ACHILLES_TENDINOPATHY_PTIS

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6 Physical The
Glenn Hunter
MSc, MCSP, SRP,
CertEd, FE,
Department of
Allied Health
Sciences, Faculty of
Health and Social
Care, Glenside
Campus, University
of West England,
Blackberry Hill,
Bristol BS16 1DD
particularly with regards to the chronic,
overuse aspects of the pathology. Current
dif®culties are well summarized by Kahn and
Maffulli (1998) and are adapted by the author
in Figure 1.
This paper expresses the approach favored by
the author for the management of Achilles
tendinopathies, and in particular Achilles
tendonosis. The reader is reminded that the
management evidence presented in this article
should be viewed as descriptive in nature,
based on testimony and empirical evidence
only, and not of a causative nature.
that in¯uence the tensile strength of the tendon
(Currier & Nelson 1992).
The ground substance, consisting of
glycosaminoglycans (GAGs), proteoglycans
and glycoproteins, in¯uences the mechanical
properties of tendon (O'Brien 1992). In
particular, the GAGs are negatively charged
and appear to interact with the collagen ®bres
and proteoglycans to in¯uence collagen ®bre
orientation, the restoration of collagen ®bre
length after tensile load has been applied, and
to regulate the amount of inter-collagen cross
links by in¯uencing the inter-®bre distance
The conservative
of Achilles tendin
Glenn Hunter
Through seeking we may learn and know
things better. But as for certain truth, no man
hath known it, for all is but a woven web of
guesses
Xenophanes, 6th Century BC
Introduction
The conservative management of Achilles
tendinopathy provides the therapist with
fascinating and frustrating opportunities.
Fascinating on the basis that there are many
plausible hypothesis in the literature suggesting
ideal management protocols, and frustrating in
that the majority of these hypotheses lack
scienti®c credibility and provide evidence
which is in the main anecdotal. While anecdotal
evidence contributes to the creative process of
clinical reasoning, it does not provide evidence
that can be used con®dently as the most reliable
predictor of an outcome.
This speculative nature of the management of
Achilles tendinopathy has developed from the
lack of precise, controlled, objective and
reproducible scienti®c data on which to base
clinical reasoning. This situation is
compounded by the methodological and ethical
dif®culties facing the researcher in this ®eld,
Master Class
rapy in Sport (2000) 1, 6±14
management
opathy
Anatomy and biomechanics of
the Achilles tendon
The Achilles tendon is a remarkable tendon,
being able to sustain loads up to 17 times body
weight, with only 13% the oxygen supply of
muscle and a remodeling rate of 4100 days
(Khan & Maffulli 1998). The structural
components enabling it to do this are regulated
by the main cellular component of connective
tissue, the ®broblast, called in tendons the
tenoblast (Van Wingerden 1995). The tenoblast
produces the ®bres, ground substance and
proteins that are required for the continuous
turnover of extra-cellular components which
maintain the mechanical properties of the
tendon.
The main extra-cellular component is
collagen accounting for 70±80% of the dry
weight (O'Brien 1992). The collagen is
predominantly type I, which is well suited to
resisting tensile but not shear forces. A small
amount of type III collagen which lacks the
tensile properties of type I collagen, is also
present. The collagen ®bres are regularly
arranged along lines of tension in tendons
subjected to uni-directional loading (O'Brien
1992), and the amount, type, orientation and
cross links between ®bres are important factors
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1998).
The mechanical properties of a tendon are
commonly investigated by the use of load
deformation analysis (Fig. 2).
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Achilles tendinopathy
(Van Wingerden 1995). GAGs also appear to
in¯uence collagen ®bre diameter with larger
concentrations of GAGs and proteoglycans
being correlated with smaller diameter ®brils
(Curwin 1998).
The extra-cellular matrix by virtue of its
structural and material properties in¯uences the
mechanical properties of the tendon with the
structural properties being size dependent
features such as length, number of ®bres
orientated in the direction of the stress applied,
and cross sectional area (Curwin 1998), and the
material properties relating to tendon
composition, for example, the amount and type
of collagen, and number of cross links (Curwin
The load deformation curve is typically
divided into four regions (Fig. 2). The key
clinical features relating to the load deformation
curve are:
1. Regions 1 and 2 represent the zone of
physiological loading. Here loading
produces a straightening of the wavy
collagen ®bres at approximately 2% change
in length (Hess et al. 1989).
2. If the tissue is elongated to between 4 and
8% change in length, microscopic failure
may occur, with collagen ®bres starting to
slide past one another and failing (O'Brien
1992). This would equate to the overuse,
micro-traumatic etiology of Achilles
Fig. 1 Current dif®culties in the management of Achilles tendinopathy. Adapted from Khan and Maffulli 1998.
dysfunction (Micheli & Fehlandt 1992).
3. The slope of the linear portion of the curve
(2) represents the tissue's stiffness; the stiffer
the tissue, the steeper the slope. The stiffness
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is a variable phenomenon and is in¯uenced
by the tendon's visco-elastic properties
(Threlkeld 1992). Visco-elasticity is a
property of soft tissues whereby the strain
induced in the tissue is dependent on the
rate of loading of the applied stress
(Burnstein & Wright 1994; Archambault et al.
1995), and the response allows the tendon to
withstand greater force with faster rates of
loading (Oakes 1994). The visco-elastic
response has implications to management of
tendon dysfunction in that controlling the
rate of loading during rehabilitation will
alter the stiffness and hence the strain in the
tissue. This helps prepare the tissue for the
variable loading rates experienced during
functional activity.
4. The area under the curve represents the
energy in the tissue (Burnstein & Wright
py in Sport
Fig. 2 Load deformation curve illustrating the four main
regions of the curve. 1 ˆ toe region; 2 ˆ linear region;
3 ˆ ®bre failure point; 4 ˆ ultimate failure point.
1994). The area under the toe and linear
supply is divided into three regions:
. Proximal ± from the musclotendinous unit
junction.
rapy in Sport (2000) 1, 6±14
. Distal ± from the tendoperiosteal junction.
. Mid portion ± this is the area of irregular and
sparse vascularity with the blood supply
being predominantly from the paratenon.
Inadequate blood supply to the tendon has
been suggested as an etiological factor in
relation to Achilles tendinopathy (Kannus &
Josza 1991).
Pathophysiology of Achilles
tendinopathy
The term Achilles tendinopathy represents a
spectrum of overuse conditions that may effect
the Achilles tendon, and encompasses a range
of histological labels termed paratendonitis,
paratendonitis with tendonosis, tendonosis and
tendinitis (Leadbetter 1992).
This article will focus on Achilles tendonosis
which manifests as non-in¯ammatory intra-
tendinous collagen degeneration resulting in
®bre disorientation, a relative absence of
tenocytes, scattered vascular in-growth
increased inter-®brilar glycoaminoglycans
(Jozsa & Kannus 1997; Movin et al. 1997).
Collagen ®bres become thin and frayed and
lose their parallel orientation (Astrom &
Rausing 1995) and tenocytes isolated from these
areas produce increased quantities of type III
collagen which does not have the load bearing
capacity of type I collagen, and consequently
failsearlier in response to mechanical loading
(Fyfe & Stanish 1992; Chan et al. 1997). The
increase in matrix GAGs may reduce the inter-
®bre cross links between collagen ®bres
resulting in reduced tensile properties in the
tendon (Movin et al. 1997).
Etiology of Achilles tendonosis
Injury is a failure of the cell and matrix to adapt
to either sudden or gradual load exposure.
Current hypotheses regarding why the cell and
matrix may fail to relate to blood ¯ow (O'Brien
1992), hypoxic (O'Brien 1992) and thermal
denaturation mechanisms (Wilson & Goodship
1994). These mechanisms may be in¯uenced by
region represents the energy that may
contribute to improved performance, for
example as part of the stretch shorten cycle,
i.e. concentric to eccentric activity (Blanpied
et al. 1995). In contrast, the area under the
®bre failure and ultimate failure points
represents the energy that may produce
tendon pathology, depending on the tensile
properties of the tendon (Wilson &
Goodship 1994).
Of critical importance to the maintenance of the
tendon's mechanical properties is the blood
supply to the tendon (O'Brien 1992). The blood
mechanical loading with regards to the
magnitude, frequency, duration and rate of
application of the load, however, establishing
causal relationships with regards to the etiology
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of Achilles tendonosis is extremely conjectural
due to the multi-factorial nature of the plausible
mechanisms (Meeuwisse 1994). Allowing for
these limitations, etiological factors should be
explored in relation to intrinsic, extrinsic and
task related factors; Watson (1997) provides an
excellent review of this area. It should be
remembered that rather than excessive load
being the etiological factor, the loading
parameters may be optimal but the mechanical
properties of the tendon may reduce due to
genetic disorders, ageing, vascular changes,
endocrine in¯uences, nutritional de®ciencies,
inactivity, and exercise (O'Brien 1992;
Archambault et al. 1995).
Management of Achilles
tendonosis
This aspect of tendon dysfunction is currently
the most dif®cult and unscienti®c area of the
study of tendon dysfunction. Conservative
treatment proceeds on the basis of hypothetico-
deductive reasoning, whereby hypotheses are
generated regarding the proposed pathology, a
treatment is applied on the basis of its proposed
favorable in¯uences on the pathology and its
effectiveness is evaluated in terms of its effect
on subjective and objective markers. If no
change occurs then a new hypothesis is
generated and tested again on subjective and
objective markers, and so on.
The author's preference for the management
of Achilles tendinosis typically involves
addressing the following areas:
. Identi®cation and correction etiological
factors.
. Speci®c soft tissue mobilization protocols.
. Eccentric muscle control protocols.
While these areas are being addressed, it is
important to modify the patient's activity to
avoid the possibility of excessive loading
parameters sabotaging any treatment effect.
Identi®cation and correction of
etiological factors
The process of trial and error is used to correct
intrinsic, extrinsic and task related factors that
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relate to the magnitude, frequency, duration
and rate of loading on the tendon. Attention is
paid to periods of transition where a change in
the training protocol without suf®cient time to
adapt has occurred. These periods may result in
transient mechanical weakness with increased
collagen turnover, decreased mature cross link
content, and decreased GAG concentration
(Archembault 1995), thus weakening the tensile
properties of the tissue.
Evidence of excessive eccentric or ballistic
activity is sought and corrected because the
higher tensile forces placed on the tendon
during these activities may produce tendon
dysfunction (Curwin 1998).
If the rate of loading appears to be excessive,
it may be controlled by the use of orthotics.
There is currently debate over the mechanism of
action of orthosis in relation to their effect on
range of motion, the rate of loading, or both
(Rogers & Leveau 1982; Norvick & Kelly 1990;
Baitch et al. 1991; McCulloch et al. 1993).
However, reducing both the range and in
particular the rate of loading is likely to be
bene®cial with regards to affecting the visco-
elastic, and hence strain response in the tendon.
If the rate of loading is not controlled, repeated
loading of the tendon may increase the stiffness
of the tendon which may cause micro-failure to
occur at stresses normally within a physiologic
range (Nordin 1989). On the basis of this
rationale the author would consider using an
orthotic in the following situations:
. To `raise the heel' to reduce the rate and
range of eccentric load on the Achilles
tendon.
. To wedge the heel medially to control the
rate of subtalar joint pronation, particularly
in patients with excessive medial tenderness
on the tendon (Fig. 3).
A reduction in the rate of pronation may reduce
the shear forces within the tendon, which may
be important as type I collagen is poorly
adapted to sustain shearing forces.
In relation to the sub-talar joint, a restriction
Achilles tendinopathy
in its range of motion of inversion may
in¯uence loading patterns in the Achilles
tendon, and sub-talar joint mobilization
techniques may be valid on this basis.
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Speci®c soft tissue mobilization
protocols
The pathology of Achilles tendinosis is
traditionally addressed with the use of electro-
y in Sport
Fig. 3 Medial calcaneal wedge to control the amount or
rate of sub-talar pronation.
therapeutic modalities, but their clinical
evidence basis is sparse. There is uncertainty
over the mode of action of these modalities in
this case because the majority of evidence is
justify this approach is of an empirical nature
and testimony as there are currently no clinical
trials into the clinical effectiveness of this
particular approach.
rapy in Sport (2000) 1, 6±14
In short, speci®c soft tissue mobilization
techniques involve tensioning the tissue using
physiological joint movement, accessory soft
tissue movement, combinations of the previous
two, and dynamic soft tissue mobilization. The
therapeutic intention of this approach in the
acute phase post injury is to in¯uence the
mechanical properties of healing tissue by
in¯uencing the process of collagen and ground
substance synthesis following injury. In relation
to Achilles tendinopathy, patients often present
in the chronic remodeling phase post injury
where the time for peak collagen and ground
substance synthesis has passed. Here the
therapeutic intention is to affect the mechanical
response of the tissue to loading by altering the
compliance of the tendon and calf complex.
The initial assessment involves assessing
physiological, accessory and combined soft
tissue mobility to identify the range,
quality and limiting factors for the movement
(Figs 4±6).
On the basis of observation only, which is
open to bias and incorrect conclusion, the
author has noticed that the restoration of the
accessory movement to the tendon appears to
be critical to the recovery of the patient. In
many cases it appears that the physiological
movement has full range and quality, but the
accessory movement is limited. It may be
reasonable to speculate that the force used to
restore the tendon's accessory motion initiates a
strain response in the tendon that produces an
in¯ammatory and hence healing response at the
site of the previously non-in¯ammatory
degenerative pathology. However, the effect of
tendon mobilization on the tendon's
mechanical and histological properties are
currently unknown.
Soft tissue mobilizations are typically applied
witha sustained load for ®ve times 30 s in a
treatment session, with the patient stretching
the area for �30 s three times every waking
3±4 h.
Once it is established that the tendon is
responding to passive soft tissue mobilization,
`non-weight bearing' dynamic soft tissue
mobilization is introduced with the patient
currently based on the chemical mediators
present during acute in¯ammation. The
pathology of Achilles tendonosis in contrast
relates to a degenerative and chronic pathology
which may be associated with an absence of
in¯ammation (Khan & Maffulli 1998) for which
theoretical modes of electro-therapeutic action
have yet to be established. Though they are not
mutually exclusive, the author's preference is to
use a manual/exercise approach to address the
soft tissue dysfunction rather than an electro-
therapeutic approach.
The mobility of the Achilles tendon and calf
complex area are addressed by using the
principles of speci®c soft tissue mobilization,
details of which have been presented elsewhere
(Hunter 1994, 1998). The evidence used to
loading the calf complex while the accessory
mobilizations are applied to the tendon (Fig. 7).
This serves as a progression towards the next
phase of treatment.
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related dysfunction which is important as
fatigue reduces the ability of the muscle tendon
unit to attenuate strain energy which may
increase the strain in the tendon. Eccentric
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Achilles tendinopathy
Eccentric control protocols
Eccentric exercise regimes have become popular
for the management of Achilles tendinopathy
on the basis that the resultant active
`lengthening' of the muscle tendon unit and
high tensile forces results in increased tensile
strength in the tendon (Stanish et al. 1996). This
allows for more storage of elastic energy in the
tendon during a stretch shorten cycle (Kannus
1997). Their use may also address fatigue-
exercise may also prepare the tendon for rapid
unloading which has been associated with
injury as sudden force release is hypothesized
to break inter-®brilar adhesions as the shearing
forces within the tendon are large (Curwin
1998).
Their clinical use was pioneered in the
literature by Stanish et al. (1986). The authors
reported a prospective study on 200 patients
suffering from chronic Achilles tendonitis with
a mean duration time from onset of 18 months.
Fig. 4 Physiological soft tissue mobilization of the calf complex. Figures i, ii, iii indicate the physiological positions used to assess the
soleus, deep posterior calf muscles and Achilles. Figures iv, v, vi indicate the physiological positions used to assess the gastrocnemius and
Achilles. It is important to note that the position of the foot in terms of pronation or supination appears to in¯uence the symptomatic
response and hence loading within the tendon. Figures iii, v & vi illustrate the effect of altering the knee (ii, iii) and hip (v, vi) position on
the foot position ± these positions should be assessed in the initial examination of the patient and the approach used for treatment
should be the position which produces the most symptomatic response. The use of wedges to evert the sub-talar joint may make the
stretch more speci®c. Sometimes the use of wedges to evert the sub-talar joint and at the same time prevent mid-tarsal joint pronation
produces the most symptomatic response. The calcaneal wedge everts the sub-talar joint, increasing the strain in the tendon. The forefoot
wedge controls the amount of mid-tarsal joint pronation, which may help to concentrate the strain produced by this movement in
the tendon.
They reported at a mean follow-up of 16
months that 44% had complete pain relief and
return to function, 43% had a marked decrease
in their symptoms, 9% had no change in their
Physical Therapy In Sport (2000) 1, 6±14 11
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experimental design, without any
randomization or control, and therefore claims
for causation are ill founded. It is also worth
noting that the treatment intervention used in
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clinical state, 2% were worse after the exercise
program, and 2% were undisclosed. This study
may be interpreted as eccentric exercise having
a favorable effect in 87% of the patients, but it
should be recognized that this study has a pre-
Fig. 6 Combined soft tissue mobilization. The
physiological positions illustrated in Fig. 4 are used to
reproduce the patient's symptoms and then shear forces
(arrow) are applied to the tendon. This can be performed
in weight bearing as above, or in non-weight bearing.
Fig. 5 Accessory soft tissue mobilization. The mobility of
the Achilles tendon is assessed by subjecting the tendon
to shearing movements. Beginning distally with the
ankle/foot complex in the neutral position, the distal
aspect of the tendon is moved in one direction while the
more proximal 'segment' is moved in the opposite
direction. The shearing movements are applied
incrementally up the tendon to assess the range, quality
and limiting factors to the movement.
the study involved the use of static stretching
pre exercise, both concentric and eccentric
Fig. 8 Eccentric exercise regimes. The 'non-weight
bearing' exercises illustrated in Fig. 7 are progressed to
weight bearing eccentric protocols, beginning with pure
eccentric control exercises. Here the patient rises on the
good side and lowers the body weight on the affected
side. Progression is by increasing the resistance via
weights and the speed of the drop. Further progression is
from pure eccentric exercise to eccentric drops followed
by immediate concentric activity and then to more
functional ballistic type activity.
Fig. 7 Dynamic soft tissue mobilization. Once the
symptoms are reducing with the use of passive soft tissue
mobilization techniques, the tendon is subjected to
dynamic loading via the use of isometric, concentric and
eccentric exercise. Whilst the patient performs these
resisted exercises against, typically, some elastic
resistance, the therapist performs accessory movement
(arrow) on the tendon as illustrated in Fig. 5.
exercise, more static stretching, followed by
ice, and hence the suggestion that eccentric
exercise was the most bene®cial component is
tenuous.
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Following on, Niesen-Vertommen et al.
(1992) took 17 patients with a duration range of
Achilles tendonitis from 4 weeks to 2.6 years.
Subjects were randomly allocated to either a
concentric or eccentric group and patients were
tested at 0, 4, 8, and 12 weeks. No statistically
signi®cant difference was evident between the
two groups in terms of the outcome measures
but the small sample size and therefore power
may have yielded a type II error. The main
conclusion of the study was that the subjective
pain measurers favored the use of eccentric
exercise, but this study used the extensive
multiple intervention programs as used by
Stanish et al. (1986), and therefore limited
conclusions can be drawn.
More recently, Alfredson et al. (1998),
prospectively studied the effect of heavy load
eccentric calf muscle training in 15 patients with
Achilles tendonosis. Patients were selected from
a group waiting for Achilles tendon surgery
and were treated with an eccentric exercise
program. This group was compared to a group
that proceeded to surgery. The study found that
all the eccentric group at 12 weeks were back to
their pre-injury levels with full running activity
and the effect in terms of pain reduction and
prevention of strength de®cits were better than
those that went on to surgery. The eccentric
group also achieved better results in half the
time of the surgical group (12 weeks vs 24
weeks, respectively). In comparison to previous
studies this study used purely eccentric
exercises with the patientsrising using the good
side and eccentrically controlling the movement
on the bad side, and therefore may be able to
claim more bias to an effect being due to
eccentric exercise. A weakness in the study is
the sampling procedure used, where no
randomization is evident.
A summary is that there is evidence of a pre-
experimental nature to suggest that eccentric
exercise may be bene®cial in the management
of Achilles tendinosis. Better research designs
using a true experimental design are required to
give more causal inference to the data currently
presented and the exact mechanism of action
requires further study.
The author's preference is to introduce
eccentric loading programs once the patient is
pain free on non-weight bearing dynamic soft
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tissue mobilization, and to give the patient
eccentric exercise as follows (Fig. 8):
. Raise on the good side and control the
movement own with the bad side.
. 3 � 20 repetitions with the knee straight per
day.
. 3 � 20 repetitions with the knee bent per
day.
. Vary the speed and resistance to progress the
exercises.
As the symptoms resolve, the progression is
towards more functional loading patterns.
Conclusion
The management of Achilles tendinopathy is
currently frustrating due to the slow response
of the tissue to treatment, and due to the
speculative and sparse nature of the evidence
on which to base clinical reasoning. The authors
preference is to bias the conservative
management towards orthotic, eccentric
exercise and in particular the use of speci®c soft
tissue mobilization. In the uncontrolled and
biased clinical setting, soft tissue mobilizations
appear to have some clinical bene®t, however
the reader is cautioned against viewing this
approach as the `holy grail' on the basis that the
evidence presented is biased and descriptive in
nature. Also bearing in mind the large tensile
properties of this tendon, it is hard to
understand what possible effect these relatively
small mobilization loads are having on the
mechanical or histological properties of the
tendon. An exciting area for researchers lies
ahead in this ®eld.
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	The conservative management of Achilles tendinopathy
	Introduction
	Anatomy and biomechanics of the Achilles tendon
	Pathophysiology of Achilles tendinopathy
	Etiology of Achilles tendonosis
	Management of Achilles tendonosis
	Identification and correction of etiological factors
	Specific soft tissue mobilization protocols
	Eccentric control protocols
	Conclusion
	References
	Figures
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