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Achilles tendinopathy: understanding the key concepts to improve clinical management


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Introduction Achilles tendinopathy is commonly encountered in clinical practice yet can be quite difficult 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 deficits, which can leave the individual vulnerable to recurrence. Insertional tendinopathy requires a tailored management that avoids dorsiflexion, 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 fibres in the context of tendinopathy. Implications Rehabilitation should be tailored to address identified 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 specific load, and carefully introduces movements that require energy storage and release within the tendon.
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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
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
dierential 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 ecient 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).
Introduction: Achilles tendinopathy is commonly
encountered in clinical practice yet can be quite dicult 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 decits, which can leave the individual
vulnerable to recurrence. Insertional tendinopathy requires a
tailored management that avoids dorsiexion, 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
identied 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
specic load, and carefully introduces movements that require
energy storage and release within the tendon
Ganderton et al
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 inuenced 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-
inammatory 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
dicult 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 signicant (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 dierent stages of pathology all require dierent
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 stiness) 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 quantied 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.
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.
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).
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.
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)
Figure 4: Schematic representation of a change from a degenerative
tendon to a reactive on degenerative tendinopathy.)
Ganderton et al
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 dierential
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
Eccentric training in Achilles tendinopathy
Eccentric training is a common intervention when
rehabilitating Achilles tendinopathy35, however, systematic
reviews have identied 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-specic 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 dierent presentations and for dierent 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 aect 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.
impairment Exercise Aim Example Exercise
Stage 1
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
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
exercise with
emphasis on energy
storage and release
Gradually increase sports-specic
load to the tendon and monitor
reaction to higher impact loading
Acceleration activities
Change of direction activities
Ganderton et al
Australasian Musculoskeletal Medicine • Vol 19, No. 2 • Aug 2015
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
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
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
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 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
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 decits (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, decits identied 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 dierence 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 dorsiexion. Applying the concept clinically,
insertional Achilles tendinopathy presents with pain occurring in
dorsiexion based activities but less so in plantarexion. 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 dorsiexion) (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:
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 inammatory 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
Australasian Musculoskeletal Medicine • Vol 19, No. 2 • Aug 2015
Figure 7: Achilles stretch causing maximal compression in
There may be important dierences 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 cu60 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 dierences 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 dierences 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 eective means of
addressing both contributors is a graded loading program that
reduces fear of loading, addresses decits 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 ineective 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 eectiveness, 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.
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... Tendon pain after loading has been described in both the absence or presence of imaging abnormalities and degeneration (Maffulli et al., 2004;Mascar o et al., 2018;Rio et al., 2014). While some studies connect ATP with degenerative structural changes within the tendon, others argue that the mechanism of ATP is related with peripheral and central mechanisms of nociception modulation suggesting pain system changes (Ganderton et al., 2015;Plinsinga et al., 2015;Tompra et al., 2016;van Sterkenburg and van Dijk, 2011). Nervous system sensitization, both peripherally and centrally, in response to nociceptive input or inflammation can be protective in the short term (Latremoliere and Woolf, 2009). ...
Abstract Background/purpose Cervical and thoracic spine manipulation has been found to reduce tendon pain and disability in lateral epicondylalgia and rotator cuff tendinopathy. Based on these findings, the application of lumbar spine manipulation may also provide similar improvements in Achilles tendinopathy (AT). Therefore, the purpose of this study was to evaluate the effect of lumbar spine manipulation on pain and disability in a patient experiencing AT. Case description A 44 years old male ex-football player presented with a 20-year history of persistent Achilles tendon pain (ATP) consistent with AT diagnosis. The patient attended 12 treatment sessions receiving a high-velocity, low amplitude lumbar spine manipulation. Outcome measures were collected at baseline, 2 weeks, 4 weeks, 3 months and 6 months and included pain in visual analogue scale, the American Orthopedic Foot and Ankle Score, the 36-Item Short Form Health Survey and the Victorian Institute of Sport Assessment-Achilles questionnaire. Pressure pain threshold was also assessed using an electronic pressure algometer. Outcomes Improvement in all outcome measures was noted 6-months post intervention. Outcome measures indicated substantial improvements in both the patient’s pain and disability. The patient was able to perform activities of daily living without difficulties, suggesting higher level of function and quality of life at 6-months post initial evaluation. Conclusion These findings have demonstrated the positive effects of lumbar spine manipulation on ATP and disability. Further studies, specifically clinical trials investigating the effect of lumbar spine manipulation or combining this technique with exercises and functional activities are suggested. Keywords Achilles tendontendinopathymanipulation
... There are a number of events that require running on sand. This has been reported to increase the risk of soft tissue injury [1], particularly in the mid-portion of the Achilles tendon [2,3], but also includes foot blisters for bare feet, excessive ankle flexion, etc. The beach events include: ...
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Sand sports include running, volleyball, soccer, beach flags, ironman, and fitness training. An increased amount of soft tissue injuries have been widely reported. A novel technique of determining the surface stiffness of beach sand in-situ used a simple drop-test penetrometer. The relationship between drop height and the depth of penetration squared was linear (Pearson’s correlation coefficient r2 > 0.92). The stiffness ratio between the soft dry sand and ocean-saturated wet sand compacted by eight hours of coastal water exposure was approximately seven, which was similar to previously reported stiffness measurements in a sand box. However, the absolute stiffness values were much smaller. While this technique was manually operated, an automatic system is postulated for future studies.
... Since exercise has been reported to be the best intervention for other lower limb tendons (Achilles 13 and patellar tendinopathy 14 ), a similar treatment algorithm for the gluteal tendons may be effective in reducing pain and dysfunction. Both eccentric and heavy slow resistance exercise have been shown to be beneficial 15,16 for rehabilitating tendon conditions. ...
Objectives: The aim of the current study was to determine the effects of education with targeted or sham exercise on pain and function in postmenopausal women with greater trochanteric pain syndrome (GTPS). Background: Conservative management of GTPS is poorly described, and to date, there have been no studies on education with exercise as an intervention for GTPS. Ninety-four postmenopausal women with GTPS were recruited to participate in this study. Materials and methods: Participants were randomized to receive one of two 12-week exercise programs (GLoBE vs. sham). Participants received education on avoiding tendon compression with appropriate activity modification. The Victorian Institute of Sport Assessment-Gluteal tendon (VISA-G) was examined at baseline, 12, and 52 weeks. Secondary outcomes included hip pain and function questionnaires (Hip dysfunction and Osteoarthritis Outcome Score (HOOS), Oxford Hip Score (OHS), and Lateral Hip Pain questionnaire), a global rating of change in symptom questionnaire, and a quality of life measure (Assessment of Quality of Life [AQoL]-8D). Differences between groups were analyzed using intention to treat with analysis of covariance, per-protocol analysis, and responder analysis. Results: Responders to the GLoBE intervention had significantly better VISA-G, HOOS, OHS, and lateral hip pain questionnaire scores compared to responders in the sham group. However, intention to treat analyses showed no between-group differences for the GLoBE intervention and sham exercise groups. Significant improvement in VISA-G score was found for both programs at 12- and 52-weeks time points (p < 0.001). Conclusion: Lack of treatment effect was found with the addition of an exercise program to a comprehensive education on GTPS management. The improved outcomes of the responders in the GLoBE group indicate that there may be a subgroup of patients with a GTPS diagnosis that benefit from a GLoBE intervention program.
... Since exercise has been reported to be the best intervention for other lower limb tendons (Achilles 13 and patellar tendinopathy 14 ), a similar treatment algorithm for the gluteal tendons may be effective in reducing pain and dysfunction. Both eccentric and heavy slow resistance exercise have been shown to be beneficial 15,16 for rehabilitating tendon conditions. ...
Introduction Greater trochanteric pain syndrome (GTPS) is an umbrella term used to describe several pathologies contributing to lateral hip pain. The most prevalent pathology is gluteal tendinopathy. Conservative management of GTPS is predominantly now focused on the use of corticosteroid injections (CSIs) and gluteal exercises. Aim To compare CSIs and gluteal exercises on pain in adults with GTPS. Method A systematic search of AMED, CINAHL, MEDLINE, EMBASE, TRIP and the Cochrane Library was conducted from inception to January 2021. Critical appraisal was completed using the Critical Appraisal Skills Programme tool. Data were extracted to obtain population characteristics and procedural details. Results Seven articles met the eligibility criteria out of a total of 336; five articles were randomised control trials (RCT) and two were cohort studies, equivalent to 758 and 70 participants, respectively. Studies generally reported significant benefits of CSIs <12 weeks and gluteal exercises >8 weeks for the reduction in lateral hip pain (p < .05). Critical appraisal demonstrated varied study quality and significant heterogeneity. Conclusion CSIs appear to be a successful treatment intervention in the short-term to decrease lateral hip pain but not in the long-term. Gluteal exercises plus education on avoiding tendon compression appears to be as successful as CSIs in the short and superior in the long-term.
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Background: Tendon pain occurs in individuals with extreme cholesterol levels (familial hypercholesterolaemia). It is unclear whether the association with tendon pain is strong with less extreme elevations of cholesterol. Objective: To determine whether lipid levels are associated with abnormal tendon structure or the presence of tendon pain. Methods: We conducted a systematic review and meta-analysis. Relevant articles were found through an electronic search of 6 medical databases-MEDLINE, Cochrane, AMED, EMBASE, Web of Science and Scopus. We included all case-control or cross-sectional studies with data describing (1) lipid levels or use of lipid-lowering drugs and (2) tendon structure or tendon pain. Results: 17 studies (2612 participants) were eligible for inclusion in the review. People with altered tendon structure or tendon pain had significantly higher total cholesterol, low-density lipoprotein cholesterol and triglycerides, as well as lower high-density lipoprotein cholesterol; with mean difference values of 0.66, 1.00, 0.33, and -0.19 mmol/L, respectively. Conclusions: The results of this review indicate that a relationship exists between an individual's lipid profile and tendon health. However, further longitudinal studies are required to determine whether a cause and effect relationship exists between tendon structure and lipid levels. This could lead to advancement in the understanding of the pathoaetiology and thus treatment of tendinopathy.
Conference Paper
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Introduction An association between tendinopathy and diabetes mellitus (DM) has been noted across multiple studies; see review by.1 This review aimed to identify and synthesise all available data on this topic. Methods Nine databases were comprehensively searched for English language journal articles reporting both a tendon and diabetes related variable. Reference lists and citation tracking were used to increase the sensitivity of the search. Articles were excluded if they were: case reports, conference proceedings, animal studies or if they lacked a control group. Results The search yielded 680 papers of which 33 were included in the final review. Meta-analysis of 4 studies identified a greater prevalence of diabetes in people with tendinopathy (OR 1.37, CI 1.05, 1.80, Figure 1). Similarly, meta-analysis of 12 studies identified an increased prevalence of tendinopathy in people with DM compared to controls (OR 4.93, CI 2.93, 5.55, Figure 2). Meta-analysis of 8 studies showed that individuals who had both tendinopathy and DM had a longer duration of disease than those who had diabetes but not tendinopathy (eight studies, mean difference: 4.75 yrs, CI 3.45, 6.05, Figure 3). Discussion The findings of this review suggest that tendinopathy should be considered in management of diabetes, particularly as duration of disease increases. This is clinically relevant as unmanaged tendinopathy can limit exercise capacity, which is an accessible means of glycaemic control in diabetes.2 In addition, management of tendinopathy can include exercise therapy to reduce pain and induce healing.3 Exercise therefore represents a mutually beneficial intervention for people suffering from DM and tendinopathy. References
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Vice Versa: Stellen Sie sich vor, Sie behandeln einen Fußballer Anfang zwanzig mit schmerzhafter Achilles­-sehne und kehren den pathologischen Prozess einfach um. Geht das? Charlotte Ganderton und ihre Kollegen meinen, ja. Vorausgesetzt, man erkennt anhand des Kontinuumsmodells die pathologische Phase der Sehne. Das ist allerdings nur einer von mehreren therapeutischen Schlüsseln...
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Being overweight or obese is associated with an elevated risk of tendon pathology. However, for sportspeople the epidemiological data linking weight or adiposity on one hand, and risk of tendon pathology on the other, are less consistent. Indeed, the mechanistic links between diet, adiposity and tendon pathology remain largely unexamined. Recent studies have begun to examine the effects of dietary interventions on outcomes such as tendon biomechanics or pain. Oxidised low-density lipoprotein has been shown to (A) accumulate in the tendon tissues of mice that eat a fatty diet and (B) induce a pathological phenotype in human tendon cells. This paper addresses the current debate: is excessive body mass index (causing increased load and strain on tendon tissue) per se the underlying mechanism? Or do local or systemic influences of fat on tendons predispose to tendon pathology? This narrative review argues that excessive blood lipids may be an important avenue for clinical investigations. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to
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[Rudavsky A, Cook J (2014) Physiotherapy management of patellar tendinopathy (jumper's knee).Journal of Physiotherapy60: xxx-xxx].
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Achilles tendinopathy (AT) is a common painful and disabling condition and current understanding of its pathophysiology is incomplete. Widespread hyperalgesia as a clinical manifestation of central sensitisation has emerged as a possible contributor to the pain state in chronic musculoskeletal injuries. Eight AT participants and eight healthy, gender, age and activity matched participants were recruited to participate in a case-controlled repeated measures study. Pressure pain threshold (PPT) was measured with a manual electronic algometer at four sites bilaterally; tibialis anterior (TA), patella tendon (PT), common wrist extensor tendon (CWET), and first dorsal interosseous (1DI). We hypothesised a reduction in PPT scores in the AT group at locations remote to the Achilles tendon compared to the healthy group. A linear mixed model analysis was used to compare the groups with age and gender adjustment. No significant difference was found between groups at any of the locations investigated: TA p= 0.638, PT p= 0.334, CWET p= 0.474, 1DI p= 0.056. Central sensitisation as represented through widespread hyperalgesia was not demonstrated in participants with AT. Our results must be treated with caution given the small number of participants tested. We also expect that the younger average age of our participants combined with a possible predisposition for decreased PPT scores secondary to high training loads may have influenced our results. Further research into pain processing changes with AT patients should be pursued with larger sample sizes and careful attention to participant matching. This will assist in developing the current understanding of pain mechanisms and guide treatment approaches in patients with AT.
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Context: Fluoroquinolone antibiotics have been used for several decades and are effective antimicrobials. Despite their usefulness as antibiotics, a growing body of evidence has accumulated in the peer-reviewed literature that shows fluoroquinolones can cause pathologic lesions in tendon tissue (tendinopathy). These adverse effects can occur within hours of commencing treatment and months after discontinuing the use of these drugs. In some cases, fluoroquinolone usage can lead to complete rupture of the tendon and substantial subsequent disability. Objective: To discuss the cause, pharmacology, symptoms, and epidemiology of fluoroquinolone-associated tendinopathy and to discuss the clinical implications with respect to athletes and their subsequent physiotherapy. Data sources: We searched MEDLINE, Cumulative Index to Nursing and Allied Health (CINAHL), Allied and Complementary Medicine Database (AMED), and SPORTDiscus databases for available reports of fluoroquinolone-related tendinopathy (tendinitis, tendon pain, or rupture) published from 1966 to 2012. Search terms were fluoroquinolones or quinolones and tendinopathy, adverse effects, and tendon rupture. Included studies were written in or translated into English. Non-English-language and non-English translations of abstracts from reports were not included (n = 1). Study selection: Eligible studies were any available reports of fluoroquinolone-related tendinopathy (tendinitis, tendon pain, or rupture). Both animal and human histologic studies were included. Any papers not focusing on the tendon-related side effects of fluoroquinolones were excluded (n = 71). Data extraction: Data collected included any cases of fluoroquinolone-related tendinopathy, the particular tendon affected, type of fluoroquinolone, dosage, and concomitant risk factors. Any data outlining the adverse histologic effects of fluoroquinolones also were collected. Data synthesis: A total of 175 papers, including 89 case reports and 8 literature reviews, were identified. Conclusions: Fluoroquinolone tendinopathy may not respond well to the current popular eccentric training regimes and may require an alternative, staged treatment approach. Clinicians, athletes, athletic trainers, and their medical support teams should be aware of the need to discuss and possibly discontinue these antibiotics if adverse effects arise.
Overuse Achilles tendon disorders are frequently seen in middle-aged, active people. Achilles tendon injuries are also common in elite-level football and result in the longest absences from playing. These tendon injuries are currently referred to as ‘tendinopathy’, a clinical diagnosis that can be made in the presence of pain, swelling of the Achilles tendon and an impaired load-bearing capacity. Histopathological studies have shown that chronic tendinopathy is frequently characterised by degeneration of the tendon tissue and not inflammation. When evaluating tendinopathies, it is important to differentiate between midportion and insertional disorders and to separate acute from chronic injuries. These injury characteristics will mainly guide treatment options and affect prognosis. For both insertional and midportion acute tendinopathies, the first treatment of choice is a symptom-based reduction in load and NSAIDs. For chronic midportion Achilles tendinopathy, the cornerstone of treatment is currently eccentric exercise therapy. Efficacy of other treatment options needs to be proven. Chronic insertional tendinopathy can be treated with anti-inflammatory treatment if a bursitis is present. In cases of intratendinous pathology, eccentric exercise therapy from a flat ground is proposed and extracorporeal shock wave therapy might be another promising option. Surgery might be considered for both insertional and midportion tendinopathies if conservative treatment fails. The prognosis for chronic tendinopathies is currently disappointing and difficult to predict, regardless of treatment.
Background—There is no disease specific, reliable, and valid clinical measure of Achilles tendinopathy. Objective—To develop and test a questionnaire based instrument that would serve as an index of severity of Achilles tendinopathy. Methods—Item generation, item reduction, item scaling, and pretesting were used to develop a questionnaire to assess the severity of Achilles tendinopathy. The final version consisted of eight questions that measured the domains of pain, function in daily living, and sporting activity. Results range from 0 to 100, where 100 represents the perfect score. Its validity and reliability were then tested in a population of non-surgical patients with Achilles tendinopathy (n = 45), presurgical patients with Achilles tendinopathy (n = 14), and two normal control populations (total n = 87). Results—The VISA-A questionnaire had good test-retest (r = 0.93), intrarater (three tests, r = 0.90), and interrater (r = 0.90) reliability as well as good stability when compared one week apart (r = 0.81). The mean (95% confidence interval) VISA-A score in the non-surgical patients was 64 (59–69), in presurgical patients 44 (28–60), and in control subjects it exceeded 96 (94–99). Thus the VISA-A score was higher in non-surgical than presurgical patients (p = 0.02) and higher in control subjects than in both patient populations (p<0.001). Conclusions—The VISA-A questionnaire is reliable and displayed construct validity when means were compared in patients with a range of severity of Achilles tendinopathy and control subjects. The continuous numerical result of the VISA-A questionnaire has the potential to provide utility in both the clinical setting and research. The test is not designed to be diagnostic. Further studies are needed to determine whether the VISA-A score predicts prognosis.
Background Few interventions reduce patellar tendinopathy (PT) pain in the short term. Eccentric exercises are painful and have limited effectiveness during the competitive season. Isometric and isotonic muscle contractions may have an immediate effect on PT pain. Methods This single-blinded, randomised cross-over study compared immediate and 45 min effects following a bout of isometric and isotonic muscle contractions. Outcome measures were PT pain during the single-leg decline squat (SLDS, 0–10), quadriceps strength on maximal voluntary isometric contraction (MVIC), and measures of corticospinal excitability and inhibition. Data were analysed using a split-plot in time-repeated measures analysis of variance (ANOVA). Results 6 volleyball players with PT participated. Condition effects were detected with greater pain relief immediately from isometric contractions: isometric contractions reduced SLDS (mean±SD) from 7.0±2.04 to 0.17±0.41, and isotonic contractions reduced SLDS (mean±SD) from 6.33±2.80 to 3.75±3.28 (p<0.001). Isometric contractions released cortical inhibition (ratio mean±SD) from 27.53%±8.30 to 54.95%±5.47, but isotonic contractions had no significant effect on inhibition (pre 30.26±3.89, post 31.92±4.67; p=0.004). Condition by time analysis showed pain reduction was sustained at 45 min postisometric but not isotonic condition (p<0.001). The mean reduction in pain scores postisometric was 6.8/10 compared with 2.6/10 postisotonic. MVIC increased significantly following the isometric condition by 18.7±7.8%, and was significantly higher than baseline (p<0.001) and isotonic condition (p<0.001), and at 45 min (p<0.001). Conclusions A single resistance training bout of isometric contractions reduced tendon pain immediately for at least 45 min postintervention and increased MVIC. The reduction in pain was paralleled by a reduction in cortical inhibition, providing insight into potential mechanisms. Isometric contractions can be completed without pain for people with PT. The clinical implications are that isometric muscle contractions may be used to reduce pain in people with PT without a reduction in muscle strength.