. 5C),
which is stripped and freed from the fat of Kager’s triangle.
Our minimal invasive technique reduce the risks
of infection, is technically easy to master, and inexpensive.
It may provide greater potential for the management
of recalcitrant AT by breaking neovessels and the accom-
panying nerve supply to the tendon. It can be associated
with other minimally invasive procedures to optimize the
results.
FIGURE 5. A mosquito is inserted in the proximal incisions (Fig. 5A). The Ethibond is retrieved from the distal incisions (Fig. 5B).
The Ethibond is slid over the anterior aspect of the Achilles tendon with a gentle see-saw motion (Fig. 5C).
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The pathogenetic significance of the neovascularization is
unknown, but several theories can be proposed. The
increased vascularization often seen in biopsies from
patients with chronic painful tendinopathy of tendo Achillis
who underwent surgery is a part of a reparative response in
the tendon.
128,129
Reparative processes associated with
neovascularization are probably inadequate.
25,126
Surgery
is successful in up to 85% of patients,
25
even though
postoperative US examination often shows a widened
tendon with hypo-echoic areas. This has led to hypotheses
of a possible denervation of the tendon as one of the
explanations to the frequently favorable effect of surgery.
130
Our rationale behind the present management mod-
ality is that the sliding of the Ethibond breaks the
neovessels and the accompanying nerve supply, therefore
decreasing the pain in patients with chronic Achilles
tendinopathy.
Percutaneous Longitudinal Tenotomy
We have used multiple percutaneous longitudinal
tenotomies when conservative management has failed in
patients with isolated tendinopathy with no involvement of
the paratenon and a well-defined nodular lesion less than
2.5 cm long.
45
US can be used to confirm the precise
location of the area of tendinopathy. If the multiple
percutaneous tenotomies are performed in the absence of
chronic paratendinopathy, the outcome is comparable to
that of open procedures. It is a simple procedure and can be
performed in the clinic under local anesthesia without a
tourniquet, but attention to detail is necessary, as even in
minimally invasive procedures complications are possible.
Percutaneous longitudinal US-guided internal teno-
tomy of the tendo Achillis is simple and can be performed
on an outpatient basis. It, however, requires the use of high-
resolution US to properly locate the tendinopathic area and
to place the initial stab wound. Also, with this technique, it
is not possible to collect samples of tendon material for
biopsy, even though recent work has shown that sympto-
matic intratendinous areas are hypo-echoic at US show
tendinosis. Complications were minimal and led to no long-
term morbidity. In our hands, it is an intervention in the
management of chronic Achilles tendinopathy when con-
servative treatment has failed. The technique is not as
effective in patients with pantendinopathy.
Operative Technique
The patient lies prone on the examination couch with
the feet protruding beyond the edge, and the ankles resting
on a sandbag. A bloodless field is not necessary. The tendon
is accurately palpated, and the area of maximum swelling
and/or tenderness marked, and checked by US scanning.
The skin is prepped with an antiseptic solution, and a sterile
longitudinal 7.5-MHz probe is used to image again the
area of tendinopathy. Before infiltrating the skin and the
subcutaneous tissues over the tendo Achillis with 10 mL of
1% lignocaine (Pierrel, Milan, Italy), 7 mL of 0.5%
lignocaine is used to infiltrate the space between the tendon
and the paratenon, to try and distend the paratenon and
break the adherences that may be present between the
tendon and the paratenon. Under US control, a number 11
surgical scalpel blade (Swann-Morton, London, UK) is
inserted parallel to the long axis of the tendon fibers in the
center of the area of tendinopathy, as assessed by high-
resolution US imaging. The cutting edge of the blade points
caudally and penetrates the whole thickness of the tendon.
Although keeping the blade still, a full passive ankle flexion
is produced. The scalpel blade is then retracted to the
surface of the tendon and inclined 45 degree on the sagittal
axis, and the blade is inserted medially through the original
tenotomy. Although keeping the blade still, a full passive
ankle flexion is produced. The whole procedure is repeated
inclining the blade 45 degree laterally to the original
tenotomy, inserting it laterally through the original
tenotomy. Although keeping the blade still, a full passive
ankle flexion is produced. The blade is then partially
retracted to the posterior surface of the tendo Achillis,
reversed 180 degree, so that its cutting edge now points
caudally, and the whole procedure repeated, taking care to
dorsiflex the ankle passively. A Steristrip (3M United
Kingdom PLC, Bracknell, Berkshire, UK) can be applied
on the stab wound, or the stab wound can be left open. The
wound is dressed with cotton swabs, and a few layers of
cotton wool and a crepe bandage are applied.
OPEN SURGERY
Surgical Technique
The prone position allows excellent access to the
affected area. Alternatively, the patient can be positioned
supine with a sandbag under the opposite hip and the
affected leg positioned in a figure-of-four position. Open
surgery for tendinopathy of the main body of the tendo
Achillis involves a longitudinal incision. Generally the
incision is made on the medial side of the tendon to avoid
injury to the sural nerve and short saphenous vein. A
straight posterior incision may also be more bothersome
with the edge of the heel counter pressing directly on the
incision. Preoperative imaging studies can guide the
surgeon in the placement of the incision. The skin edge of
the incision should be handled with extreme care through-
out the procedure, as wound-healing problem are possible
and potentially disastrous. The paratenon is identified and
incised. In patients with evidence of coexisting paratendi-
nopathy, the scarred and thickened tissue is generally
excised. Care should be taken to minimize dissection and
excision on the anterior side of the tendon. The fatty tissue
anteriorly is thought to contain much of the vascular supply
to the tendon. On the basis of preoperative imaging studies,
the tendon is incised sharply in line with the tendon fiber
bundles. The tendinopathic tissue can be identified as it
generally has lost its shiny appearance, and frequently
contains disorganized fiber bundles that have more of a
‘‘crabmeat’’ appearance. This tissue is sharply excised. The
remaining gap can be repaired using a side-to-side repair. If
significant loss of tendon tissue occurs during the debride-
ment, consideration could be given to a tendon augmenta-
tion or transfer, even though we rarely undertake this
additional procedure. A tendon turn-down flap has been
described for this purpose. With a turn-down procedure, 1
or 2 strips of tendon tissue from the gastrocnemius tendon
is dissected out proximally whereas leaving the strip
attached to the main tendon distally. It is then flipped 180
degree and sewn in to cover and bridge the weakened defect
in the distal tendon. A plantaris weave has also been
reported for this purpose. The plantaris tendon can be
found on the medial edge of the tendo Achillis. It can be
traced proximally as far as possible and detached as close as
possible to the muscle tendon junction to gain as much
length as possible. It can be left attached distally to the
calcaneus, looped, and weaved through the proximal tendo
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Achillis and sewn back onto the distal part to the tendon.
Alternatively, the plantaris can be detached distally as well
and used as a free graft. Finally, transfer and augmentation
with the flexor hallucis longus tendon has been reported.
21
Open surgery for tendinopathy of the main body of the
AT can be considered if prolonged nonoperative manage-
ment fails. However, patients should be informed of the
potential failure of the procedure, risks of wound complica-
tions and at times prolonged recovery time.
131
The surgical
procedure is relatively straightforward, but on occasion
may require concomitant transfer of tendon tissue to
reinforce the weakened tendon. Rehabilitation is focused
on early motion and avoidance of overloading the tendon
in the initial healing phase.
Other Operative Techniques
Muscle Transfer to the Body of the Tendon
Longitudinal tenotomies increase the blood supply of
the degenerated area. Recently, in a rabbit model, after
longitudinal tenotomy we performed a soleus pedicle graft
within the operated tendon, and showed that the trans-
planted muscle was viable and had integrated well within
the tendon tissue 3 months after the transplant, without
transforming into connective tissue. The transplanted
muscle fibers integrated with the tendon but remained
distinct from it. Hypervascularization of the graft tissue,
probably owing to the operation, was also observed,
together with neoangiogenesis up to 3 months after the
operation.
132
OUTCOME OF SURGERY
We performed a systematic review of the available
published literature covering the years from 1966 to 1999 to
identify all studies that reported the outcome of surgery for
Achilles tendinopathy as their primary aim.
133
Keywords
used in the search were tendo Achillis, tendinitis, tendon,
postoperative complications, tendon injuries, and tendino-
pathy. Subheadings used in the search were surgery,
pathology, physiology, and imaging. All journals were
considered and all relevant articles were retrieved. Most of
the articles that reported surgical success rates revealed
successful results in over 70% of cases. However, this
relatively high success rate is not always observed in clinical
practice. The articles that reported success rates higher than
70% actually had poorer methods scores. This finding
could be used as evidence that the discrepancy between
published and actual outcomes is due to the deficiencies in
methods; this also points the way for developing a set of
criteria that should be used to plan future surgical studies.
GENETICS
A genetic component has been implicated in tendino-
pathies involving the AT.
134,135
An underlying genetic
factor as a contributing cause to AT injury was originally
proposed because of an association between the ABO blood
group and the incidence of AT ruptures or chronic Achilles
tendinopathy evident in Hungarian and Finnish popula-
tions with blood group O.
136
The distribution of the ABO and Rh blood groups was
determined in 832 patients with a tendon rupture. Among
these, the frequency of blood group O (52.8%) was
significantly higher than in the general population of
Hungary (31.1%) and the frequency of group A was
significantly lower. Of the 83 cases of multiple ruptures or
rerupture, 57 patients (68.7%) had blood group O. The
dominance of group O was found for all sites of tendon
rupture, but there was no significant association with the
Rh groups. Individuals with blood group O seemed to have
an increased risk of tendon rupture.
136
The distribution of the ABO blood groups was studied
in Finland in 917 patients with specific musculoskeletal
diagnoses. The ABO blood group distribution of patients
with rupture of the AT (P= 0.030) and of patients with
chronic Achilles tendinopathy (P= 0.10) differed from the
controls. The ABO blood group distribution was not
associated with other musculoskeletal injuries studied. The
blood group A/O ratio was 1.42 in the control population.
In the group with rupture of the AT this ratio was 1.0, and
in the group with Achilles tendinopathy it was 0.70.
137
These studies implied that ABO or closely linked genes on
the tip of the long arm of chromosome 9 could be
associated with tendinopathy or tendon injuries. The gene
for ABO on chromosome 9q34 encode for transferases,
which apart from determining the structure of glycoprotein
antigens on red blood cells, may also determine the
structure of some proteins of the ECM of tendons.
136
To
test whether the association between blood groups and
AT rupture reported in Finland and in Hungary was
present in Scotland, the distribution of ABO blood groups
of 78 patients was compared with that found in 24,501
blood donors typed at the Blood Transfusion Centre during
the same period. Overall, 47 of 78 (60%) of patients with an
AT rupture belonged to blood group O, compared with
51% of the population as a whole. Only 22 (28%) of the
AT rupture patients belonged to blood group A, whereas
35% of the general population were members of this group
(NS). The A/O ratio was 0.47 for the tendon rupture
patients, compared with 0.68 for the general population.
The authors could not demonstrate any significant associa-
tion between the proportions of ABO blood groups and
ATR in the Grampian Region of Scotland.
138
The findings
in other studies could be due to peculiarities in the
distribution of the ABO groups in genetically segregated
populations.
138
Polymorphisms within the COL5A1 and tenascin-C
(TNC) genes have been associated with AT injuries in
a physically active population.
134,135
The COL5A1 gene,
which is in close proximity to the ABO genes on
chromosome 9q34
139
encodes for a structural component
of type V collagen which forms heterotypic fibers with type
I collagen in tendons and possibly plays an important role
in regulating fibrillogenesis and, therefore, tendon
strength.
140,141
COL5A1 gene has a role in the pathogenesis
of Achilles tendinopathy and it has been observed that
South African individuals with the A2 allele of this gene are
less likely to develop Achilles tendinopathy.
135
Although no
direct link with COL5A1 gene has been demonstrated, the
genes encoding for collagen I and III, namely COL1A1
and COL3A1, show relatively high but variable levels of
expression in normal tendon, and significantly increased
expression of both genes in painful tendinopathy.
142
This
correlation needs to be investigated further. TNC is a
modular and multifunctional ECM glycoprotein that is
exquisitely regulated during embryonic development and in
adult tissue remodeling.
143
The TNC gene, which encodes
for the ECM glycoprotein TNC in tendons, is also closely
linked to the ABO genes on chromosome 9q32 to q34.
144
The TNC gene is expressed in regions of the tendon
predominantly responsible for transmitting high levels of
Longo et al Sports Med Arthrosc Rev Volume 17, Number 2, June 2009
122 |www.sportsmedarthro.com r2009 Lippincott Williams & Wilkins

mechanical force, such as the myotendinous and osteoten-
dinous junctions,
145
and is regulated by mechanical loading
in a dose dependent manner.
145,146
The TNC protein is
involved in regulating cell-matrix interactions.
147
It inter-
acts with fibronectin, aggrecan, versican, brevican, neuro-
can, integrins, cell adhesion molecules and annexin II.
134
Allele distribution of the guanine-thymine (GT) dinucleo-
tide repeat polymorphism in the TNC gene is associated
with AT injury.
134
Alleles containing 12 and 14 GT repeats
were significantly higher in patients with AT injuries,
whereas alleles containing 13 and 17 GT repeats were
higher in the asymptomatic controls.
134
A possible biologic
explanation for TNC involvement in the etiology of AT
injuries could be explained by abnormal mechanical
loading leading to altered synthesis of TNC,
148
which
could disrupt the regulation of cell-matrix interactions in
the tendon,
147
with the onset of apoptotic changes in the
tenocytes.
149
The exact role of COL5A1 and TNC genes in
the pathogenesis of tendinopathy is still debated, and the
current evidence does not allow to clarify whether or not
COL5A1 and TNC genes are the ideal markers of
tendinopathy.
135
A negative association of a particular
gene, such as with the ABO system,
138
does not necessarily
mean that there is absolutely no association with that
particular gene(s) at that locus. The fact that certain studies
have found an association with the ABO system and tendon
injuries
138,150
warrants further investigation at that parti-
cular locus. It is also possible that other genes, yet to be
determined, may contribute towards the pathogenesis of
tendinopathy, which could be a polygenic condition, given
the multitude of the genes involved in maintaining normal
tendon homeostasis. On the basis of current evidence, it is
difficult to conceive that only a single gene and not multiple
genes are involved in the pathogenesis of Achilles tendino-
pathy. Thus, additional investigation needs to be performed
to identify these genes.
134,135,151
CONCLUSIONS
Achilles tendinopathy gives rise to significant morbidity,
and, at present, only limited scientifically proven manage-
ment modalities exist. The management of this condition
remains a challenge, especially in athletes, in whom the
physician often tries to be innovative. In many instances,
this carries with it an unquantifiable risk.
24
A better
understanding of tendon function and healing will allow
specific management strategies to be developed.
64,65,152
Many interesting techniques are being pioneered.
33,58,66,153
Although these emerging technologies may develop into
substantial clinical management options, their full impact
needs to be evaluated critically in a scientific fashion.
Future trials should use validated functional and clinical
outcomes, adequate methodology, and be sufficiently
powered. Clearly, studies of high levels of evidence, for
instance large randomized trials, should be conducted to
help answer many of the unsolved questions in this field.
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