Content uploaded by James E Gaida
Author content
All content in this area was uploaded by James E Gaida on Jul 09, 2017
Content may be subject to copyright.
12
Australasian Musculoskeletal Medicine • Vol 19, No. 2 • Aug 2015
Achilles tendinopathy: understanding the key
concepts to improve clinical management
Charlotte Ganderton1, Jill Cook2, Sean Docking2, Ebonie Rio2,
Mathijs van Ark2,3, Jamie Gaida2,4
1. La Trobe University, College of Science, Health and Engineering, Melbourne, Australia
2. Monash University, Department of Physiotherapy, Melbourne, Australia
3. University of Groningen, University Medical Center Groningen, Center for Sports Medicine, Groningen, The Netherlands
4. Canberra University, Discipline of Physiotherapy, Canberra, Australia
Introduction
Treating achilles tendinopathy requires great clinical skills
applied by thoughtful practitioners. Although often thought of
as a simple diagnosis with straightforward treatment, it can be a
complex and challenging condition to manage. The pathology, the
dierential diagnoses of mid and insertional Achilles tendinopathy
and the role of eccentrics need to be considered for every individual
you see with this condition.
Tendons are specialised connective tissue structures that
transfer forces produced by contractile cells of muscles to bone.
The Achilles tendon has an additional specialised function to
provide shock absorption and energy storage (e.g. while hopping)
to facilitate ecient movement.1 The Achilles mid-portion is
between 2cm and 6cm from the calcaneus; the Achilles insertion
less than 2cm from the calcaneus.2
Tendon pathology continuum model
Tendon is comprised of cells (tenocytes) embedded in an
extracellular matrix of collagen, elastin and ground substance
(proteoglycans, glycoproteins and water) (Figure 1). Tendon cells
are responsive to load, and will adapt the extracellular matrix to
withstand the loading environment.3 Disruption to this process
through relative overload alters the proteins produced by the cell
4, which can result in tendon pathology that ultimately decreases
the capacity of the tendon to tolerate loading.
Figure 1: Normal tendon histology (H&E stain, 100x)
This article is an updated re-publication of an article64 in the
German language journal SportsPhysio (published by Thieme)
and is reproduced with their kind permission.
Professor Cook is supported by the Australian Centre for
Research into Sports Injury and its Prevention, which is one
of the International Research Centres for Prevention of Injury
and Protection of Athlete Health supported by the International
Olympic Committee (IOC). Prof. Cook is supported by a NHMRC
practitioner fellowship (1058493).
Abstract
Introduction: Achilles tendinopathy is commonly
encountered in clinical practice yet can be quite dicult to
successfully treat. Relative overload is the precursor to most
presentations, while systemic conditions can decrease the amount
of load that triggers overload. While there is evidence for the
use of eccentric exercise, it is not recommended in isolation for
most presentations of Achilles tendinopathy as it fails to address
strength and kinetic chain decits, which can leave the individual
vulnerable to recurrence. Insertional tendinopathy requires a
tailored management that avoids dorsiexion, as this position
compresses the tendon onto the calcaneus.
Purpose: This masterclass summarises the tendinopathy
continuum and articulates the authors’ clinical reasoning and
hands-on experience managing Achilles tendinopathy. We outline
graded loading concepts while emphasising that relying on recipes
is likely to fail. We also provide a perspective on the role of central
pain processing and peripheral input from nociceptive bres in
the context of tendinopathy.
Inplications: Rehabilitation should be tailored to address
identied impairments (muscle bulk asymmetries, kinetic chain
dysfunction, tolerance of energy storage and release in the Achilles
tendon), and progressively work toward movements and activities
relevant for the individual’s sport or daily activities. Within the
three-stage rehabilitation sequence, stage 1 aims to reduce pain
and increase calf muscle bulk; stage 2 focuses on improving
power within the whole kinetic chain, and movement control
during jumping and landing; and stage 3 begins to retrain sport
specic load, and carefully introduces movements that require
energy storage and release within the tendon
Ganderton et al
13
Australasian Musculoskeletal Medicine • Vol 19, No. 2 • Aug 2015
The transition from normal tendon to pathology has been
described in the tendon pathology continuum model by Cook
and Purdam5 (Figure 2). It describes three overlapping stages
within a continuum – reactive tendinopathy, tendon dysrepair and
degenerative tendinopathy. These stages have increasing degrees
of pathology and decreasing capacity of the pathological area to
recover. Progression is inuenced by change in tendon load and
intrinsic factors, including genetics6, adiposity7, cholesterol8, 9,
insulin resistance10, diabetes 11 and menopause.12
Reactive tendon pathology: A short term adaptive, non-
inammatory response of the cell (activation and proliferation)
in response to acute overload. The extracellular matrix is altered
with increased proteoglycan content but with little change in the
collagen. The proteoglycans produced (predominantly aggrecan
& versican) bind more water and cause tendon thickening that is
commonly seen in response to an acute tensile or compressive
overload.13 This increase in cross-sectional area reduces tendon
stress by decreasing force per unit area.5 This process occurs in
response to i) acute overload, ii) return to loading after a rest,
or iii) following a direct blow to the tendon and is reversible if
appropriately managed.5
Tendon dysrepair: An attempt of the tendon to regain
extracellular matrix structure through ongoing cell activation,
resulting in greater disruption of the extracellular matrix and
possible vascular and neuronal ingrowth.14 These tendons are
dicult to distinguish clinically but are more common in a young
person with a chronically overloaded tendon.15
Degenerative tendon pathology: The tendon often remains
hypercellular but there is little capacity for reversal of pathology
due to signicant (collagen) brillar disorganisation. Areas of cell
death due to apoptosis, trauma or tenocyte exhaustion may be
apparent on biopsy.16 Islands of degenerative tendon
are interspersed between other stages of pathology and normal
tendon5 (Figure 3). Typically, these tendons are seen in active
middle age people, and clinically they may have focal nodular
areas in the tendon.5
Other pathology: Combinations of pathology can occur, the
most common being a reactive on degenerative pathology, where
there is reactive pathology in the remaining normal part of the
tendon, while the degenerative part remains unchanged (Figure 4).
These dierent stages of pathology all require dierent
rehabilitation, as there is no ‘one size ts all’ exercise program.
Assessment for tendinopathy
The subjective assessment should include a thorough
history of loading patterns, 24-hour response to loading (i.e. pain
and stiness) and whether known tendinopathy risk factors are
present (diabetes, rheumatological conditions, uoroquinolone
antibiotics17, 18). The clinician needs to be aware that a player who
has recently returned to sport after time o with an injury may be
susceptible to tendinopathy, especially if they rapidly return to full
load.19, 20 Physical examination of Achilles tendinopathy should
involve assessment of calf muscle bulk and strength, kinetic chain
function and the capacity of the tendon to store and release elastic
energy.21 In addition to a complete biomechanical analysis22, the
patient’s pain level during graded functional tasks (i.e. double
heel rise followed by single-leg heel raise and/or repeat single-leg
hops) should be quantied using a pain scale (numerical rating
scale). Dysfunction should be assessed using a validated outcome
measures such as the Victorian Institute of Sport Assessment –
Achilles (VISA-A) questionnaire.23 It is important to note that
It is proposed that reactive tendinopathy, a non-inflammatory
proliferative response in the cell and matrix, occurs with acute
tensile or compressive overload. This results in a short-term
adaptive and relatively homogeneous thickening of a portion of
the tendon that will either reduce stress (force/unit area) by
increasing cross-sectional area or allow adaptation to compres-
sion. This differs from normal tendon adaptation to tensile load,
which generally occurs through tendon stiffening with little
change in thickness.
14
Thus, reactive response is a short-term adaptation to overload
that thickens the tendon, reduces stress and increases stiffness.
The tendon has the potential to revert to normal if the overload
is sufficiently reduced or if there is sufficient time between
loading sessions.
Imaging
The tendon is swollen in a fusiform manner; the diameter is
increased on both magnetic resonance imaging (MRI) and
ultrasound (US) scans. Ultrasound shows reflection from intact
collagen fascicles, with diffuse hypoechogenicity occurring
between intact collagen structures. Magnetic resonance imaging
will show minimal or no increased signal at this stage. The
change in imaging appearance is mainly derived from the
increase in bound water within the proteoglycans (fig 2).
Clinical
Reactive tendinopathy is seen clinically in an acutely overloaded
tendon and is more common in a younger person. For example,
a young jumping athlete who dramatically increases the
number of jumping/landing repetitions a week may develop
patellar tendon swelling and pain.
Tendons chronically exposed to low levels of load (e.g. in the
detrained athlete returning from illness or injury, or a sedentary
person) may also be vulnerable to this stage of tendinopathy
when exposed to moderate increase in load. In addition it may
occur as a result of direct trauma to tendon, to which the
Achilles, patellar and elbow tendons are particularly exposed.
2. Tendon dysrepair
Tendon dysrepair describes the attempt at tendon healing,
similar to reactive tendinopathy but with greater matrix
breakdown. There is an overall increase in number of cells,
which are mainly chondrocytic, as well as some myofibroblasts,
resulting in a marked increase in protein production (proteogly-
can and collagen). The increase in proteoglycans results in
separation of the collagen and disorganisation of the matrix.
Figure 1 Pathology continuum; this model embraces the transition
from normal through to degenerative tendinopathy and highlights the
potential for reversibility early in the continuum. Reversibility of
pathology is unlikely in the degenerative stage.
410
Figure 2: The tendon pathology continuum model. Reproduced from ‘Is
tendon pathology a continuum? A pathology model to explain the clinical
presentation of load-induced tendinopathy’, J L Cook and C R Purdam,
43, 409-416, 2009 with permission from BMJ Publishing Group Ltd.
Figure 3: Degenerative tendon histopathology (H&E stain, 100x)
Commonclinicalpresenta/ons
Degenera/vearea
Reac/vetendon
Degenera/vearea
Normaltendon
Figure 4: Schematic representation of a change from a degenerative
tendon to a reactive on degenerative tendinopathy.)
Ganderton et al
14
Australasian Musculoskeletal Medicine • Vol 19, No. 2 • Aug 2015
tendons may be painful to palpation (especially in athletes) in
people who do not have tendinopathy, and that palpation pain
does not help predict prognosis.24 Pain localisation depends on
whether the presentation is mid-substance – where people pinch
with two ngers either side of the mid tendon, or insertional –
where people point with one nger near the Achilles insertion.
These pain presentations do not refer and vague pain is likely
to be associated with another diagnosis. Potential dierential
diagnoses include seronegative arthropathies25, sural nerve
irritation or neuroma26, os trigonum syndrome27, and peroneal
tendon subluxation or dislocation.28 The presence of an invaginated
plantaris tendon29 or a plantaris tendon that is rmly attached to the
Achilles tendon via a retinacular-like structure30 may be detected
in cases of recalcitrant medial-sided mid-portion tendinopathy.
When retrocalcaneal bursitis is diagnosed, usually via imaging,
it best to consider the entire enthesis organ.31 That is, the bursa
and tendon should not be considered in isolation.32-34 Finally, it
should be recalled that pathology can exist on imaging without
the tendon being the source of symptoms, and therefore a clinical
diagnosis incorporating the above pain localisation patterns and
the presence of load-related pain should form the basis for client
management.
Eccentric training in Achilles tendinopathy
Eccentric training is a common intervention when
rehabilitating Achilles tendinopathy35, however, systematic
reviews have identied low methodological quality among studies
on this intervention.36, 37 Additionally, there is substantial variability
in the protocol used for eccentric training, for example i) 3x15
knee straight, 3x15 knee bent, twice daily ii) gradual increase up
to 3x15 over 1-2 weeks, iii) 1x15 knee straight, 1 x 15 knee bent,
iv) once daily, v) thrice daily, vi) addition of 10-second hold.38
There are unique characteristics of eccentric exercise that may
have important implications for tendinopathy. These include
modulation the neurological stretch response39; perturbations
of tendon force40-42; increased shear forces between the tendon
and paratendon structures; pain modulation43; or adaption of
mechanotransduction signalling in passive tendon structures.39
Despite these data, it is unclear whether it is important to isolate
the eccentric component of the exercise rather than performing
a concentric-eccentric exercise.
The number of repetitions, sets and frequency of calf
exercises in the Alfredson program (3 sets of 15 repetitions of
heel drops o a step with the knee straight and knee bent, at
slow speed, twice daily)35 do not correlate with guidelines for
strength training to achieve hypertrophy and contractile strength
in the triceps surae muscle.44 Thus, a functional strengthening and
endurance program that includes loading into the stretch shortening
cycle (SSC) should also be used in conjunction with an eccentric
program39, 45, 46 when rehabilitating an Achilles tendinopathy. The
next section provides further detail of how eccentrics may t
within a graded loading program.
Exercise therapy for Achilles tendinopathy
Once Achilles tendinopathy is diagnosed, a rehabilitation
program should be commenced with the primary focus of
decreasing or abolishing pain during tendon loading activities and
improving function. The program should be designed around an
individual’s pre-injury function and sporting level with the ultimate
goal of treatment being full return to activity. Essential elements
include: regular increases in weight/resistance to progressively
load muscle tendon unit (low repetition, high load) followed by
increased speed of exercises to load the tendon. A three stage
progressive loading rehabilitation program has been described
by Kountouris and Cook47 that involves addressing functional
impairments, from muscle-tendon strength, to power (including
kinetic chain and lumbo-pelvic control), to sport-specic exercise.
Not only does the calf and Achilles complex need full scrutiny
and rehabilitation, but the strength and function of the kinetic
chain must be treated as well. The program should be adapted
for dierent presentations and for dierent stages of pathology.
Rehabilitation should be continued until the tendon regains full
capacity to store and release energy without immediate or latent
pain, and then be followed by a maintenance program if returning
to competitive sport.47 The energy storage activities used at the
end of the rehabilitation program should match those required
in the individual’s sport or in a patient-centred goal. Ongoing
monitoring with clinical tests and standardised outcome measures
should be undertaken throughout the rehabilitation process.
Exercise is the best intervention for tendinopathy48-50, and
is the only stimulus with the capacity to positively aect tendon
matrix.4, 51 While exercise is the cornerstone of rehabilitation for
all stages of pathology, its application should vary according to
presentation. Reactive tendinopathy requires relative rest from
high tendon load activities (energy storage and release activities
such as running) and prescription of isometric exercise for pain
reduction.52 In contrast, dysrepair and degenerative pathology
require progressive loading to moderate cell response and address
Table 1: Rehabilitation exercises to restore functional impairments in rehabilitation stages. Adapted from ‘Rehabilitation of Achilles and patellar
tendinopathies’, A Kountouris and J Cook, 21(2), 295-316, 2007 in Best Practice & Research Clinical Rheumatology.
Rehabilitation
Stage
Functional
impairment Exercise Aim Example Exercise
Stage 1
Muscle-tendon
function
Decrease pain, improve Achilles –
calf strength
Heavy sustained isometric contractions (preferably single leg),
progressing on to heel raise exercise on a step or at oor (note
that insertional presentations should not be given exercises
below neutral o a step due to compression 53)
Stage 2
Power and lower
limb kinetic chain
function
Improve capacity and control during
faster movements. Promote smooth
movements at the hip, knee and ankle
during impact and load
Skipping – commence with two legs and stop between each
skip; progress to continuous; progress to single leg and then
add speed
Stage 3
Sport-specic
exercise with
emphasis on energy
storage and release
Gradually increase sports-specic
load to the tendon and monitor
reaction to higher impact loading
Sprinting
Jumping/landing
Acceleration activities
Change of direction activities
Ganderton et al
15
Australasian Musculoskeletal Medicine • Vol 19, No. 2 • Aug 2015
Tendon
musculotendinous junction of normal Achilles tendon showed
good correlation of fl ow between sites (Astrom & Westlin
1994b). These studies suggest that the blood supply at rest is
not compromised at a particular point of the Achilles tendon.
Tendons have a rich, almost exclusively afferent nerve supply
that mediates proprioception (O’Brien 1997). Encapsulated
and nonencapsulated nerve endings in tendon include type I
Ruffi ni corpuscles, pressure receptors (stretch sensitive), type
II Paccinian corpuscles, type III Golgi tendon organs (mech-
anoreceptors) and type IV free nerve endings (pain) (O’Brien
1997). Most afferent nerve endings are near the muscle tendon
junction (Kirkendall & Garrett 1997). Hence, the nerve supply
of the midtendon may be minimal and pain sensitivity to early
pathological processes may be compromised.
The enthesis and myotendinous junction are two important
structures of tendon.
Tendon insertion into bone (the enthesis) is a point of change
in tissue fl
exibility from tendon to bone. T
wo types of enthe-
sis have been described: the fi brocartilaginous enthesis and the
fi brous enthesis. Fibrous enthesis occurs when the superfi cial
tendon inserts into the periosteum and occurs in metaphyseal
and diaphyseal attachments (Benjamin & Ralphs 1996).
The fi brocartilaginous enthesis is a transitional zone where
tendon graduates to bone through the sequence of layers, from
normal tendon to fi brocartilage, through mineralized fi brocarti-
lage and fi nally bone. This transition occurs within a variable dis-
tance (200–400 m to several millimeters) (Benjamin & Ralphs
1998) and the thickness may be related to the amount of move-
ment and load that occurs between the bone and tendon.
The unmineralized fi brocartilage region has rows of rounded
cells between bundles of type II collagen. Unlike tendon cells,
these cells do not have connective arms to other cells (Benjamin
& Ralphs 1998), hence there is no communication between bone
and tendon cells. A distinct border (the blue line) separates min-
eralized from unmineralized fi brocartilage (Ferretti et al 1985).
The blue line is composed of densely packed, randomly oriented
collagen of various diameters that are continuous with both the
mineralized and unmineralized fi brocartilage (O’Brien 1997).
The enthesis allows a gradual change in mechanical proper-
ties from the fl exible tendon to the rigid bone. The fi brocarti-
lage controls bending of fi bers and distributes force to the bone
(Kraushaar & Nirschl 1999). The more bending of fi bers that
occurs in a tendon due to load, the more fi brocartilage is present
at the enthesis. The enthesis also protects the tendon insertion
from narrowing when the tendon is stretched, thus restricting
the decrease in cross-sectional area (Benjamin & Ralphs 1998).
It is important to consider other structures associated with
fi brocartilaginous tendon insertions, including bursae and car-
tilaginous adaptations on both apposing bone and tendon (Fig.
3.3). This has been termed the ‘enthesis organ’ by Benjamin et al
(2004). Hence the presentation of a bursitis at a tendon attach-
ment (gluteus medius, tibial patellar tendon attachment) is likely
refl ective of an enthesis problem rather than an isolated bursitis,
and should be treated as such. The Achilles tendon insertion and
the effect of calcaneal shape on the enthesis structures has been
well described by Rufai et al (Rufai et al 1995). Diagnoses such
as Haglund’s deformity are merely variation of enthesis anatomy
that predispose an individual to pathology and pain.
Myotendinous junction
The myotendinous junction is also a specialized anatomical area
that allows transmission in force as well as the change in tissue
fl exibility and size. Because of these tissue changes it is a com-
mon site of injury, usually termed a muscle strain (Clancy 1990).
The amount of folding increases the surface area by tenfold. At
this junction, the tendon bundles are invaginated, but separate
from the muscle sarcomeres by an aponeurosis. Similar to the
bone–tendon junction, the connective tissue of muscle and ten-
don blend together. As tendon collagen extends into the muscle
at the musculotendinous junction, it provides more extensive
attachment of tendon to muscle (O’Brien 1997) There may
be some structural differences in the myotendinous junctions
between type 1 and type 2 muscle fi bers (Kvist et al 1991).
Biomechanical properties of
tendons
Tendons act as springs to store energy in locomotion and as a
result, the elastic properties of tendon are essential in athletic
function. At the same time, tendons must transfer force effi -
ciently to bone with minimal energy loss. Thus, the mechanical
Figure 3.3 • Normal tendon enthesis.
Normal tendon enthesis
TendonBursa Fibrocartilage on the bursal
side of the tendon
Calcified
fibrocartilage
Bone
Unmineralized
fibrocartilage
Fibrocartilage
on the bursal
side of the bone
21/02/2007 10:57:08
Figure 5: Tendon attachment to bone and the enthesis organ. Schematic
representation demonstrating the complex nature of the tendon attachment
to the bone and the brocartilage where the tendon and bone are adjacent.
Reproduced from Cook JL. Tendon. In: Kolt G, Snyder-Mackler L,
editors. Physical Therapies in Sport and Exercise. London: Churchill
Livingstone; 2007
functional decits (e.g. strength and kinetic chain function).47
A common clinical presentation is reactive on degenerative
tendinopathy (Figure 4). In these cases, the rst aim is to settle
symptoms. Once that is achieved, decits identied in the
examination should be addressed with a strength and graded
loading program. There is no recipe program for Achilles
tendinopathy, the program should be tailored to the person’s
presentation, their risk factors, their aims for activity, and the
capacity and pathology in the tendon. It is irrational to consider
that the same exercise program would be appropriate for a young
sprinting athlete and an elderly post-menopausal woman who
wants to play golf.
Diagnostic and therapeutic dierence between treating mid-
portion and insertional Achilles tendinopathy
Normal tendon attaches to bone through the enthesis organ.31
This complex attachment allows compression of the tendon against
the upper aspect of the calcaneus to reduce load on the insertion
and provide a mechanical advantage to the muscle-tendon unit.54
This area of compression proximal to the tendon insertion
is where pathology most commonly occurs and compression
is maximal in dorsiexion. Applying the concept clinically,
insertional Achilles tendinopathy presents with pain occurring in
dorsiexion based activities but less so in plantarexion. Thus,
stretching the Achilles over a step or completing the original
Alfredson program may provoke pain as will running up hills
or on soft surfaces such as the beach (the heel digs into the sand
which increases dorsiexion) (Table 1 & Figure 6). In addition
to aggravating activities, the key diagnostic feature separating
mid-portion Achilles from insertional Achilles is the area of pain,
remembering that tendon pain is always well localised and the
area indicated as their main site of pain is a good diagnostic sign.
Insertional Achilles tendinopathy should be treated by
keeping the tendon out of compression, i.e. progressive loading
in more plantar exion.53 Pain relief can be achieved with a
substantial heel raise (preferably added to the outside of the shoe,
in-shoe raises are often poorly tolerated) for everyday activity. As
pain reduces and tendon capacity improves, compressive loads
can be gradually re-introduced if required.
Figure 6: 1. A sagittal section of an Achilles tendon insertion, the gure
on the left demonstrates a tendon inserting inferior to a prominent
superior tuberosity on the calcaneus, the gure on the right shows
a tendon that inserts on the posterior surface of the calcaneus that
lacks a prominent superior tuberosity. Compression will occur at the
superior aspect of the calcaneus in the tendon in the left gure, but not
in the tendon in the right gure. Reproduced with permission from A.
Rufai, J. R. Ralphs, M. Benjamin, Journal of Orthopaedic Research,
‘Structure and histopathology of the insertional region of the human
Achilles tendon’, 13, 4, 585-593, 2005, Wiley Online Library DOI:
10.1002/jor.1100130414
Tendon pain: Peripheral vs. central sensitisation
Tendinopathy is the clinical presentation of pain and
dysfunction in a tendon. Like other chronic pain conditions,
there can be a disconnect between clinical presentation and
abnormalities on imaging. That is, pain may be present without
imaging change and vice versa.43 Tendinopathy typically presents
with localised pain on loading45, tenderness to palpation55 and
impaired function.56 However, the pain experienced does not t
with a triphasic inammatory process. Nociception from vascular
structures, tenocytes, biochemical changes, cell activation, ion
channel and matrix changes may contribute to the development
of a painful tendon.43, 57
Some features of tendon pain are physiological whereas
others are pathophysiological, and both peripheral and central
input contribute to the clinical features of tendinopathy.43
Localised pain in response to tendon loading appears to have a
physiological mechanism driven by primary nociceptive factors
.58 Many tendinopathies, especially in the lower limb, have a
relatively simple pain presentation without typical chronic pain
features such as spreading, despite a long duration of pain.
Ganderton et al
16
Australasian Musculoskeletal Medicine • Vol 19, No. 2 • Aug 2015
Figure 7: Achilles stretch causing maximal compression in
dorsiexion
There may be important dierences between upper and lower
limb tendinopathies in terms of the contribution from peripheral
tissue or central drivers.59 While the role of central sensitisation has
been highlighted for rotator cu60 and lateral elbow61 tendinopathy,
there is preliminary evidence that central sensitisation does not
occur in Achilles tendinopathy.62 The importance of upper limb
function for self-care and occupational activities, might contribute
to these dierences in central sensitisation between upper and
lower limb tendinopathies. As all nociceptive input is evaluated
in terms of threat63, the increased threat associated with upper-
limb tendinopathy (e.g. negative thoughts and feelings arising
due to fear of pain with daily activities, fear of tendon rupture,
fear of unemployment) likely amplify the pain experience. We
should keep these dierences in mind and be careful of applying
research ndings from the rotator cu to Achilles tendinopathy.
Fundamentally, a thorough assessment of all contributions
to tendon pain should be undertaken when diagnosing and treating
tendon injury. In light of the current literature, clinicians should
consider the impact that both peripheral and central mechanisms
have on tendon injury. Perhaps the most eective means of
addressing both contributors is a graded loading program that
reduces fear of loading, addresses decits and incorporates
education within the rehabilitation process.
What should physiotherapy for patients with Achilles
tendinopathy look like in 2015 and beyond?
Physiotherapy for tendinopathy should move to a thoughtful
and planned loading intervention that is tailored to each person’s
presentation. Reliance on recipe programs is ineective and not
suitable for clinical practice. Referral for considered interventions
should be based on a failure to progress with an adequate
conservative program, rather than a knee jerk response to tendon
pain. Tendon pain appears to be tissue protecting and interventions
that completely remove neural input might be dangerous. Adjunct
treatments such as electrotherapy and massage have limited
evidence for their eectiveness, however may be used as needed
but should never form the basis of a tendon treatment. Furthermore,
progression to surgery or invasive procedures should not be
based on failure to improve from passive therapies. Patience of,
and education for, the person with tendinopathy is essential and
should be central to a physiotherapy program.
References
1. Benjamin M, Ralphs JR. Tendons in health and disease. Man
Ther. 1996;1(4):186-91.
2. Clain MR, Baxter DE. Achilles tendinitis. Foot Ankle.
1992;13(8):482-7.
3. Benjamin M, Kaiser E, Milz S. Structure-function relationships
in tendons: a review. J Anat. 2008;212(3):211-28.
4. Kjaer M, Langberg H, Heinemeier K, et al. From mechanical
loading to collagen synthesis, structural changes and function
in human tendon. Scand J Med Sci Sports. 2009;19(4):500-10.
5. Cook JL, Purdam CR. Is tendon pathology a continuum? A
pathology model to explain the clinical presentation of load-
induced tendinopathy. Br J Sports Med. 2009;43(6):409-16.
6. Collins M, Posthumus M. Type V collagen genotype and
exercise-related phenotype relationships: a novel hypothesis.
Exerc Sport Sci Rev. 2011;39(4):191-8.
7. Gaida JE, Ashe MC, Bass SL, Cook JL. Is adiposity an under-
recognized risk factor for tendinopathy? A systematic review.
Arthritis Rheum. 2009;61(6):840-9.
8. Scott A, Zwerver J, Grewal N, et al. Lipids, adiposity and
tendinopathy: is there a mechanistic link? Critical review. Br J
Sports Med. 2014.
9. Tilley B, Cook JL, Docking SI, Gaida JE. Is higher serum
cholesterol associated with altered tendon structure or tendon
pain? A systematic review. Br J Sports Med. 2015.
10. Gaida JE, Alfredson L, Kiss ZS, Wilson AM, Alfredson H,
Cook JL. Dyslipidemia in Achilles tendinopathy is characteristic
of insulin resistance. Med Sci Sports Exerc. 2009;41(6):1194-7.
11. Ranger TA, Wong AMY, Cook JL, Gaida JE. Is there an
association between tendinopathy and diabetes mellitus? A
systematic review with meta-analysis. 2015.
12. Cook JL, Bass SL, Black JE. Hormone therapy is associated
with smaller Achilles tendon diameter in active post-menopausal
women. Scand J Med Sci Sports. 2007;17(2):128-32.
13. Parkinson J, Samiric T, Ilic MZ, Cook J, Handley CJ.
Involvement of proteoglycans in tendinopathy. J Musculoskelet
Neuronal Interact. 2011;11(2):86-93.
14. Andersson G, Danielson P, Alfredson H, Forsgren S. Nerve-
related characteristics of ventral paratendinous tissue in chronic
Achilles tendinosis. Knee Surg Sports Traumatol Arthrosc.
2007;15(10):1272-9.
15. Cook JL, Khan KM, Kiss ZS, Griffiths L. Patellar
tendinopathy in junior basketball players: a controlled clinical
and ultrasonographic study of 268 patellar tendons in players
aged 14–18 years. Scand J Med Sci Sports. 2000;10(4):216-20.
Ganderton et al
17
Australasian Musculoskeletal Medicine • Vol 19, No. 2 • Aug 2015
16. Lian Ø, Scott A, Engebretsen L, et al. Excessive apoptosis
in patellar tendinopathy in athletes. Am J Sports Med.
2007;35(4):605-11.
17. Stephenson AL, Wu W, Cortes D, Rochon PA. Tendon Injury
and Fluoroquinolone Use: A Systematic Review. Drug Saf.
2013;36(9):709-21.
18. Lewis T, Cook J. Fluoroquinolones and tendinopathy: a guide
for athletes and sports clinicians and a systematic review of the
literature. J Athl Train. 2014;49(3):422-7.
19. Myer GD, Faigenbaum AD, Cherny CE, Heidt RS, Jr., Hewett
TE. Did the NFL Lockout expose the Achilles heel of competitive
sports? J Orthop Sports Phys Ther. 2011;41(10):702-5.
20. Woods C, Hawkins R, Hulse M, Hodson A. The Football
Association Medical Research Programme: an audit of injuries
in professional football-analysis of preseason injuries. Br J Sports
Med. 2002;36(6):436-41.
21. Cook JL, Khan KM, Maulli N, Purdam C. Overuse
tendinosis, not tendinitis part 2: applying the new approach to
patellar tendinopathy. Phys Sportsmed. 2000;28(6):31-46.
22. Cook JL, Khan KM, Kiss ZS. Posterior leg tightness and
vertical jump are associated with US patellar tendon abnormality
in 14–18-year old basketball players: A cross-sectional
anthropometric and physical performance study. J Sci Med Sport.
2002;5(4):121-.
23. Robinson JM, Cook JL, Purdam C, et al. The VISA-A
questionnaire: a valid and reliable index of the clinical severity
of Achilles tendinopathy. Br J Sports Med. 2001;35(5):335-41.
24. Cook JL, Khan KM, Kiss ZS, Purdam CR, Griths L.
Reproducibility and clinical utility of tendon palpation to detect
patellar tendinopathy in young basketball players. Victorian
Institute of Sport tendon study group. Br J Sports Med.
2001;35(1):65-9.
25. Benjamin M, McGonagle D. The anatomical basis for disease
localisation in seronegative spondyloarthropathy at entheses and
related sites. J Anat. 2001;199(Pt 5):503-26.
26. Cook JL, Khan KM, Purdam C. Achilles tendinopathy. Man
Ther. 2002;7(3):121-30.
27. Khan K, Brown J, Way S, et al. Overuse injuries in classical
ballet. Sports Med. 1995;19(5):341-57.
28. Roth JA, Taylor WC, Whalen J. Peroneal tendon subluxation:
the other lateral ankle injury. Br J Sports Med. 2010;44(14):1047-
53.
29. Spang C, Alfredson H, Ferguson M, Roos B, Bagge J,
Forsgren S. The plantaris tendon in association with mid-portion
Achilles tendinosis: tendinosis-like morphological features and
presence of a non-neuronal cholinergic system. Histol Histopathol.
2013;28(5):623-32.
30. van Sterkenburg MN, Kerkhos GM, Kleipool RP, Niek van
Dijk C. The plantaris tendon and a potential role in mid-portion
Achilles tendinopathy: an observational anatomical study. J Anat.
2011;218(3):336-41.
31. Benjamin M, Moriggl B, Brenner E, Emery P, McGonagle
D, Redman S. The “enthesis organ” concept: why enthesopathies
may not present as focal insertional disorders. Arthritis Rheum.
2004;50(10):3306-13.
32. Gheno R, Nico MA, Buck FM, Trudell DJ, Haghighi P,
Resnick D. Edematous processes within Kager fat pad: magnetic
resonance imaging, gross anatomical, and histological studies
in cadavers with clinical correlation. J Comput Assist Tomogr.
2010;34(4):621-5.
33. Lohrer H, Arentz S, Nauck T, Dorn-Lange NV, Konerding
MA. The Achilles tendon insertion is crescent-shaped: an in vitro
anatomic investigation. Clin Orthop Relat Res. 2008;466(9):2230-
7.
34. Theobald P, Bydder G, Dent C, Nokes L, Pugh N, Benjamin
M. The functional anatomy of Kager’s fat pad in relation to
retrocalcaneal problems and other hindfoot disorders. J Anat.
2006;208(1):91-7.
35. Alfredson H, Pietilä T, Jonsson P, Lorentzon R. Heavy-load
eccentric calf muscle training for the treatment of chronic Achilles
tendinosis. Am J Sports Med. 1998;26(3):360-6.
36. Kingma JJ, de Knikker R, Wittink HM, Takken T. Eccentric
overload training in patients with chronic Achilles tendinopathy:
a systematic review. Br J Sports Med. 2007;41(6):e3.
37. Woodley BL, Newsham-West RJ, Baxter GD. Chronic
tendinopathy: eectiveness of eccentric exercise. Br J Sports
Med. 2007;41(4):188-98.
38. Habets B, van Cingel RE. Eccentric exercise training in
chronic mid-portion Achilles tendinopathy: a systematic review
on dierent protocols. Scand J Med Sci Sports. 2015;25(1):3-15.
39. Allison GT, Purdam C. Eccentric loading for Achilles
tendinopathy-strengthening or stretching? Br J Sports Med.
2009;43(4):276-9.
40. Rees JD, Lichtwark GA, Wolman RL, Wilson AM. The
mechanism for ecacy of eccentric loading in Achilles tendon
injury; an in vivo study in humans. Rheumatology (Oxford).
2008;47(10):1493-7.
41. Henriksen M, Aaboe J, Bliddal H, Langberg H. Biomechanical
characteristics of the eccentric Achilles tendon exercise. J
Biomech. 2009;42(16):2702-7.
42. Grigg NL, Wearing SC, O’Toole JM, Smeathers JE. The eect
of exercise repetition on the frequency characteristics of motor
output force: implications for Achilles tendinopathy rehabilitation.
J Sci Med Sport. 2014;17(1):13-7.
43. Rio E, Moseley L, Purdam C, et al. The pain of tendinopathy:
physiological or pathophysiological? Sports Med. 2014;44(1):9-
23.
44. ACSM. ACSM’s guidelines for exercise testing and
prescription. 8th ed. Philadelphia: Wolters Kluwer Health/
Lippincott Williams & Wilkins; 2010.
45. Cook JL, Purdam C. Rehabilitation of lower limb
tendinopathies. Clin J Sport Med. 2003;22(4):777-89.
46. Kongsgaard M, Aagaard P, Kjaer M, Magnusson SP. Structural
Achilles tendon properties in athletes subjected to dierent exercise
modes and in Achilles tendon rupture patients. J Appl Physiol.
2005;99(5):1965-71.
47. Kountouris A, Cook J. Rehabilitation of Achilles and patellar
tendinopathies. Best Practice & Research Clinical Rheumatology.
2007;21(2):295-316.
48. Gaida JE, Cook J. Treatment options for patellar tendinopathy:
critical review. Curr Sports Med Rep. 2011;10(5):255-70.
49. Rudavsky A, Cook J. Physiotherapy management of patellar
tendinopathy (jumper’s knee). J Physiother. 2014;60(3):122-9.
50. de Vos RJ, d’ Hooghe PPRN, de Leeuw P, Kerkhos GMMJ.
Achilles tendinopathy. In: d’Hooghe P, Kerkhos GMMJ, editors.
Ganderton et al
18
Australasian Musculoskeletal Medicine • Vol 19, No. 2 • Aug 2015
The ankle in football. Paris: Springer; 2014.
51. Ingber DE. Mechanobiology and diseases of
mechanotransduction. Ann Med. 2003;35(8):564-77.
52. Rio E, Kidgell D, Purdam C, et al. Isometric exercise induces
analgesia and reduces inhibition in patellar tendinopathy. Br J
Sports Med. 2015.
53. Jonsson P, Alfredson H, Sunding K, Fahlstrom M, Cook J.
New regimen for eccentric calf-muscle training in patients with
chronic insertional Achilles tendinopathy: results of a pilot study.
Br J Sports Med. 2008;42(9):746-9.
54. Cook JL, Purdam C. Is compressive load a factor in the
development of tendinopathy? Br J Sports Med. 2012;46(3):163-8.
55. Maulli N, Kenward MG, Testa V, Capasso G, Regine R, King
JB. Clinical diagnosis of Achilles tendinopathy with tendinosis.
Clin J Sport Med. 2003;13(1):11-5.
56. Maulli N, Khan KM, Puddu G. Overuse tendon conditions:
time to change a confusing terminology Arthroscopy.
1998;14(8):840-3.
57. Danielson P. Reviving the “biochemical” hypothesis for
tendinopathy: new ndings suggest the involvement of locally
produced signal substances. Br J Sports Med. 2009;43(4):265-8.
58. Kettunen JA, Kvist M, Alanen E, Kujala UM. Long-term
prognosis for jumper’s knee in male athletes. A prospective
follow-up study. Am J Sports Med. 2002;30(5):689-92.
59. Baron R, Hans G, Dickenson AH. Peripheral input and its
importance for central sensitization. Ann Neurol. 2013;74(5):630-
6.
60. Littlewood C, Malliaras P, Bateman M, Stace R, May
S, Walters S. The central nervous system - An additional
consideration in ‘rotator cu tendinopathy’ and a potential basis
for understanding response to loaded therapeutic exercise. Man
Ther. 2013;18(6):468-72.
61. Heales LJ, Lim EC, Hodges PW, Vicenzino B. Sensory
and motor decits exist on the non-injured side of patients with
unilateral tendon pain and disability--implications for central
nervous system involvement: a systematic review with meta-
analysis. Br J Sports Med. 2014;48(19):1400-6.
62. Skinner IW, Debenham JR, Krumenachera S, Bulsarab MK,
Wand BM. Chronic mid portion Achilles tendinopathy is not
associated with central sensitisation. Pain and Rehabilitation -
the Journal of Physiotherapy Pain Association. 2014;37:34-40.
63. Moseley GL. Reconceptualising pain according to modern
pain science. Phys Ther Rev. 2007;12(3):169-78.
64. Ganderton C, Cook J, Docking S, Rio E, van Ark M,
Gaida J. Therapeutische Schlüsselkonzepte für Patienten mit
Achillessehnentendinopathie. Sportphysio. 2014;2(3):112-7.
Ganderton et al