©Journal of Sports Science and Medicine (2011) 10, 238-253
http://www.jssm.org
Review article
Current opinions on tendinopathy
Jean-François Kaux 1
Jean-Louis Croisier 1
, Bénédicte Forthomme 1, Caroline Le Goff 2, Jean-Michel Crielaard
1
Physical Medicine Service and Department of Motility Sciences, and
Sciences, University Hospital, University of Liege, Liège Belgium
Abstract
Tendinopathy is characterized by pain in the tendon and impaired performance sometimes associated with swelling of the
tendon. Its diagnosis is usually clinical but ultrasonography and
magnetic resonance imaging can refine the diagnosis. Tendinopathy is highly prevalent and is one of the most frequently
self reported musculoskeletal diseases in physical workers and
sports people. Nevertheless, it is very difficult to carry out general epidemiologic studies on tendinopathy because of the varying sports cultures and sports habits in different countries. The
aetiology of tendinopathy seems to be multi-factorial, involving
intrinsic and extrinsic factors. The role of inflammation is still
debated but the absence of inflammatory cells does not mean
that inflammatory mediators are not implicated. Different theories have been advanced to explain pain and chronicity mechanisms, but these mechanisms remain largely unknown. “Conventional” treatments are generally employed empirically to
fight pain and inflammation but they do not modify the histological structure of the tendon. However, these treatments are
not completely satisfactory and the recurrence of symptoms is
common. Currently, eccentric training remains the treatment of
choice for tendinopathy, even though some studies are contradictory. Moreover, many interesting new treatments are now
being developed to treat tendinopathy, but there is little evidence
to support their use in clinical practice.
Key words: Aetiology, epidemiology, inflammation, tendinopathy, therapeutic advances, treatments.
Introduction
Musculoskeletal diseases are a heterogeneous group of
conditions. The description and definition of different
musculoskeletal diseases will differ, between medical
specialists and the general population, and also between
different cultures and languages. Self reported musculoskeletal diseases are highly prevalent and are estimated
at between 2% and 65% (depending on survey design
factors and the age of the study population) (Forde et al.,
2005). The number of overuse injuries is not exactly
known, but in sports medicine, they account for 30 to
50% of all injuries (Scott and Ashe, 2006). Generally, for
physical workers, the prevalence of musculoskeletal
symptoms increases with duration of employment (Forde
et al., 2005). Age-adjusted logistic regression analyses
have shown that people who have worked for 25 to 35
years are more likely to develop tendinopathy (Forde et
al., 2005).
Tendinopathy is a common overuse injury in the
athletic and working populations; it is the main reason for
2
1
and
Department of Biomedical and Preclinical
consultation for a musculoskeletal complaint, and corresponds to around 30% of all such consultations with a
general practitioner (Forde et al., 2005; Riley, 2008).
Secondary referral rates vary widely, but one study reported that 17% of new patients seen in a locomotor clinic
had soft-tissue complaints (Riley, 2008).
In the last twenty years, sports activities have become increasingly important in our modern society.
Moreover, much attention has been paid to high level
athletes in competitive sports, which has increased the
demand on sports performance. Unfortunately, this has
increased the risk of injuries, especially of overuse injuries, which result from the necessity to train more often,
for longer periods of time, and more intensively. Moreover, in leisure sports, there are greater numbers participating, starting younger or continuing for longer, this
includes an increasing number of women, who are spending greater amounts of time participating in sports. In
more the equipment of these people is not always adapted
to the sports person, thus increasing the risk of tendinopathy (Maffulli et al., 2003). Sixty percent of overuse injuries sustained in running are experienced by the male
population; women under the age of 30 are at the greatest
risk of overuse injuries (Maffulli et al., 2003).
A few years ago the word “tendinitis” was widely
employed to designate pain located at the tendon. This
term corresponds to a histopathological description of
tendon impairment associated with an intratendinous
inflammation (Khan et al., 2002; Maffulli et al., 2003). By
contrast, “tendinosis” has been employed to describe a
histopathological state of degenerative tendon without
inflammatory signs or correlation with clinical symptoms
(Khan et al., 2002; Maffulli et al., 2003). More recently,
this concept has evolved and the word “tendinopathy” has
been proposed for the clinical diagnosis of pain accompanied by impaired performance, and sometimes swelling in
the tendon (Khan et al., 2002).
Currently, the most employed clinical and functional classification for tendinopathy remains the one
proposed by Blazina et al. (1973). This classification
distinguishes 4 stages: 1) pain after sports activity; 2) pain
at the beginning of sports activity, disappearing with
warm-up and sometimes reappearing with fatigue; 3) pain
at rest and during activity; 4) rupture of the tendon. It also
seems useful to classify the chronology of symptoms into
3 stages: when symptoms have been present for 0 to 6
weeks, the tendinopathy is characterized as “acute”, between 6 to 12 weeks, it is regarded as “sub-acute” and
after more than 3 months, it may be considered as
Received: 03 January 2011 / Accepted: 21 February 2011 / Published (online): 01 June 2011
Kaux et al.
239
Table 1. Classification systems of tendinopathy developed by Nirschl et al. (2003).
Pathologic stages:
Stage I: temporary irritation (chemical inflammation?)
Stage II: permanent tendinosis – less than 50% tendon cross-section
Stage III: permanent tendinosis – greater than 50% tendon cross-section
Stage IV: partial or total rupture of tendon
Phases of pain:
Phase I: mild pain after exercise activity, <24 hours
Phase II: pain after exercise activity, >48 hours, resolves with warm-up
Phase III: pain with exercise activity, does not alter activity
Phase IV: pain with exercise activity that alters activity
Phase V: pain caused by heavy activities of daily living
Phase VI: intermittent pain at rest that does not disturb sleep; pain
caused by light activities of daily living
Phase VII: constant rest pain and pain that disturb sleep
“chronic”.
However Nirschl et al proposed other staging systems and pain phase systems based on the observed histology at the time of surgery for tennis elbow and derived
from the patient’s description of the duration and intensity
of pain (Table 1) (Nirschl and Ashman, 2003).
The aim of this review is to present a critical analysis of the current opinion on tendinopathy, from physiopathology to treatments.
Histology and physiopathology
Compared with the normal tendon, which is glistening
white and has a firm fibroelastic texture, tendinopathy
induces specific modifications: the tendon appears grey or
yellow-brown and is soft, friable, fragile and thin or oedematous (Nirschl and Ashman, 2003; Scott and Ashe,
2006).
Under light microscopy, tendinopathy shows:
• disrupted collagen with fibres thinner than normal
and loss of the classical hierarchical structure
(Nirschl and Ashman, 2003; Riley, 2008). Tenocytes
located at the site of tendinopathy produce abnormal
amounts of collagen III, commonly associated with
wound healing (Cook et al., 2002).
• increased ground substance with high concentrations
of glycosaminoglycans and proteoglycans. (Sharma
and Maffulli, 2005; Rees et al., 2009). This increased
proteoglycan turnover is likely required to maintain
normal tendon homeostasis, with perturbations in
proteoglycan metabolism contributing to tissue dysfunction, resulting in chondrogenic differentiation (de
Mos et al., 2009; Rees et al., 2009).
• changes in cellularity with more prominent and numerous tenocytes with more rounded nuclei, and
without a fine spindle shape (Cook et al., 2002;
Nirschl and Ashman, 2003; Riley, 2008).
• an increase in apoptosis or programmed cell death
possibly explained by oxidative stress (Millar et al.,
2009) and loss of cellular homeostatic tension (Cook
et al., 2002; Egerbacher et al., 2008).
• neovascularization demonstrate on color and power
Doppler US, a process which could be associated
with tendon repair (Alfredson et al., 2006; Riley,
2008; Ackermann et al., 2009) or chronic pain
(Knobloch, 2008). In a recent study, US confirmed
• neovessels in the majority of Achilles tendinopathy
cases but the severity of symptoms was not correlated
with a neovascularization score (Sengkerij et al., 2009).
Electron microscopy has demonstrated that some vascular buds do not possess a lumen; this granulation-like
tissue has been termed angiofibroblastic hyperplasia
(Nirschl and Ashman, 2003).
In summary, changes in the tendinous matrix composition are in part mediated by inflammatory mediators
and metalloproteinase enzymes and are consistent with
changes in cell-mediated matrix remodelling that precede
the onset of clinical symptoms, as shown in Figure 1
(Bard, 2003; Cook and Purdam, 2009; Riley, 2008). Thus,
it seems that part of the treatment of tendinopathy should
focus on correcting intratendinous modifications.
The aetiology of tendinopathy seems to be a multifactorial process, involving promoting factors that are
intrinsic or extrinsic, working either alone or in combination (Fredberg and Stengaard-Pedersen, 2008; Jarvinen et
al., 2005; Nirschl and Ashman, 2003; Scott and Ashe,
2006). Aetiological factors are summarized in Table 2,
where we distinguish between innate general factors,
acquired general factors and acquired local factors.
In particular, it seems that after repetitive mechanical loads and/or when the load exceeds the strength of the
tendon, the tendon can become progressively micro- and
macroscopically damaged. Collagen fibres begin to denature, causing progressively a focal area of intratendinous
degeneration, partial tears, and ruptures (Bard, 2003;
Jarvinen et al., 2005; Sharma and Maffulli, 2005) (Figure
1). Indeed, excessive load of the lower extremities and
training errors have been shown to be present in 60 to
80% of patients who have Achilles tendon overuse injuries (Jarvinen et al., 2005). Regarding blood circulation of
a tendon, overuse may cause damage at both the microand the macrovasculature (Rees et al., 2006). Impaired
metabolic activity including disturbed oxygen transport is
likely to be detrimental to molecular cross-linking and
tissue repair. The ageing tendon is characterized by a low
rate of metabolism, a progressive decrease in elasticity
and tensile strength and a decreasing tendon blood flow
(Figure 1 & Table 1); thus, age would be regarded as an
important predisposing factor in the occurrence of tendinopathy.
However, contrary to previous articles, a study of
Master track and field athletes did not detect any influence of age, gender, weight, height, or impact profile on
240
Current opinion on tendinopathy
Figure 1. Physiopathology of tendinopathy (inspired from Finley and Rodgers, 2004; Forde et al., 2005).
the development of Achilles tendinopathy (Longo et al.,
2009). This conclusion certainly needs to be confirmed.
Although the role of inflammation is still debated
(Sharma and Maffulli, 2005; Riley, 2008; Millar et al.,
2009), animal and human studies support both the overload theory and the notion that inflammation may play a
role in the aetiology of acute tendinopathy. However, a
degenerative process soon supersedes this (Rees et al.,
2006). More recently, it has been shown that an inflammatory process may be related to the development of
chronic tendinopathies (Fredberg and StengaardPedersen, 2008; Millar et al., 2009). The absence of inflammatory cells in or around the lesion does not mean
that inflammatory mediators are not implicated in tendinopathies (Rees et al., 2006; Riley, 2008; Millar et al.,
2009). Biochemically, endothelial cells express and respond to a network of inflammatory mediators such as
interleukins (IL-1β, IL-6), prostaglandins (PGE1, PGE2),
nitric oxide synthetase (NOS), growth factors (PDGF,
TGF-β, b-FGF, EGF, VEGF, IGF-1) and other potential
modulators of tendon cell activity (glutamate, substance
P) (Ackermann et al., 2009; Millar et al., 2009; (Sharma
and Maffulli, 2005; Riley, 2008). The balance between
these growth factors (GFs) may have important implications in the control of tendon healing (Anitua et al., 2007).
The GFs also increase the production of COX-2, the
Table 2. Aetiology of tendinopathy: proposals for predisposing factors (Alfredson et
Bard, 2009; Forsgren et al., 2009; Fournier and Rappoport, 2005).
Innate general factors
Acquired general factors
- age (> 40 years)
- nutrition (excess of protein)
- male gender
- excessive force
- anatomic variants
- body composition (adiposity)
- blood type O
- new physical activities
- poor technique
- genetic factors
- training errors
- high body weight/adiposity
- weakness
- environmental conditions
- running surface
- hyperthermia
- drugs (oral corticosteroid or contraception,
fluoroquinolones, cannabis, heroin, cocaine)
- infectious diseases
- general diseases (RA, psoriasis, SLE, neurological conditions, hyperuricemia, AHT, CRF,
diabetes, insulin resistance, hypothyroidism, arteriosclerosis, hyperparathyroidism, glycogen
storage disease)
al., 2006; Andres and Murrell, 2008;
-
Acquired local factors
decrease in local vascular
perfusion
repetitive loading
excessive loading
abnormal and unusual movements
impingement
new/old shoes and equipment
RA = rheumatoid arthritis; SLE = systemic lupus erythematosus; AHT = arterial hypertension; CRF chronic renal failure.
Kaux et al.
expression of cytosolic phospholipase-A2 and the activation of stress-activated protein kinase (Fredberg and
Stengaard-Pedersen, 2008). Deposits of fibrinogen or
fibrin have also been described in chronic Achilles tendinopathy. Experimental evidence indicates that bioactive
peptides released in the formation and degradation of
fibrin increase vascular permeability, exerting a chemotactic effect on fibroblasts and inflammatory cells.Tendon
integrity depends on the extracellular matrix metabolism,
which is regulated by proteolitic enzymes (Karousou et
al., 2008). In tendinopathy, there are changes in the expression and activity of various matrix-degrading enzyme
metalloproteinases, particularly the collagenases (MMP-1,
MP-3, MMP-8, MMP-13) (Sun et al., 2008) and gelatinases (MMP-2, MMP-9) (Orchard et al., 2008). Changes
in the level of tissue inhibitors of metalloproteinase
(TIMPs), which are consistent with increased proteolytic
activity in degenerate tendons, are also reported
(Karousou et al., 2008; Riley, 2008). Quinolones enhance
interleukin-1-mediated MMP3 release, inhibit tenocyte
replication, and reduced collagen and matrix synthesis
(September et al., 2009).
One recently-described concept is the ‘cholinergic
anti-inflammatory pathway’ and the proliferative and
tissue reorganization process via autocrine and paracrine
effects that may be implicated in tendinopathy (Forsgren
et al., 2009). This concept refers to the occurrence of the
immunomodulatory effects of acetylcholine (ACh) released from cholinergic nerves. The neuronal inputs to
immune cells thus control cytokine production via an
inflammatory reflex. There is an attenuation in the release
of TNF-α and other pro-inflammatory cytokines and in
macrophage activation, in response to electrical stimulation of the vagus nerve (Forsgren et al., 2009).
Pain mechanisms and causes of chronicity
Surprisingly, the pain mechanism has not been wholly
elucidated. Classical theories state that inflammation and
its mediators (prostaglandins, thromboxanes, prostacyclines) lead to pain, or in severe chronic forms, pain is
due to separation of collagen fibres (Sharma and Maffulli,
2005). Biochemical stimulation of the nociceptors due to
extravasation of glucosaminoglycans (chondroitin sulphates) and other biochemical irritants (substance P, glutamate and its receptor NMDAR1) has been suggested in
more recent theories (Ackermann et al., 2009). On the
other hand, tenocytes produce ACh and immunoreactions
are possible with the ACh-receptor M2 of nerve fibres
which accompany blood vessels into the pathological
tendon (Fredberg and Stengaard-Pedersen, 2008; Forsgren
et al., 2009; Knobloch, 2008), yet the presence of neovascularization does not predict pain or functional outcomes
(de Jonge et al., 2008). The non-neuronal cholinergic
system may be involved in the establishment of a “cholinergic anti-inflammatory pathway”. Newly obtained
information suggests that this system plays an important
functional role in chronically painful tendons and in inflammatory conditions (Forsgren et al., 2009).
However, evidence of local, non-neuronal production of catecholamines (not ACh), has been recently demonstrated in fibroblasts at the muscle origin of the lateral
241
and medial epicondyles, in patients with tennis and golf
elbow. This production of catecholamines might have an
influence on blood vessel regulation and pain mechanisms
in these conditions (Zeisig et al., 2009).
Nevertheless, chronic pain or repeated tendinopathies could result from the absence of consensus in
treatment. Indeed, if the cause of tendinopathy is the inability of the tendon to bear constraints, passive treatments, generally purely analgesic and anti-inflammatory,
could remain ineffective. Only active treatments, such as
eccentric exercises, or new therapies, such as platelet-rich
plasma or extracorporeal shock waves, would have an
actual action on structure and adaptation of tendons to
stress (Khan and Scott, 2009). Indeed, the term “mechanotransduction” refers to the process by which the body
converts mechanical loading into cellular responses
which, in turn, promote structural changes (Khan and
Scott, 2009). Thus, the process enhances collagen fibril
alignment with increased tensile strength, encourages
fibroblast activity and collagen cross-linkage formation,
and prevents adhesions between the healing tendon and
adjacent tissue (Barone et al., 2008; Cook et al., 2002;
Petersen et al., 2007; Stasinopoulos et al., 2005). Another
cause of tendinopathy recurrence could be the absence of
clearly defined and evidence-based return to play criteria.
Indeed, a too early return to playing sport could deprive
the injured tendon of the opportunity to adapt to conditions faced in training or competition. Consequently,
assessing treatment effectiveness on the basis of precise
criteria seems logical. Currently, there is a lack of consensus regarding these criteria and research needs to be undertaken to clarify this point.
Diagnosis
Generally, the reason a patient seeks medical treatment is
due to pain or functional limitations. The diagnosis of
tendinopathy is primarily clinical. The differential diagnosis for tendinopathy is listed in the Table 3.
Tendinopathies are clinically characterized by a
gradual onset of stiffness in the tendon, activity-related
pain, decreased function, and sometimes localized swelling and palpable crepitations (Andres and Murrell, 2008;
Fredberg and Stengaard-Pedersen, 2008). Usually, clinical
examination reveals pain with the following 3 tests:
stretching, isometric contractions and palpation of the
pathological area.
Although usually not required, diagnostic imaging
may assist in diagnosing tendinopathy and choosing an
appropriate treatment regimen. However, due to the poor
correlation between diagnostic imaging and symptoms,
the role of serial diagnostic imaging is limited (Khan et
al., 2003).
Several imaging modalities can be used to evaluate
tendinopathy. For instance, US (with color Doppler) and
MRI are considered superior to conventional radiography
or CT-scanners; they are usually prescribed when tendinopathy is unresponsive to treatment and entails lingering
symptoms (Fredberg and Stengaard-Pedersen, 2008;
Khan et al., 2003). However US, which is interactive, and
certainly very operator-dependent, provides excellent
morphological detail of tendons. It is also relatively
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Current opinion on tendinopathy
Table 3. Differential diagnosis of tendinopathy depending on localization (except for traumatic, tumoral and infectious diseases).
Localization (% incidence)
Risk factors
Differential diagnosis
- Wrist and hand (4 to 56% in - house cleaner
- De Quervain’s disease
physical workers)
- physical workers
- other wrist tendinopathies
- rowing
- carpal tunnel syndrome
- skiing
- rhizarthrosis
- golf
- radial styloiditis
- tennis
- intersection syndrome
- joint hypermobility
- Guyon’s canal syndrome
- rheumatoid arthritis
- Wartenberg’s syndrome
- diabetes
- hypothyroidism
- Elbow (9 to 40% in tennis - tennis
- tennis elbow
players)
- golf
- golf elbow
- physical workers
- C5-C6 radiculopathy (lateral)
- C8-T1 radiculopathy (medial)
- posterior interosseous nerve compression
- radiocapitellar osteoarthritis/chondromalacia
- osteochondritis dissecans capitellum
- rheumatic enthesopathy
- Shoulder (15 to 20% in physi- - volleyball
- rotator cuff tendinopathy
cal workers and athletes, from - baseball
- frozen shoulder
31 to 73% in the wheelchair - javelin
- omarthrosis
population)
- swimming
- acromio-clavicular pathology
- tennis
- instability of the shoulder
- American football
- labrum / SLAP lesions
- wheelchair population
- C4-C5-C6 radiculopathy
- painter
- nerve lesion (suprascapular, thoracic longus, axil- clerical work (computer)
laris nerves)
- Hip (around 0,5% around - excess weight
- gluteus medius tendinopathy
general population)
- skiing
- greater trochanteric bursitis
- ice-skating
- coxarthrosis
- roller-skating
- coxitis (spondylarthropathy)
- ilio-tibial band tenderness
- hip osteonecrosis
- pubalgia
- sacroiliac pathology
- labral lesion
- villonodular synovitis
- osteochondromatosis
- stress fracture of the femur or pelvis
- femoroacetabular impingement
- Knee (7 to 40% in sportsmen)
- basketball
- patellar tendinopathy
- volleyball
- quadriceps tendinopathy
- soccer
- hamstring tenosynovitis
- long-distance running
- patellofemoral pain syndrome
- orienteering
- prepatellar bursitis
- ice hockey
- Osgood-Schlatter disease
- cycling
- Sinding-Larsen-Johansson Disease
- track and field
- meniscal lesion
- plica
- Hoffa’s inflammation
- stress fracture of the tibia or fibula
- Ankle (5.9% in sedentary - running
- Achilles tendinopathy
people and around 50% in en- - soccer
- Ligament injuries
durance athletes)
- track and field
- Anterior or posterior impingement
- jumping
- gout
- volleyball
- retrocalcaneal bursitis
- badminton
- rheumatoid arthritis
- orienteering
- rheumatic fever
- sero-negative arthropathies
- Sever's Disease
- stress fracture of the calcaneus
inexpensive and has several significant advantages over
MRI in showing the fine internal structure of tendons
(showing neovascularization, thickening of the tendon,
discontinuity of fibres, focal hypoechoic intratendinous
areas…) (Fredberg and Stengaard-Pedersen, 2008). The
extreme sensitivity of MRI means that structural abnor-
Kaux et al.
malities detected by imaging may not correlate precisely
with symptoms (Khan et al., 2003). A careful clinical
correlation with imaging findings is therefore needed
(Cook et al., 2001; Khan et al., 2003). For example, in
one study, the sensitivity and specificity of US for patellar
tendinopathy were calculated to be 58% and 94% respectively; for MRI, sensitivity and specificity were 78% and
86%, respectively (Warden and Brukner, 2003). Even if
imaging adds little information of use for expert sports
medicine clinicians in diagnosing tendinopathy, it may be
useful in decision-making regarding surgical treatment or
for inexperienced clinicians who are unsure of their diagnoses or unfamiliar with grading schemes (Khan et al.,
2003). It is generally acknowledged that imaging shows
poor predictive value in terms of development of symptoms and clinical findings (Khan et al., 2000). A recent
theory explains that severe tendinopathies can be asymptomatic for a long period before the appearance of symptoms (Cook et al., 2001). Thus, chronic tendinopathies
can be compared with an iceberg where pain represents
the tip. It has also been suggested that through US examination of the Achilles tendons of asymptomatic athletes, it
would be possible to predict a group with a risk of developing symptoms; the use of the technique thus would
reduce the risk of developing chronic tendinopathies or
tendon ruptures (Fredberg et al., 2008). Further studies
are needed to confirm these studies and to investigate
which prophylactic treatments might reduce the risk of
tendinopathy occurrence (Fredberg et al., 2008).
On the other hand, no study has confirmed that radiological monitoring of patient progress has a clinical or
cost benefit (Khan et al., 2003). Moreover, tendon imaging abnormalities persist even when patients have made a
good functional recovery. For example, US images have
been shown to remain both qualitatively and quantitatively abnormal 12 months after patellar tendon surgery,
even in athletes who have returned pain-free to full competition. In terms of MRI, tendon appearance does not
return to normal after successful surgery, and thus this
imaging technique is not able to distinguish patients
whose surgical outcome was good from those whose
outcome was bad (Warden and Brukner, 2003). Consequently, imaging does not appear to have a major role to
play in monitoring outcomes following surgical intervention for tendinopathy (Khan et al., 2003; Warden and
Brukner, 2003).
In conclusion, clinical assessment remains the cornerstone of appropriate diagnosis and management of
tendinopathy (Cook et al., 2001). US and/or MRI could
be useful for confirming the diagnosis where there is
some doubt, but these imaging techniques are not recommended for monitoring treatment (Khan et al., 2000).
Epidemiology
Because of differences in national sports cultures and
sports habits, it is very difficult to undertake a general
epidemiologic study on tendinopathies. Thus, national
epidemiological studies are important in each country in
order to plan prevention programmes for sports injuries.
With respect to physical workers, the prevalence of
self-reported musculoskeletal symptoms has been shown
to be high for the lower back (56%), wrist/hands/fingers
243
(40%), knees (39%), and shoulders (17-36%) (Forde et
al., 2005). The most commonly diagnosed musculoskeletal disorders were tendinopathies (19%) and ruptured
disks in the back (18%), shoulder bursopathies (15%), and
carpal tunnel syndrome (12%) (Forde et al., 2005). Common upper extremity tendinopathies include rotator cuff
injury, lateral and medial epicondylitis and De Quervain’s
tenosynovitis (Werner et al., 2005). The incidence of
shoulder tendinopathies in physical workers is estimated
at 15 to 20% and ranges from 4 to 56% for hand and wrist
tendinopathies (Werner et al., 2005). The risk is increased
when there is a combination of high force, repetition, or
exposure to vibration during repetitive work (Werner et
al., 2005).
The online supplementary material 2 shows differential diagnosis and proposed risk factors for tendinopathy for each joint. We have limited ourselves to the tendinopathies of the upper and lower limbs because tendon
pathologies of the trunk are definitely more difficult to
isolate from other local pathologies (e.g. athletic groin
pain) (Tibor and Sekiya, 2008).
Upper limb tendinopathies
Lateral epicondylitis (tennis elbow) is common in athletes
of all ages participating in sports involving overhead or
repetitive arm actions (Hume et al., 2006). Its incidence in
tennis players is as high as 9 to 40% (Maffulli et al., 2003;
Scott and Ashe, 2006). It is 2 to 3.5 times more frequent
in people over the age of 40, in particular if playing tennis
more than 2 hours per day. The condition affects approximately 1 to 3% of the general population. The extensor carpi radialis brevis is the most frequently involved
tendon but some patients also have involvement of the
extensor digitorum communis (Scott and Ashe, 2006). In
tennis, lateral epicondylitis is 5 to 10 times more common
than medial epicondylitis (golfer’s elbow) (Hume et al.,
2006; Maffulli et al., 2003; Scott and Ashe, 2006). In the
case of golfer’s elbow, which is a typical complaint in
javelin throwing, baseball and golf, coexistence of ulnar
nerve pathology can be expected in up to 50% of cases
with anterior subluxation of the ulnar nerve with elbow
flexion (in 10 to 15% of cases), and may exaggerate or
even mimic the symptoms of golfer’s elbow (Maffulli et
al., 2003; Scott and Ashe, 2006).
One potential cause of rotator cuff tendinopathy is
shoulder impingement. This condition represents 18% of
overuse injuries in adult athletes and, if untreated, may
result in rotator cuff rupture (Maffulli et al., 2003). The
supraspinatus is the most commonly injured muscle and
Bigliani types II or III acromion are associated with increased incidence of rotator cuff tears (Scott and Ashe,
2006). Such complaints of the anterior shoulder are often
present in swimmers. Anterior shoulder pain due to rotator cuff tendinopathy is often present in swimmers (until
71% of elite swimmers) (Scott and Ashe, 2006). Other
throwing sports such as javelin, baseball, tennis, volleyball, or American football may also be associated with
anterior shoulder pain (Kaplan et al., 2005). The shoulder
is the most common site of pain reported in the wheelchair population (from 31 to 73%). Bicipital tendinopathy
has also been cited as the most commonly occurring pathology in this population (Finley and Rodgers, 2004).
244
The incidence of biceps pathology is directly proportional
to the extent of rotator cuff disease (41%) and may be the
result of a combination of a primary change from the
impingement process and a secondary change after loss of
overlying coverage by the rotator cuff (Chen et al., 2005).
De Quervain’s disease, caused by stenosing tenosynovitis
of the first dorsal compartment of the wrist (abductor
pollicis longus and extensor pollicis brevis), is probably
the best known form of paratendinopathy of the wrist and
hand and is approximately six times more common in
women than in men (Maffulli et al., 2003). Patients with
this condition usually report pain at the dorsoradial aspect
of the wrist, with referral of pain toward the thumb and/or
the lateral forearm. People may develop De Quervain's
tenosynivitis following excessive use of the wrist or
thumb (e.g. skiing, wringing out wet clothes, hammering,
lifting heavy objects…). This condition remains the third
most reported tendinopathy of the upper extremity in
physical workers and it is promoted by diabetes or rheumatoid arthritis (Werner et al., 2005).
Lower limb tendinopathies
Achilles tendinopathy is the most prevalent lower extremity tendinopathy, with a 5.9% frequency in sedentary
people and around a 50% frequency in elite endurance
athletes (Scott and Ashe, 2006; Fredberg and StengaardPedersen, 2008). Most common clinical Achilles disorders are mid-portion tendinopathies (55-65%), followed
by insertional problems (insertional tendinopathy and
retrocalcaneal bursitis; 20-25%) (Jarvinen et al., 2005).
Eleven percents of soccer players report having an Achilles tendinopathy but middle- and long-distance running,
track and field (7-9% of top-level runners), orienteering
and jumping (volleyball, basketball, badminton) are the
main sports practised by patients with Achilles tendon
injury (53%), emphasizing the aetiological role of running
and jumping (Maffulli et al., 2003; Jarvinen et al., 2005).
Men have a higher prevalence of Achilles tendinopathy
than women do before menopause (Scott and Ashe,
2006), probably due to a greater level of exercise. One
study showed that forty-one percent of patients who had
had an Achilles tendinopathy developed symptoms in the
contralateral leg during an 8-year follow-up (Jarvinen et
al., 2005). The natural history of Achilles tendinopathy
remains unclear: around 30% of Achilles tendinopathies,
which are resistant to conservative management undergo
operative management (Maffulli et al., 2003; Paavola et
al., 2000).
About one third of sports injuries treated in sports
clinics concern the knees and one quarter of athletes
treated for a knee injury are diagnosed with tendinopathy
(Maffulli et al., 2003). The highest incidences appear in
soccer (21%), basketball (13.6%), long-distance running
(13%), volleyball (12%), orienteering (8%) and ice
hockey (7%). The most common knee disorder is
jumper’s knee, and its incidence is reported to be in the
range of 7 – 40% (Fredberg and Stengaard-Pedersen,
2008; Scott and Ashe, 2006). Patellar tendinopathies
represent two thirds of all pathologies of the knee induced
by volleyball or basketball practice (Scott and Ashe,
2006). Other tendon complains are ilio-tibial band friction
syndrome and hamstring tenosynovitis. Ilio-tibial band
Current opinion on tendinopathy
friction represents approximately 14% of overuse injuries
of the knee and is associated with cyclers, long-distance
runners or joggers (55%), and skiers (15%). Hamstring
tenosynovitis (3% of knee problems) is present in patients
active in sprinting, hurdling or jumping (50%), and soccer
(22%) (Maffulli et al., 2003).
Tendinopathy of the gluteus medius tendon is the
main cause of greater trochanter pain syndrome (Bard,
2009). The incidence of greater trochanteric pain is reported to be approximately 1.8 patients per 1000 per year
with the prevalence being higher in women and in patients with coexisting low back pain, osteoarthritis, iliotibial band tenderness, and obesity (Williams and Cohen,
2009). The fact that greater trochanteric pain is more
common in women is perhaps due to the specific morphology of the pelvis (Tibor and Sekiya, 2008). Great
trochanteric pain seems to be increasing in younger patients.
Treatments
Choices of treatment often change in parallel with
physiopathological discoveries regarding tendinopathies.
On the one hand, classic treatments, based on antalgic and
anti-inflammatory drugs and passive physiotherapy, are
often not sufficient. On the other hand, more advanced
treatments exist, which have an impact on tendon structure and can lead to lasting recovery (Table 4, Figure 2).
a. Conventional treatments
Conventional treatments are generally employed empirically to fight pain and inflammation but they do not modify the histological structure of the tendon (Croisier et al.,
2001). These treatments such as relative rest or modified
activity, cold, stretching, braces, antalgic physiotherapy
and correction of provoking gestures are usually initially
employed in acute and in the most hyperalgic phase of
tendinopathy (Alfredson, 2005; Fournier and Rappoport,
2005). In a recent study using a rat model, it was demonstrated that 2 weeks of rest was often sufficient to recover
from the molecular and biomechanical effects of 2 and 4
weeks of overuse (Jelinsky et al., 2008). Such findings
could represent a scientific basis for the use of rest or the
removal of the cause of the tendinopathy (repeated gestures), and such an approach is rational.
Anti-inflammatory drugs: The goal of non-steroidal
anti-inflammatory drugs (NSAIDs) is to reduce inflammation through the inhibition of the synthesis of inflammatory factors (inflammatory cells, prostaglandins, interleukins…) and their use has been popular for many years
in the management of tendinopathy (Glaser et al., 2008).
Evidence cited in the literature suggests that both oral and
local NSAIDs are a reasonable option for the control of
acute pain associated with tendon overuse but that they
are not effective long term (Alfredson, 2005; Magra and
Maffulli, 2006; Hennessy et al., 2007; Andres and
Murrell, 2008; Glaser et al., 2008). In addition, long-term
use of NSAIDs, even of COX-2 selective, increases the
risk of gastrointestinal, cardiovascular and renal side
effects associated with these medications. Although
NSAIDs appear to be effective for pain control, this analgesic effect could lead patients to ignore early symptoms,
entailing further damage on the affected tendon and
Kaux et al.
245
Table 4. Therapeutic effects of different treatments for chronic tendinopathies.
Treatment
Efficacy on pain (short-term)
Efficacy on pain (long-term)
Rest & ice
++
NSAIDs
++
- to ±
Passive physiotherapy (US,
± to +
DTFM, acupuncture…)
Orthotic devices
+
±
Corticosteroid injections
+++
- to ±
Eccentric training
+
+++
ESWT
++
++ to +++
Sclerosant injections
++
++ (?)
BTA injections
++
+ (?)
Injections of blood or PRP
± to +
+++ (?)
Topical NO therapy
++
+++ (?)
Injections of MMP-inhibitor
++
++ (?)
Stem-cell or gene therapy
?
?
Effect on recidivation
++
+ (?)
?
?
?
?
?
?
-: no efficacy; ±: little efficacy; +: good efficacy; ++: very good efficacy; +++: excellent efficacy; (?): need more trials; ?: efficacy unknown
delaying definitive healing (Magra and Maffulli, 2006).
On the other hand, studies on acute tendon injuries in a rat
model showed that NSAID administration did not prevent
collagen degradation or loss of tensile force in tendons
(Hennessy et al., 2007). However, the role of NSAIDs is
still being discussed with regard to the controversy relating to inflammation in tendinopathies (Magra and
Maffulli, 2006; Rees et al., 2006; Hennessy et al., 2007;
Fredberg and Stengaard-Pedersen, 2008). Indeed, animal
and human studies support both the overload theory and
the notion that inflammation may play a role in the aetiology of acute tendinopathy. However, a degenerative process soon supersedes this (Rees et al., 2006). Moreover, it
has recently been shown that an inflammatory process
may be related to the development of chronic tendinopathies (Rees et al., 2006; Fredberg and StengaardPedersen, 2008).
Classical physiotherapy: There is controversy in
the literature and little evidence to support the use of
conservative treatments such as ultrasound (US), iontophoresis with NSAIDs, deep transverse friction massage
(DTFM), or acupuncture (Brosseau et al., 2002; Green et
al., 2005; Andres and Murrell, 2008). While frequently
proposed in clinical settings, these modalities are reported
to be effective, but only one (methodological limitations)
scientific clinical study has confirmed their effects
(Alfredson, 2005). However, in some studies these treat-
Figure 2. Treatments for tendinopathies.
ments show positive effects in the reduction of pain or in
improvement in the function of patients with tendinopathies (e.g. lateral epicondylitis) (Fournier and
Rappoport, 2005; Rees et al., 2006; Hennessy et al., 2007;
Andres and Murrell, 2008). Further research is required to
verify whether these modalities should remain a part of
tendinopathy treatment.
Orthotic devices: Different sorts of orthotic devices
exist but it is difficult to accurately assess their effectiveness in tendinopathy. Orthotics can be useful by modifying the vector strength transmitted on osseous insertion,
by reinforcing proprioceptive stimulus or by correcting a
static disorder (Fournier and Rappoport, 2005).
Orthotics are widely used in conservative management of tendinopathy but there is little evidence to
support their effectiveness (Hennessy et al., 2007). A
Cochrane review on the use of orthotic devices for epicondylitis failed to demonstrate their effectiveness (Struijs
et al., 2002).
Corticosteroid injections: At the cellular level, the
anti-inflammatory and immunosuppressive activities of
corticosteroids are currently considered to be attributable
to the inhibition of the synthesis of cytokine genes and
proinflammatory factors. In addition, the repression of
genes encoding cell surface receptors and adhesion molecules in the activation, migration, and recruitment of
lymphocytes mediates the anti-inflammatory effect of
246
corticosteroids (Paavola et al., 2002).
In tendinopathy, changes in the composition of the
tendinous matrix are in part mediated by inflammatory
mediators and metalloproteinase enzymes and are consistent with changes in cell-mediated matrix remodelling,
which precedes the onset of clinical symptoms. Corticosteroids could mediate their own effect thorough alterations in the release of these harmful chemicals agents, the
behaviour of their receptors, or both (Fredberg and
Stengaard-Pedersen, 2008). CSIs aim to achieve a reduction in inflammation, neo-vascularization and tendon
thickness but there are also other unknown effects such as
the general inhibition of protein synthesis (Fredberg et al.,
2004). For these reasons, corticosteroid injections (CSIs)
are commonly and successfully used to control painful
tendinopathies in many common conditions (Andres and
Murrell, 2008; Fredberg et al., 2004; Hennessy et al.,
2007) where there is the risk of tendon rupture (Hennessy
et al., 2007). Moreover, it seems that the claimed good
clinical effects of local corticosteroid injections could be
mediated, at least partially, through their effect on the
connective tissues and adhesions between the tendon and
peritendinous tissue. This would inhibit synthesis of collagen and other extracellular matrix molecules as well as
the forming of granulation tissue in these sites (Paavola et
al., 2002).
Although CSIs are commonly used to treat tendinopathy, there is a lack of controlled clinical series defining the exact indications for and determining the effects
of such injections. Subsequently, many recommendations
for using local injections of corticosteroid are not based
on scientific evidence (Paavola et al., 2002). Indeed,
many studies have noted an early significant improvement
after a steroid injection in the short term, up to 6 weeks,
but recurrences are common and in the long term (beyond
6 months) a “wait-and-see” policy or NSAID therapy can
have the same results (Andres and Murrell, 2008). Thus in
good practice medicine, the steroid injection would be
made only to decrease pain in order to get through this
hyperalgic phase in order to start physiotherapy and/or
eccentric training (Andres and Murrell, 2008; Stanish et
al., 1986) as soon as possible.
To summarize, there are a wide variety of conventional treatments for the management of tendinopathy,
both pharmacological and non-pharmacological. These
treatments have, beyond a doubt, a therapeutic interest
and a relative efficacy. This efficacy would appear to be
more important in the acute phase of tendinopathy, and
regularly as adjuvant treatment with other techniques.
However, these treatments are not completely satisfactory
and the recurrence of symptoms is common. Moreover,
there is little evidence to support the use of these treatments, and more controlled trials are needed.
b. Eccentric training
A few decades ago, Stanish (Stanish et al., 1986) was one
of the pioneers of progressive eccentric exercise therapy
(EET) in chronic tendinopathies, especially in Achilles
tendinopathies (Alfredson, 2005; Glaser et al., 2008).
More recently, eccentric programmes have been developed for the management of patellar tendinopathies
Current opinion on tendinopathy
(Stanish et al., 1986; Peers and Lysens, 2005; Visnes and
Bahr, 2007) and lateral epicondylitis (Stasinopoulos et al.,
2005; Croisier et al., 2007). Specific modalities of eccentric intervention are slow speed, low intensity and gradual
intensification. Such active treatment induces a progressive action on the tendon structure, which can lead, after a
certain length of time (minimum 20 to 30 sessions of
exercises), to the healing of tendinopathies, but it can also
prevent relapse and chronicity (Croisier et al., 2001; Khan
and Scott, 2009). However, this treatment should be painful at the beginning.
“Mechanotransduction” initiated by EET refers to
the process by which the body converts mechanical loading into cellular responses which, in turn, promote structural changes (Khan and Scott, 2009). Thus, the process
enhances collagen fibril alignment with increased tensile
strength, encourages fibroblast activity and collagen
cross-linkage formation, and prevents adhesions between
the healing tendon and adjacent tissue (Barone et al.,
2008; Stasinopoulos et al., 2005). Recently, it has been
shown that endurance and resistance training induces
tendon tissue remodelling (increase in collagen fibre content and reduction in the number of cell nuclei), which
depends on the length and the intensity of workload rather
than on training type (running or climbing) (Barone et al.,
2008). It has also been proposed that positive effects of
EET may be attributable either to the effect of stretching,
with a lengthening of the muscle-tendon unit and consequently less strain experienced during joint motion, or to
the effects of loading within the muscle-tendon unit, with
hypertrophy and increased tensile strength in the tendon
(Allison and Purdam, 2009; Stasinopoulos et al., 2005).
Some theories propose that during EET, the blood flow is
either stopped in the area of damage, which leads to neovascularization and improves blood flow as well as causing healing in the long term (Boesen et al., 2006), or have
found that EET reduces paratendinous capilliary blood
flow, consistent with a decrease in pain (Rees et al.,
2008). Recently, a new theory has suggested that highfrequency oscillations in tendon force occur during EET
by increased force fluctuations, rather than by force magnitude (featuring less in concentric exercises), providing
the mechanism to explain the therapeutic benefit of eccentric loading (Rees et al., 2008).
Several studies have demonstrated that treatment
leads to good clinical results both with (Croisier et al.,
2001; 2007; Frohm et al., 2007a; 2007b) or without the
use of a heavy load (Norregaard et al., 2007; Stanish et
al., 1986). EET has superior short-term results compared
to concentric training (Mafi et al., 2001). Some authors
have demonstrated better results with EET on corporeal
tendinopathies in comparison with enthesopathies
(Andres and Murrell, 2008; Glaser et al., 2008). New
research has shown that good clinical results can be expected without loading in dorsiflexion to avoid impingement between tendon, bursa and bone in the case of
Achilles tendinopathy (Jonsson et al., 2008). Other studies in the short term showed greater clinical gains, better
results in terms of pain reduction and a better return to
function after using a decline protocol compared with a
step protocol and produced (Visnes and Bahr, 2007).
Kaux et al.
Patients are also recommended to take 4 to 10 weeks of
rest from sport for optimal reduction of tendinosis symptoms (Visnes and Bahr, 2007).
The benefits of isokinetic devices are well known,
particularly for delivering eccentric exercises. These devices have also proven to be advantageous for the management of tendinopathies, in comparison with manual
strengthening or isotonic exercises (Croisier et al., 2001;
2008). The risk of worsening a tendinopathy with eccentric overload training under these controlled circumstances seems to be reduced with the use of isokinetic
dynamometer (Croisier et al., 2001; Frohm et al., 2007b).
As a result, EET has become the treatment of
choice for chronic tendinopathy (Achilles, patellar and
epicondylitis) (Allison and Purdam, 2009; Glaser et al.,
2008; Hennessy et al., 2007) even though in real life, and
despite appropriate compliance, only about 60% of the
patients benefit from EET (Sayana and Maffulli, 2007).
Combining EET and stretching could perhaps improve
results in decreasing pain; indeed, stretching seems to
have similar effects to EET at 1-year follow-up in the case
of Achilles tendinopathy (Norregaard et al., 2007). It has
also been suggested that, in combination with EET, rehabilitation should incorporate sports-specific stretch shortening cycle and strengthening programmes (Allison and
Purdam, 2009).
In summary, EET is currently considered to be the
most efficient treatment for tendinopathy, even though
some studies are contradictory. Nevertheless, in order to
be effective, this treatment needs specific modalities: slow
speed, low intensity and gradual intensification, with
minimum 20 to 30 sessions of exercises often being
needed.
c. More recent advances in treatment
Extra-corporeal shock wave therapy: Over the last
ten years, many clinical trials have evaluated the use of
extra-corporeal shock waves therapy (ESWT) for treating
patients with chronic tendinopathies. Multiple variables
are associated with this therapy, such as type of shock
wave generator (electrohydraulic, electromagnetic or
piezoelectric), type of wave (radial or focal), intensity
(total energy per shock wave/per session), frequency of
the shock waves, and the protocol of application and
repetitions (number of shocks) (Rompe and Maffulli,
2007). This makes the comparison of trials difficult and
ESWT thus remains a controversial form of treatment.
However, some studies have shown that ESWT is as
effective as surgery, but cheaper, and this treatment appears to be a supplement for the treatment of those tendinopathies that are refractory to conventional therapies
(Rasmussen et al., 2008). The only common factor is that,
in most studies, it is necessary for the patient to experience pain during treatment, and local anaesthesia may
therefore decrease the effectiveness of the treatment
(Furia, 2006). Studies using high-energy ESWT have
better results in tendinopathy than those using low-energy
ESWT (Furia, 2006).
As explained above, in the case of tendinopathy,
the damaged tendon contains disrupted and thinner collagen fibres, and there are changes in cellularity and an
increase in apoptosis. The aim of ESWT seems to be to
247
stimulate cell activity and increase blood flow, but the
mechanism for this is not very clear or well understood.
Possible stimulatory effects on neovascularization and
inhibition of nociception with liberation of pain inhibiting
substances (endorphins) are expected to occur
(Mouzopoulos et al., 2007). An increase in the permeability of neuron cell membranes and cellular damage could
create immediate analgesia (Andres and Murrell, 2008).
Other biological effects, through the induction of specific
growth factors (TGF-β1 and IGF-1) playing an important
mitogenic and anabolic role, increased blood flow, inflammatory-mediated process and liberation of hydroxyproline and increased tenocyte proliferation and
collagen synthesis, could induce a long term beneficial
effect (6 to 8 weeks) (Chao et al., 2008). Histological
observations have demonstrated that ESWT resolves
oedema, swelling and inflammatory cell infiltration in
injured tendons (Chao et al., 2008). The mechanisms of
the therapeutic effect of ESWT on calcific tendinopathies
are also uncertain. It has been proposed that increasing
pressure within the therapeutic focus causes fragmentation and cavitation effects inside amorphic calcifications
and leads to disorganization and disintegration of the
deposit (Mouzopoulos et al., 2007). This mechanical
irritation can activate an inflammatory response and neovascularization, with leukocyte recruitment, extravasation, chemotaxis and phagocytosis (Mouzopoulos et al.,
2007). There is some evidence to support the use of
ESWT in calcific tendinopathies of the rotator cuff, especially with an exact focusing of the ESWT (Mouzopoulos
et al., 2007) but US-guided needling in combination with
ESWT seems to be more effective (Cacchio et al., 2006).
The literature is not clear on the treatment of chronic
tennis elbow with ESWT (Andres and Murrell, 2008;
Rompe and Maffulli, 2007) but studies show that after 3
to 6 treatment at weekly intervals, with a clinical focusing, there are good results after a follow-up of more than
3 months (Rompe and Maffulli, 2007). There is no evidence supporting the use of ESWT in the treatment of
medial epicondylitis (Werner et al., 2005). Studies are
controversies and thus there is little evidence to justify the
use of ESWT in Achilles (Furia, 2006; Glaser et al., 2008;
Hennessy et al., 2007) and patellar tendinopathies (Peers
and Lysens, 2005; Vulpiani et al., 2007). Recently, a case
control study has demonstrated a good evolution of
greater trochanteric pain syndrome after low-energy
ESWT (Furia et al., 2009).
It has been demonstrated that high-energy shock
waves from 0.42 to 0.54 mJ·mm-2 can induce tendon lesion. Thus it is recommended not to use shock waves with
energy flux densities of over 0.28 mJ·mm-2 in the treatment of tendinopathies. Local complications reported are
usually not serious: soft tissue swelling, cutaneous erosions, haematoma, local pain (Mouzopoulos et al., 2007).
Recently, a comparative study between EET and
ESWT for chronic Achilles tendinopathy has shown better results with ESWT, but these findings need to be confirmed with more robust research (Hart, 2009). However,
in our opinion, ESWT could be a good complementary
treatment to EET for Achilles tendinopathies, as confirmed by a new article (Rompe et al., 2009). However,
other series are needed to prove the real efficacy of
248
ESWT to treat other tendinopathies.
Sclerosant injections: These injections of 5 mg/mL
polidocanol (sclerosing agent usually use to treat varicose
veins) have been used to block target tendon blood flow,
resulting in sclerosis in small blood vessels, sometimes
termed “neovessels”. This neovascularization, which is
seen under high resolution US with color Doppler, could
be associated with tendon repair (Alfredson and Ohberg,
2006) or chronic pain (Knobloch, 2008). Indeed, these
“neovessels” could be associated with in-growth of nerves
in areas of pathologic tendons (Rabago et al., 2009) and it
is possible that theses nerve fibres are the generator of
pain in chronic tendinopathies (Scott et al., 2008). These
injections of polidocanol might not only sclerose the
vessels, but may also eradicate the pain-generating nerve
fibres (Andres and Murrell, 2008). Although polidocanol
injections appear to provide pain relief, it is unclear what
role they may play in tendon healing in tendinopathy
(Andres and Murrell, 2008). Even though capilliary blood
flow may decrease by around 25% (Knobloch et al.,
2007), some authors say that there is no relationship between changes shown in US and tendon function after
sclerosing treatment. Moreover, after the injection, there
is initially an unexplained increased intratendinous vascularity. Some clinical series with sclerosing injections
(from 2 to 7 treatments at 2-6 week intervals) report good
short- and/or long-term result with an increase in strength
and a decrease in pain in epicondylitis, midportion Achilles, patellar and quadriceps tendinopathies or in shoulder
impingement syndrome but the same results are not found
with non-sclerosing injections (Andres and Murrell, 2008;
Rabago et al., 2009). Studies associating sclerosing injections and eccentric training have demonstrated a decrease
in pain during eccentric training, resulting in a complete
resolution of pain in the short term (Alfredson, 2005).
Other studies are needed to evaluate the safety (possible
sural nerve injury) and efficacy of this technique and the
standardized the protocol of injection (volume, concentration) and its combination with other therapies (Rabago et
al., 2009).
Botulinum toxin injections: Few articles from the 5
last years (Wong et al., 2005; Placzek et al., 2007) have
considered the possibility of making botulinum toxin
injections (BTA) injections in the extensor radiali carpi
brevis muscle to treat epicondylitis. This treatment is
based on the fact that the paralysis caused by BTA involves a reduction in tensile stress on the enthesis. It
seems that other factors are important, such as the inhibition of algogene substances (i.e. glutamate, substance P)
and a destruction of pre-ganglionic sympathetic fibres,
which could explain the antalgic effect of BTA injections
(Wong et al., 2005; Placzek et al., 2007). Results are
contradictory and, furthermore, the treatment is expensive.
Injections of blood or platelet-rich plasma: Injections of autologous whole blood or the blood product
platelet-rich plasma (PRP) have been used for tendinopathy with the aim of providing cellular and humoral mediators to induce healing in areas of degeneration. PRP is
prepared from autologous whole blood, which is centrifuged to concentrate platelets in plasma (Kaux et al.,
2007; Kajikawa et al., 2008; Rabago et al., 2009). There
Current opinion on tendinopathy
are different techniques for preparing PRP and thus different volumes of PRP are obtained and variable platelets
concentrations collected (Leitner et al., 2006; Kaux et al.,
2007; 2009). The intention is to augment the natural healing process at the site of pain through the action of growth
factors (GFs) (PDGF, IGF-1, VEGF, bFGF, TGF-β1,
EGF…) to promote matrix synthesis and wound healing
(Anitua et al., 2007; Andres and Murrell, 2008; Kaux et
al., 2007; Rabago et al., 2009). The balance between these
GFs may have important implications in the control of
angiogenesis and fibrosis (Anitua et al., 2007). Moreover,
locally injected PRP has been shown to enhance the contribution of circulation-derived cells to tendon healing in
the early phase of the healing process (Kajikawa et al.,
2008). Some studies in laboratories have shown that PRP
increases the healing of tendons and ligaments and that
the different GFs have a specific action during healing
(Anitua et al., 2007; Kaux et al., 2007). In vitro studies
confirm the efficacy of PRP injections with improvements
in Achilles tendon repair and a stronger tendon in rats
(Virchenko and Aspenberg, 2006). A study on athletes
confirms that, where a surgically repaired Achilles tendon
tears, the use of PRP may present new possibilities for
enhanced healing and functional recovery (Anitua et al.,
2007). There have been only a few clinical studies, in the
last 3 years, regarding the use of PRP injections for elbow
tendinopathies, patellar tendinopathies and rotator cuff
tears, with good results, but in vitro studies are encouraging (Mishra and Pavelko, 2006; Mishra et al., 2009;
Suresh et al., 2006). Protocols include restriction from
taking NSAIDs 1 to 2 days before treatment and for 10 to
14 days after treatment (Kaux et al., 2007). Other controlled trials are needed and better technique standardization could improve therapeutic efficacy.
Topical glyceryl trinitrate therapy: Recent studies
have shown that oxygen free radicals, in the correct dose,
can stimulate fibroblast proliferation (Murrell, 2007).
More recently NO has shown its capacity to enhance
tendon healing and extracellular matrix synthesis (Andres
and Murrell, 2008; Glaser et al., 2008; Murrell, 2007).
Thus NO enhances collagen synthesis and results in the
injured tendon having better material and mechanical
properties (healing tendons are stronger on a per-unit area
basis than those not exposed to additional NO) (Hennessy
et al., 2007; Murrell, 2007; Paoloni and Murrell, 2007).
Few clinical trials have demonstrated a beneficial effect
of NO on patient-determined pain, function, and loss of
symptoms of Achilles tendinopathy, chronic supraspinatus tendinopathy and tennis elbow (Murrell, 2007;
Paoloni and Murrell, 2007). The most commonly described side effect seen with NO treatment is headaches,
which can be severe enough to cause cessation of treatment (Andres and Murrell, 2008). As it stands, more
double-blind studies would be useful to standardize this
treatment (dosage, modalities of treatment….). Moreover,
this therapy could be a good treatment in combination
with others i.e. eccentric reeducation or ESWT but proof
of its efficacy in combination is needed.
Injection of MMP-inhibitor: Aprotinin is a broad
spectrum serine proteinase inhibitor (including matrix
metalloproteinase MMP) with a likely mechanism of
inhibition of the plamin-activation pathway of MMPs
Kaux et al.
(Orchard et al., 2008). Tendon integrity depends on extracellular matrix metabolism, which is regulated by proteolitic enzymes. In tendinopathies, there are changes in
the expression and activity of various matrix-degrading
enzyme metalloproteinases, that are consistent with increased proteolytic activity in degenerate tendons (Andres
and Murrell, 2008). The possibility of inflammatory suppression may not fully inhibit MMP-based tendon degradation, while therapies directly aimed at MMPs may be
more effective. Indeed, in the last 5 years, aprotinin injections have been shown to lead to good clinical improvement: in clinical series, mild-Achilles tendinopathy patients were treated more successfully than patellar tendinopathy patients (Hennessy et al., 2007; Orchard et al.,
2008) and aprotinin injections appeared superior to both
corticosteroid and saline injections (Orchard et al., 2008).
The major side effect of aprotinin (bovine-derived) is
anaphylaxis, which is seen particularly after repeated use
of the drug.
Table 5. Effective treatments for usual chronic tendinopathies.
Tendinopathies
Proposed treatments
- (Orthotic)
Tennis elbow
- (US)
- (Corticosteroid injection)
- Eccentric training
- Sclerosant injection
- BTA injections
- Injection of blood or PRP
- Topical NO therapy
Rotator cuff tendinopathy - US (calcific tendinopathy)
- (Corticosteroid injection)
- ESWT (calcific tendinopathy)
- Sclerosant injection
- Topical NO therapy
- Eccentric training
Jumper’s knee
- ESWT
- Sclerosing injection
- Injection of blood or PRP
- Injections of MMP-inhibitor
- (Orthotic)
Achilles tendinopathy
- Eccentric training
- ESWT
- Sclerosing injections
- Topical NO therapy
- Injections of MMP-inhibitor
Stem-cell or gene therapy: In vitro research, with
encouraging results, has just begun on stem-cell and gene
therapy technologies for the treatment of degenerative
conditions of the musculoskeletal system such as tendinopathy (Sharma and Maffulli, 2008). In theory, pluripotent stem cells can be isolated and then delivered to an
area of need such a degenerative tendon. Once the stem
cells are in the desired location, either local signalling or
the addition of exogenous factors can lead the pluripotent
cells to differentiate into the needed cell line (Andres and
Murrell, 2008). Animal studies suggest that gene therapy
together with adenovirus-mediated gene therapy may also
improve the capacity of the injured tendon to heal (Bolt et
al., 2007).
In conclusion, many interesting new treatments are
now being developed to treat tendinopathy, but currently
249
there is little evidence to support their use in clinical practice. More well-designed controlled trials are greatly
needed.
In Table 5, we would like to develop the therapeutically approach, based on the available data, for each
type of frequently occurring tendinopathy.
Conclusion
Chronic tendinopathy is a condition that causes many
patients significant pain and disability. We focus on the
importance of differential diagnosis according to localization of the problem (online supplementary material 2).
Although usually not required, diagnostic imaging may
assist in diagnosing tendinopathy and choosing an appropriate treatment regimen. However, due to the poor correlation between diagnostic imaging and symptoms, the
role of serial diagnostic imaging is limited
Currently, the aetiology of tendinopathy is still unclear. However, it seems to be multi-factorial, involving
multiple intrinsic and extrinsic factors. The role of inflammation is still debated but it seems that the absence of
inflammatory cells does not mean that inflammatory mediators, such as cytokines, metalloproteinases or growth
factors, are not involved in tendinopathy. These can also
be implicated in the pain mechanism as well as in neovascularization. Tendinopathy often becomes chronic because the exact pathogenesis remains largely unknown.
The majority of patients will have resolution of
their symptoms with classical treatments, which include
rest, NSAIDs, orthotic devices, passive physiotherapy or
corticosteroid injections. If, however, pain persists, active
treatment (eccentric reeducation) or the use of more recently developed treatments are an option. These include
ESWT, sclerosant injections, topical glyceryl trinitrate
therapy, and injections of MMP-inhibitor, botulinum
toxin, autologous whole blood or PRP. However, there is
a need for further research into these newer treatments
and further clinical series would be useful. Physicians
have a variety of therapeutic options available to treat
tendinopathies but, in each case, there is a lack of evidence supporting their use as the gold standard treatment,
except perhaps in the case of eccentric reeducation where
there is more proof of efficacy. Another approach, which
is too little developed in the literature, is the use of a
combination of different therapies. None of the developed
treatments is now sufficient to treat tendinopathy alone.
In addition, in our opinion, one of the causes
(which can be corrected) of chronicity or repeated tendinopathies is the absence of consensus regarding treatment
and the return to play criteria: the absence of rest, a lack
of mechanotransduction (Khan and Scott, 2009) or a too
early return to playing sport does not allow the injured
tendon to be adapted to conditions faced in training or
competition. It is also important to consider criteria to
evaluate treatment efficacy. Should they be based only on
pain and ability to restart physical activity or is there a
new place for imaging examination (US or MRI), though
we know that abnormalities persist after that patients have
good functional recovery? Currently, there is a lack of
discussion in the literature regarding these criteria, and
further research needs to be undertaken.
250
Acknowledgement
The Léon Frédéricq Funds and the Lejeune-Lechien grants contributed
to this work.
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Key points
• The word “tendinopathy” is the correct term for the
clinical diagnosis of pain accompanied by impaired
performance, and sometimes swelling in the tendon.
• The aetiology of tendinopathy seems to be a multifactorial process, involving promoting factors that
are intrinsic or extrinsic, working either alone or in
combination.
• US (with color Doppler) and MRI are usually prescribed when tendinopathy is unresponsive to treatment and entails lingering symptoms.
• Eccentric training is currently considered to be the
most efficient treatment for tendinopathy; nevertheless, in order to be effective, this treatment needs
specific modalities: slow speed, low intensity and
gradual intensification, with minimum 20 to 30 sessions of exercises often being needed.
• Many interesting new treatments are now being developed to treat tendinopathy, but currently there is
little evidence to support their use in clinical practice.
AUTHORS BIOGRAPHY
Jean-François KAUX
Employment
University of Liège and University Hospital of Liège (Belgium)
Degree
Medical Doctor
Research interests
Tendon and treatments of tendinopathies,
sports pathologies
E-mail: jfkaux@chu.ulg.ac.be
Bénédicte FORTHOMME
Employment
University of Liège and University Hospital of Liège (Belgium)
Degree
Physiotherapist, PhD, Professor.
Research interests
Shoulder pathologies
E-mail: bforthomme@chu.ulg.ac.be
Kaux et al.
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Caroline Le GOFF
Employment
University Hospital of Liège (Belgium)
Degree
Pharmacist
Research interests
Sports and metabolism
E-mail: c.legoff@chu.ulg.ac.be
Jean-Michel CRIELAARD
Employment
University of Liège and University Hospital of Liège (Belgium)
Degree
MD, PhD, Professor
Research interests
Sports pathologies
E-mail: jmcrielaard@ulg.ac.be
Jean-Louis CROISIER
Employment
University of Liège and University Hospital of Liège (Belgium)
Degree
Physiotherapist, PhD, Professor
Research interests
Isokinetic, sports pathologies
E-mail: jlcroisier@ulg.ac.be
Dr Jean-François Kaux
Physical Medicine Service and Department of Motility Sciences,
University Hospital, University of Liege, Avenue de l’Hôpital,
B35, B-4000 Liège Belgium