2003, Vol.22, Issues 4, Current Concepts in Tendinopathy

Clin Sports Med 22 (2003) xi
Foreword
Current concepts in tendinopathy
Mark D. Miller, MD
Consulting Editor
Tendinopathy? How can we devote an entire issue to tendinopathy? What ever

happened to tendonitis, anyway? Well, for those of you asking questions like that,
read on! Within the last decade, researchers, including many of the authors of
articles appearing in this issue of the Clinics in Sports Medicine, have made
major strides in our understanding of tendinopathy. There is much more to it than
just changing the name from tendonitis to tendinopathyit represents a whole
new approach to our understanding and treatment of this disorder.
Dr. Ben Kibler has assembled an impressive group of experts for this issue. It
is a virtual whos who of tendinopathy. Put aside your biases and distaste for
this diagnostic entity, take a new look at an old problem, and learn something
that will help some of your most difficult patients. This issue has already helped
me in my own clinical practice. Who knows, with a fresh understanding and
approach, you might not need to change the Kleenex in your treatment rooms
quite so often!
Mark D. Miller, MD
Department of Orthopedic Surgery
University of Virginia
Charlottesville, VA 22903-0753, USA
E-mail address: mdm3p@hscmail.mcc.virginia.edu
0278-5919/03/$ see front matter D 2003 Elsevier Inc. All rights reserved.
doi:10.1016/S0278-5919(03)00050-4
Clin Sports Med 22 (2003) xiii
Preface
Current concepts in tendinopathy
W. Ben Kibler, MD
Guest Editor
I am pleased to serve as the Guest Editor for this issue of the Clinics in Sports
Medicine. It has been 11 years since the landmark two-part series on tendinopathy
appeared in this publication. That series produced a basis for better understanding
of tendon injury and treatment; this issue is designed to produce further updates on
current concepts concerning tendinopathy.
An internationally recognized group of authors have contributed articles that
examine possible modes of cellular injury from tension to compression; anatomic
and physiologic factors that underlie the clinical presentation of symptoms; sitespecific examples of tendinopathy; and guidelines and protocols for rehabilitations.
This bench to bedside approach gives the sports medicine clinician a basic
understanding upon which to implement clinical treatment of this common and
often difficult-to-treat injury.
I would like to thank Deb Dellapena and the editors of the Clinics in Sports
Medicine for their support and work in producing this issue, as well as the authors
for their scholarship, interest, and enthusiasm for this subject. Through these
efforts will come a better understanding and more efficacious treatment for
tendon injuries.
W. Ben Kibler, MD
Lexington Clinic Sports Medicine Center
1221 S. Broadway
Lexington, KY 40504, USA
E-mail address: wkibler@aol.com
doi:10.1016/S0278-5919(03)00069-3
Clin Sports Med 22 (2003) 675 692
Types and epidemiology of tendinopathy

Nicola Maffulli, MD, MS, PhD, FRCS(Orth)a,*,
Jason Wong, MRCSb, Louis C. Almekinders, MDc
a
Department of Trauma and Orthopaedic Surgery, Keele University School of Medicine,

North Staffordshire Hospital, Thornburrow Drive, Hartshill, Stoke on Trent,
Staffordshire, ST4 7QB, UK
b
Department of Orthopaedic Surgery, University of Aberdeen Medical School, Polwarth Building,
Foresterhill, Aberdeen AB25 2ZD, UK
c
Department of Orthopaedic Surgery, Sports Medicine Section,
University of North Carolina School of Medicine, Chapel Hill, NC, USA
Over the course of the last two decades, athletes have received increased
demands on their performance. This has determined an increase in the risk of
acute and overuse sport injuries, as they are required to train more often, more
intensely and for longer. Until the recent past, sports and physical activities
involved mainly young and middle-aged people. Today, with an increase in
leisure time, a greater number of individuals spend time practicing recreational or
competitive sports [1,2].
During physical exercise, much stress and force are exerted on the tendon,
increasing the risk of injury. In repetitive hopping in place, a force of about 4000 N
has been measured in the Achilles tendon. The force measured from the Achilles
tendon is about twice the ground-reaction force. In hopping, most of the elastic
energy is stored in the tendon itself. The contribution of the elastic energy in
hopping is about 40% of the total mechanical work [3]. This implies that the
tendon plays an important role as an active element of the muscle-tendon unit
during sport.
This article is divided into separate but interconnected parts. First we discuss
tendinopathy from a histopathological viewpoint. We then describe the basic
epidemiological issues facing physicians when dealing with such conditions.
Some forms of tendinopathies are discussed, but we stress that these are not
detailed, in-depth descriptions, and that the conditions selected, though representative, are only a small cross-section of clinically relevant tendinopathies
* Corresponding author. Nicola Maffulli, Department of Trauma and Orthopaedic Surgery, Keele
University School of Medicine, North Staffordshire Hospital, Thornburrow Drive, Hartshill, Stoke on
Trent, Staffordshire, ST4 7QB, UK.
E-mail address: n.maffulli@keele.ac.uk (N. Maffulli).
doi:10.1016/S0278-5919(03)00004-8
676
N. Maffulli et al / Clin Sports Med 22 (2003) 675692
(Table 1). We stress that reliable, well-conducted epidemiological studies are not
available for most tendinopathies.
Basic pathology of overuse tendon conditions

The most common tendon injuries in sports are presented in Table 1. Any
tendon and its surrounding tissues can undergo a tendinopathic process, however.
The intrinsic and extrinsic factors have varying significance in the background of
different tendon problems in sports, but some can be discussed in general.
Lack of consistent nomenclature for histopathological findings has limited
progress in understanding the pathological basis of tendon conditions [4,5]. The
understanding that the pathological bases of overuse tendon conditions is
tendinosis has induced Khan et al [4] to adapt the histopathological classification
based on the work of several authors [6 8] (Table 2). The finding that clinical
tendon conditions in athletes result from tendinosis is not new. Perugia et al [9]
noted the remarkable discrepancy between the terminology generally adopted for
these conditions (which are erroneously thought to be inflammatory because the
ending itis is used) and their histopathological substratum, which is largely
degenerative [9].
Tendinosis
Although the term tendinosis was first used by German workers in the 1940s, its
recent usage comes from the work of Puddu et al [10]. In tendinosis, there is tendon
degeneration without clinical or histological signs of inflammation. Tendinosis can
be associated with paratenonitis [10]. Thus, although there is a wide range of
tendon pathologies, it appears that the majority of overuse tendinopathies in
Table 1
Common sites of overuse tendon injuries
Tendon involved
Injury
Achilles
Achilles tendinopathy, Achilles paratendinopathy,

tendon rupture, calcaneal apophysitis (Severs disease)
Patellar tendinopathy, patellar peritendinopathy, patellar
apicitis (jumpers knee), Osgood-Schlatter lesion,
Sinding-Larsen-Johansson lesion
Medial tibial syndrome
Iliotibial tract syndrome
Hamstring syndrome
Patella
Posterior tibial
Iliotibial tract
Biceps femoris, semitendinosus,
semimembranosus
Supraspinatus
Other rotator cuff tendons (infraspinatus,
subscapularis, teres minor)
Common wrist extensors
Common wrist flexors
Supraspinatus syndrome (impingement syndrome,

swimmers shoulder)
Rotator cuff tendinopathy or tear
Lateral epicondylitis (tennis elbow)
Medial epicondylitis (throwers elbow,
golfers elbow, little league elbow)
677
Table 2
Histopathological classification of tendon disorders (Khan et al (1999) modification of Clancy, 1990)
Pathological diagnosis
Macroscopic pathology
Histopathological findings
Tendinosis
Intratendinous degeneration
(commonly due to ageing,
microtrauma, vascular
compromise)
Tendinitis
Symptomatic degeneration
of the tendon with vascular
disruption and inflammatory
repair response
Paratenonitis
Inflammation of the
outer layer of the tendon
(paratenon) alone, whether
or not the paratenon is
lined by synovium
Paratenonitis associated with
intratendinous degeneration
Collagen disorientation,
disorganization and fiber separation
by an increase in mucoid ground
substance, increased preponderance
of cells and vascular spaces with
or without neovascularization
and focal necrosis or calcification
Degenerative changes as noted
above with superimposed evidence
of tear, including fibroblastic and
myofibroblastic proliferation,
hemorrhage and organizing
granulation tissue.
Mucoid degeneration if the areolar
tissue is seen. A scattered mild
mononuclear infiltrate with or
without focal fibrin deposition and
fibrinous exudate
Degenerative changes as noted in
tendinosis with mucoid degeneration
with or without fibrous and scattered
inflammatory cells in the paratenon
alveolar tissue
Paratenonitis
with tendinosis
athletes are due to tendinosis, with collagen degeneration and fiber disorientation,
increased mucoid ground substance, and an absence of inflammatory cells [4].
At light microscopy, tendinosis shows changes in collagen among tenocytes
and also within the matrix or ground substance [11]. Some collagen fibers
separate and lose their parallel orientation, with a decrease in fiber diameter and
in overall density of collagen. Collagen microtears also occur, and these may be
surrounded by erythrocytes, fibrin, and fibronectin deposits. Within collagen
fibers there are unequal and irregular crimping, loosening, and increased
waviness, in contrast to the normal tight, parallel, bundled appearance. There
is an increase in type III (reparative) collagen. These changes lead to decreased
birefringence under polarized light microscopy [11]. Special stains demonstrate
increase in mucoid ground substance (proteoglycans) [12,13].
There is much variation in cellular density in tendinosis. In some areas,
tenocytes are abnormally plentiful, with rounded nuclei and ultrastructural
evidence of increased production of proteoglycan and protein, which gives them
a chondroid appearance. In contrast, other areas of the tendon may contain fewer
tenocytes than normal, with small, pyknotic nuclei [11]. Rarely, there is infiltration of lymphocytes and macrophage-type cells, which may be part of a healing
process [11]. A characteristic feature of tendinosis is proliferation of capillaries
and arterioles.
678
Several subcategories have been identified by electron microscopy: (1) hypoxic

degeneration, (2) hyaline degeneration, (3) mucoid or myxoid degeneration, (4)
fibrinoid degeneration, (5) lipoid degeneration, (6) calcification, and (7) fibrocartilaginous and bony metaplasia [6,9]. These pathologies can coexist, and their
prevalence varies, possibly depending on the anatomical site and the nature of the
insult that caused them (eg, hypoxia versus mechanical loading; acute versus
chronic injury). Thus, tendinosis is the end result of a number of etiologic processes
with a fairly small spectrum of histological manifestations. The essence of
tendinosis is degeneration in tendon cells, collagen fibers, and the subsequent
increase in noncollagenous matrix [6] (see Table 2).
A major issue is that tendinosis is not necessarily symptomatic. For example, in
a 4-year longitudinal study of 46 patellar tendons, 18 tendons had hypoechoic
lesions at baseline, and 28 were ultrasonographically normal. Five tendon lesions
resolved ultrasonographically in the study period, and magnetic resonance imaging
in 4 of these tendons was normal. Seven normal patellar tendons at baseline
developed a hypoechoic area, but only 2 became symptomatic. There was no
association between baseline ultrasound changes and symptoms at follow-up, and
there was no statistically significant relationship between ultrasonographic patellar
tendon abnormalities and clinical outcome in elite male athletes [14]. The presence
of an ultrasonographic hypoechoic area is associated with a greater risk of
developing symptoms of patellar tendinopathy [15], however, and an ultrasonographic tendon abnormality is three times as common as clinical symptoms [16].
The role of physical activity on the presence of tendinosis is not clear, even though
it appears that sonographic hypoechoic areas are present in asymptomatic patellar
tendons of a proportion of elite athletes, but rarely present in controls [17]. In the
Achilles tendon, following a rupture, the patients asymptomatic contralateral
tendons had a greater prevalence of intratendinous alterations [18].
Tendinitis
Tendinitis is a condition in which the substance of tendon exhibits inflammation. Many physicians and scientists with an interest in tendon pathology
understand that when the term tendinitis is used in a clinical context, it refers to a
clinical syndrome, not to a specific histopathologic entity [19,20]. Some argue
that this accepted misuse of the term does not warrant alteration. As long as
tendinitis remains in use for what is truly tendinosis, however, some clinicians,
athletes, coaches and patients will underestimate the implications of the condition. Hence, we recommend that the use of the misnomer tendinitis in the
context of overuse tendon conditions be abandoned [5,21].
Paratenonitis
Paratenonitis occurs where a tendon rubs over a bony protruberance. The term
includes what was previously called peritendinitis, tenosynovitis (single layer of
areolar tissue covering the tendon), and tenovaginitis (double-layer tendon
679
sheath). Examples include paratenonitis of the abductor pollicis longus and extensor pollicis longus (de Quervains disease), and of the flexor hallucis longus as it
passes the medial malleolus of the tibia [6,22].
Clinically, paratenonitis presents with acute edema and hyperaemia of the
paratenon with infiltration of inflammatory cells (see Table 2). After a few hours to
a few days, a fibrinous exudate fills the tendon sheath and causes the crepitus that
can be felt on clinical examination. When acute paratenonitis becomes chronic,
fibroblasts appear, along with a perivascular lymphocytic infiltrate. Peritendinous
tissues become macroscopically thickened and new connective tissue adhesions
occur [11]. Myofibroblastscells with cytoplasmic myofilamentsalso appear
and make up about 20% of the noninflammatory cells. Myofibroblasts are capable
of active contraction, indicating that scarring and shrinkage associated with
paratenonitis is an active, cell-mediated process [11]. Blood vessels proliferate.
Marked inflammatory changes are seen in more than 20% of the arteries in the
paratenon [23]. Thus, in paratenonitis, inflammatory cells are found both among
the cellular elements of the paratenon and in the vascular ingrowth.
Tendinopathies: new definitions

We have recently advocated the use of the term tendinopathy as a general
clinical descriptor of tendon injuries in sport [21]. In overuse clinical conditions in
and around tendons, frank inflammation is infrequent, and, if seen, is associated
mostly with tendon ruptures [24 26]. Tendinosis implies tendon degeneration
without clinical or histological signs of intratendinous inflammation, and is not
necessarily symptomatic [21]. When the term tendinitis is used in a clinical context,
it does not refer to a specific histopathological entity. Tendinitis is commonly used
for conditions that are truly tendinoses, however, and leads athletes and coaches to
underestimate the proven chronicity of the condition. Paratenonitis is characterized
by acute edema and hyperaemia of the paratenon, with infiltration of inflammatory
cells, and possibly with production of a fibrinous exudate within the tendon sheath,
causing the typical crepitus be felt on clinical examination. The term partial tear of a
tendon should be used to describe a macroscopically evident partial tear of a
tendon. This is an uncommon acute lesion. Most articles describing the surgical
management of partial tears of a given tendon in reality deal with degenerative
tendinopathies. The combination of pain, swelling, and impaired performance
should be labeled tendinopathy. According to the tissues affected, the terms
tendinopathy, paratendinopathy, or pantendinopathy (when both the tendon and
the surrounding tissues are involved) should be used.
Epidemiologic approach to sports injuries

Many studies on sports injuries are based on reports from outpatient or accident
and emergency departments, whereas others have been based on reports from
680
specialist sports centers. Often studies cannot be compared, due to lack of

uniformity in definitions of injuries, level of sports participation, insufficient
information on the population at risk and on the exposure time to the sport, and
variability in study design and data collection [27 29].
The epidemiological approach in sports traumatology aims to quantify the
occurrence of sports injuries in relation to who is affected by injuries, where
and when these injuries occur, and what their outcomes are (descriptive
approach). This is an effort to explain why and how such injuries occur, and
to develop strategies to prevent them (analytical approach) [28]. Preventing
sports injuries is important to reduce the short- and long-term social and
economic consequences of injuries [27]. The epidemiological approach implies
that injuries do not happen purely by chance [30]. Epidemiological techniques
have been applied to sports injury problems since the 1960s [28]. This marked
a transition from the clinical series, which were numerator-based, to denominator-based data.
Incidence of injuries
Two types of incidence rates have been reported: case rate and athlete
rate. Case rates, the most common type of incidence rates reported in the
literature, are given by the total number of reported injuries occurring during
the study period divided by the total number of athletes exposed to the sport
considered [28]. Athlete rates are obtained by dividing the total number of
athletes injured by the total number of athletes participating, and often include
more than one injury to the same athlete [28]. Therefore, their use can give
spurious values.
Sports injuries are often presented as sports injuries per 100 athletes. Incidence
rates can also be expressed as rate per season, rate per practice, or rate per game
[31]. A more precise way of qualifying exposure is a rate per athlete exposure
(AE). An AE is defined as one athlete participating in one practice or game in
which there is the possibility of sustaining an athletic injury. The rate per element
exposure, where one element exposure is defined as one athlete participating in
one element of activity in which there is a possibility of sustaining an athletic
injury, has also been used. Examples of exposure elements are vaults, pitches,
bicycle trips, etc.
Incidence of injury has been reported in various forms. For instance, in club
gymnastics, injury rates vary between 2 to 4 [32] and 39.9 per 100 school
children per year [33].The frequency of injury in a given sport depends entirely
on the participation rate and popularity of a given sport. Incidence rate is affected
by numerous factors, such as level of training and competition, chronological
and biological age of the athletes, the proficiency of the coach, etc [28]. Baseball
and American football are popular in the United States. Soccer, field events, and
rugby are played more in Europe, cricket has the maximum number of
participants in the Commonwealth countries, and many countries have their
indigenous sports.
681
Injury characteristics
This aspect of epidemiology deals with factors such as injury onset, injury
type, injury location, and injury mechanism [28]. When planning the collection of
such data, great care should be exerted in the strict definition of each of the above
categories. For example, in the Training of Young Athletes (TOYA) Study, we
defined an acute injury as an injury arising because the musculo-skeletal system
was exposed to a single episode of stress exceeding its level of intolerance, and
an overuse injury as an injury which arose because the limits of tolerance of the
musculo-skeletal system had been exceeded by repetitive submaximal loading
[34]. Prospective and retrospective studies are a good source of injury characteristics. Injuries can either occur acutely or suddenly, and are associated with a
macrotraumatic event, such as an Achilles tendon rupture, or arise gradually as a
microtraumatic event, such as Achilles tendinopathy [35].
Injury severity
The severity of injuries ranges broadly from sprains and contusions to death. It
is represented and accounted for in the epidemiological literature as injury type,
time lost from sport, residual symptoms, financial costs, nature and duration of
treatment, or absence from school [36]. 75% of sports injuries are abrasions,
sprains, strains and contusions [33], and do not require medical treatment. Very
serious sports accidents in youth, such as brain or spinal cord damage, lesions of
the heart, or submersions leading to invalidism or death, are exceptional [27]. The
severity of an injury is most often calculated by measuring the time lost due to the
injury. Ekstrand and Gillquist [37] classified injury-induced absence from sports
activity into minor, moderate, and major, according to whether the required
absence from sport was less than a week, more than a week but less than a month,
or more than a month, respectively. In general, these three grades correspond to
codes 1, 2 and 3 of the Abbreviated Injury Scale (AIS). AIS 4, 5, and 6 injuries,
ranging from life-threatening to fatal, were exceptional [38,39]. Motorcycling,
skiing, and horse riding [40] caused the costliest injuries. To our knowledge, there
are no such studies of overuse tendon injuries.
Injury risk factors

An important part of sports injury epidemiology is the identification of factors
that contribute to the occurrence of athletic injuries [41]. This process is complicated by many risk factors that play a role before the actual occurrence of injury
events. These have been classically divided into two typesintrinsic and extrinsic
[36,41], which interact to make the athlete more susceptible to injury [42].
Intrinsic risk factors:
Malalignment (ie, excessive pronation, femoral neck anteversion, etc)
Limb length discrepancy
682
Muscular imbalance
Muscular insufficiency
Extrinsic risk factors:
Training errors (ie, distance, intensity, hill work, technique, fatigue, etc)
Training surfaces
Environmental conditions
Footwear and equipment
Injury prevention
Most of the preventive measures suggested in the literature have arisen from
descriptive research, and have not been derived from risk factors that have been
substantiated as defensible injury predictors through correlational or experimental
research [28]. Once the analytical evidence points to an association between
certain risk factors and injury, thereby establishing a degree of predictability for
those participants who are likely to sustain injury, a method of intervention can be
devised to prevent it [42]. Good descriptive data can lead to suggestions for
injury prevention that, once implemented, help to control the occurrence of
severe sports injuries. Intervention can be either therapeutic, using tapes or braces
to an injured area resulting in reduction in reinjuries, or preventive, in which an
agent or procedure is tried on athletes free from injury and is evaluated by
recording the reduction of risk of injury. Certain injury prevention procedures are
time-tested, and include preparticipation screening, warming up sessions, regular
systematic and scientific training, safe environment, adequate standard protective
equipment, adaptation of rules, and appropriate health education by physical
education teachers [33].
In sports medicine, epidemiological studies are important when planning
prevention programs for sports injuries. Individual national sports cultures and
different sports habits in different countries also mean that national epidemiologic
studies are of importance in each individual country. In many European countries,
about 50% of all sports injuries are caused by soccer. In many tendon injury
reports, the diagnosis is based on clinical examination.
Age
In children, tendons and ligaments are relatively stronger than the epiphyseal
plate, and considerably more elastic. Therefore, in severe trauma, the epiphyseal
plate, being weaker than the tendons and ligaments, gives way. As a result,
growth plate damage is more common than ligamentous and tendon injuries
[43,44].
Injuries to the insertions of tendons onto bone are more frequent than injuries
to the main body of the tendon [45]. The Osgood-Schlatter lesion is by far the
most common tendon ailment in young athletes (at least 10% of all sport overuse
683
injuries) [43,44]. Calcaneal apophysitis (Severs disease) is another common

overuse injury in adolescents (around 8% of all overuse problems in this age
group) [46]. In elderly athletes, overuse injuries are more common, possibly
because most of them are involved in endurance sports. Rotator cuff injuries
(18%) and Achilles tendon and calf injuries (20%) are more common in this age
group than in younger athletes [45].
Gender
Most tendon injuries occur in males. Male predominance in tears of the
Achilles tendon varies between 7 to 1 and 4 to 1 [47]. Although 60% of overuse
injuries sustained in running occur in men, women under the age of 30 are at the
greatest risk for overuse injuries. The proportion of female participants in sports
injury surveys has increased dramatically during the past few decades [48]. The
reasons for the increased female proportion are probably the increased female
participation in physical activity. Also, more women now undertake sports at high
risk not only of acute but also of overuse injury [49].
Blood group distribution

Josza et al [50] reported a significant association between the increased risk
of tendon ruptures and the blood group O in Hungary, where they found that in
over 800 patients with tendon rupture, 53% had blood group O. The distribution
in the normal Hungarian population was 31%. The ratio of blood groups A to O
(A/O ratio) was 0.51 (1.36 in the normal population). Of the patients with
multiple tendon ruptures or rerupture, 68% had blood group O, and the A/O
ratio was 0.25.
In Finland, a similar blood group O dominance was found in patients with
Achilles tendon rupture (A/0 ratio, 1.0) and with chronic Achilles peritendinopathy (A/O ratio, 0.70) when compared with the blood group distribution of the
Finnish population (A/O ratio, 1.42) [51].
We studied 78 patients treated at a large hospital in Scotland for an acute
Achilles tendon tear, and compared their distribution of ABO blood groups with
that found in 24,501 blood donors typed at the blood transfusion center in the
same hospital during the same 6-year period. Overall, 47 of the 78 patients
(60%) belonged to blood group O, compared with 51% of the population as a
whole. Only 22 (28%) of the Achilles tendon rupture patients belonged to blood
group A, whereas 35% of the general population were members of this group
(NS). The A/O ratio was 0.47 for the tendon rupture patients, a difference
which was not statically significant when compared with the A/O ratio of 0.68
for the general population [52]. The findings in Finnish and Hungarian studies
could result from peculiarities in the distribution of the ABO groups in
genetically segregated populations.
684
Specific tendinopathies
Achilles tendinopathy
The etiology of Achilles tendon overuse injuries is multifactorial [53]. Training errors have been reported in 60% to 70% of the running injuries [54]. Rapid
increase in mileage, increased interval training, and running on sloping and
slippery roads are associated with Achilles paratendinopathy [55]. In a report on
698 patients with Achilles tendon injuries, 66% had paratenonitis and 23% had
Achilles tendon insertional problems. In 8% of the patients, the injury was
located at the myotendineal junction, and 3% of patients had a complete tendon
rupture. Of the patients with Achilles tendon problems, 89% were men. Running
was the main sport in 53% of patients with an Achilles tendon injury. Running
sports patients were 27% of all patients studied [56]. Two thirds of Achilles
tendon injuries in competitive athletes involve the paratenon, and 20% involve
the insertion. Malalignent of the lower extremity was found in 60% of patients
with Achilles tendon overuse injury [57]. It should be noted, however, that up to
now only statistically significant associations have been found, and no study has
identified a definite cause-effect relationship.
Excessive repetitive overload of the Achilles tendon is, however, regarded as
the main pathological stimulus which leads to tendinopathy [53]. In 455 athletes
with Achilles tendon problems, Kvist found that 53% were involved in running
sports and 11% were soccer players, emphasizing the etiological role of running
[57]. The rest of the patients were involved in other sports in which running was
an important training means. Achilles tendinopathy is not always associated with
excessive physical activity, and in one series 31% of 58 Achilles tendinopathy
patients did not participate in sports or vigorous physical activity [58].
Forefoot varus correlated significantly with Achilles paratendinopathy.
Decreased subtalar joint and ankle motion were more frequent in athletes with
Achilles paratendinopathy and insertional tendinopathy than in other athletes
[56]. This contrasts with the findings by Segesser et al, who found ankle joint
instability and hyperpronation to predispose to Achilles tendon disorders [59].
Different malalignments and biomechanical faults seem to play an etiologic role
in 60% to 70% of the athletes with Achilles tendon overuse injuries [57]. These
injuries occur at a higher rate in older athletes. In 470 patients with Achilles
paratendinopathy and insertional tendinopathy, about 25% were young athletes,
with 10% younger than 14, and there was a significant connection with the
calcaneal apophysitis (Severs disease) in this age group [56].
The natural history of Achilles tendinopathy is still unclear: 24% to 45.5% of
the subjects with Achilles tendinopathy who fail to respond to conservative
management undergo operative management [60,61]. In an 8-year longitudinal
study of conservative management of Achilles tendinopathy patients, 24 of the
83 patients (29%) had to be operated on. Seventy patients (84%) had full
recovery of their activity level. At 8 years, 78 patients (94%) were asymptomatic
or had only mild pain with strenuous exercise; however, 34 patients (41%) started
685
to suffer from Achilles tendinopathy in the initially uninvolved contralateral tendon [62,63].
Patellar tendinopathy
About one third of sports injuries treated on an outpatient basis in sports clinics
concern the knees [64]. In Europe, the highest incidences were in soccer (21%),
long-distance running (13%), volleyball (12%), orienteering (8%), and ice hockey
(7%). The most common knee disorders were jumpers knee (20%) and OsgoodSchlatter disease (10%). Other tendon complaints were patellar paratendinopathy
(6%), hamstring tendinopathy (3%), and iliotibial band syndrome (2%) [65].
Volleyball and soccer were the sports in which two thirds of all their patients with
patella tendinopathy were involved [66]. In a classic study, patients suffering from
jumpers knee were usually tall athletes [67], but Martens et al did not find this
correlation [66]. The classic site is the lower patellar pole, with well localized
tenderness. Lesions of the mid one third of the tendon have been described [68],
and their management and outcome may well differ from those of classical
jumpers knee [69].
In children and adolescents, tendons are relatively stronger than the bones in
which they insert. Osgood-Schlatter lesions and Sinding-Larsen-Johansson
lesions are traction apophysitis of the tibial tubercle, and at the inferior pole of
the patella, respectively. Both present as localized tenderness and radiographic
fragmentation in athletic adolescents aged 11 to 13 [70]. These lesions are
typically self-limiting [43]. Both the Sinding-Larsen-Johansson lesions and the
Osgood-Schlatterlesions occur between ages 8 to 13 in girls, and 10 to 15 in
boys. Boys are affected nearly twice as often than girls, possibly because of their
higher activity levels [44]. There may be pain at that site without fragmentation of
the tibial tubercle during a growth spurt, and occasionally there is local
inflammation around a separate ossicle at maturity [71]. Over the past few years,
the rate of reported cases of patellar tendinopathy seems to have increased [72],
probably because athletes undergo more strenuous and prolonged periods of
training and competition, and because of the higher awareness of both athletes
and health care professionals [72].
Kujala et al, studying the role of different anatomic factors relative to patellar
apicitis and tendinopathy, found a significant correlation between leg length
inequality and patella alta. Increased laxity of the knee joint correlated with
patellar chondropathy [73]. The pathologic changes are most often located at the
insertional areas, and microlesions caused by repeated jumping are often found at
histology [72]. The role of repeated direct trauma over the anterior aspect of the
knee is still unclear [74,75].
Iliotibial tract friction syndrome
Iliotibial band (ITB) friction syndrome results from excessive friction between
the ITB and the lateral femoral epicondyle. Most frequent in distance runners and
686
military recruits, the ITB syndrome can occur with any activity requiring
repetitive knee flexion and extension [76], and has been reported in cyclists
and athletes involved in sports requiring repetitive knee flexion [77]. ITB
syndrome presents with exertional pain over the lateral femoral condyle associated with hard running [76]. At 20 to 30 of knee flexion, the ITB rubs against
the lateral femoral epicondyle. In runners, impingement occurs near foot strike,
predominantly in the foot contact phase of the gait cycle, or in the deceleration
phase [78], and the repetitive microstrains in the ITB may lead to degenerative
changes. Although it has never been proven scientifically, running on roads might
cause excessive pronation of the foot on the high side, resulting in injury [79].
Approximately 14% of patients with overuse injuries of the knees had iliotibial
band syndrome [65]. In Oravas report of 88 patients, 55% were long-distance
runners or joggers, and 15% were skiers [77]. Genu varum, excessive pronation, a
lateral condylar spur, or leg length discrepancy can all increases the tension in the
ITB or create friction against the epicondyle. Athletes who abruptly increase the
running load have a higher incidence of ITB syndrome [79]. It is unknown whether
increased thickness of the ITB is a risk factor or a secondary phenomenon. Training
errors may also be responsible for predisposing to ITB syndrome. Inexperienced
runners who abruptly increase their weekly mileage have a higher incidence of ITB
syndrome. A more recent hypothesis proposes that hip abduction weakness leads to
ITB syndrome. Fatigued runners with hip abduction weakness are prone to
increased thigh adduction and tension on the ITB.
Quadriceps tendinopathy
The superior strength, mechanical advantage, and better vascularity of the
quadriceps tendon make quadriceps tendinopathy much less common than patellar
tendinopathy. In adolescent athletes, avulsion injuries of the proximal patella
apophysis are more common than tendinopathy of the quadriceps mechanism [80].
Patients with quadriceps tendinopathy report pain at the proximal pole of the
patella. The pain is insidious, and often associated with a recent increase in
jumping, climbing, kicking or running. Physical examination reveals tenderness
over the superior pole of the patella and discomfort with resistance to extension
when the knee is in maximum flexion. Malalignment, such as femoral anteversion,
increased Q angle, and tibial torsion, should be evaluated, together with quadriceps
strength and hamstring flexibility. In older individuals with quadriceps tendinopathy, degenerative changes such as calcification in the tendon or spur formation at
the superior pole of the patella may be present. When extension strength is
maintained, an MRI may show degeneration of the posterior insertion of the
tendon [74].
Hamstring syndrome
In hamstring syndrome, pain is felt over the ischial tuberosity and radiates
along the posterior aspect of the thigh [81]. Normally, the sciatic nerve lies
687
lateral to biceps femoris near the ischial tuberosity, and then under the thigh
muscles. The hamstrings have thick tendinous structures near their site of
origin. In the hamstring syndrome, this fibrous region is distinct, scarred and
fibrotic. Some patients present adhesions between the sciatic nerve and the
tendon. Most athletic patients are active in sprinting, hurdling, or jumping
(50%), and soccer (22%).
Tennis elbow
Tennis elbow, also known as lateral epicondylitis, follows excessive use of
wrist extensors and forearm supinators. Up to 40% of tennis players suffer from
it. Tennis elbow affects approximately 1% to 2% of the population and is between
5 to 9 times more common than medial epicondylitis [82]. Although any of the
common extensor origin tendons can be involved in this condition, the extensor
carpi radialis brevis tendon is the most commonly involved specific site [83].
Patients most commonly present with lateral elbow pain that frequently radiates
into the proximal extensor forearm musculature. Most patients relate symptoms
to activities that stress the wrist extensor and supinator muscles, and especially to
activities that involve forceful gripping, or lifting of heavy objects. The incidence
of tennis elbow is 2 to 3.5 times higher in the over-40 age group than for those
under 40, and higher among the athletes who played more than 2 hours a day than
among those who play less than 2 hours a day [84].
Golfers elbow
Golfers elbow, also known as medial epicondylitis, is a typical complaint in
javelin throwing, baseball, and golf. In the majority of cases, it results from
overuse of the forearm wrist and finger flexor muscles, and in particular of the
pronator teres and flexor carpi radialis muscles [82]. Occasionally, symptoms
develop as a result of a direct injury to the medial epicondyle. In other patients,
the causative factors may be difficult to identify, and this latter group of patients
may fall into the mesenchymal syndrome category of patients [85]. In the
majority of cases, the pathological changes observed within the common flexor
origin mirror those seen with lateral epicondylitis, both macroscopically and
microscopically. Clinical examination findings reveal localized tenderness most
evident over the anterior and medial aspects of the medial epicondyle and
medial epicondylar ridge. Coexistence of ulnar nerve pathology can be expected
in up to 50% of cases [86]. The medial elbow discomfort is exaggerated by
activities that involve active contraction of the wrist and finger flexors, and
pronation of the forearm. In 10% to 15% of individuals, the ulnar nerve
subluxes anteriorly with elbow flexion, and may exaggerate or even mimic
the symptoms of golfers elbow, assuming that ulnar nerve pathology exists, or
may even trick the clinician into assuming that the individual does not have
coexisting ulnar nerve pathology, due to the absence of tenderness posterior to
the medial epicondyle [87].
688
Paratendinopathy of flexor carpi radialis

The flexor carpi radialis tendon sharply angulates over the anterior aspect of
the trapezium within its tight fibrous sheath to be inserted into the base of the
index metacarpal. This tendons close proximity to the trapezium results in
anchoring of the tendon sheath to the trapezium, and makes the tendon prone to
injury. Typically the patient is a middle-aged woman who presents with pain that
develops spontaneously in the region of the scaphoid tubercle and is exacerbated
by resisted flexion and radial deviation of the wrist. The clinical diagnosis is not
always clear-cut, however, due to the high incidence of degenerative changes
present within the basal joint of the thumb in this patient group [88]. If surgical
release of the tendon sheath is indicated, the sheath should be released proximally
and distally to the trapezial tubercle. The tendon should also be mobilized from
the volar aspect of the trapezium, allowing inspection of the trapezial groove.
Any sharp osteophytes should be excised and the sheath left open.
De Quervains disease
De Quervains disease is probably the best known form of paratendinopathy,
causing wrist and hand pain. Patients typically present with pain in the radial aspect
of the distal forearm exacerbated by ulnar deviation of the wrist. Usually, it has an
insidious onset frequently associated with activities that involve frequent abduction
of the thumb. Direct trauma can be the initiating factor in some patients, however,
with the condition later being accentuated by constant use. The underlying
pathology is identical to any form of paratendinopathy, although many authors
have suggested that the presence of multiple aberrant tendons and other variations
of the tendon sheath may increase the likelihood of an individual developing this
condition. This commonly held view is probably erroneous, especially because
others have demonstrated, through anatomical studies, that only 20% of the
population have normal tendon anatomy [89]. It is perhaps more important to
identify these variants to ensure that all subcompartments of this combined tendon
sheath are fully decompressed surgically. In the younger person, the diagnosis is
usually easy to make, based on the history and following clinical examination.
Most patients with the condition present in the fourth and fifth decades, however,
and other common causes for radial wrist pain, such as arthritis of the carpometacarpal joint of the thumb must be considered, especially because de Quervains
disease is approximately six times more common in women than in men [90].
Recently, we compared the efficacy of conservative management of de
Quervains disease in 30 postpartum women and 30 nonpregnant women. Conservative management gave good results in patients in the first group. At the 6-month
follow-up, a significant difference between the two groups on pain and function
was evident. Only one patient among the postpartum women underwent surgery
because of failure of conservative management, versus 25 nonpregnant women
patients [91]. This suggests that hormonal status may play a role in the etiopathogenesis of the condition.
689
Summary
During the last few decades, the role of sports and physical activity has
become more and more important in all modern communities. The risk of
tendon injury has thus increased, and prevention has become important.
Epidemiologic studies are important when planning prevention programs for
tendon injuries. Because of individual sport cultures and different sport habits in
different countries, national epidemiologic studies are of importance in each
individual country.
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Clin Sports Med 22 (2003) 693 701
Cell death and tendinopathy

Jun Yuan, MBBS, PhD, Min-Xia Wang, MD,
George A.C. Murrell, MBBS, DPhil*
Orthopaedic Research Institute, St. George Hospital Campus, University of New South Wales,
Sydney, NSW 2217, Australia
Apoptosis is an active, often physiological, process distinguished from necrosis,

the other form of cell death, in that the cells themselves decide to undergo
apoptosis, or programmed cell death. Recently we have found that the cells of
injured rotator cuff tendons have much higher rates of apoptosis than the cells of
uninjured tendonsan observation that may help explain why tendons exposed to
excessive strain may become tendinopathic.
Modes of cell death

Cell death is an integral part of the normal life of complex organisms [1,2]. Two
alternative modes of cell death can be distinguished: apoptosisprogrammed cell
death, and necrosisaccidental cell death [3 6].
Necrosis
Any cell can be killed by the application of some noxious compound or
treatment. Most often, these cells die by necrosis, a pathological response involving
a dramatic increase in cell volume and lysis [7]. Necrosis is a passive, catabolic
process, occurring in acute, nonphysiological injury, which, unlike apoptosis, does
not require the expression of new mRNA and protein [8,9].
Necrosis is morphologically characterized by the swelling of mitochondria,
early rupture of the plasma membrane, with release of cytoplasmic and nuclear
contents into the intercellular milieu with an inflammatory response and secondary
damage [7,10].
* Corresponding author. Orthopaedic Research Institute, St George Hospital Campus, University

of New South Wales, 4-10 South Street, Kogarah, Sydney, NSW 2217, Australia.
E-mail address: murrell.g@ori.org.au (G.A.C. Murrell).
doi:10.1016/S0278-5919(03)00049-8
694
J. Yuan et al / Clin Sports Med 22 (2003) 693701
Table 1
Criteria distinguishing apoptosis from necrosis
Features
Necrosis
Apoptosis
Stimuli
Toxins, hypoxia, trauma
Energy requirement
None
Physiological and pathological conditions

without ATP depletion
ATP-dependent
Histology
Cellular swelling,
Chromatin condensation, apoptotic bodies,
disruption of organelles,
death of single isolated cells
death of patches of tissue
DNA breakdown pattern
Randomly sized fragments Ladder of fragments in internucleosomal
multiples of 185 base pairs
Plasma membrane
Lysed
Intact, blebbing, with molecular alterations
Phagocytosis of dead cells Immigrant phagocytes
Neighboring cells
Tissue reaction
Inflammation
No inflammation
From Hetts SW. To die or not to die: an overview of apoptosis and its role in disease. JAMA
1998;279(4):300 7; with permission.
Apoptosis
In 1972, Kerr et al [11] coined the term apoptosis, after the Greek word
meaning leaves falling from a tree, to describe an intrinsic cell suicide program
involved in the normal turnover of hepatocytes. Apoptosis has become a major
focus of research on cancer and immunological and neurodegenerative disorders.
Apoptosis is a highly regulated form of cell death that is distinctive from
necrosis [10] (Table 1). Cells undergoing apoptotic cellular suicide rapidly shrink
Fig. 1. Comparison of proportion (%) of apoptotic cells in supraspinatus rotator cuff tendon (RCT)
from rotator cuff-ruptured patients and subscapularis tendon (control) from rotator cuff-normal
patients. All tissues were stained by DNA end labeling assay. Blinded assessment of percentage of
apoptotic cells was performed. In each section, 500 cells were counted in tendinous, cellular, and
vascular areas. Mean SEM; n = 25 for rotator cuff tear (RCT) group; n = 6 for control group; ***,
P < 0.001 when compared with control group using students unpaired two-tailed t-tests. (From Yuan J,
Murrell GA, Wei AQ, et al. Apoptosis in rotator cuff tendonopathy. J Orthop Res 2002;20(6):1372 9;
with permission.)
695
and lose their normal intercellular contacts, and subsequently exhibit dense
chromatin condensation, nuclear fragmentation, cytoplasmic blebbing, and cellular
fragmentation into small apoptotic bodies. These apoptotic bodies are quickly
phagocytosed by neighboring cells or macrophages. As no cytosolic contents are
released into the intercellular medium during apoptosis, inflammation is not
triggered. The characteristic internucleosomal cleavage of nuclear DNA of
apoptosis is a biochemical hallmark of apoptosis [7,12].
Biological significance of apoptosis

Apoptosis is essential for the normal development of multicellular organisms
and is involved in cell turnover in healthy adult tissues [13]. In mature animals,
cell death balances cell division, maintaining the constancy of tissue mass.
Fig. 2. Apoptosis in rotator cuff tendon was assessed by in-situ DNA end labeling assay. (a) Subscapularis tendon from a rotator cuff-normal patient showing only a few apoptotic cells. (b) A large
number of apoptotic cells were identified in degenerative supraspinatus rotator cuff tissue (arrows).
(c) Negative control section of degenerative supraspinatus tendon tissue from a ruptured rotator cuff
patient generated by omitting TdT from reaction. (From Yuan J, Murrell GA, Wei AQ, et al. Apoptosis
in rotator cuff tendonopathy. J Orthop Res 2002;20(6):1372 9; with permission.)
696
Apoptosis also plays a critical role in removing unwanted, injured, or potentially

dangerous cells, such as tumor cells and virus-infected cells.
Apoptosis in degenerative diseases

Abnormal regulation of apoptosis has been implicated in the onset and
progression of an ever broader range of diseases, which include cancer [14],
Alzheimers disease [15], Parkinsons disease [16], retinal degeneration [17],
osteoarthritis [18 20], and most recently tendinopathy [21].
Tendinopathy
Intratendinous changes of both extracellular matrix and cellular components are
consistently found in the various tendinopathies (Achilles, patellar tendon, flexor,
and extensor, or the elbow and rotator cuff) [22,23]. The histological characteristics
include collagen degeneration and fiber disorientation, increased mucoid ground
substance, and an absence of inflammatory cells [24,25]. Tenocytes are abnormally
plentiful and alterations in the size and shape of the mitochondria and nuclei have
been noted [24].
Fig. 3. Comparison of proportion (%) of apoptotic cells in supraspinatus rotator cuff tendon (RCT)
and normal subscapularis tendon (RCN) from the same patients. Paired RCT and RCN were collected
from the same rotator cuff-ruptured patients. All tissue was stained by DNA end labeling assay, and
the percentages of apoptotic cells were calculated. Mean SEM; n = 6 for each group; ***, P < 0.001
when compared with RCN group using students paired two-tailed t-tests. (From Yuan J, Murrell
GA, Wei AQ, et al. Apoptosis in rotator cuff tendonopathy. J Orthop Res 2002;20(6):1372 9;
with permission.)
697
Fig. 4. Comparison of proportion (%) of apoptotic cells in subscapularis tendon from rotator cuff
ruptured patients and rotator cuff normal patients. Subscapularis tendon tissues collected from the
patients with (+RCT) or without ( RCT) rotator-cuff tear were stained by DNA end labeling assay.
The percentage of apoptotic cells was calculated. Mean SEM; n = 6 for + RCT group; n = 6
for -RCTgroup; *, P < 0.05 when compared with -RCT group using students unpaired two-tailed
t-tests. (From Yuan J, Murrell GA, Wei AQ, et al. Apoptosis in rotator cuff tendonopathy. J Orthop Res
2002;20(6):1372 9; with permission.)
Fig. 5. DNA laddering assay. (a) Laddering bands (arrows) unique for apoptosis were detected in
degenerative supraspinatus tendon tissues from rotator cuff ruptured patients (lane 2-3). Subscapularis
tendon (control) from a rotator cuff normal patient did not show the laddering patterns (lane 1).
(b) Paired subscapularis tendon and supraspinatus tendon from three rotator cuff-ruptured patients were
analyzed. Laddering bands (arrows) were detected in degenerative supraspinatus tendon tissue of
patient (lane 2), but not in normal subscapularis tendon tissue of the same patient (lane 1). (From Yuan J,
Murrell GA, Wei AQ, et al. Apoptosis in rotator cuff tendonopathy. J Orthop Res 2002;20(6):1372 9;
with permission.)
698
Apoptosis in tendinopathy
The authors were the first to report excessive apoptosis in degenerating tendon
[21]. A significant finding in the study was that there were twice as many apoptotic
cells in ruptured supraspinatus tendon than in normal subscapularis tendon using
in-situ, terminal transferase-mediated, nick-end labeling (TUNEL) assays (Fig. 1).
The apoptotic cells were distributed evenly through the torn edges of the
degenerative tendon (Fig. 2). We also collected torn degenerative supraspinatus
tendon and normal subscapularis tendon from the same patients and performed a
paired experiment. Degenerative tendon had a much higher proportion of apoptotic
cells than normal tendon, which had relatively normal histology (Fig. 3). The
proportion of cells undergoing apoptosis also increased with age (Fig. 4). The
specificity of apoptotic cell death was confirmed by DNA laddering assays (Fig. 5).
Fig. 6. Immunohistochemical identification of fibroblast-like cells and macrophages. (a) In

degenerative supraspinatus tendon from a rotator cuff-ruptured patient, fibroblast-like cells (arrows)
were positive for the anti-human fibroblast antibody. (b) CD-68 stained a few macrophages (arrows) in
degenerative supraspinatus tendon from a rotator cuff-ruptured patient. (From Yuan J, Murrell GA, Wei
AQ, et al. Apoptosis in rotator cuff tendonopathy. J Orthop Res 2002;20(6):1372 9; with permission.)
699
Using specific cell markers, the apoptotic cells in the rotator cuff were identified as
fibroblasts or fibroblast-like cells [21]. Only a few cells were positive for a
macrophage marker (Fig. 6), confirming an absence of inflammation during the
tendon degeneration process [21].
Mechanisms involved in apoptosis in tendinopathy

Apoptosis can be initiated by a wide variety of stimuli [26]. The precise
mechanism of initiation of apoptosis in tendon degeneration in vivo is still unclear.
Studies from our group indicate that oxidative stress induces apoptosis in primary
cultured human tendon fibroblasts in vitro [27]. The pathways of apoptosis induced
by oxidative stress may involve the release of cytochrome c from mitochondria to
cytosol and the activation of caspases.
Arnoczky et al [28] have demonstrated that cyclic strain is associated with
an activation of stress-activated protein kinases (SAPKs) in several cell lines,
including tendon fibroblasts. These SAPKs have been shown to be important
upstream regulators of a variety of cell processes, including apoptosis.
We can hypothesize, therefore, that tendinopathy may follow a pathway
illustrated in Fig. 7 [29]. An increase in the amount and duration of load that a
tendon cell sees may result in activation of intracellular stress-activated protein
kinases, which when persistently activated cause the tendon cells to undergo
apoptosis or programmed cell death. Increased cell death results in a collagenous
matrix that is weaker and more prone to tearing. With time, this tendon may
rupture. The cellular and molecular aspects of tendon apoptosis and their role in
the disease are still unclear.
Fig. 7. Schematic illustration regarding the possible pathogenesis of tendinosis. (From Murrell GAC.
Understanding tendinopathies. Br J Sports Med 2002;36:392 3; with permission.)
700
Summary
Apoptosis and necrosis are presently recognized as the two major types of
physiological and pathological cell death. Apoptosis is a tightly regulated cell
deletion process that differs morphologically and biochemically from necrotic
cell death. Tendinopathy is defined as a tendon injury that originates from
intrinsic and extrinsic etiological factors. Excessive apoptosis has recently been
described in degenerative tendon. The increased number of apoptotic tendon cells
in degenerative tendon tissue could affect the rate of collagen synthesis and
repair. Impaired or dysfunctional protein synthesis may lead to weaker tendon
tissue and eventually increase the risk for tendon rupture. Clearly, there are many
details to insert into this pathway, but there is hope that if the fine details of
the pathway can be fleshed out, then strategies may be able to be developed
to break the cycle at one or more points and prevent or treat tendinopathy
more effectively.
Acknowledgments
Supported in part by South Eastern Sydney Area Health Service/St George
Hospital and NiCox Corporation.
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Clin Sports Med 22 (2003) 703 710
Compression etiology in tendinopathy

Louis C. Almekinders, MDa,*, Paul S. Weinhold, PhDb,
Nicola Maffulli, MD, PhD, MS, FRCS(Orth)c
a
Division of Orthopaedic Surgery, North Carolina Orthopaedic Clinic, 4309 Medical Park Drive,
Suite 100B, Durham, NC 27704, USA
b
Department of Orthopedic Surgery, Sports Medicine Section,
University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA
c
Department of Trauma and Orthopedic Surgery, Keele University School of Medicine,
North Staffordshire Hospital, Thornburrow Drive, Hartshill, Stoke on Trent,
Staffordshire, ST4 7QB, UK
Chronic tendon problems or tendinopathies remain a common problem for

both elite and recreational athletes. Although acute, traumatic conditions such as
ligament and muscle tears receive much attention in the lay press and scientific
literature; chronic tendon problems account for much of the lost time in practice
and competition [1,2]. These conditions have generally been grouped together
with the term tendinitis. The suffix -itis indicates an inflammatory condition
of the tendon, but biopsy studies have clearly shown that classic inflammatory
changes are not frequently seen in these chronic tendon conditions [3 5]. Yet,
the histopathlogic features of these tendon disorders are clearly different from
normal tendon. The exact pathophysiologic processes that can occur within
tendon have yet to be determined and some are discussed in other articles in this
issue. Because of the lack of understanding, the term tendinopathy has been
coined to designate tendon disorders [6,7]. Several different forms of tendinopathy have been described. At this point, the anatomic location of the tendinopathy within the tendon plays a role in determining the type of tendinopathy.
Chronic tendon abnormalities consistent with tendinopathy can be found in the
midsubstance of the tendon, the insertion site on the bone, and the tenosynovium
surrounding the tendon. These different types can coexist within one tendon
as well.
It appears that tendons throughout the body can be affected by tendinopathies
[8]. The supraspinatus, common wrist extensor, quadriceps, patellar, posterior
tibialis, and Achilles tendons are probably the most commonly affected tendons.
Again, different type of tendinopathies are possible within these tendons;
* Corresponding author.
E-mail address: almek002@mc.duke.edu (L.C. Almekinders).
doi:10.1016/S0278-5919(03)00067-X
704
L.C. Almekinders et al / Clin Sports Med 22 (2003) 703710
however, the tendinopathy affecting the insertion site into the bone or enthesis
appears to one of the most common types. In particular, the supraspinatus,
common wrist extensor, quadriceps, and patellar tendon are almost exclusively
affected by insertional tendinopathy. This article focuses on this type of
tendinopathy and discusses the possible pathomechanics in the etiology of these
tendon disorders.
Traditional concept
Chronic tendon problems have generally been described as overuse injuries.
The traditional concept of overuse injuries involves the excessive loading of the
tendon and subsequent mechanical breakdown of the loaded tendon [9]. The
excessive loading can theoretically occur in many ways. Training errors have
frequently been mentioned as etiologic factor in tendon overloading [10,11].
A given tendon has a baseline mechanical strength. The mechanical strength may
be dependent on the loading history of the tendon, as the tendon will adapt to the
loads placed upon it. If the loading has been low or limited in frequency or
duration, the mechanical strength of the tendon will be relatively limited. Once a
rapid increase in training load, frequency, or duration occurs, the tendon may not
be able to adapt fast enough to this change. The mechanical strength of the
tendon may be exceeded and a small injury may ensue. Exactly how this small
injury progresses is not well studied. Theoretically, microinjuries in the tendon
occur repeatedly. The tendon may be able to heal a certain level of microinjury;
however, as the training and heavy loading of the tendon continues, this healing
process may be overwhelmed and a more major injury develops. At some point
the injury becomes clinically apparent through pain in the involved tendon. This
scenario is often considered a consequence of training error. Slow and moderate
increases in training are thought to allow for healing and adaptation of the tendon
and thereby avoid clinical injuries.
There are other factors besides training errors that may lead to increased loading
of the tendon. Poor technique in athletes is one of the possible factors [12,13]. For
instance, throwing athletes may place increased load on their supraspinatus tendon
if the throwing motion is mostly generated in the shoulder, and jumping athletes
may place abnormal stress on their patellar tendon if their landing from a jump is
not biomechanically sound. Athletic equipment may be another factor that
increases the load on the tendon. Shoe wear in running and jumping athletes is
frequently mentioned, as is the choice of racquet in tennis players [14,15]. Finally,
internal factors may play a role in the level of the load on the tendon. Internal factors
involve the status of the muscles, ligaments, and bones surrounding the tendon.
Some of these, such as strength of the musculature and flexibility of the ligaments
and muscle-tendon units, are quite variable. Lack of flexibility and muscle
imbalances are frequently mentioned as etiologic factors in chronic tendinopathies
[16,17]. Other internal factors are more or less fixed; limb alignment and body
habitus are examples.
705
Regardless of the factors involved in the development of a chronic tendon

problem, the traditional concept centers around increased loads on the tendon as a
result of these factors. These offending loads are thought to be tensile loads. It is
known that excessive tensile loads are capable of causing plastic deformation and
eventually rupture of the tendon [18]. In a chronic tendinopathy, the tensile loads
are presumed to be large enough to cause plastic deformation but not complete
failure. The plastic deformation is the biomechanical equivalent of a microinjury.
Repeated episodes of plastic deformation may add up to a clinically significant macroinjury.
Clinical challenges to the traditional concept

The traditional view of an overuse injury as a result of tensile overload appears
plausible at first glance. In spite of the fact that this view is widely accepted, the
clinical and scientific basis for this concept is incomplete at best. As mentioned
before, many clinical cohort studies mention the etiologic factors leading to
overuse, such as training errors, poor technique, inadequate equipment, inflexibility, and muscle imbalance. Without a prospective design and adequate control
groups, however, any conclusion regarding the etiologic role of these factors is
purely speculative. Only a few studies have attempted to study these factors in a
controlled, prospective manner and these have shown conflicting results.
Lysholm et al [19] recorded the mileage that the runners in his prospective study
completed and were able to show a moderate relation between injury rates and
mileage. The groups were not comparable with regards to their demographics,
however, and therefore the results could also be explained on the basis of age and
gender differences. Using a different approach, Popovich et al [20] found no
protective effect of rest on overuse running injuries in a prospective study on
military recruits. Witvrouw et al [21] studied intrinsic factors such as alignment,
flexibility and strength in relation to the development of patellar tendinopathy.
They were unable to detect a significant relation between patellar tendinopathy
and most variables including anthropometric variables, alignment and strength.
Only a moderate relation between this condition and quadriceps and hamstring
flexibility was found. Hartig et al [22] as well as Soderman et al [23] were able to
correlate flexibility with overuse injuries in a prospective study; however their
overuse injury groups included mostly non-tendinopathic conditions. Equipment
studies have been focused on shoes and inserts. Controlled studies on shoe
modifications [24,25] have been able to show differences in stress fracture rate
but not for chronic tendon problems.
Epidemiological studies have also made some interesting observations. In a
prospective study, Kannus et al [26] found that overuse injuries, including tendon
problems, were significantly more common in elderly athletes compared with
young athletes. Fahlstrom et al [27] made a similar observation and at the same
time were unable to relate Achilles tendon problems to other factors such as
training quantity and years of playing.
706
Biomechanical challenges to the traditional concept

As tendons transfer the force generated by the contractile elements within
muscle to the bone, there is no question that tensile loads are placed on the tendon.
The ultrastructural design of tendon is uniquely suited to withstand those tensile
loads. Biomechanical studies on failure modes of muscle-tendon units have clearly
shown that failure will occur within the muscle near the muscle tendon junction
[28,29] and not in the tendon. Although these load-to-failure studies do not study
repetitive submaximal loads, they do point out how healthy tendon is biomechanically overdesigned compared with its attached muscle. Load-to-failure studies on
isolated tendon specimens have shown plastic deformation or a decline in
mechanical properties to occur at 2% to 4% grip-to-grip strain [30,31]. Recent
studies in our laboratory with new specimen gripping techniques have suggested
that tendon behaves elastically to much higher strain values that approach failure
strains (Weinhold, work in progress, October 2002). Thus, the loads required to
cause mechanical changes in healthy tendons are quite large. It is not entirely clear
whether in-vivo loads can approach those values, as in-vivo measurements have
used rather large transducers that may significantly alter the normal anatomy [32].
As mentioned before, insertional tendinopathy is an extremely common form of
tendinopathy. In insertional tendinopathy, the pathologic tendon lesion is found at
or very close to the insertion site or enthesis. Insertional tendinopathy is commonly
seen in the supraspinatus (rotator cuff tendinopathy), common wrist extensor
(lateral epicondylitis), patellar (Jumpers knee) and Achilles tendon. Imaging and
surgical studies of these conditions reveal several common features [33 36]. These
tendons are relatively thick, with a broad insertion site. The tendons tend to insert at
an oblique angle to the bone, although this angle changes with movement of the
joint. Possibly most important, the pathology is predominantly found at the joint
side of the enthesis. Initial or partial tearing of the supraspinatus is found generally
on the humeral side rather than bursal side [37]. Lateral epicondylitis and jumpers
knee can be approached from the joint side with arthoscopic techniques [38,39].
Finally, tendon pathology in insertional Achilles tendinopathy is generally found at
the calcaneal or ankle-joint side of the tendon [40].
The enthesis is designed to transfer the mechanical tensile loads generated by
the muscle-tendon unit onto the bone. It has to carry out this function with a thick
tendon that inserts at a varying, oblique angle dependent on the position of the joint.
The architecture of these tendon insertion sites is complex. Anatomic studies by
Benjamin et al [41] have shown a cartilaginous transition zone most pronounced on
the joint side of the tendon. Work by Vogel et al [42] on the increase of
proteoglycans within the posterior tibialis tendon indicates that the cartilaginous
changes can occur as an adaptive response to mechanical compression on the
tendon. These histologic findings question whether the tendon insertion site is
uniformly subjected to tensile loads. This has led to various biomechanical studies
on the strains near the tendon insertion sites.
Bey et al [43] use an MRI-based technique to determine strains in the supraspinatus insertion onto the greater tuberosity. Strains were measured at various
707
glenohumeral positions. In general, the strain of the supraspinatus tendon on the

joint side of the insertion was significantly lower than the values found on the
bursal side.
In a biomechanical study of the patellar tendon origin near the inferior pole, the
tendon was instrumented with strain sensors and taken through range-of-motion
while the tendon was loaded [44]. Longitudinal strains in the tendon were measured
just distal to the inferior pole of the patella. The highest tensile strains were found
on the anterior side of the tendon. The lowest strains were found on the posterior,
joint side, where the changes with patellar tendinopathy or jumpers knee are routinely found. In a study by Basso et al [45], seemingly conflicting results were
found when they studied the biomechanical behavior of the patellar tendon. Strains
were measured over the length of the tendon, rather than local strain, as reported by
Almekinders et al [44]. Measured in this manner, the strains were actually greater
posteriorly in the tendon, and failure occurred at higher strains posteriorly. This
may not reflect what is actually occurring close to the insertion site, where the
pathology is almost exclusively found, however. Basso et al [46] also reported on
the compressive load in the patellar tendon as it courses over the inferior pole of the
patella. They found significant compressive loads at this location and felt that the
bone of the inferior pole of the patella exerted this compressive load through an
impingement on the tendon.
Most recently, a study has been completed on the Achilles tendon insertion site
[47]. The tendon was instrumented with strain sensors just proximal to the
calcaneus. Again, the lowest strains were found on the calcaneal side, where the
pathological changes of Achilles insertional tendinopathy are generally found.
Although not all biomechanical studies report the exact same results, a
consistent pattern appears to emerge from these studies. It seems clear that the
strains within the tendons near their insertion sites are not uniform. The significance of this cannot be fully appreciated until we have more knowledge of the
material properties of tendons as well. If we assume that the material properties are
similar throughout the tendon, this would mean that any muscle force transferred
through the insertion site preferentially loads the side of the tendon that is usually
not affected initially in tendinopathy. In that case, the side affected by tendinopathy
is generally stress-shielded. Thus, the presence of differential strains opens the
possibility of a different biomechanical explanation of the pathology found in these
regions of the tendon. The traditional concept of tensile failure may not be the
essential feature of the pathomechanics.
Alternative biomechanical theories in insertional tendinoapthy

The recently reported biomechanical data suggest a different biomechanical
etiology of insertional tendinopathy. The stress-shielded and transversely-compressed side of the enthesis has a distinct tendency to develop cartilage-like or
atrophic changes in response to the lack of tensile load [40 42]. Over a long
period, this process may develop a primary degenerative lesion in that area of the
708
tendon. This may explain why the tendinopathy is not always clearly activityrelated, but sometimes more strongly correlated with age. In this manner, it could
almost be considered an underuse injury rather than an overuse injury as a result
of stress-shielding.
The formation of cartilage-like changes in the enthesis in many ways can be
considered a physiologic adaptation to the compressive loads. It may not allow
the tendon to maintain its ability to withstand high tensile loads in that region of
the tendon, however. It seems possible that in athletes, certain joint positions will
occasionally still place high tensile loads on this region of the tendon. As the
stress-shielding may have led to tensile weakening over time, an injury may
occur more easily in this region. In this manner, insertional tendinopathy could
be considered an overuse injury, but predisposed by pre-existing weakening of
the tendon.
Finally, we should consider the effects of differential strains within the tendon.
As the joint changes position, strains in one section of the tendon could be
changing in opposite directions. Internal shear forces and heat could be generated
that injure cellular or matrix components in the tendon. Accumulation of these
injuries could lead to significant tendon destruction. This could be the biomechanical explanation of some of the intratendinous degeneration seen in certain
forms of tendinopathy.
Summary
Recent studies have emphasized that the etiology of tendinopathy is not as
simple as was once thought. The etiology is likely to be multifactorial. Etiologic
factors may include some of the traditional factors such as overuse, inflexibility,
and equipment problems; however, other factors need to be considered as well,
such as age-related tendon degeneration and biomechanical considerations as
outlined in this article. More research is needed to determine the significance of
stress-shielding and compression in tendinopathy. If they are confirmed to play a
role, this finding may significantly alter our approach in both prevention and in
treatment through exercise therapy. The current biomechanical studies indicate
that certain joint positions are more likely to place tensile stress on the area of
the tendon commonly affected by tendinopathy. These joint positions seem to be
different than the traditional positions for stretching exercises used for prevention and rehabilitation of tendinopathic conditions. Incorporation of different joint positions during stretching exercises may exert more uniform,
controlled tensile stress on these affected areas of the tendon and avoid stressshielding. These exercises may be able to better maintain the mechanical
strength of that region of the tendon and thereby avoid injury. Alternatively,
they could more uniformly stress a healing area of the tendon in a controlled
manner, and thereby stimulate healing once an injury has occurred. Additional
work will have to prove if a change in rehabilitation exercises is more efficacious that current techniques.
709
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Clin Sports Med 22 (2003) 711 725
The painful nonruptured tendon:

clinical aspects
Karim Khan, MD, PhD, FACSP, FACSM,
Dip Sport Med (CASM) (Assistant Professor)a,b,*,
Jill Cook, PhD, PT, Grad Dip Manip Therc
a
Department of Family Medicine, The University of British Columbia, 211-2150 Western Parkway,
Vancouver, BC, Canada V6T 1V6
b
School of Human Kinetics, The University of British Columbia, War Memorial Gymnasium,
210-6081 University Boulevard, Vancouver, BC, Canada V6T 1Z1
c
School of Physiotherapy, Faculty of Health Sciences, LaTrobe University, Kingsbury Drive,
Bundoora, Victoria, Australia 3086
Tendon injuries account for a substantial proportion of overuse injuries in

competitive and recreational sports participants, as well as in individuals whose
jobs require repetitive activity. Overuse type injuries account for 30% to 50% of
all sports injuries, and in many endurance and power sports tendon injuries are
clearly the most frequent reason for interruptions to training and competition [1].
Because tendon problems are so common, and not easily managed, this issue of
Clinics is devoted to them. This article aims to provide an understanding of the
pathology underlying the conditions before outlining current evidence for clinical
assessment and treatment of tendinopathies.
Tendon pathology: the myth of tendinitis

So the reader can better understand the abnormalities found in symptomatic
tendons, we first review the macroscopic and light microscopic appearance of normal tendon. More detailed descriptions of tendon anatomy exist elsewhere [2,3].
Normal tendon
Tendons are anatomic structures interposed between muscles and bones that
transmit the force created in muscle to bone and make joint movement possible.
* Corresponding author. 211-2150 Western Parkway, Vancouver, BC, Canada V6T 1V6.
E-mail address: kkhan@interchabnge.ubc.ca (K. Khan).
doi:10.1016/S0278-5919(03)00035-8
712
K. Khan, J. Cook / Clin Sports Med 22 (2003) 711725
The basic elements of tendon are collagen bundles, cells, and ground substance or
extracellular matrix, a viscous substance rich in proteoglycans. Collagen provides
tendon with tensile strength; ground substance provides structural support for the
collagen fibers and regulates the extracellular assembly of procollagen into
mature collagen [4]. Tenocytes are flat, tapered cells sparingly distributed among
the collagen fibrils that synthesize both the ground substance and the procollagen
building blocks of protein.
Collagen is arranged in hierarchical levels of increasing complexity, beginning
with tropocollagen, a triple-helix polypeptide chain, which unites into fibrils,
fibers (primary bundles), fascicles (secondary bundles), tertiary bundles, and
finally the tendon itself [2,3].
The entire tendon is covered by the epitenon, a fine, loose connective tissue
sheath containing the vascular, lymphatic and nerve supply. More superficially,
the epitenon is surrounded by paratenon, a loose areolar connective tissue
consisting essentially of type I and type III collagen fibrils, some elastic fibrils,
and an inner lining of synovial cells. Together, the paratenon and epitenon are
sometimes called the peritendon [2].
The classic two-layered synovial tendon sheath is only present in certain
tendons as they pass areas of increased mechanical stress. The outer layer is the
fibrotic (ligamentous) sheath and the inner layer is the synovial sheath, which
consists of thin visceral and parietal sheets [2]
The myotendinous junction is a highly specialized anatomic region in the
muscle-tendon unit where tension generated by muscle fibers is transmitted from
intracellular contractile proteins to extracellular connective tissue proteins (collagen fibrils) [2]. As this region is rarely affected by tendinopathy, its complex
ultrastructure is not discussed further here, but the interested reader is referred
elsewhere [2].
The osteotendinous junction is a specialized region in the muscle-tendon unit
where the tendon inserts into a bone. In the osteotendinous junction, the
viscoelastic tendon transmits the force into a rigid bone. The region has been
described as containing four light-microscopic zones: (1) tendon, (2) fibrocartilage, (3) mineralized fibrocartilage, and (4) bone [5].
Under the light microscope, normal tendon consists of dense, clearly defined,
parallel and slightly wavy collagen bundles. Collagen has a characteristic
reflective appearance under polarized light. Between the collagen bundles there
is a fairly even sparse distribution of cells with thin wavy nuclei. There is an
absence of stainable ground substance and no evidence of fibroblastic or
myofibroblastic proliferation. Tendon is supplied by a network of small arteries
oriented parallel to the collagen fibers in the endotenon [2,3].
The myth of tendinitis
Until recently, if a patient presented with a history of exercise-related pain and
tenderness at one of the common sites of tendinopathy (the Achilles, patellar,
rotator cuff, or elbow tendons), and if history and examination features suggested
713
that pain was emanating from the tendon, the patient would most likely have been
diagnosed as having tendinitis, an inflammatory condition of the tendon. This
was proven not to be the case as long ago as 1976, when Giancarlo Puddu of
Rome examined the Achilles tendon of symptomatic runners and showed that
inflammatory cells were absent. This research finding has not been widely
incorporated into clinical practice, however, until more recent years [6 10].
Here we summarize the findings of histopathological examination at commonly
reported sites of tendon pain.
Achilles tendon
Histopathologic examination of symptomatic Achilles tendons reveals degeneration and disordered arrangement of collagen fibers. Collagen fibers are thinner
than normal and separated by large mucoid patches and vacuoles. In addition to
collagen fibers in symptomatic Achilles tendons being abnormal in themselves,
the characteristic hierarchical structure is also lost [6]. Also, there is an increase in
Alcian-blue-staining ground substance. Whether this precedes or follows the
collagen separation is currently under investigation. Symptomatic Achilles tendons reveal increased vascularity [11]. It is important to note that inflammatory
lesions [6,11], intracellular lipid aggregates, and acellular necrotic areas were
exceptional and not regarded as normal elements of the degenerative process
[6]. The authors concluded that the absence of inflammation and the poor healing
response demonstrate a state of degeneration that conforms to the histopathology
described by previous authors in total ruptures and in chronic tendinopathy [6].
With respect to the paratenon, Kvist et al [12,13] found evidence of mucoid
degeneration, fibrosis, and vascular proliferation, with only a slight inflammatory
infiltratesimilar to other series. Astrom and Rausing [6] found virtually no
evidence of paratenonitis in their series of Achilles tendon specimens. These
differences may be explained by the fact that Kvist et al did not report pathology
of the tendon itself, and studied more active, younger patients. Thus, paratenonitis is not a prerequisite for Achilles tendon symptoms in a population of
recreational sportspeople and office workers. The major lesion in chronic
Achilles tendinopathy is a degenerative process characterized by a curious
absence of inflammatory cells and a poor healing response [6].
Patellar tendon
Macroscopically, the patellar tendon of patients with patellar tendinopathy
(also commonly called jumpers knee) contain yellow-brown and disorganized
tissue in the deep posterior portion of the patellar tendon adjacent to the lower
pole of the patella [14 16]. Under the light microscope, the tendons of patients
suffering jumpers knee do not consist of tight parallel collagen bundles, but
instead are separated by increased mucoid ground substance that gives them a
disorganized and discontinuous appearance. Clefts in collagen and occasional
necrotic fibers may suggest microtearing. There is loss of the characteristic
714
reflective polarized light appearance [17]. A consistent feature across studies of

the patients with chronic patellar tendinopathy was the finding of mucoid
degeneration with variable fibrosis and neovascularization. The collagen producing tenocytes themselves lost their fine spindle shape and nuclei were more
rounded and sometimes chondroid in appearance, amounting to fibrocartilaginous
metaplasia. Small vessel ingrowth was also evident. As with Achilles tendinopathy, patellar tendinopathy occasionally revealed erythrocytes and positive
staining for iron pigment, but the histopathology remained identical to those
cases without rupture [17]. As with the Achilles tendon pathology described
above, myofibroblasts are prominent [18,19] and board-certified pathologist
authors have found inflammatory cells to be absent [17,18]. In addition, there
is disruption of the bone tendon junction and a propensity to develop cystic
lesions where active repair is not occurring.
Extensor carpi radialis brevis tendon
The term tennis elbow was used for 100 years before the pathology of the
extensor carpi radialis brevis tendon was associated with lateral tennis elbow [20].
At surgery the symptomatic extensor carpi radialis brevis contained disrupted
collagen fibers, increased cellularity, and neovascularisation [20]. Acute inflammatory cells were almost always absent from the tendon, but a mild sprinkling of
chronic inflammatory cells were noted in supportive or adjacent tissues. When
chronic inflammatory cells were present, they resulted from repair of partial tears
[20]. A recent study in 20 cases of chronic (6 48 months) lateral epicondylitis
confirmed that there was no histopathologic evidence of either acute or chronic
inflammation in any of the specimens [21]. The histopathology reported in lateral
tennis elbow also exists in medial tennis elbow [22,23]. As at the patellar tendon,
there is disruption of the bone tendon junction, as well as a propensity to develop
cystic lesions where active repair is not occurring.
Rotator cuff
Histopathology of symptomatic rotator cuff tendons reveals collagen disruption and fibrocartilaginous metaplasia [24,25], as well as cellular distortion
and necrosis, calcium deposition, fibrinoid thickening, hyalinization, fibrillation,
and microtears. There is loss of the characteristic crimped pattern of tendon, and
parallel bundles of collagen separate and become disorganized [24 26]. Characteristically, the symptomatic rotator cuff reveals disruption of fascicles, formation
of foci of granulation tissue, dystrophic calcification, thinning of fascicles,
associated with cell and vessel proliferation [24]. Hypervascularity of the
degenerative rotator cuff has also been reported by others [27,28].
Tendinosis
These data clearly indicate that painful, overuse tendon injury is due to
tendinosisthe histologic entity of collagen disarray, increased ground sub-
715
Table 1
Bonars classification of tendinopathies [7]
Pathological
diagnosis
Concept
(macroscopic pathology)
Tendinosis
Intratendinous degeneration
(commonly due to aging,
microtrauma, vascular
compromise)
Tendinitis/Partial
rupture
Symptomatic degeneration of
the tendon with vascular
disruption and inflammatory
repair response
Paratenonitis
Inflammation of the outer

layer of the tendon (paratenon)
alone, whether or not the
paratenon is lined by synovium
Paratenonitis associated with
intratendinous degeneration
Paratenonitiswith
tendinosis
Histologic finding
Collagen disorientation, disorganization
and fiber separation by an increase
in mucoid ground substance, increased
prominence of cells and vascular spaces
with or without neovascularization and
focal necrosis or calcification
Degenerative changes as noted above with
superimposed evidence of tear, including
fibroblastic and myofibroblastic
proliferation, hemorrhage and organizing
granulation tissue.
Mucoid degeneration in the areolar tissue
is seen. A scattered mild mononuclear
infiltrate with or without focal fibrin
deposition and fibrinous exudate
Degenerative changes as noted in tendinosis
with mucoid degeneration with or without
fibrosis and scattered inflammatory cells in
the paratenon alveolar tissue
From Khan KM, Cook JL, Bonar F, Harcourt P, Astrom M. Histopathology of common overuse
tendon conditions: update and implications for clinical management. Sports Med 1999;27:393 408;
with permission.
stance, neovascularization, and increased prominence of myofibroblasts. Bonars

classification is tabled (Table 1).
Although the term tendinosis was first used by German workers in the
1940s, its recent usage results from the work of Puddu et al [29]. Tendinosis is
tendon degeneration without clinical or histological signs of an inflammatory
response. It may result from the pathological process of apoptosis [30] or other
mechanisms of failed healing. It appears that tendinosis is the major, and perhaps
Table 2
Implications of the diagnosis of tendinosis compared with tendinitis
Trait
Overuse tendinosis
Overuse tendinitis
Prevalence
Time for full recovery
(initial presentation)
Time for full recovery (chronic)
Likelihood of full recovery to
sport from chronic symptoms
Focus of conservative therapy
Common
2 3 mos
Rare
Several days to 2 wks
3 6 mos
80%
4 6 wks
99%
Encourage collagen synthesis,

maturation, and strength
Excise abnormal tissue
70% 85%
4 6 mos
Anti-inflammatory modalities
and drugs
Not known
95%
3 4 wks
Role of surgery
Prognosis for surgery
Time to recover from surgery
716
the only clinically relevant chronic tendon lesion [7], although minor histopathologic variations may exist in different anatomical sites.
The finding that the clinical tendon conditions in sportspeople are due to
tendinosis is not new. Writing about the tendinopathies in 1986, Perugia et al noted
the remarkable discrepancy between the terminology generally adopted for these
conditions (which are obviously inflammatory because the ending -itis is used)
and their histopathologic substratum, which is largely degenerative [31]. Table 2
summarizes the main differences that a presumptive diagnosis of tendinosis
implies, compared with a diagnosis of tendinitis.
Clinical assessment of the painful tendon

As in all branches of medicine, the keys to diagnosis remain history and
physical examination. Imaging has an important, but secondary role [32,33].
History
The diagnosis of tendon pain is generally straightforward, but exceptions
exist. The classic presentation is one of increasing pain at the site of the offending
tendon, often with recognition that there has been an increase inactivity. The pain
is usually load-related. In very early tendinopathy, pain may be present at the
beginning of an activity and then warm-up (disappear) during activity itself,
only to reappear when cooling down if the activity is prolonged, or to be more
severe on subsequent attempts to be active. The patient can usually localize the
pain rather clearly and the pain is described as severe or sharp during the
early stages and sometimes as a dull ache once it has been present for some
weeks. Pain that is vague in nature and distribution or referred to as tingling or
as a numb feeling should alert the physician that the problem may not
primarily emanate from tendon. Tendon pain itself usually does not radiate,
although referred pain can contribute to the development of a secondary tendon
problem (classically, a neck problem contributing to elbow pain; see below).
Aggravating activities generally are those that increase load on the tendon in
question, relieving factors include relative rest, ice, and nonsteroidal antiinflammatory drugs and other analgesic medications. In any case of suspected
tendinopathy, the history should include questions about general health, not only
because this is a good clinical practice, but also because tendinopathy can mark
the presence of an underlying spondyloarthropathy (eg, psoriasis) [34]. Symptoms such as previous gastrointestinal infection or sexually transmitted diseases
should alert the clinician to the possibility of a secondary tendinopathy. Many
patients who have well-established psoriasis are not aware that tendinopathy is an
extradermal manifestation of this condition.
Specific differential diagnoses to consider at various anatomical regions are
listed in Table 3. The specifics of these conditions are outside the scope of this
article but can be found elsewhere [35].
717
Table 3
Specific differential diagnoses to consider when patients present with tendinopathy at various anatomical regions
Region
Achilles
Patellar
Lateral elbow
Rotator cuff
Tibialis posterior
medial ankle
Differential diagnoses
to consider
Posterior impingement, bursitis,
referred pain (less common)
Patellofemoral pain
Referred pain from the cervical
spine (common), nerve
entrapments in the forearm
AC joint pain and osteolysis
of the distal clavicle, shoulder
instability, and glenoid labral
tears
Flexor hallucis longus
tendinopathy
Keys to correct diagnosis

Careful palpation, passive plantarflexion
test for posterior impingement
Careful palpation
Careful examination of the cervical
spine, awareness of forearm nerve
entrapments
Examination of the AC joint,
assessment for instability, and labral
tests
Careful palpation FHL tendinopathy
is generally at the tunnel; tibialis
posterior tendinopathy is generally at
the navicular insertion
Physical examination
Physical examination must include tests that load the tendon to reproduce pain
and other loading tests that load alternative structures. After consideration of the
history and the behavior of the tendon pain under load, careful palpation together
with knowledge of surface anatomy allows a confident clinical primary diagnosis
of tendinopathy. Palpation should reveal focal tenderness that essentially reproduces the patients pain. At the Achilles this may be 3 cm to 5 cm above the
calcaneal insertion (classic midportion tendinopathy), or less commonly at the
insertion (insertional tendinopathy) itself. Many experienced clinicians find
the latter condition responds less well to treatment, and thus distinguish these
two types of Achilles tendinopathy because of their very different prognoses.
Insertional tendinopathies at less commonly affected sites (eg, Achilles insertion,
patellar tendon distal insertion) should increase the clinicians index of suspicion
to the possibility that a spondyloarthopathy is involved (see history, above) [34].
The tenderness of patellar tendinopathy is generally found on the deep surface of
the proximal attachment of the patellar tendon. This can be palpated when the
knee is in about 30 of flexion and the quadriceps muscle is totally relaxed. Note
that some tenderness is usual at this location, but moderate or severe tenderness is
associated with pathology [36]. Similarly, the cardinal signs of lateral and medial
elbow tendinopathy is tenderness at the origins of the elbow extensors and
flexors, respectively. As mentioned above (history), the prevalence of cervical
pathologies (such as joint hypomobility) means that the neck must be examined
carefully in all cases of shoulder and elbow tendinopathy. A skilled physical
therapist or clinician aware of upper limb tension tests [37] should examine
718
difficult cases of elbow tendinopathy, as referred pain and cervical contribution is

often not in the classic radicular pattern. The clinician must understand the role of
somatic pain in both the upper and lower limbs so that somatic pain is not
overlooked inadvertently. Once this diagnosis has been made, however, further
examination should aim to identify why the tendinopathy has arisen, and this
generally requires expertise in understanding sporting biomechanics.
Imaging assessment
In apparently straightforward cases of tendinopathy, many expert clinicians
feel that the diagnosis can be made confidently clinically, thus obviating the need
for any investigation. In cases where the history and examination may not be
typical, or the clinical recovery is not as expected, both ultrasound and magnetic
resonance (MR) imaging provide a great deal of morphological information about
tendons. Although there is an association between tendon morphology and
symptoms, there are many cases where structure does not parallel pain, so the
clinician must interpret imaging findings bearing symptoms in mind. Detailed
discussion of this topic is beyond the scope of this section, but the reader is
referred elsewhere for further discussion of lack of clinical correlation between
tendon imaging and symptoms [38 43].
Achilles tendon degeneration is evident as increased signal on MR imaging [44]
and hypoechoic regions on ultrasound [45 47]. Regions of tendinosis produce
increased signal on MR imaging [17,18] and hypoechoic regions on ultrasound
[17,47]. At the shoulder, elbow, and patellar tendons, MR delineates tendon
pathology [21], but ultrasound can be technically challenging, as the tendon
insertion is adjacent to bone, which limits image quality [48]. At the shoulder,
however, ultrasound comes into its own, as the skilful operator can use the dynamic
capacity of the investigation to assess the rotator cuff in great detail. Regions of
tendon degeneration produce high-intensity signal on MR imaging [49]. A high
proportion of asymptomatic volunteers (89% 100%) have regions of high signal
in the rotator cuff tendon [43,50]. This suggests, but does not prove, that
subclinical tendon degeneration may be a relatively common phenomenon
amongst asymptomatic individuals. The take-home message for physicians is that
patients must be managed on clinical grounds, not according to a predetermined,
imaging-driven algorithm. If imaging reveals normal morphology but symptoms
have been present for some time and are moderately severe, however, the diagnosis
of tendinopathy is less likely and other pathologies should be considered.
Conservative management of tendinopathies

Although many conservative treatments have been used to treat tendinopathies, there have been few randomized controlled trials. In this section we review
the evidence that supports common methods used to treat tendinopathies in
clinical practice.
719
Relative rest
Relative rest may be an important component of treatment of tendinopathy,
given that there is frank structural damage to the tendon. Collagen healing may
require longer than has traditionally been afforded a patient with tendinopathy. In
sports, tendons must often sustain more than 10 times body weight [51], yet the
tissue has a slow metabolic rate, as evidenced by its having only 13% of the
oxygen uptake of muscle and requiring more than 100 days to synthesize collagen
[52]. Thus, symptom relief in tendinosis may take months rather than weeks.
There are no objective guidelines as to how much rest is optimal. Traditionally, pain has been used as a guide. Thus, the patient is generally advised to
undertake relative rest until he or she can perform activities of daily living
essentially free of pain. After that time, strengthening (see below) can begin.
Continued rest allows a decrease in musculotendinous strength and less ability for
the unit to function optimally. Alfredson has postulated that pain is a normal part
of the healing process, however, and encourages patients to perform certain
strengthening exercises unless they have debilitating pain [53].
Strengthening
Strengthening, particularly eccentric strengthening, has been advocated as a
treatment of tendon overuse conditions since the early 1980s [54 56]. Clinical
studies point to the efficacy of eccentric strengthening regimens [54,56 59].
Mechanical loading accelerates tenocytes metabolism and may speed repair [60].
These data provide rationale for judicious, progressive strengthening in the
treatment of tendinosis [9,61,62].
Nonsteroidal anti-inflammatory drugs (NSAIDs)
On theoretical grounds one would predict that the anti-inflammatory action of
NSAIDs would have no therapeutic effect in tendinosis, a noninflammatory
condition. Furthermore, the analgesic effect of NSAIDs [63] may permit patients
to ignore early symptoms, further damage tendon, and thus delay definitive
healing. In practice, there is little evidence that NSAIDs should play a role in
management of tendinopathy [64], and Astrom et al found no beneficial effect of
NSAIDs in patients with Achilles tendinopathy [65]. Until there is evidence to
suggest otherwise, it seems that NSAIDs are inappropriate in the management of
uncomplicated tendinopathy.
Corticosteroids
The role of corticosteroids in treatment of tendon conditions has been the
subject of considerable debate [66,67] but very few well-designed studies [68].
Further studies are desperately needed. It is clear that corticosteroid injection that
inadvertently enters into tendon tissue leads to cell death and tendon atrophy [69].
As tendinosis is not an inflammatory condition, the rationale for using cortico-
720
steroids needs reassessment, particularly as corticosteroids inhibit collagen

synthesis [70,71] and decrease load to failure [72]. Corticosteroids, however,
provide short-term pain reduction by mechanisms that are poorly understood [40].
Other pharmaceutical agents
The protease inhibitor aprotinin and other drugs such as low-dose heparin
have been used in the management of peri- and intratendinous pathology [73].
More recently, researchers have used a sclerosing agent, poldicanol, better known
for its role in treatment of varicose veins and esophageal varices, to ablate the
neovessels associated with tendinopathy [74,75]. Although preliminary results
are encouraging, these results must be considered preliminary at the time this
journal goes to press.
Modalities
Physiotherapists employ a wide variety of modalities, including ultrasound,
laser, and heat, to treat tendinopathies [76]. Modalities are proposed to decrease
inflammation and promote healing, but there is very limited evidence to support
these claims. Studies of severed tendons have shown that ultrasound increases
collagen synthesis in fibroblasts [77] and increases tensile strength of healing
tendon [78,79] and has little effect on inflammation [80,81]. After rabbit
Achilles tenotomy there was a 26% greater collagen concentration in tendons
that had received laser photostimulation compared with those that received sham
laser [82]. Biomechanical and biochemical measures of tendon healing were
improved by a combination of ultrasound, laser, and electrical stimulation of
rabbit Achilles tendons after tenotomy and suture repair [83]. All of these effects
would help to reverse the pathology of tendinosis by stimulating fibrosis and
repair; however, relevant human data are required.
Cryotherapy
Cryotherapy may decrease the extravasation of blood and protein from the
neovessels found in painful tendons [74,76]. It would also be expected to decrease
the metabolic rate of tissue and decrease tendon temperature after exercise. Thus,
ice may play a role in treating tendinosis. Ice would be particularly effective
in treating tendinopathies where paratenonitis is associated with tendinosis
(eg, some Achilles tendinopathies). As ice may mask pain in tendinosis and
increases tissue stiffness, it ought not be used before sports participation.
Braces and supports
Braces and supports are used as an adjunct to treatment of elbow and knee
tendinopathies. Braces may act to keep the tendon warm during sporting
performance but would not be expected to protect the tendon, except by
aiding proprioception.
721
Orthotics
Orthotics are commonly prescribed in the treatment of Achilles tendinopathy,
and less commonly for jumpers knee. Ankle plantarflexion peak torque differs
between patients with Achilles tendinopathy and controls [84], and this would
provide a rational mechanism of action for orthotics in this condition. Further
studies of biomechanics in athletes with tendinopathies and the role of orthotics
are required.
Technique correction
As technique correction aims to decrease the load that is placed through a
tendon, it clearly has a place in managing the tendinosis associated with overuse
conditions [9,85]. For example, attention to a tennis players backhand drive
technique can play a major role in treating tendinosis at the lateral elbow [86],
and adjusting jumping technique in volleyballers may contribute to treatment of
patellar tendinosis [87].
Surgery
The aims of surgery have been outlined elsewhere [88], and clinical research
suggests it can be effective in a proportion of cases [89,90]. Why surgery promotes
healing of tendon is still not understood. It has been argued that perhaps the
postoperative healing response and the careful progression of rehabilitation after
surgery rather than the surgery itself causes improvement in the patients
condition, but the time course of healing after surgery in Colemans study [91]
argues against this being the only cause. An important point for clinicians to
remember and to emphasize to patients is that surgery, when successful, does not
permit immediate return to sport. Prospective outcome studies (likely to be more
accurate on this than retrospective studies or clinical impression) indicate that
elbow surgery may permit patients return to sport in 4 to 6 months [20], Achilles
surgery may do so in 6 to 9 months [92], and patellar tendon surgery may do so in
9 to 12 months [93]. Rotator cuff surgery is difficult to categorize, as the time to
recover depends on the type of surgery, and there are many different procedures
for shoulder tendinonpathy. Nevertheless, an elite throwing or racquet sports
player is unlikely to return to full competition at the same level after a
tendinopathy procedure (eg, repair of partial tear) for a minimum of 6 to 9 months.
Summary
Tendon conditions cause a great deal of morbidity in both elite and
recreational athletes, and outcome of treatment is often unsatisfactory. Evidence
that the common clinical conditions (eg, Achilles, patellar, elbow and rotator cuff
tendinopathies) are due to tendinosis has been present for many years, yet the
misnomer tendinitis is still widely used for these conditions in clinical
722
practice. Clinical practice remains very different from evidence-based recommendations [8], but this is a common challenge in medical practice. Thus, in
addition to further research in an area of medicine rife for such endeavor, there
must be attention to knowledge translationensuring that the patient benefits
from what is already known.
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Clin Sports Med 22 (2003) 727 741
Chronic midportion Achilles tendinopathy:

an update on research and treatment
Hakan Alfredson, MD, PhD
Sports Medicine Unit, Department of Surgical and Perioperative Science, Umea University,
901 87 Umea, Sweden
Chronic painful conditions in the midportion of the Achilles tendon, often

referred to as Achilles tendinopathy, are relatively common, especially among
recreational athletes in the age group between 30 and 60. In the athletic population,
the etiology is considered to be associated with overuse of the aged tendon, but
scientifically, the etiology and pathogenesis are unknown. In general, Achilles
tendinopathy has been considered to include an inflammatory component, and the
nomenclature often used (tendinitis, tendonitis) implies inflammatory involvement. Recent research using microdialysis technique and gene technology, however, has clarified that there is no chemical inflammation in chronic midportion
Achilles tendinosis (tendinopathy with ultrasonographically verified tendon
changes). Interestingly, the neurotransmitter glutamate and its NMDAR1 receptor
were found for the first time in human tendons by using microdialysis and
immunohistochemical techniques. The concentrations of glutamate were significantly higher in painful tendons with tendinosis than in normal, pain-free tendons.
Treatment of Achilles tendinopathy is considered difficult, and in chronic
Achilles tendinosis surgery is often needed. Recent research, however, has shown
promising clinical results using nonsurgical methods. Painful eccentric calf
muscle training as treatment of painful midportion chronic Achilles tendinosis
has been demonstrated to give good short-term clinical results. Also, in a very
recent pilot study, sclerosing of neovessels in the area with pain and tendon
changes showed promising short-term clinical results.
The Achilles tendon has a high capacity to withstand tensional forces, and is
the strongest tendon in the human body. Chronic painful conditions in the tendon
are relatively common, especially among middle-aged recreational athletes [1].
The etiology and pathogenesis are unknown. There is a wide range of suggested
etiological factors, but the scientific background to most of these suggestions is
E-mail address: hakan.alfredson@idrott.umu.se

doi:10.1016/S0278-5919(03)00010-3
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H. Alfredson / Clin Sports Med 22 (2003) 727741
lacking, and they are to be characterized as unproven theories. An association

with overuse from repetitive loading is most often stated as being the etiologic
factor [2 4]; however, these conditions are also seen in physically inactive
individuals [5,6]. This was further emphasized in a study on a large group of
patients with chronic Achilles tendinopathy (342 tendons with tendinosis), where
it was demonstrated that physical activity was not correlated to the histopathology, suggesting that physical activity could be more important in provoking the
symptoms than being the cause of the actual lesion [7]. Among other suggested
etiological factors to be mentioned are: aging, with a decreased blood supply and
decreased tensile strength; muscle weakness and imbalance; and insufficient
flexibility [8 12].
Clinically, it is important to establish a correct diagnosis. In scientific studies,
an accurate clinical examination, ultrasonography [13 15], magnetic resonance
imaging (MRI) [13 15], and biopsy [16] have been shown to be helpful tools for
a correct diagnosis. Most commonly the patients with Achilles tendinopathy
present a history with a gradual onset of pain during tendon loading, and morning
stiffness in the tendon [6,17,18]. The common findings during clinical examination are an area with tenderness, and often, but not always, a localized swelling in
the tendon (Fig. 1). There are quite a few possible differential diagnoses, such as
os trigonum syndrome, tenosynovitis or dislocation of the peroneal tendons,
tenosynovitis of the plantar flexors, an accessory soleus muscle, tumors of the
Achilles tendon (xanthomas), and neuroma of the suralis nerve, that have to be
kept in mind. The clinical examination can be combined with imaging of the
tendon. Hypoechoic areas on ultrasound and areas with increased signal intensity
on MRI have been shown to correspond to areas of altered collagen fiber
structure and increased interfibrillar ground substance (hydrophilic glycosamino-glycans) [5]. A condition combining chronic pain symptoms from a tender
area in the midportion of the Achilles tendon and images showing corresponding
changes in the tendon is commonly named chronic Achilles tendinosis [5,18].
Fig. 1. A localized swelling at the 2 6 cm level (from the calcaneal insertion) in the Achilles tendon
is shown.
729
The primary aim of this article is to review recent research on painful chronic
midportion Achilles tendinosis, and its implications on nonoperative and operative treatment.
Terminology
Painful conditions in the Achilles tendon have been given many names, and the
definition of the same condition is often different in different studies. The
nomenclature for the chronic painful condition often does not reflect the pathology
of the tendon disorder [5], making it difficult to evaluate scientific articles and to
compare the results of different treatment regimens. Quite often, the terms
tendinitis and tendonitis are used [19 22], despite the absence of scientific
evidence demonstrating chemical inflammation. The term chronic tendinopathy
is often used for patients with a long duration of a painful condition located in the
Achilles tendon region [5,17,18]. That term only indicates a condition with pain,
however, and says nothing about its character. Puddu et al have suggested the term
tendinosis to be used for local degenerative changes in the Achilles tendon [23].
The term degenerative, however, does not have a standard description,
but is associated with a variety of histological entities, such as: hypoxic degeneration, mucoid or myxoid degeneration, hyaline degeneration, fatty degeneration,
fibrinoid degeneration, fibrocartilaginous metaplasia, bony metaplasia, calcification, abnormal tendon structure, nodular thickening, irregular fiber structure, poor
fiber orientation, grayish discoloration of ground substance and tendon edema,
focal hypercellularity, vascular proliferation in the tendon, or different combinations of these entities [4,19,21,23 26]. Recently, the characteristic morphological
features of tendinosis were demonstrated to be changes in the collagen fiber
structure and arrangement, and an increased amount of interfibrillar glycosaminoglycans (GAGs) [5].
In summary, I suggest that the term chronic tendinopathy be used when
discussing chronic painful conditions in the midportion of the Achilles tendon. If
the following examination (ultrasound, MRI, or possibly biopsy) shows tendon
changes corresponding to the painful area in the tendon, the condition could be
defined as chronic Achilles tendinosis.
Recent research on pathogenesis

It is well known that in vivo investigations of metabolic events in human
tendons are difficult to perform, and therefore, there is relatively sparse knowledge
about the normal and injured tendon. In situ microdialysis has been shown to be a
useful technique to study metabolism of substances in different types of human
tissue [27,28], but the method had, to our knowledge, never before been used in
human tendon tissue. The microdialysis technique allows continuous measurements of concentrations in vivo of substances with molecular size below the cutoff
730
limit (20 kD) of the dialysis membrane. Therefore, it was of interest to investigate
whether the microdialysis technique could be used to study certain metabolic
events in the Achilles tendon. In patients with chronic painful conditions in the
Achilles tendon, it has been commonly believed that there is involvement of an
inflammatory reaction, despite the absence of inflammatory cell infiltration in
tendon biopsies [1,22,29,30]. Prostaglandins are well known to play a central role
in inflammatory reactions [31], and treatment is often focused on medication with
prostaglandin antagonists. In recent years, however, the role of inflammation in this
condition is being questioned. Therefore, we decided to study the concentrations of
PGE2, which is well known to be involved in chemical inflammation, in tendinosis
and normal Achilles tendons. We also decided to investigate whether the excitatory
neurotransmitter glutamate, known to be a potent and very important painmodulator in the central nervous system [32] but never identified in human
tendons, could be found in the Achilles tendon. Recently, for the first time,
glutamate receptors have been found in human peripheral tissue (bone) [33]. Here,
we describe what is to our knowledge the first experiment using the microdialysis
technique to detect and study the local concentrations of PGE2 and glutamate in
human tendons (patients with painful midportion chronic Achilles tendinosis and
normal pain-free Achilles tendons) [34]. A microdialysis catheter (CMA 60 CMA/
Microdialysis AB, Stockholm) with a diameter of 1.4 mm and a 30 mm length of
the membranous covered active part was introduced into the tendon under visual
control through a small skin incision (Fig. 2), and placed longitudinally and parallel
to the tendon fibers into the area of tendon changes/tendinosis, and into the central
part of the tendon in the controls. The microdialysis pump has a fixed infusion rate
of 0.3mL/min (Ringer solution), and samples were taken every 15 minutes during a
4-hour period. Prostaglandin E2 was analyzed using RIA technique, and glutamate
was analyzed with HPLC technique. In four patients (mean age 40.7 years) with
chronic symptoms from a painful nodular thickening in the Achilles tendon
corresponding to tendon changes on ultrasonography, and in five controls (mean
age 37.2 years) with normal Achilles tendons (verified by ultrasonography), the
local concentrations of glutamate and prostaglandin E2 (PGE2) were registered
during 4 hours under resting conditions. The results showed that there were
no significant differences in the mean concentrations of PGE2 (83 22 versus
54 24 pg/mL) between tendons with tendinosis and normal tendons. Surprisingly,
Fig. 2. A microdialysis catheter placed in the Achilles tendon through a 1 cm-long skin incision.
731
glutamate was found in the Achilles tendons, and there were significantly higher
concentrations of glutamate in tendons with tendinosis compared with normal
tendons (35 6 versus 9 0.8 mmol/L [mean SD], P < 0.05). There were no
significant changes of the glutamate concentration over the time of investigation.
The finding of the excitatory neurotransmitter glutamate in a human tendon has
never before been reported. In recent years, the importance of glutamate as a
mediator of pain in the human central nervous system has been emphasized [32],
and from animal studies, it is known that glutamate receptors, including the
ionotrophic glutamate receptor N-metyl-D-aspartate (NMDA), are present in
unmyelinated and myelinated sensory axons [35]. Furthermore, peripherally
administered NMDA and non-NMDA glutamate receptor antagonists have been
demonstrated to diminish the response to formalin-induced nociception in the rat
[36]. In conclusion, the microdialysis technique can be used for in vivo studies in
the human Achilles tendon, and the results showed that there were no signs of
chemical inflammation (normal PGE2 levels), but that there were high levels of the
excitatory neurotransmitter glutamate in tendons from patients with chronic painful
Achilles tendinosis. These results further underline that there is no chemical
inflammation involved in the chronic stage of this condition. There might well
be a so-called neurogenic inflammation, however, involving neuropeptides like
substance P and calcitonin gene related peptide (CGRP), among others. The
possibility of using the microdialysis technique to study metabolic events in
tendons is an interesting field for future research.
In a follow-up study, immunohistochemical analyses and enzyme histochemistry were used to investigate the occurrence of glutamate NMDA-receptors
in Achilles tendon tissue [37]. The results showed, for the first time, the occurrence of glutamate NMDAR1-receptors in Achilles tendon tissue. Furthermore,
the NMDAR1-immunoreaction was confined to acetylcholinesterase-positive
structures, implying that the receptors were localized in association with
nerve structures.
Recently, the microdialysis technique was used to study the concentrations of
lactate in Achilles tendons with painful midportion tendinosis, and in normal
pain-free tendons. The results showed that the tendons with tendinosis had
significantly higher concentrations of lactate compared with the normal tendons
[38]. The findings indicate that there might be anaerobic conditions, expressed as
higher lactate levels, in tendons with painful tendinosis. Whether ischemia
precedes the start of tendinosis, or the tendinotic tendon changes cause ischaemia,
has yet to be investigated, however.
Another possibility for studying possible differences between Achilles tendons
with painful tendinosis and normal pain-free tendons, is to use ultrasonography and
color Doppler. On a study of consecutive patients with painful midportion Achilles
tendinosis, the results showed that in 28 consecutive tendons with painful
tendinosis, but not in any of the normal pain-free tendons, there was a neovascularisation outside and inside the ventral part of the area with tendon changes
[39]. These findings might have implications for the pathogenesis of chronic
painful midportion Achilles tendinosis.
732
The rapidly growing area of gene technology has created possibilities for
studying the expression of genes involved in pathological and normal conditions
in different tissues. The cDNA-array technique allows for studies of a large amount
of gene expressions, and by also using real-time PCR technique, more precise
measurements of mRNA expression levels can be done. Ireland et al. have found a
down-regulation of matrix-metallo-proteinase-3 (MMP-3) and an upregulation of
Type I and Type III collagen, in tendons from patients with chronic Achilles
tendinopathy compared with normal tendons from autopsies [40]. Very recently, in
a study in which tendinosis tissue was compared with control tissue from the same
Achilles tendon, we found an upregulation of MMP-2 (destructive enzyme), FNRB
(fibronectin receptor involved in healing processes), and VEGF (vascular endotelial growth factor), in painful tendinosis tissue [41]. The findings indicate the
presence of concomitantly ongoing destructive and healing processes. Also, in our
study, there was no major regulation of the genes for a variety of different cytokines
known to be involved in inflammatory processes. This finding further support the
view that there is no inflammation in the chronic stage of Achilles tendinosis.
Although there are some difficulties that need to be taken into account, these
new techniques will most likely be very useful in future research.
Treatment
A chronic painful condition in the Achilles tendon is associated with a huge
variety of proposed treatment regimens. It is important to know that there is
sparse scientific evidence for most of the conservative and surgical treatments
proposed and used. The few scientific prospective studies, and the absence of
studies comparing different types of conservative and surgical treatment regimens
in a randomized manner, are major disadvantages when evaluating the effects of
specific treatment regimens.
Nonoperative treatment
A nonoperative (conservative) treatment regimen is recommended as the
initial strategy by most authors [1,2,4,6,8 10,18,42,43]. This strategy includes
identification and correction of possible etiological factors, and also a symptomrelated approach.
Biomechanical abnormalities [8,9,11,44,45], training errors [8,11,46,47],
muscle weakness [2,4,48 50], decreased flexibility [2,4,8,9,45,51,52], and poor
equipment [42,46,53] have all been proposed as possible etiological factors. But
again, it is important to know that these proposals rest on poor scientific grounds,
and are to be characterized as unproven theories.
Nonsteroidal anti-inflammatory drugs (NSAIDs) are most often used as one
part of the initial treatment [8,9,11,22,29,54 57], despite the absence of scientific
evidence for an ongoing chemical inflammation [18,26,34,41]. Consequently,
with the latest research findings in mind, the use of NSAIDs with the purpose of
733
diminishing chemical inflammation in chronic painful Achilles tendinopathy cannot be justified. This was already indicated in a randomized, double-blind,
placebo-controlled study consisting of 70 patients with chronic painful Achilles
tendinopathy, where it was demonstrated that oral medication with piroxicam
gave similar results as placebo [58].
The use of corticosteroid injections is controversial [4,29,30], and there are
many different opinions on this type of treatment. Several authors have found frequent partial ruptures after steroid injections in the treatment of chronic painful
conditions in the Achilles tendon [7,12,24,29,59], and treatment with steroid
injections in patients with chronic Achilles tendinopathy has been shown to predict
a partial rupture [7]. Also, in a relatively large group of patients surgically treated
for chronic Achilles tendon pain, 42% of the patients had previously been treated
with corticosteroid injections, indicating a poor effect of steroids on this condition [52].
So-called treatment modalities like cold therapy [9], heat [60], massage [61],
ultrasound [62], electrical stimulation [63], and laser therapy,[64] are often
included in the treatment. These treatment modalities have all been suggested to
be effective, but there are, to my knowledge, no scientific clinical studies that
confirm their effects.
Most commonly the initial treatment consists of a multioriented approach,
including combined rehabilitation models. There are many different designs of
combined rehabilitation models; most often they include a combination of rest
(complete or modified), medication (NSAIDs, corticosteroids), orthotic treatment
(heel lift, change of shoes, corrections of malalignments), stretching and massage,
and strength training [2,4,8,9,11,12,43].
Recent research on nonoperative treatment
As early as 1984 Curwin and Stanish stressed the importance of eccentric
training as a part of the rehabilitation of tendon injuries [2]. Influenced by their
theories, my colleagues and I designed a special type of eccentric calf muscle
training regimen to be used on a well-defined diagnosis. We decided to study
patients with chronic painful midportion Achilles tendinosis, as the midportion of
the Achilles tendon is an area that can be relatively easily examined clinically and
visualized with ultrasound or MRI. First, in a prospective pilot study on
recreational athletes, we reported good clinical results with treatment consisting
of heavy-load eccentric calf-muscle training [42]. All 15 patients in that study had
localized changes in the tendon (at the 2 cm to 6 cm level from the insertion into
the calcaneus) corresponding to the painful area (verified with ultrasonography).
In all patients the conventional treatment (rest, NSAIDs, change of shoes,
orthoses, physical therapy, ordinary training programs) had been tried without
any effect on the Achilles tendon pain, and all patients were on the waiting list for
surgical treatment. The patients performed their eccentric exercises (Fig. 3A C)
3 15 repetitions, 2 times daily, 7 days a week, for 12 weeks. It needs to be
mentioned that this type of tendon loading is painful, and the patients were told to
734
Fig. 3. From an upright body position and standing with all body weight on the ventral half-part of the
foot, with the ankle joint in plantar flexion lifted by the noninjured leg, the calf-muscle is loaded
eccentrically by having the patient lower the heel beneath the lever. Eccentric calf-muscle loading with
the knee straight (A) and to maximize the activation of the soleus muscle, eccentric calf-muscle
loading with the knee bent (B). When the exercises can be done without experiencing pain in the
tendon, the load should be increased to reach a new level of painful training, by using a back-pack
that is gradually filled with weights, or a by using a weight machine (C).
continue their exercises despite experiencing pain or discomfort from the tendon.
In fact, the exercises were supposed to be painful, and when there was no tendon
pain during exercise, the load was gradually increased to reach a new level of
painful training. The results showed that after the 12-week training regimen, all
15 patients were satisfied and back to their previous (before injury) activity level.
No patient was operated on. The pain score (VAS scale) during activity (running)
decreased from an average of 81.2 before eccentric training regimen, to 4.8 after
training. We have now followed this group of patients for 4 years or more
(unpublished data), and in only 1 patient has surgical treatment been needed due
to the recurrence of Achilles tendon pain. All the other 14 patients are still
satisfied with the result of treatment. At our clinic, we now routinely treat all
patients with the diagnosis of chronic Achilles tendinosis (at the 2 cm to 6 cm
level) with this type of painful training, and of the last 100 consecutive tendons,
only 10 tendons have needed surgical treatment (unpublished data).
735
Fig. 3 (continued).
In addition, to find out if treatment with painful concentric calf-muscle training

could also give a good clinical result, we performed a randomized prospective
multicenter study in which patients with painful chronic Achilles tendinosis at the
2 cm to 6 cm level in the tendon were randomized to either concentric or eccentric
training [65]. The eccentric training program was the same as previously described
[42], whereas the concentric training program was designed to include exercises
containing mainly concentric calf-muscle action. For both programs, training was
encouraged despite experiencing pain or discomfort in the tendon. The results
showed that the eccentric training regimen produced significantly better clinical
results (81% of patients satisfied and back to previous activity level) than the
concentric training regimen (38% satisfied patients) [65].
We cannot yet explain the basis for the good clinical results achieved with
painful eccentric calf-muscle training. Theoretically there are several possible
explanations. The results could be effects of loading-induced hypertrophy and
increased tensile strength in the tendon, or perhaps an effect of stretching, with a
lengthening of the muscle-tendon unit and consequently less strain during ankle
joint motion. Also, the eccentric training regimen is painful to perform, and
maybe this type of painful loading is associated with some kind of alteration of
pain perception from the tendon. In a study using ultrasonography and color Doppler, we have recently demonstrated that in Achilles tendons with chronic pain-
736
Fig. 3 (continued).
ful tendinosis, but not in normal pain-free tendons, there is a neovascularisation

(Fig. 4) outside and inside the ventral part of the area with tendon changes [39].
By using ultrasonography and color Doppler during eccentric calf-muscle
contraction, we observed that the flow in the neovessels disappeared in the
position with the ankle joint in dorsiflexion. These observations raised the questions of whether the good clinical effects demonstrated with eccentric training
could be due to action on the neovessels, and whether the neovessels and accompanying nerves were the main source of pain. In a following experiment, we
injected local anesthesia into the area with neovessels outside the tendon. This
resulted in a pain-free tendon; the patients could load their Achilles tendon
without experiencing any pain from the tendon. These findings, taken together,
raised the hypothesis that the neovessels and accompanying nerves were responsible for the pain in the area with tendinosis. To test this hypothesis, in a
noncontrolled pilot study we injected a sclerosing agent in the area with neovessels on the ventral side of the tendon. The short-term (6 months) results were
very promising, and 8 out of 10 patients were pain-free and satisfied with treatment after a mean of two treatments (injections) [66]. At follow-up, in the successfully treated patients there were no neovessels outside or inside the tendon,
737
Fig. 4. Gray-scale ultrasonography and color Doppler examination (a longitudinal view) of an Achilles
tendon with tendinosis located at the 2 6 cm level in the tendon. The affected area of the tendon is
thick, irregular and echo poor. There is a neovascularization outside and inside the ventral part of the
area with tendon changes.
but in the two unsuccessfully treated patients there were remaining neovessels.
The results of this new type of treatment are promising, but longer follow-ups and
randomized controlled studies are needed for further evaluation.
Operative treatment
Chronic painful tendon conditions are in general considered difficult injuries
to treat. It has been a general opinion that in about 25% of patients with chronic
painful conditions located in the Achilles tendon, nonsurgical treatment is not
successful and surgical treatment is needed [1]. Frequency of surgery has been
shown to increase with patient age, duration of symptoms, and occurrence of
tendinopathic changes [1].
Varying surgical techniques are being used. Most commonly, a straight
longitudinal skin incision [19,21,25,59,67 71] is used to identify the affected
part of the tendon. Next, the paratenon is incised, macroscopically hypertrophic
parts of the paratenon are excised, [19,21,24,25,68 71], and through a central
longitudinal tenotomy the tendon area with tendinosis is visualized and the
macroscopic abnormal tissue is excised [19,21,25,29,59,67 72]. Promising
clinical results have also been achieved using a method consisting of percutaneous longitudinal tenotomy [73]. The surgical technique used in that method is
described as the performance of multiple longitudinal incisions in the area of
maximum tendon-swelling (checked by ultrasonography). The authors suggest
that the effect achieved with multiple longitudinal incisions in the tendon is an
improvement of the local circulation, and thereby a return to a normal biochemistry in the tendon.
Postoperative rehabilitation
The methods used for rehabilitation after surgery to the Achilles tendon are
varying, and unfortunately, there is often sparse information in the descriptions of
738
the methods being used. At our clinic, we have closely followed all surgically
treated patients during the period of postoperative rehabilitation, and particularly
investigated the time it takes to recover calf-muscle strength and to get back to
previous (before injury) activity level. In two prospective studies [68,69], we
demonstrated that despite the patients undergoing a supervised stepwise training
program increasing flexibility and strength (concentric and eccentric) during the
first year postoperatively, it took a long time to recover both concentric and
eccentric calf muscle strength on the injured side. The injured side was
significantly weaker compared with the noninjured side for 6 to 12 months
postoperatively. There was no obvious advantage in recovery of muscle strength
with a shorter immobilization time (2 weeks) [69] versus a longer (6 weeks) [68]
period. Furthermore, in another prospective study, we demonstrated that there
was a prolonged progressive calcaneal bone loss on the operated side in patients
surgically treated for chronic Achilles tendinosis [74]. Around the time when the
patients were pain free and returned to their sports (6 to 12 months), the calcaneus
had a relatively low bone mass (16% to 18% lower on the injured side). During
that period (6 to 12 months postoperatively) the calcaneus might possibly be
vulnerable to heavy loads. There were no signs, however, of a permanent
decrease in bone mass (no side-to-side differences in bone mass of the calcaneus
2 years after surgery).
The short-term results after surgical treatment of chronic Achilles tendinosis
have in general been reported to be good in 70% to 100% of patients. It needs to
be emphasized, however, that there are few prospective studies on well-defined
groups of patients and very few studies with long-term follow-ups. The basis of
the relatively good results after surgical treatment is unknown, but the most stated
theory is that the revision of the tendon improves the local circulation and creates
better possibilities for tissue repair. At our clinic, we have followed our operated
patients with repeated ultrasonography examinations. We have found that the
tendon changes demonstrated with ultrasonography postoperatively are most
often more pronounced than the tendon changes demonstrated before operation
(unpublished data). These findings have led us to propose that the good effect of
surgical treatment might be due to a denervation caused by the often extensive
revision of the tendon.
Summary
Chronic painful midportion Achilles tendinosis has been known as a difficult condition to treat, and surgical treatment was often needed. In recent scientific studies, however, treatment with painful eccentric calf muscle training has
shown very good short-term clinical results and significantly reduced the need
for surgical treatment. Also, very recently, a new method consisting of sclerosing of neovessels in the area with painful tendinosis showed promising shortterm results. Ongoing and future research will evaluate the potential of these
treatment models.
739
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Clin Sports Med 22 (2003) 743 759
Patellar tendinopathy
Stuart J. Warden, BPhysio (Hons), PhDa,b,
Peter Brukner, MBBS, FACSPa,*
a
Centre for Sports Medicine Research and Education, The University of Melbourne,
Victoria 3010, Australia
b
Department of Orthopedic Surgery, Indiana University School of Medicine, 1120 South Drive,
Indianapolis, IN 46202-5114, USA
Patellar tendinopathy is a common and significant syndrome encountered in

sports medicine. Referring to a clinical condition characterized by activity-related,
anterior knee pain associated with focal patellar-tendon tenderness [1 3], patellar
tendinopathy is believed to result from repeated loading of the knee extensor
mechanism, and is thus most prevalent in sports involving some form of jumping
[4]. In recognition of this association with jumping, patellar tendinopathy was first
described as and is commonly referred to as jumpers knee [4 8]. This term is
misleading, however, as the condition is found in a wide variety of sports people,
including those who do not participate in sports involving jumping [4,9 11].
Another traditionally popular term to describe the clinical condition is patellar
tendinitis. Histopathological studies, however, have consistently shown the
pathology underlying patellar tendinopathy to be degenerative rather than inflammatory [10,12 14]; thus, the suffix -itis, implying the presence of inflammation, is
inaccurate. To describe the histopathological presentation of the condition the term
tendinosis is preferred [2,3,10]. This distinction is important, as the correct
labeling and understanding of the pathology has repercussions for management and
the outcome expectations of both the clinician and athlete [2].
To clarify the terminology surrounding the syndrome, it has been advocated that
the term patellar tendinopathy be used clinically to describe overuse conditions of
the patellar tendon [1 3]. Alternative terms such as tendinosis and tendinitis
should only be applied following pathologist examination of tissue biopsies, as
these refer to distinct histopathological conditions that cannot be assessed clinically. In line with these recommendations, the term patellar tendinopathy is used in
Dr. S.J. Warden is supported by a National Health and Medical Research Council (Australia) CJ
Martin Fellowship (Regkey no. 209169).
E-mail address: p.brukner@unimelb.edu.au (P. Brukner).
doi:10.1016/S0278-5919(03)00068-1
744
S.J. Warden, P. Brukner / Clin Sports Med 22 (2003) 743759
the following discussion, which overviews current understanding of the pathology,

pathophysiology, and pathogenesis of patellar tendinopathy, and discusses aspects
of its clinical examination, imaging, and management.
Pathology and pathophysiology

The predominant pathological feature of patellar tendinopathy is tendinosis,
typically in the deep posterior portion of the patellar tendon adjacent to the lower
pole of the patella [13]. Tendinosis is characterized by progressive tissue degeneration with a failed reparative response and the complete absence of inflammatory
cells [10,12,14]. Macroscopically, this makes the afflicted region of the tendon soft
and gives it a yellow-brown, disorganized appearancean appearance that is
commonly labeled mucoid degeneration [15 18]. This contrasts with the
normal appearance of a glistening, stringy, parallel-organized, white tendon.
When viewed microscopically, the pathological region is distinct from normal
tendon, with both matrix and cellular changes. Instead of clearly defined, parallel,
and slightly wavy collagen bundles, tendinopathy is associated with relative
expansion of the tendinous tissue, loss of the longitudinal alignment of collagen
fibers, and loss of the clear demarcation between adjacent collagen bundles [4,10,
12 14,19]. The tissue has lost its normal reflective appearance under polarized
light, and there is gradual and increasing separation of collagen fibers that distorts
the normally dense homogenous polarization pattern [4,10]. Occasional clefts in
the collagen suggest microtears that may be interpreted as microscopic partial
ruptures [20]. In addition, there are frequently focal regions of intratendinous
calcification [10,21 24]. The latter may arise due to traction injury to the inferior
pole of the patella [10,24]; however, recent evidence has shown the calcification to
have formed discretely via endochondral ossification [21].
Multiple cellular changes coexist with the matrix changes in tendinopathy. The
most obvious of these changes is hypercellularity resulting from an increase in
cellular proliferation [25]. There is atypical fibroblast and endothelial cellular
proliferation [12,19,26], and extensive neovascularization [10,14,19,22,27].
These changes represent an attempt at healing. The collagen-producing tenocytes
lose their fine spindle shape, and their nuclei appear more rounded and
sometimes chondroid in appearance, indicating fibrocartilaginous metaplasia
[13]. Of note is the consistent finding of a clear absence of inflammatory cells
[4,10,12,14].
Despite the absence of inflammatory cells in patellar tendinopathy, mediators in
the inflammatory cascade appear to be involved in its pathophysiology. Of
particular note is the involvement of cyclooxygenase-2 (COX-2). COX-2 is an
inducible enzyme that rate-limits the production of proinflammatory prostaglandins, such as PGE2. In tendons harvested from patients with patellar tendinopathy,
both the tendon tissue itself and harvested cells expressed higher levels of COX-2
than healthy control patellar tendons [12]. In addition, the harvested cells produced
greater in-vitro quantities of PGE2 [12], although this has yet to be confirmed in
745
vivo [28]. The potential involvement of inflammatory pathways in patellar

tendinopathy has implications with regard to the use of anti-inflammatory agents
in its management (discussed later).
Pathogenesis
To prevent patellar tendinopathy and to develop appropriate treatment strategies
when it does occur, an understanding of the pathogenesis is required. Unfortunately, the precise mechanism by which patellar tendinopathy develops is currently
unknown. As with most overuse conditions, the development of patellar tendinopathy is likely to be due to a range of factors, with the relative contribution of each
factor varying among individuals. These factors can be grouped into two categories: extrinsic and intrinsic.
Extrinsic factors are the most commonly indicted in the pathogenesis of patellar
tendinopathy, with the most frequently reported causative factor being mechanical
overload. For patellar tendinopathy to develop, repeated heavy loading of the
tendon is required [6,29]. This explains its prevalence in sports involving some
form of jumping, such as basketball and volleyball. In volleyball, a direct relationship exists between the number of training sessions (number of jumps) and the
development of patellar tendinopathy [6].
As the characteristic lesion in patellar tendinopathy typically occurs in the deep
posterior portion of the patellar tendon adjacent to the lower pole of the patella, it
has been hypothesized that loading exposes this region to the most strain. This
hypothesis has contrasting evidence, with two cadaver studies reporting opposing
results [30,31]. One found greater strain in the anterior portion of the tendon [30],
whereas the other reported greater strains in the posterior portion [31]. Although the
latter study did find evidence to support the hypothesis of greater strains in the
posterior portion of the tendon, the authors also found the posterior portion of
the patellar tendon to be more adapted to loading, as evident by its enhanced
mechanical properties. Thus, it is not clear whether patellar tendinopathy is purely a
strain-related phenomenon.
Although extrinsic factors may be the most consistent causative factor in the
development of tendinopathy, the development of patellar tendinopathy in some
athletes while others with equivalent loading are spared signals that intrinsic factors
must also contribute. Johnson et al [32] hypothesized that impingement of the
inferior pole of the patella onto the tendon may contribute to the pathogenesis. This
is supported by the findings of altered patella anteroposterior tilt [33] and a long
inferior pole [18,34] in many knees with tendinopathy. Recent research, however,
found no difference between symptomatic and asymptomatic knees in terms of the
tendon-patella angle during flexion, suggesting that impingement is not an
important contributing factor [35]. The long inferior pole found in some symptomatic athletes may merely represent a traction osteophyte caused by repeated
high-tensile forces in this area [34], and may not have been a pre-existing
contributory abnormality.
746
Other intrinsic factors that have been postulated as causes of patellar tendinopathy include malalignment, patella alta, abnormal patellar laxity, and muscular
tightness and imbalance [36]. Of these, only muscle tightness has prospectively
been shown to be a predisposing factor. In particular, Witvrouw et al [36] found
decreased flexibility of the quadriceps and hamstring muscles to be significantly
associated with the subsequent development of patellar tendinopathy.
How extrinsic and intrinsic factors combine to trigger the generation of patellar
tendinopathy is not established. It is possible that the pathological changes are
initially triggered by matrix changes. Heavy loading may cause tensile failure of
tendon fibers, resulting in microdamage. When this occurs, tenocytes must increase
their production of collagen and matrix. This is a slow process, however, due to the
inherently slow turnover rate of collagen. With further loading, an area of
tendinosis may develop due to progressive microdamage and subsequent failed
healing attempts.
An alternative to matrix-mediated changes is the possibility of cellular-triggered
pathological changes. Recent research has shown a direct relationship between the
amount of stress that tendon cells are exposed to and the induction of a stressactivated protein kinase, c-Jun N-terminal kinase (JNK) [37]. Although transient
activation of JNK is associated with normal cell processes, persistent JNK
activation has been linked to the initiation of programmed cell death or apoptosis.
Although yet to be shown in patellar tendinopathy, increased cellular apoptosis has
been shown in supraspinatus tendons with tendinosis [38].
History and clinical examination

A solid history and clinical examination are cornerstones to the diagnosis of
patellar tendinopathy. Patellar tendinopathy presents subjectively as well-localized
anterior knee pain related to activity levels [5,39]. Pain is usually insidious and
gradual in onset, and may be precipitated by an increase in the frequency or
intensity of repetitive ballistic movements of the knee. Initially pain may present as
a dull ache at the beginning of or after strenuous activity. This initial symptom may
be ignored as it warms up with further activity [40]. With continued use, however,
pain can progress to be present during activity and can ultimately interfere
significantly with performance. In some cases there is a constant ache at rest and
night pain that disturbs sleep [10,27,34]. Other common complaints are pain when
seated for long periods, and when ascending and descending stairs [29].
On clinical examination, the most consistent finding is patellar tendon tenderness [29,41]. This is typically located at the inferior pole of the patella; however, it
is influenced by knee position [42]. With the knee flexed to 90 the tendon is placed
under tension, and tenderness significantly decreases and may disappear altogether.
Thus, the patellar tendon should be palpated in relaxed full-knee extension.
Pressure on the superior border of the patella should be applied to tilt the inferior
pole anteriorly, enabling palpation of the tendon origin. Using this method, pain on
palpation can reliably be graded as either mild, moderate, or severe [43]. Undue
747
significance should not be attached to mild pain in isolation of other signs and
symptoms of patellar tendinopathy, as it may be a normal finding in active athletes
[43,44].
In addition to palpation, other features to note on clinical examination are
muscle size and functional strength. Patients with chronic symptoms may exhibit
wasting of the quadriceps, with the vastus medialis obliquus portion most
commonly affected. Overall thigh circumference may be reduced and calf atrophy
may also be present. Functional strength testing of the quadriceps may be
performed by asking the patient to perform 15 one-legged step-downs in which
the non-weight bearing foot is not allowed to touch the ground between cycles
[45]. The work capacity of the calf can be assessed by performing single-legged
heel raises. A jumping athlete should be able to perform a minimum of 40 raises
[45]. During both activities the onset of fatigue and the quality of movement should
be monitored, and both activities should be performed bilaterally.
To reproduce symptoms of patellar tendinopathy a useful functional test is the
decline (30) squat test. This places greater load on the patellar tendon than does a
squat on level ground [45]. Objective measurement during this test can obtained by
determining the number of decline squats before the onset of pain, and by asking
the athlete to indicate the level of pain on a visual analog or verbal reporting scale.
An alternative method of objectively assessing an athlete with patellar tendinopathy is to implement the Victorian Institute of Sport Assessment (VISA) scale
[46]. This scale provides a numerical index of the severity of patellar tendinopathy
by assessing both symptoms and function. A maximum score of 100 indicates full,
pain-free function.
The key differential diagnosis in patellar tendinopathy is patellofemoral pain
syndrome. This is usually straightforward to differentiate, as the subjective and
objective features of patellar tendinopathy are generally distinctive. In some
cases, however, differential diagnosis may be difficult and the two conditions
may coexist. One method to aid differentiation is to perform functional testing
(ie, decline squat test) with and without the use of taping to influence the
patellofemoral joint. At least, this may indicate whether the patellofemoral joint
should also be treated.
In addition to patellofemoral pain syndrome, patellar tendinopathy needs to be
differentiated from fat-pad syndromes, and assessment of other potential coexisting conditions such as meniscal tears and cartilage degeneration may need to
be considered where indicated [22]. Also, the potential of pain referral to the knee
should not be ignored [47].
Imaging
Imaging can be used to confirm the clinical diagnosis of patellar tendinopathy
with the techniques of choice being ultrasonography and magnetic resonance
imaging (MRI). Both provide excellent anatomic representation of the patellar
tendon, and histopathologic studies have shown that the characteristic tendino-
748
pathy appearances observed with both forms of imaging are due to the underlying
tendon pathology [10,14,19,26,48,49].
Ultrasonography
Ultrasonography provides a readily available, quick, and inexpensive method of
imaging the patellar tendon. The tendon is readily examined using high-frequency
linear array transducers with the knee flexed or semiflexed, and by obtaining both
longitudinal and transverse images [50]. In suspected cases of patellar tendinopathy, ultrasonography can be used to confirm the existence and location of
intratendinous lesions. These lesions are reflected by decreased echogenicity,
evident by either diffuse hypoechogenicity or a focal sonolucent region, typically
in the deep posterior portion of the tendon adjacent to the lower pole of the patella
[8,10,27,39,50 55] (Fig. 1). The decrease in echogenicity represents a decrease in
the ultrasound attenuative properties of the tendon, resulting from the disruption of
the collagen bundles. Other common findings on ultrasonography include tendon
thickening [8,24,27,44,53,56], irregularity of the tendinous envelope [8,53],
intratendinous calcification [8,24,44,51,57,58], and erosion of the patellar tip
[8]. The primary disadvantages of ultrasonography are its operator-dependency
and somewhat limited soft-tissue contrast [40].
Magnetic resonance imaging
MRI provides high spatial resolution that allows detailed anatomic structures to
be identified, and it provides high intrinsic tissue contrast that allows normal
tendons to be distinguished from abnormal tendons. On MRI, patellar tendinopathy
is characterized by a focal increase in signal within the tendon as well as an
alteration in its size [14,19,26,27,32,34,59,60]. The later is necessary with some
sequences, as the magic angle phenomenon associated with MRI can artificially
increase signal intensity, resulting in false-positive findings [61 63]. El-Khoury
Fig. 1. Ultrasound appearance of patellar tendinopathy. On the left side of the figure, the right tendon
shows a large area of decreased echogenicity (blackened area) associated with tendon thickening. On
the right side, the left tendon shows a normal appearance of the patellar tendon.
749
et al [59] suggest an anteroposterior diameter cutoff point of 7 mm between

symptomatic and asymptomatic tendons; however, more recent authors have
shown considerable overlap and variation in tendon thickness [34,64,65]. The
primary disadvantages of MRI are its relatively high cost, limited availability in
some regions, and lengthy time for scanning.
Limitations of imaging
Although both ultrasonography and MRI are useful in imaging patellar
tendinopathy, neither can be labeled as the gold standard for its diagnosis. Positive
ultrasonography and MRI images for patellar tendinopathy have been shown in
asymptomatic tendons [10,39,44,51,58,60,65 69]. Similarly, symptomatic tendons can have the imaging appearance of normal asymptomatic tendons
[32,39,43,44,54,69]. Using currently available data, the sensitivity and specificity
of ultrasonography can be calculated at 58% and 94%, respectively (Table 1). For
MRI, the sensitivity and specificity can be calculated at 78% and 86%, respectively
(Table 2). Thus, although ultrasonography and MRI may accurately reflect tendon
morphology, the imaging appearance may not necessarily reflect clinical symptoms. Further confirming this, numerous authors have shown no correlation
between the severity of tendinopathy symptoms on clinical grading systems and
tendon appearance on ultrasonography [44,57,68].
Table 1
Results of ultrasonography assessment in symptomatic and asymptomatic patellar tendons
Total tendons
Cook et al [4]
Cook et al [39]
Cook et al [58]
Cook et al [66]
Davies et al [27]
Fredberg and Bolvig [67]
Fritschy and de Gautard [8]
Khan et al [10]
Khan et al [70]
Lian et al [44]
Myllymaki et al [54]
Panni et al [68]
Terslev et al [69]
Summary
Symptomatic tendons
Asymptomatic tendons
Total
Total
+/
57
176
374
46
16
98
47
63
23
81
62
84
18
57
19
0
0
16
3
32
28
8
30
62
46
4
57
15
0
4
13
3
32
28
8
23
31
46
3
0
0
0
0
0
7
31
0
1
1145
305
259
43
Calculations
Sensitivity = 58%
Specificity = 94%
Positive predictive value (PV+) = 86%
Negative predictive value (PV ) = 77%
Abbreviations: +, positive ultrasonography finding;
unequivocal ultrasonography finding; nr, not reported.
0
157
374
46
0
95
15
35
15
51
0
38
14
840
+/
34
71
18
123
303
28
15
nr
6
8
12
80
nr
29
7
39
14
12
24
2
190
635
, negative ultrasonography finding; +/
750
Table 2
Results of MRI assessment in symptomatic and asymptomatic patellar tendons
Total tendons
Davies et al [27]
Johnson et al [32]
Khan et al [10]
Major and Helms [60]
McLoughlin et al [64]
Popp et al [19]
Schmid et al [35]
Shalaby and Almekinders [34]
Yu et al [14]
Summary
Symptomatic tendons
Asymptomatic tendons
Total
+/
Total
0
14
35
34
0
0
32
17
0
16
38
63
34
15
11
51
29
11
16
24
28
0
15
11
19
12
11
14
19
28
0
5
0
15
11
18
7
11
0
0
1
3
0
252
120
109
Calculations
Sensitivity = 78%
Specificity = 86%
Positive predictive value (PV+) = 93%
Negative predictive value (PV ) = 61%
Abbreviations: +, positive ultrasonography finding;
unequivocal ultrasonography finding; nr, not reported.
2
2
132
+/
0
nr
8
14
nr
26
23
4
9
5
35
54
, negative ultrasonography finding; +/ ,
In addition to being unable to reflect clinical symptoms, ultrasonographic and

MRI appearances cannot be used to distinguish outcome following intervention for
tendinopathy. Ultrasound images remain both qualitatively and quantitatively
abnormal 12 months after surgery, even in athletes who have returned pain-free
to full competition [24]. With longer follow-up after surgery, no correlation exists
between the area of the hypoechoic region and either function or time after surgery
[57]. In terms of MRI, tendon appearance does not return to normal after successful
surgery, and thus it is not able to distinguish patients whose surgical outcome was
excellent from those whose outcome was poor [24]. Consequently, imaging does
not appear to have a major role to play in monitoring outcomes following
intervention for tendinopathy.
As tendons can have asymptomatic lesions on imaging, and these lesions in
symptomatic tendons have been shown to be an area of histological degeneration, it
is reasonable to question whether imaging can be used to predict future prognosis.
At this stage this is not completely clear, although based on current longitudinal
data using ultrasonography a trend does appear (Table 3). In one study, a 4.2 times
greater risk of developing symptoms was identified in asymptomatic tendons with
imaging abnormalities than in those without such abnormalities [51]. Because
asymptomatic tendinosis can lead to spontaneous tendon rupture [23], the relevance of asymptomatic lesions on imaging needs further investigation.
As imaging does not reflect symptoms or indicate outcome, it remains a
supplemental aid to clinical examination in the assessment of patellar tendinopathy. Imaging is very sensitive to abnormal tendon morphology [24]. Given the
751
Table 3
Ability of ultrasonography to predict future prognosis
Reference
Total
tendons
Cook et al [51]
52
16 months
Cook et al [66]
46
4 years
Fredberg and Bolvig [67]
98
11 months
Khan et al [70]
46
> 12 months
Follow-up time
Totals
Ultrasonography
at baseline
10
42
18
28
18
80
23
23
abnormal
normal
abnormal
normal
abnormal
normal
abnormal
normal
69 abnormal
173 normal
Clinically symptomatic
at follow-up
3
3
4
2
3
0
8
2
18 (26%)
7 (4%)
high positive-predictive value of imaging (Tables 1,2), it is of use in patellar

tendinopathy, as it can confirm the clinical diagnosis and increase the overall
likelihood of diagnosis. If imaging reveals characteristic features of patellar
tendinopathy that fit the clinical presentation, then treat as such; however, if
imaging is normal, then other causes of anterior knee pain need to be further
considered. Imaging should not be used to determine management, and it does
not appear to have a major role postoperatively. Whether imaging findings in
asymptomatic tendons are predictive of future prognosis should be a focus of
further research.
Conservative treatment
Despite the morbidity associated with chronic patellar tendinopathy, there is a
surprising lack of scientific evidence directing the management of this condition.
This lack of evidence results from a dearth of methodologically sound, randomized-controlled trials of clinically implemented treatments, and has resulted in
vastly contrasting treatment choices among clinicians. In spite of this, what is
currently agreed upon is that initial management should be conservative rather than
surgical. This reasoning is based on the facts that the time course of recovery with
appropriate conservative management is equivalent to that following surgery, and
that the outcome of conservative management is equal to, if not better than, that
following surgery [2].
For appropriate conservative management, the aforementioned underlying
pathology of patellar tendinopathy needs to be understood by both the treating
clinician and athlete. The pathology is degenerative by nature and this degeneration
was most likely taking place before the onset of symptoms. This means that the
pathology is typically quite advanced before clinical presentation. The advanced
degeneration before the onset of symptoms, combined with the slow metabolic rate
of tendon, means that recovery can be prolonged. In chronic cases, this recovery
752
can take in the vicinity of 4 to 6 months [2]. In athletes with a short duration of
symptoms, recovery to full sporting capacity may take 2 to 3 months [2]. It is with
these latter athletes that special care needs to be taken, as they may be able to warm
up the injury, enabling full sporting capacity, further mechanical overload, and
further tendon degeneration.
The focus of any conservative management program should be to deload the
tendon and to encourage collagen synthesis, maturation, and strength [2]. At all
times, progression through the program should be directed by the athletes
symptoms. Common reasons why conservative treatment programs fail are too
rapid a progression through rehabilitation, lack of monitoring of an athletes
symptoms during and after therapy, and inappropriate loads [45].
Relative load reduction and biomechanical correction
As patellar tendinopathy is predominantly a strain-related phenomenon, initial
conservative management should involve some form of load reduction to limit
progression of the pathology. Given the detrimental effects of complete immobilization, load reduction should be achieved by relative rest rather than complete
cessation of activity. Relative rest means that the athlete may be able to continue
playing or training, if it is possible to reduce the amount of loading through
modification of pain-provoking activities and reduction in total training hours.
In addition to changing training activities and durations, patellar tendon loading
may be reduced through biomechanical correction. Correcting biomechanics of the
lower limb kinetic chain can improve its energy-absorbing capacity and redistribute forces from the knee and patellar tendon. Biomechanical correction can be as
simple as training how to land so that greater load is absorbed by distal and
proximal joints. When landing, the ankle and calf are critical in absorbing the initial
load and reducing load being transmitted to the knee [71]. Approximately 40% of
landing energy is transmitted proximally, and thus a functioning calf complex is
required to absorb the major portion of the initial load [45]. Similarly, functioning
of the hip complex is important. When a large range of hip flexion is combined with
forefoot landing, vertical ground reaction forces can be further reduced [72].
To assist distal and proximal joints in absorbing more load, correction of
anatomical and functional abnormalities may be needed. Inflexibility of the
quadriceps, hamstrings, iliotibial band, or calf has the potential to restrict rangeof-motion at the knee and ankle, and to increase the load on the patellar tendon.
Similarly, weakness of the gluteal, lower abdominal, quadriceps, and calf muscles
may lead to fatigue-induced aberrant movement patterns that may alter forces
acting on the knee [45]. Forces on the knee may also be influenced by foot
mechanics, and thus shoe orthoses may be indicated in some athletes.
Strengthening exercises
Although mechanical loading is implicated in the etiology of patellar tendinopathy, loading is known to be beneficial to tendon health, and strengthening
753
exercises are recommended in its management. Exercise may influence the structure, chemical composition, and mechanical properties of a tendon [73]. Animal
studies have shown loading of tendon improves collagen alignment and stimulates
collagen cross-linkage formation [74]. In tendinopathy, mechanical loading may
speed repair, as it increases tenocyte metabolism [75].
Clinical studies point to the efficacy of eccentric strengthening regimes in the
treatment of tendinopathies [76 78]. This has been supported by recent scientific
evidence [79,80], although studies in patellar tendinopathy are currently lacking
[9]. Initial exercises should focus on strength and endurance gains before
progressing to speed gains. Both pain and the ability of the musculotendinous
unit to do work should guide the amount of strengthening activity, and during all
exercises quality of movement should be emphasized.
Pharmacological intervention
Anti-inflammatory agents are the most common pharmacological interventions
in patellar tendinopathy, with the two most common agents being oral nonsteroidal
anti-inflammatory drugs (NSAIDs) and local injection of corticosteroids. The use
of both has been debated, considering that tendinopathy has a noninflammatory
pathology. In a thorough review of the role of NSAIDs in the treatment of
tendinopathy, Almekinders and Temple [81] found little evidence that they were
helpful. In terms of corticosteroid injection directly into the tendon tissue, it has
been found to inhibit collagen synthesis [82] and lead to cell death and tendon
atrophy [83], and a reduction in load-to-failure [84].
Although inflammatory cells do not appear to be present in patellar tendinopathy, inflammatory pathways may still be involved, and thus anti-inflammatory
agents may have a role in management. This potential role needs to be further
explored. It is possible that NSAIDs benefit tendinopathy via alternate mechanisms, such as accelerated formation of cross-linkages between collagen fibers
[85,86]. Similarly, corticosteroids, when injected peritendinous rather than intratendinous, could possess beneficial effects, mediated through effects on the
connective tissue and peritendinous adhesions by inhibiting the production of
collagen, other extracellular matrix molecules, and granulation tissue [87].
Electrophysical modalities
A range of electrophysical modalities have been employed to treat patellar
tendinopathy. These include ultrasound, laser, and electrical stimulation. Currently
there is only circumstantial evidence supporting the use of these modalities and
further research is required. Ultrasound can stimulate in-vitro collagen production
from fibroblasts [88,89], and increases mechanical strength return during repair of
acute tendon injuries [90,91]. Laser has been shown in a rabbit Achilles tenotomy
model to increase collagen content [92]. Biomechanical and biochemical measures
of tendon healing were improved by a combination of ultrasound, laser, and
electrical stimulation of rabbit Achilles tendons after tenotomy and suture repair
754
[93]. Whether beneficial effects of these modalities are present in degenerative

patellar tendinopathy and in humans has not been investigated.
Cryotherapy
Icing may have a role in the management of patellar tendinopathy, particularly
when applied post-loading. Icing reduces blood flow and may help to reduce the
pathological neovascularization associated with tendinopathy. Whether it also
reduces tenocyte collagen production requires consideration. Icing may also be
used as an analgesic; however, this role should only be used following exercise, as
it may mask symptoms enabling tissue overload [13].
Massage
Massage therapy is used in patellar tendinopathy to promote repair and to
decrease adhesions between the tendon fibers [29]. Research in healing rodent
tendons showed soft-tissue mobilization to increase fibroblast recruitment and
promote healing [94,95]. Clinically, in tendinopathy the most effective form of
massage appears to be digital ischemic pressure followed by deep transverse
friction throughout the entire tendon. Massage should also be performed on both
the calf and quadriceps muscles to maintain their compliance [29,45]. This may
take the form of sustained myofascial tension.
Surgical treatment
Surgery for patellar tendinopathy is only indicated after a prolonged (6 months)
and well-supervised conservative treatment program fails. Surgery may involve
excision of degenerated areas, arthroscopic debridement, repair of macroscopic
defects, multiple longitudinal tenotomies, drilling of the inferior pole of the patella,
resection of the tibial attachment of the patellar tendon with realignment, percutaneous needling, or percutaneous longitudinal tenotomy [29,41]. As the pathophysiology of patellar tendinopathy is not known, the exact surgical technique
chosen is based on the surgeons opinion and experience [29]. There is no
consensus as to the optimal surgical technique to use.
Surgery is not indicated in the initial management of patellar tendinopathy, as
surgical outcomes are rather unpredictable and recovery can be extended. A review
of 23 papers found that the outcome following surgery was either excellent or good
in 46% to 100% of cases, with an overall success rate of 75% to 85% being a verybest-case estimate [96]. Thus, 15% to 25% of patients will experience persistent or
recurrent tendon pain following surgery. The recovery following surgery, even with
a good or excellent result, can take 6 to 12 months [40,57], and many athletes will
not be able to return to their previous level of sport [97]. Consequently, surgery
should only be considered after a thorough, high-quality, conservative management program has been attempted.
755
Summary
Patellar tendinopathy is a common and serious condition in athletes. Although
there have been many advances in the understanding of the histopathology,
imaging, and surgical outcomes in this condition in the past decade, successful
management of athletes with patellar tendinopathy remains a major challenge
for both the practitioner and patient. There is a definite need for further
prospective studies into etiological factors and randomized controlled trials into
treatment choices.
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Clin Sports Med 22 (2003) 761 776
Rupture of the Achilles and patellar tendons

Nicola Maffulli, MD, MS, PhD, FRCS (Orth)a,*,
Jason Wong, MRCS (Edin)b
a
Department of Trauma and Orthopaedics, Keele University School of Medicine,

Thornburrow Drive, Hartshill ST47QB, UK
b
Department of Plastic and Reconstructive Surgery, Royal Victoria Infirmary,
Newcastle Upon Tyne NE, UK
Extension of the knee and plantarflexion of the ankle produce the powerful
motion required to initiate gait. The powerhouse of lower limb locomotion is
predominantly transmitted through two vulnerable major tendinous structures.
With such dependency of lower limb function on the Achilles and patellar
tendons, rupture can be catastrophic.
Tendon ruptures typically affect men in their third or fourth decade who are
active in sport. Achilles tendon rupture is common and becoming more frequent.
There has been an increase in the incidence over the last 20 years, 60% to 75% of
which can be related to sports [1,2]. Patellar tendon rupture is far less common, as
the bone substance of the patella marks the weakest component of the knee
extensor mechanism. A tendon rupture is usually an indicator of intratendinous
degenerative changes [2].
In competitive sports, acute injuries in these two tendons are relatively
infrequent, although they occur in an unpredictable fashion and can be devastating to athletes. This article provides sports physicians an overview of these
problems, drawing from the authors own experience and the recent literature.
Epidemiology
The Achilles tendon is strongest tendon in the body, closely followed by the
patellar tendon. Many possible etiological factors have been involved in its
rupture, and these can broadly be divided into high-energy disruptions, degenerative changes, and mechanical imbalance. Injuries acquired from participation
* Corresponding author. Department of Trauma and Orthopaedics, Keele University School of

Medicine Thornburrow Drive, Hartshill ST47QB, UK.
E-mail address: n.maffulli@keele.ac.uk (N. Maffulli).
doi:10.1016/S0278-5919(03)00009-7
762
N. Maffulli, J. Wong / Clin Sports Med 22 (2003) 761776
in sports account for the majority of ruptures [2]. Acute injuries result from rapid
force shifts to the lower limb in sports like football, basketball, track and field,
volleyball, squash, and badmintonthese present high risk for rupture in the
Achilles and patellar tendons [2 4]. Due to the unique mechanical properties and
helical and cross-linking structure of tendons, forces generated through the
movement of the lower limb are rarely enough to rupture the Achilles or patellar
tendon on their own. Although the etiology is not entirely clear, degenerative
changes are found in most ruptured tendons, suggesting that there exists a
prerupture phase and even a predisposition to rupture [5]. Variations from relative
inactivity to active training may explain why white collar professionals who
partake in the occasional sporting pursuit are typically at particular risk. Direct
injection of steroids [6,7] and administration of systemic corticosteroids [8,9] and
fluoroquinolones [10,11] are associated with an increase in the risk of Achilles
and patellar tendon rupture. Other disease processes such as rheumatoid arthritis
[12], systemic lupus erythematosus [13,14], chronic renal failure [15], hyperuricaemia [16], genetically-determined collagen abnormalities, infectious disease,
neurological conditions, hyperthyroidism, hyperthermia, arterioscleroisis, and
diabetes mellitus have also been implicated as risk factors for rupture [17].
Achilles tendon
Risk factors for rupture of the Achilles tendon include poor tendon vascularity,
degeneration, gastronemius-soleus dysfunction, poorly conditioned musculotendinous unit, changes in training pattern, and poor footwear [18]. Mechanical
imbalance and microtears have also been reported [19].
Patellar tendon
Direct trauma to the patellar tendon provides an obvious means of disruption.
Rupture of the patellar tendon from indirect trauma is usually the result of chronic
degeneration within the tendon, followed by an acute or subacute force that
overwhelms the weakened fibrillar structure. There is histological evidence in
spontaneously ruptured tendons that pathological changes within the tendon are
present before rupture [20]. In the healthy knee extensor musculotendinous unit,
tensile overload usually results in a transverse fracture at the patella, further
supporting a pathological process in the tendon itself [21]. There is no evidence
of the fact that clinically evident patellar tendinopathy is a common feature
preceding patellar tendon rupture, although degenerative changes are seen in
ruptured patellar tendons [22]. Certain surgical procedures to the knee have been
associated with patellar tendon rupture. Displacement of the patellar tendon
during total knee arthroplasty and anterior cruciate ligament reconstruction using
the central third of patellar tendon are the usual culprits. Surgical procedures that
disturb the midsubstance or insertion points of the tendon, however, have also
been associated with rupture [23,24], and in some patients occur several years
after the operation [25].
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Basic science
Tendons were regarded as relatively inert tissue. The cellular elements in a
tendon are very active, however, and allow for transmission of high tensile forces,
elastic recoil, and longitudinal movement. In the response to physiological strain,
microtears can form in the tendon substance, with new collagen being formed
simultaneously, thus allowing for tendon remodeling [26]. Due to the helical
arrangement of the tendon fibrils and the actin and myosin content, tendons can
stretch up to 4% before damage. At strain levels greater than 8%, macroscopic
rupture will occur [27]. With aging, tendons stiffen from the effects of reduced
glycosaminoglycan content and increased collagen concentration [28]. Blood and
nutrient supply also reduces with age, particularly to the mid portion of the
Achilles tendon [29].
Mechanics
Achilles tendon
Tensile force normalized to subject weight can be from 2.6 kN when walking
to 9 kN when running [30], and the tendon can withstand approximately 50 to
100 N/mm. The mechanism of rupture has been classified into three main
categories [31]: (1) 53% arising from weight-bearing, forefoot pushoff with knee
in extension (eg, sprinting, jumping sports); (2) 17% occurring following sudden
unexpected dorsiflexion of the ankle, such as slipping into a hole or falling
downstairs; and (3) 10% arising following violent dorsiflexion of the plantarflexed foot, such as in falling from a height. In the remaining ruptures, the exact
mechanisms of rupture could not be identified.
Patellar tendon
Ascending-stairs forces generated across the patellar tendon are approximately
2.24 kN [32], and forces being generated during competitive weightlifting
approach 12.2 kN [33]. Diseased tendon ruptures at lower forces, and reports
of spontaneous rupture through everyday activities are frequent [34]. The
mechanism of injury is usually an eccentric overload to the extensor mechanism,
with the foot planted and the knee partially flexed.
Clinical presentation
A detailed history and comprehensive physical examination are essential
and often provide enough information for the diagnosis of lower limb tendon rupture.
764
Achilles tendon
The majority of Achilles tendon ruptures can be diagnosed clinically. Twenty
percent to 25% of Achilles tendon ruptures are missed by the first examining
doctor, however [35,36]. Longstanding ruptures pose a greater challenge in
diagnosis, and imaging techniquesincluding real-time high-resolution ultrasonography, and magnetic resonance imagingare used to aid diagnosis. The
history typically starts with sudden onset of pain in the affected leg, with
patients occasionally reporting that they thought they had been struck on the
back of the leg. Some patients hear an audible snap. Following rupture, patients
are often unable to bear weight and notice weakness in plantarflexion and
swelling of the affected ankle. Plantarflexion is usually still possible through the
use of flexor hallucis longus, flexor digitorum longus tibialis posterior, and
peroneal tendons. Patients with chronically ruptured tendons usually cannot
recall an injury or put it down to an ankle sprain. They may notice weakness of
the leg in simple day-to-day tasks like climbing up the stairs. Examination often
reveals edema and bruising over the rupture site, with a palpable gap that may
be obscured by swelling. The rupture site is usually 2 cm to 6 cm proximal to
the insertion of the tendon [37] (Fig. 1). A number of tests have been described
to demonstrate the rupture, such as the Simmonds (or Thompson) test [38,39],
Matles test [40], OBrien test [36], and Copeland test [41]. The Simmonds test is
the most frequently used and involves the patient adopting a prone position with
his ankles clear of the couch. The examiner then squeezes the fleshy part of the
calf: with an intact tendon, the ankle plantar flexes. A false positive might arise
if the plantaris tendon is intact. The affected leg should always be compared
with the contralateral limb. The other tests may be used if the Simmonds test
is equivocal.
Fig. 1. Fresh rupture of the Achilles tendon.
765
Fig. 2. Fresh rupture of the patellar tendon.
Patellar tendon
Rupture of the patellar tendon is often dramatic (Fig. 2). Sudden pain
associated with a popping or tearing sensation is usually experienced. A hemarthrosis usually follows, and causes the knee joint to swell. This must be differentiated from other knee injuries, such as a meniscal tear or cruciate ligament
rupture. In one study, almost one third of patients were misdiagnosed at first
presentation [42]. Unassisted weight bearing is near impossible. The most
important sign with patellar ruptures is the inability to actively extend the knee
and maintain the passively extended knee against gravity. If most of the retinacular
fibers remain intact, however, some extension may be possible [42]. There is often
a palpable gap at the level of the rupture, and the patella may be proximally
displaced when compared with the contralateral patella. Pain and swelling usually
limit flexion of the knee. Missed ruptures may be difficult to diagnose as
hematoma and scar formation fills the gap, although an extensor lag can usually
be demonstrated. Patients often find that stair climbing and rising from a chair are
very difficult, and elderly patients may present to the physician as off legs.
Investigations
The diagnosis of Achilles and patellar rupture is formulated on a clinical basis.
When the diagnosis is dubious, however, various investigations can clarify
the diagnosis.
766
Radiographs
Plain radiographs have little place in the diagnosis of acute Achilles tendon
rupture in modern practice, other than diagnosing associated or incidental bony
abnormalities. Subtle signs such as loss of definition in Kagers triangle may be
seen. Other signs like diminished Toygars angle and Arners sign are less reliable
[43]. Deformation of the contour of the distal segment of tendon has also been
used as a subtle indicator of rupture [31]. Radiographs in patellar tendon rupture
are helpful to exclude patella fractures, although bony fragments may be seen if
the tendon was avulsed (Fig. 3). On the lateral view, a patella alta is identified [44].
Ultrasound
Ultrasound lends itself well for the imaging of Achilles and patellar tendon
rupture due to the superficial position of both tendons. A normal Achilles tendon
appears as a hypoechogenic, ribbon-like image contained within hyperechogenic
bands [45]. Rupture produces an acoustic vacuum with thick irregular edges [46].
In patellar tendon ruptures, hypoechogenicty is noted over the entire thickness of
the tendon. In chronic tears, thickening of the tendon at the rupture site is seen,
with disruption of the normal echo pattern [47].
Fig. 3. Anterior posterior and lateral radiographs of a patellar tendon rupture; note fragments of
avulsed bone in tendon substance.
767
Magnetic resonance imaging (MRI)

The normal Achilles tendon is seen as a low signal intensity on all pulse
sequences used. The tendon is well delineated by the high signal intensity of the
fat pad of Kagers triangle. The patellar tendon on MRI is homogeneous and of
low signal intensity throughout its course on proton density images. An increase
in the intratendinous signal intensity usually indicates hematoma and edema at
the site of rupture on T2-weighted images. It is particularly of good use in
identifying associated intra-articular injuries and for neglected tears when
diagnosis is unclear.
Management
There exists an extensive variety of methods for the management of Achilles
tendon ruptures, ranging from those that are managed in an equinus cast to those
that an external fixation device are applied to. This reflects the controversy over
the best means of treatment [48]. Patellar tendon rupture is best managed by
operative reconstruction of the extensor apparatus. The method of choice depends
upon timing of repair and operator preference.
Nonsurgical management
Achilles tendon
Immobilization in a below-the-knee cast in gravity equinus position for
4 weeks, followed by placing the foot in a more neutral position for a further
4 weeks, has been described most frequently in the literature [48]. Functional
bracing was introduced to address the problems of muscle atrophy and stiffness
that followed long periods of immobilization [49 51]. The functional results are
impressive, with low complication rates. Conservative management in general
has a higher rerupture rate than operative management, however, and in our view
should not be recommended for athletes.
Patellar tendon
Conservative management by immobilization of the knee in full extension is
ineffective. Inevitably, an extensor lag ensues, and the mechanics of the knee are
not restored.
Surgical management
Achilles tendon
The diversity of different techniques reflects the imagination and ingenuity of
previous authors. It also implies that there is no universally-accepted, ideal means
of repairing Achilles tendon ruptures. Operative measures can be broadly divided
into open methods, percutaneous methods, and methods used for delayed repairs.
768
Open repair is most prevalent in the literature, with a huge number of different
methods being described. The simple end-to-end suturing of ruptured tendon is
the preferred means of repair [48]. A number of other techniques have been
described aimed at reinforcing the repair in acute ruptures. Neglected ruptures can
be repaired by similar methods [52], but may require augmentation by autograft
[53], allograft [54,55], or synthetic materials [56,57]. The period of immobilization ranges from 2 to 8 weeks. Early mobilization at 2 weeks or even sooner has
been used with good results and appears to be gaining popularity [58]. Minor
complications consist predominantly of wound problems. In a quantitative
review, we found that approximately 12.3% of immobilized open repairs had
minor wound complications and 2.3% had major wound complications; approximately 4.9% of early mobilized open repairs had minor wound complications
and 0.4% had major wound complications [48].
Patellar tendon
Repair of acute ruptures is usually performed by securing sutures through the
tendon and through transosseous tunnels in the patella, with or without reinforcing cerclage sutures. A number of variations on this simple end-to-end repair
have been described. Reinforcement is of particular use when tendon quality is
poor and in neglected ruptures. Semitendinosus or gracilis tendon can provide
local tendon stock for augmentation [59,60]. Achilles tendon allografts have been
used in neglected ruptures [61 63]. Although there is a risk of disease
transmission, and the procedure is technically demanding, the functional results
are good. Other means of reconstructing the patellar tendon include using fascia
lata [42], carbon fibers [64], nonabsorbable tape suture materials [42], and
Dacron vascular graft [65]. A more conservative approach to postoperative
management typically involves a cylinder cast with knee in extension for 4 to
6 weeks, with straight leg exercises at 3 weeks followed by controlled motion
bracing. Isokinetic training regimes following soon after repair are the becoming
increasingly popular.
How we do it
Acute Achilles tendon repair
Our method of choice for repairing acute Achilles tendon ruptures is based on
the procedure described by Webb and Bannister [17,66]. This involves a threeincision percutaneous repair under local anesthesia. After infiltration of local
anesthesia around the Achilles tendon, the patient is placed prone, and a pillow is
placed beneath the anterior aspect of the ankles to allow the feet to hang free. The
operating table is angled 20 cranially to reduce venous pooling in the feet and
ankles. Both legs are prepped to allow the tension of both Achilles tendons to be
compared intraoperatively. A tourniquet is not used. Three 3 cm transverse
incisions are made over the Achilles tendon. The first is directly over the palpable
769
defect. The other incisions are about 4 cm proximal and 4 cm distal to the first
incision. The proximal incision is made to the medial side of the tendon to reduce
the risk of damage to the sural nerve. Damage to the sural nerve results in sensory
deficit to the skin over the posterolateral aspect of the calf and over the lateral
malleolus, the lateral aspect of the foot, and the fourth and fifth toes, and can
produce a troublesome neuroma.
By placing two separate double loops of absorbable material into the proximal
and distal ends of the ruptured tendon in a modified Kessler-type suture, we
produce an eight-strand repair. The sutures are then tied with the ankle in
physiological equinus, observing the contralateral limb as the sutures are tied.
The skin wounds are closed with absorbable subcuticular suture material, and
nonadherent dressings are applied (Fig. 4). A full plaster-of-paris cast is applied
in theater, with the ankle in the equinus position.
Delayed Achilles tendon repair
Augmentation with peroneous brevis under general anesthesia and tourniquet
is our preferred method of repair for neglected Achilles tendon ruptures. The
patient is placed prone with the feet protruding over the edge of the operating
table. This will allow intraoperative comparison of both ankles when adjusting
the tension of the repair. A tourniquet is applied to the thigh of the affected leg,
and the leg is exsanguinated. Both legs are prepped and draped. A 10 cm to 12 cm
longitudinal skin incision is made just medial to the medial border of the Achilles
tendon and sharp dissection is performed through the subcutaneous fat layer. The
Achilles tendon is exposed, and the ends are freshened. The proximal stump is
gently dissected out and mobilized distally.
The peroneus brevis passes around the posterior aspect of the lateral malleolus
and above the peroneal trochlea to insert onto the styloid process of the base of
the fifth metatarsal. A 2.5 cm longitudinal incision is made over the base of the
fifth metatarsal. The peroneus brevis tendon is identified and detached from its
Fig. 4. Skin appearance following Webb and Bannister Achilles tendon repair.
770
insertion and mobilized proximally. A stay suture is placed in the distal end of the
peroneus brevis tendon and the tendon is then delivered through the posteromedial wound, using gentle continuous traction as it is pulled through the inferior
peroneal retinaculum. In this fashion, the tendon of peroneus brevis retains its
blood supply from the intermuscular septum.
The peroneus brevis tendon is then weaved through the Achilles tendon ends.
It is first passed from lateral to medial through the distal stump via coronal
incisions medially and laterally in the Achilles tendon. The edges of the coronal
incisions in the Achilles tendon are sutured to the peroneus brevis tendon to
prevent progression of the incision that would lead to the peroneal tendon
cutting out. The tendon is then passed through the proximal stump from medial
to lateral and the foot plantarflexed to achieve the correct tension. A comparison
is made with the contralateral limb to confirm that tension is equal. The peroneal
tendon is sutured to the Achilles tendon stumps using absorbable material. If
there is a very large defect, the tendon of plantaris, if present, can be harvested.
This is then used as a further reinforcement of the repair. Hemostasis is
achieved, and the paratenon is closed over the repair using absorbable material.
The skin is closed with a continuous subcuticular suture with absorbable
material. Steristrips (3M Health Care, St. Paul, MN) are applied, and the wound
is dressed and a below knee plaster-of-paris cast is applied with the ankle in
physiological equinus [53].
Acute patellar tendon repair
To repair the patellar tendon, we perform a simple end-to-end, Bunnell-type
repair with heavy absorbable sutures through transosseous tunnels with a
reinforcing absorbable suture material. Use of cerclage suture or tape for
reinforcement has also been described [22,65,67 69]. The repair is performed
under tourniquet control. A longitudinal midline incision is made from the
midpatella to the tibial tubercle. The skin is lifted laterally and medially to
expose the tendon and the adjacent retinacula. The tendon ends are debrided. If
the injury involves an avulsion off the distal pole of the patella or tibial tubercle,
the tendon is cleared of loose bone fragments too small for internal fixation.
The medial and the lateral edges of the retinacular tear are identified and
repaired. Three or four heavy absorbable sutures are passed through a transverse
hole approximately 1 cm posterior to the tibial tubercle, brought proximally, and
passed transversely through the quadriceps tendon close to the superior border of
the patella in a figure-of-eight fashion. Tension is applied to the sutures, which
are then clamped but not tied. In the North American literature, it is recommended that a lateral radiograph of the knee be obtained at this stage to assess
the patellar height compared with that on preoperative radiographs of the
contralateral knee, to ensure articular congruity. We prefer to flex the knee to
90, test the tension of the sutures, adjust them as required, and tie them. The
wound is closed in layers, and the knee is placed in a well-padded dressing,
without using braces.
771
Delayed patellar tendon repair

Simple end-to-end suture is difficult when the repair has been delayed more
than 6 weeks [42,59,70]; the longer the delay between injury and repair, the
greater the likelihood of quadriceps contracture and proximal patellar migration.
Fibrous adhesions may form between the patella and the femur. Distally, the
ruptured tendon ends retract and become embedded in scar tissue, and calcific
intratendinous deposits may develop. If possible, we prefer to perform an end-toend repair in neglected ruptures. Patients who present with superior patellar
migration, loss of passive patellar mobility, and lack of full passive knee motion
may require preoperative patellar traction [42]. To accomplish this, we place a
Steinmann pin transversely through the midportion of the patella, allowing for a
2 kg weight to distract the patella over several days to a few weeks. Lateral
radiographs of the knee are taken weekly until the patella has been returned to its
anatomical position. This process is time consuming, and can be frustrating.
Measures must be taken to prevent formation of deep vein thrombosis.
Rehabilitation after a neglected rupture is considerably more conservative than
that after repair of a fresh rupture. A brace is used for 6 weeks, during which time
gentle passive exercises are performed, followed by active range-of-motion
exercises to regain full extension. Closed manipulation of the knee is occasionally
required to increase the range of motion of the knee.
Complications
Achilles tendon
Possible early postoperative complications are sural nerve damage and
hematoma formation. Medial positioning of the incision reduces the risk of
damage to the sural nerve. Hematoma formation risk is reduced, as the procedure
is performed without tourniquet so that the surgeon will be able to deal with any
bleeding at the time of operation. Intermediate superficial and deep wound
infections can occur. A major factor in our adoption of the Webb and Bannister
technique is that the risk of wound breakdown is far lower when compared with
open repair [17].
The most important late complication is rerupture. Our quantitative review of
the literature noted rerupture rates of 10.8% in conservatively managed patients.
We reported a 2.2%risk of rerupture with operatively-treated Achilles-tendon
rupture. Using a percutaneous technique, Webb and Bannister [17] did not have a
rerupture at a median follow-up of 35 months in 27 patients. Rerupture rates of
6.6% have been reported for percutaneous repairs using other techniques,
however [48].
Patellar tendon
Early hemarthrosis occasionally develops, necessitating either aspiration or
formal drainage, and the use of a suction drain should be considered. Wound
infection or skin dehiscence may occur, usually over the distal aspect of the
772
wound where the skin is relatively thin. This complication can be avoided by
placing the skin incision lateral to the tibial tubercle, and by imparting less
tension at the suture line. Anterior knee pain can occur if there is evident articular
incongruity of the patella. Decreased quadriceps strength and loss of full knee
flexion are the most common complication after a patellar tendon repair.
Aggressive postoperative rehabilitation, with early range-of-motion and quadriceps exercises, should be implemented. Manipulation under anesthesia may be
considered if 120 of flexion are not achieved by the second or third postoperative month. Arthroscopic debridement can be considered to achieve the last
few degrees of extension if these are lacking despite appropriate rehabilitation.
Quadriceps atrophy does not compromise the final return of strength, both
subjectively and objectively [42,67].
Rerupture is occasionally seen in patients who attempt to return to running or
jumping activities before complete healing of the repaired tendon [42]. Revision
is usually successful in re-establishing knee motion and strength, as long as the
repair is performed early. When the repair has been reinforced with a cerclage
wire, wire breakage may occur. The wire may need to be removed because of
skin irritation and wire extrusion. For this reason, we use absorbable sutures as
the reinforcing material rather than metallic wire. Patella baja may occur, with
resultant motion loss and the risk of patellofemoral degeneration, if excessive
tension on the sutures causes inaccurate coaptation of the tendon ends.
Postoperative care
Achilles tendon
The operated limb is elevated on a frame. The neurovascular status of the
limb is assessed. Patients are usually discharged the same day following repair,
after assessment by the physiotherapist. The full cast is retained for 2 weeks. At
this time, patients are reviewed in the outpatient clinic, where the cast is split
and the wounds inspected. An anterior splint is worn with foot plantigrade for a
further 4 weeks. Patients are advised to mobilize partial weight bearing initially,
increasing to weight bearing as able by 4 weeks. During the period in cast,
patients are advised to perform gentle isometric contractions of the gastro-soleus
complex after weight bearing has become comfortable. The splint is then
removed, and physiotherapy follow-up for gentle mobilization is arranged.
Swimming and cycling are started 2 weeks after removal of the splint, and
patients are expected to be full weight bearing by removal of the splint, 6 weeks
after operation.
Patellar tendon
Isometric quadriceps- and hamstring-strengthening exercises are begun on the
first day after surgery, and we allow protected weight bearing with crutches from
the second postoperative day. Active flexion and extension of the knee are started
2 weeks after the operation. Mobility progresses to full weight bearing without
crutches by 4 to 6 weeks postoperatively, if good quadriceps control is shown.
773
Although isokinetic rehabilitation is very much in fashion, we prefer to

undertake functional rehabilitation with isoinertial exercises, gradually progressing to a sport-specific functional rehabilitation program. Resumption of strenuous
athletic activity is allowed 4 to 6 months postoperatively, when the patient should
have a full range of knee motion and at least 85% of the strength of the
contralateral extremity.
Summary
Certain similarities can clearly be appreciated between Achilles and patellar
tendon ruptures. Both are strong tendons that transmit force bridging at least one
joint of the lower limb. When healthy, both require massive forces to be
disrupted, and both can be weakened through certain systemic disease processes,
steroids, and fluoroquinones. Both allow for a variety of innovative management
possibilities that ultimately lend themselves to individual surgical preference. We
feel that, although surgical management plays an important role in restoring
continuity in knee extension and in plantar flexion, functional outcome inevitably
relies on patient motivation and a well-established physiotherapy regime. Sports
physicians should be able to identify both conditions early in their presentation,
but still hold a high index of suspicion for these problems in athletes who have an
acute exacerbation of ongoing tendinopathy.
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Clin Sports Med 22 (2003) 777 789
Rehabilitation of lower limb tendinopathies

Jill L. Cook, PhD, PG Manip Phys, B. App Sci (Phys)a,*,
Craig R. Purdam, M Sports Phys, Dip Physb
a
Musculoskeletal Research Centre, La Trobe University, 3086 Victoria, Australia

b
Australian Institute of Sport, P.O. Box 176, Belconnen 5616 ACT, Australia
Lower limb tendinopathy is a common clinical presentation in physically

active individuals. Elite athletes who have a high intensity of training and play
sports that involve eccentric actions appear to be at increased risk of developing
tendinopathy, but tendinopathy can affect the recreational athlete as well. The
most commonly affected tendons are the Achilles tendon, posterior tibial tendon,
patellar tendon, adductor tendons, and upper hamstring tendon. Less commonly,
the flexor hallucis longus (ballet dancers) and gluteus medius tendons (in older
athletes) present with pain.
Much of the research on lower limb tendinopathy has been conducted in the
Achilles and patellar tendons, and many of the principles of assessment and
rehabilitation outlined below are based on these tendons. The principles presented, however, are adaptable to all other tendons. Each tendon, each individual,
and each sport has unique characteristics and rehabilitation must be tailored to
suit each unique combination.
Time frames for recovery vary depending on presentation, activity levels,
injury and length of symptoms, but realistically complete rehabilitation from
long-standing tendon injury can take up to 6 months or more. An athlete may still
need to continue to exercise to regain full musculotendinous function for months
after a successful return to sport to completely reverse inhibitory and unloading
patterns, despite becoming pain free early in the rehabilitation process.
Who gets lower limb tendinopathy?

The lower limb in sport is subject to high loads, as it supports the trunk and
upper body and provides for both explosive movement and stabilization. The
* Corresponding author. Musculoskeletal Research Centre, La Trobe University, 3086 Victoria, Australia.
E-mail address: J.Cook@latrobe.edu.au (J.L. Cook).
doi:10.1016/S0278-5919(03)00007-3
778
J.L. Cook, C.R. Purdam / Clin Sports Med 22 (2003) 777789
load on the joints and tendons of the lower limb can be considerable; forces up to
14 times body weight are absorbed by the musculoskeletal system in some
gymnastic moves. As sport requires regular training and competition, these forces
are recurrent, cumulatively loading the tendons. The frequency of jumping
activity in athletes has been associated with patellar tendinopathy [1] and Achilles
tendinopathy [2].
Sport
Specific sports seem predisposed to specific tendon injury; it appears the more
load the sport induces in the tendon the more likely the injury. Jumping sports
load the patellar tendon [3] and running sports load the Achilles tendon [2]. Field
hockey players get upper hamstring tendinopathy (clinical observation) and
change of direction and kicking sports get adductor tendinopathy [4] and
associated changes in nearby structures [5]. Sports with minimal eccentric
musculotendinous activity, such as rowing and cycling, have their own subset
of injuries but appear to be less predisposed to lower limb tendinopathies.
Age
Older athletes appear susceptible to tendinopathy but not necessarily because
tendons degenerate with age [6]. Tendon pathology can be more severe in older
athletes, however, due to changes associated with aging, such as less tendon
water and increased crosslinks [7]. Studies of tendinopathy encompass subjects
from the second to the fifth decade, indicating that tendinopathy affects active
individuals regardless of age. Younger athletes seem to get tendinopathy under
higher loads (reflecting eliteness) than older athletes, who may have pain with
relatively lower loads. Tendinopathy has been reported in tendons of athletes as
young as 14 years [8].
Assessment of tendinopathy
The findings from the assessment of the athlete with lower limb tendinopathy
should lead the clinician to the appropriate rehabilitation program. The assessment must therefore be comprehensive and inclusive of the whole limb. The
sporting requirements of the limb must be examined, including endurance,
power, and strength assessments, structured to the limitations of athlete pain
and function.
Identify functional deficits
Sporting participation does not guarantee intact function, as athletes are quick
to develop strategies to unload painful structures. This can lead to specific
unloading patterns within the kinetic chain, or can cause a general unloading
pattern of the entire limb. They may consequently develop weakness in and
779
around the symptomatic musculotendinous unit. Loss of power appears to be the

primary event, followed by loss of endurance and then base strength.
Primary unloading is best identified by deficits in calf power and endurance,
reduced capacity to squat, and loss of pelvic control. Hopping on the spot is one
test that allows the clinician to assess the athletes ability to recurrently absorb
shock through the limb.
Other tests, such as hop for distance and 6 m hop [9], may also identify a side-toside difference in function. Obviously, in some athletes these high-level functional
tests are inappropriate and simpler tests with lower load may be indicated.
Identify inhibitory strategies
Unloading strategies to decrease the load on the tendon or the pain experienced under load are common in tendinopathy. Over time, these strategies can
become the normal pattern and can require attention during rehabilitation.
Landing with limited knee flexion is one such strategy that may be a result of
weakness, pain, or a combination of both.
Assess biomechanics
The biomechanics of the limb must also be examined to identify anatomical
features or dynamic movement patterns that may increase tendon loading. In the
clinical sense, examining and treating biomechanical faults is central to treating
the athlete; however, it must be acknowledged that there has not been a clear
association shown between tendinopathy and biomechanical measures [3,10].
Examine the tendon and associated structures
Examination of the tendon and the structures around the tendon is important
and should be used to confirm findings from the assessment, but not used as the
sole method to grade intensity or identify painful structures. Direct palpation of
the tendon may not indicate that the tendon is either pathological or the source of
the pain [11]. Palpation, however, is essential for differential diagnosis and to
assess alterations in tendon compliance [12].
Many problematic tendons lie near structures that are also affected by sport and
that can be a source of pain in their own right (patellofemoral joint, pubic
symphysis, sciatic nerve). Correct differential diagnosis is critical at the beginning
of rehabilitation, as other pathologies may not respond to tendon rehabilitation.
Tendon imaging
The diagnosis of tendinopathy is assisted by the presence of imaging
abnormality; however, imaging abnormalities can also exist in athletes without
symptoms [13,14]. Therefore, imaging should not be the sole basis for diagnosis,
and clinical evaluation remains the criterion measure. Similarly, tendon imaging
780
should not direct rehabilitation, as it has been shown that imaging changes are
independent of clinical recovery [15].
Principles of rehabilitation
Although tendon pain is very localized and occurs with very specific loads,
rehabilitation must be directed at the entire limb. The longer the athlete has had
pain, the more likely the rehabilitation will need to include structures above and
below the painful tendon.
Correct biomechanics
Biomechanical evaluation is an essential part of the clinical assessment and
treatment of lower limb tendinopathies, even if there is little evidence to support
this intervention. Management of this facet is designed to improve limb shock
absorption or unload stressed structures.
Structural biomechanical aberrations can be somewhat difficult to change,
such as a pes cavus or tibial varum. Dynamic changes due to strength or motor
patterning deficits may be more responsive to treatment, such as internal
femoral rotation and rapid pronation, which can be treated with taping,
orthotics, and retraining.
The foot is the most evaluated and corrected biomechanical structure, and both
the pronating foot and the supinated foot may respond to orthotic correction.
Clinically, this appears more relevant for distal lesions of the lower limb, with
progressively less impact on the proximal lesions. The type and rigidity of foot
orthotics remains debatable, but it appears that the increased proprioception from
the orthotic may be as important as its corrective structure itself [16]. Evaluating
the shoe of the athlete and assessing if it suits their foot and the forces applied to
it may also assist in controlling tendon load.
Change motor patterns
Acquired motor patterns are inherently difficult to change, but persistent
attention to correct patterns throughout the entire rehabilitation program may
translate into better patterns in sport. Changes may be assisted by increases in
strength and power during the program, control of biomechanical faults, and
increasing joint range.
Load management
Athletes with tendon pain and decreased lower limb function may need to
reduce the volume or intensity of training or increase the frequency of rest days.
This may be in combination with the rehabilitation program or occasionally as a
sole management strategy. When managing an athlete during the competitive
781
season, collaboration with the technical and strength coach is critical, to facilitate
appropriate load management.
Load management may need to continue after completion of rehabilitation
when it is apparent that there is a finite load that an individual tendon can tolerate.
Substitution of fitness drills with those that have less impact on the tendon may
be all that is required for the athlete to remain competitive. Some athletes may
need to sustain modified training for 12 or more months after rehabilitation,
whereas others may always have some limitation on tendon load.
Exercise guidelines
Load the musculotendinous unit specifically
As the limb is used as a kinetic chain, symptomatic tendons higher up the
chain can be compensated by increased attenuation of force in distal joints and
muscles. Thus strength exercise directed at the quadriceps or gluteal muscles
must be as specific to the musculotendinous unit as possible. Similarly, most
rehabilitation must be undertaken as a single-leg exercise, as double-leg exercises
allow compensation with the other leg.
Recent work by Purdam et al [17] has suggested that in performing a squat, the
knee extensor mechanism may not be subjected to maximal loads or sufficiently
isolated in its function. Passive and active calf tension have the capacity to reduce
demand on the knee extensors in the squat by limiting forward angulation of the
tibia. This may be minimized by ensuring the calf functions at a shorter length,
thereby developing less tension as the squat is performed. This can be achieved
by placing the ankle in a fixed amount of plantar flexion on a decline (Fig. 1).
When loading the gluteus medius or hamstring tendon, similar care must be
taken to ensure that the knee and ankle and associated muscles are not unloading
the targeted musculotendinous unit; for example, specifying ankle plantarflexion
to increase the demands on the hamstring in the performance of the hamstring
curl exercise.
Loading the Achilles tendon is straightforward; lifting body weight will
induce tendon load. Hopping appears to induce near maximal load; however,
the clinical perspective seems to suggest that forward hopping may induce greater
load in the Achilles, possibly because of a greater contribution of force from
proximal muscles [18].
Increase the shock absorbing capacity of the limb
Improving shock absorption includes both increasing musculotendinous
control of the antigravity units and increasing joint range. The ankle is the most
important joint to treat, as range is easily compromised with injury and
degeneration. The range of dorsiflexion is critical for Achilles [19] and patellar
tendinopathy, as it allows greater range and lower rate of shock absorption in
landing. Improving the range of motion of the stiff or cavoid foot with
mobilization or orthotics may also increase shock absorption.
782
Fig. 1. Decline squat.
Calf, quadriceps, and gluteal function are critical for adequate musculotendinous shock absorption, more critical if the tendinopathy is in one of these muscle
groups. Close attention to all these muscles during rehabilitation will maximize
improvement in shock absorption.
Exercise prescription
Exercise prescription for tendinopathy should have a bias toward eccentric
strengthening of the musculotendinous unit. The role of eccentric exercise in
successful rehabilitation has been reported for many years. Curwin and Stanish
[20] first detailed the concept in the early 1980s. Since then, most research
has supported the role of eccentric exercise in improving painful tendinopathy
[21 23]. Eccentric programs have changed over time, but little evidence exists
to suggest that one program has superior results to another.
Eccentric exercise has been best investigated in the Achilles tendon by
Alfredson and colleagues [24]. Their research indicates that a high level of
exercise with increasing musculotendinous load into pain is very beneficial. This
is a substantial difference from the eccentric program first suggested by Curwin
and Stanish, as shown in Table 1.
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Table 1
Comparison of exercise programs
Repetitions
Contraction type
Pain
Speed
Resistance
Progression
Curwin and Stanish, 1984
Alfredson et al, 1998/2000
30/day
Concentric and eccentric
Minimal pain during exercise
Increasing speed of
eccentric-concentric turnaround
Resistance to BW + 5 10 lbs single leg
Speed and load combined
180/day
Eccentric only
Exercise into severe pain
Slow
Resistance to BW + 60 kg single leg
Load
Concentric exercise appears not to effect such a change, with several studies
indicating poorer outcomes for subjects undertaking a concentric program than
those using eccentric exercise [23,25].
Most eccentric exercise involves the use of a recipe that must be followed;
however, many individuals with tendon pain require rehabilitation outside of the
prescribed program. The athlete with significant weakness and inhibition may
require exercises to build to the level able to undertake the recipe, and the elite
athlete will generally need to progress beyond the recipe to higher-level function.
Failure to progress tendon load to the point that is required for the athlete to
return to sport will result in failure of the program.
Most eccentric exercise programs are reported to induce a decrease in tendon
pain. These changes occur early in the rehabilitation time, with greatest change
appearing in the first 4 weeks of the program. This suggests that the mechanism
for improvement may not be purely structural [26].
Complete tendon rehabilitation must be progressive and logical, with realistic
time frames for each level. Each level will contain some eccentric contractions.
The program should begin with a strength bias, progress to a power program, and
finish with sport-specific load on the tendon. Progression through such a program
depends on the musculotendinous unit achieving set requirements of the level
below, assessed with definite and valid tools. For example, quadriceps strength
must be first gained in an athlete with patellar tendinopathy using exercises such
as leg press and lunges. Increasing speed with exercises such as skipping will
increase tendon load. Sport-specific loads such as jumping will complete the
program. It is essential that the endurance be an integral component of each level.
Weights versus weight-bearing exercises
Most programs these days emphasize the need for weight-bearing, functional
exercises in contrast to the open-chain exercises offered previously. Most
practitioners adhere strongly to this new dictum. Although it is imperative that
functional training is a part of any tendon rehabilitation program, we risk
abandoning useful practices in favor of in-vogue treatments.
Open-chain exercises such as leg extensions and hamstring curls are useful to
specifically target a single muscle group, something that closed-chain and
functional exercises are often unable to achieve. Weights offer excellent muscular
784
loading with minimal tendon strain, and are therefore useful in the early stages of
rehabilitation and to maintain muscle strength after return to training and sport.
Assessing progress and outcome of rehabilitation

When does the clinician progress the rehabilitation? The decision, and
therefore the measures, must be clinical and easy to apply, and must be able to
identify real change in the tendon. Therefore, neither imaging nor tenderness to
palpation can be used. It is critical that measures that account for load and pain
are used, so that the exercise prescription is accurate and induces the appropriate
load increases that the athlete and the tendon can tolerate.
Subjective scoring
The Victorian Institute of Sport Assessment (VISA) scales for the patellar and
Achilles tendons [27,28] and generic scoring systems for tendon pain and
function such as the Nirschl scale [29] are the best subjective systems for rating
change in tendon status. Obviously, a scale that is designed for a specific tendon
will be more sensitive to change than a generic scale; however, the less common
tendinopathies still do not have a specific rating tool. Other outcome measures are
not specific for tendon pain, although the patient-specific functional scale [30]
may provide some quantification of progress.
Objective scoring
Inducing a repeatable load and quantifying pain at each stage of rehabilitation
allows the clinician and athlete to assess progress. Rating pain out of 10 will
allow quantification of the pain. A test may need to be progressed in intensity as
the tendon improves; however, ideally there should be as few progressions as
possible over the course of rehabilitation.
The load can be started at a simple weight lifting for the upper limb, but the
lower limb needs a weight-bearing task. High-load functional tasks, such as
hopping for the Achilles tendon, provide an excellent test of functional capacity
before return to sport.
The decline squat for the patellar tendon may be used throughout the
rehabilitation, as it can be performed in the acutely painful athlete and is also
sensitive to change in the athlete with good function.
The painful tendon with good function

If a complete assessment reveals an athlete with good function but pain that
interferes with performance, the program outlined above may have little or no
effect. In these athletes, it may be worth trying to change tendon pain, as first
suggested by Alfredson et al [24]. In this treatment program, the athlete
785
incorporates significant pain in the exercise program. This appears to directly

affect nociceptors, and decreases in tendon pain can occur early in the program
after an initial flare-up of pain. As the source of tendon pain is unclear [31], this
indirect method of treating pain offers the best option for these athletes.
Other treatment options

Electrotherapy
The effectiveness of electrotherapy agents in the treatment of lower limb
tendinopathy has been questioned in recent years. As the theory for the use of
electrotherapy was based on an inflammatory component to the pathology and
pain, there are limited reasons for their use. Electrotherapy may offer short-term
pain relief, but overall gives poor clinical results when used as the primary
treatment [4].
Two recent randomized trials have indicated that the low frequency microwave [32] and microcurrent [33] have better effects than placebo treatment in the
Achilles tendon. The rationale behind these studies (improvement due to
increasing the blood flow to the tendon) remains at odds with other research in
the area [34].
Frictions
Frictions using a specialized treatment device have been assessed as a
positive intervention in humans; however, this study appears to have methodological limitations and the results should be interpreted with caution [35].
Certainly in rats tendon, hard friction produced a positive result, increasing
cellular output [36].
Clinically, frictions can offer pain reduction in athletes; however, they may
also increase tendon pain. The tendon that responds positively to frictions is
difficult to pick and the clinician risks aggravating some athletes. Theoretically,
frictions may be appropriate in the degenerative, relatively quiescent tendon with
pain less related to tensile load.
Tendon mobilization has been used as a treatment in the Achilles tendon [12].
This technique is restricted in other tendons because of anatomical limitations
(Fig. 2).
Surgical rehabilitation
The surgical treatment of lower limb tendinopathies is problematic for
surgeons, athletes, and rehabilitation clinicians alike. There are a plethora of
surgical options [37,38], although not all have produced clinically useful results
[39]. Similarly, different postsurgical protocols are reported and these may impact
on outcome after surgery.
786
Fig. 2. Tendon mobilization.
Outcome after surgery is reportedly good to excellent in most studies;

however, these high success rates have been linked to methodological flaws in
many studies [40,41]. This suggests that further research is needed to give a true
indication of the real clinical outcome after tendon surgery for athletes.
Although symptomatic improvement is common after tendon surgery, Coleman
et al [42] suggested that athletes require more than this, and they separately
examined sustained return to sport as an outcome. This separation of symptomatic
improvement and successful return to sport is important, because most athletes
undergo surgery to enable them to play sport without pain. Symptomatic
improvement by itself can be gained more easily by cessation of sporting activities.
Rehabilitation after surgery
The process of rehabilitation is similar to the principles outlined for conservative treatment, but exercise prescription and time frames for recovery may also be
dependent on the surgeons preferences and the type of surgery. Intratendinous
surgery has been demonstrated to induce a proliferative response in the tendon
that in turn induces tendon swelling and prolongs recovery time [43]. Many
athletes having surgery for tendinopathy have the weakness and functional
deficits outlined above before surgery, and these need to be addressed in the
context of a healing tendon. Exercise is a positive stimulus for tendon [44], and
this is still true for the postoperative tendon.
Time frames for recovery are at least that for a conservative program;
however, longer rehabilitation is not uncommon. Tendon reaction after intratendinous surgery results in massive increase in tendon size and the remodeling
process is significantly longer than clinical recovery.
Repetitive surgery to the same tendon is not uncommon, although it may not
offer increased odds of recovery unless each surgical intervention addresses
different pathological structures. These athletes have very specific, prolonged,
and difficult rehabilitation demands.
787
Difficult tendons
There are many athletes with tendon problems that present unique challenges
to the clinician, and the above guidelines may need regular modification for
each situation.
One of the most difficult rehabilitation challenges occurs in the in-season
athlete, who is continuing to train and play. The concept of a strength-driven
program seems an anathema, as the athlete is subjecting the tendon to extreme
loads during competition. Load management may be the most important
component of the program here, but strength and power through the kinetic
chain may be equally important. Proper assessment will direct the rehabilitation.
The tendon that flares up several times in a season can usually be settled with
load management and a commitment to addressing proper rehabilitation during
the off-season. Identifying the stimulus to the increase in symptoms, such as
increase in training or playing load or concurrent injuries, may help the clinician
prevent flare-ups from occurring.
Those tendons that flare up suddenly and significantly, however, are sometimes very difficult to settle, and may require an extended time off and appropriate
rehabilitation. If this occurs during the season, it may be several weeks before it is
apparent that the tendon will not settle sufficiently to continue to play.
Tendons that become painful after a direct blow seem to develop a proliferative tendinopathy, where the primary reaction in the tendon seems to be groundsubstance proliferation. These remain swollen and painful for several months,
often precluding activity, but generally settle with time. The processes of
weakness and unloading are likely, and rehabilitation should start immediately
and be as aggressive as the tendon can tolerate. Constant monitoring using a
robust scoring system is the key in these instances.
Tendons that have been painful for a long period and have not responded to
multiple treatments also cause clinical problems. Many treatments may have been
inappropriate (electrotherapy and rest-based) or of insufficient length to effect a
change. There is a subset of athletes, however, that may need surgical evaluation,
or a trial of a pain-based program, or some of the newer treatment options [34].
Some tendons have demands placed on them that exceed the capacity of the
tendon despite excellent function. This occurs most commonly in very high-level
sports that place large demands on the tendon, such as high jumping and triple
jump. If load management does not help these athletes return to sport, then they
may need to be counseled as to the ongoing role of sport in their lives.
Summary
Tendon rehabilitation requires an extensive assessment, and identification of
deficits that impact on sporting performance. Rehabilitation must address all
these deficits and may take several months. Return to sport may require short- or
long-term load modification. Surgery also requires a long recovery time, and may
not guarantee a return to sport.
788
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Clin Sports Med 22 (2003) 791 812
Etiologic and pathogenetic factors for rotator

cuff tendinopathy
Samir Mehta, MD, Jonathan A. Gimbel, MS,
Louis J. Soslowsky, PhD*
McKay Orthopaedic Research Laboratory, University of Pennsylvania, 424 Stemmler Hall,
36th and Hamilton Walk, Philadelphia, PA 19104-6081, USA
Rotator cuff tendinopathy is one of the most common causes of shoulder pain
and functional impairment [1,2]. An understanding of the anatomy, histology, and
biomechanics of the rotator cuff may provide some insight into the pathologic
process involved in this tendinopathy. Multiple factors play a role in both the
normal and pathologic rotator cuff. These factors, including muscle, tendon,
ligament, labrum, bone, and vascular supply, coalesce to create a complex
biomechanical, biochemical, and molecular biologic structure. The emergence
of appropriate animal models has given researchers the ability to address
causation of tendinopathies rather than being limited to descriptions of existing
pathology in living and cadaveric tissue. The clinical implications of these basic
science studies can further research and therapeutic modalities.
Anatomy
The shoulder joint allows the greatest range of motion of any joint in the body
[3]; it is typically able to attain elevation angles of approximately 170, extension
angles of approximately 60, abduction angles of approximately 90, and rotation
angles of approximately 90. This large amount of motion primarily consists of
movement of the scapulothoracic articulation and the glenohumeral joint. To
allow such large motions, the glenohumeral joint must be relatively unconstrained. To that end, the surface area of the glenoid is only about one third that of
the humeral head [3], and there is a moderate amount of laxity (approximate 8 mm
E-mail address: soslowsk@mail.med.upenn.edu (L.J. Soslowsky).
doi:10.1016/S0278-5919(03)00012-7
792
S. Mehta et al / Clin Sports Med 22 (2003) 791812
to 11 mm of humeral head translation in any direction) in a normal joint. The

joint is highly congruent, however. Conformity of the joint is primarily provided
by the glenoid labrum. Stereophotogrammetric studies have shown that the
curvature of the head of the humerus and the glenoid differ by as little as 1%
[4]. Despite the joints high congruency, it is still relatively unstable because of
the small surface area of the glenoid relative to the humerus. Therefore, static
stabilizers (eg, ligaments, capsule) and dynamic stabilizers (eg, tendon/muscle
units) are needed to stabilize the humerus within the glenoid. Due to its large
motions, the instability of the joints anatomy, and its repetitive use, the soft
tissues making up and surrounding the glenohumeral joint are highly susceptible
to injury. Thus, a thorough understanding of the structure and function of the
glenohumeral joint and the structures that surround the joint is essential.
Our knowledge of the gross anatomy of the shoulder has remained constant,
but our understanding of the microscopic anatomy has improved as imaging
techniques have become more precise. The rotator cuff is composed of four
muscle/tendon units: the subscapularis anteriorly, the supraspinatus superiorly,
and the infraspinatus and teres minor posteroinferiorly (Fig. 1). These four
muscle/tendon units are the primary dynamic stabilizers of the joint. The
ligaments that serve as the static stabilizers of the joint are also shown in
Fig. 1. Although the tendons and ligaments that comprise the joint are shown as
separate structures, they have actually been demonstrated to fuse into one
continuous band at or near their insertions into the tuberosities of the humerus
[5]. The fusing of the rotator cuff tendons suggests that they act more as a
combined and integrative structure than as single entities. The microstructure of
the rotator cuff tendons near the insertions of the supraspinatus and infraspinatus
has been further described as a five-layer structure (Fig. 2) [5,6]. The precise
structural and biomechanical significance of the fusing of the tendons and this
five-layer structure remains to be determined.
Although pathologic changes in any one or all of the rotator cuff tendons can
result in clinical symptoms, the supraspinatus tendon is most frequently involved
[7]. This may be partially due to the bony and ligamentous anatomy surrounding
the supraspinatus tendon, specifically the coracoacromial arch [8]. The coracoacromial arch, composed of the coracoacromial ligament and coracoid anteriorly
and the acromion posterosuperiorly, forms the outlet for the supraspinatus tendon.
The supraspinatus glides beneath this arch through all planes of humeral elevation [9] and has been shown to come into contact with this arch, depending on
the elevation and rotation of the humerus [4]. The subacromial bursa, which
serves as a barrier between the undersurface of the acromion and the supraspinatus tendon, can further decrease the outlet space. The bursa often becomes
inflamed, which further results in pain and minimization of the outlet space.
The external impingement of this arch on the supraspinatus tendon, which is
discussed in more detail later, is thought to be one of the primary causes of
tendinopathy of the supraspinatus tendon.
In addition to external impingement, the intrinsic degeneration of the structure
and composition of the tendon due to aging or other factors is also thought to be
793
Fig. 1. (A) Anterior view of the right human shoulder revealing anatomic relationship between the
acromion (a), coracoacromial ligament (b), coracoid (c), and supraspinatus tendon (d). (B) Lateral
view of the right human shoulder revealing anatomic relationship between acromion (a), coracoacromial ligament (b), and coracoid (c). (From Soslowsky LJ, An CH, Johnston SP, et al. Geometric
and mechanical properties of the coracoacromial ligament and their relationship to rotator cuff disease.
Clin Orthop 1994;304:10 7; with permission.)
associated with tendinopathy. The insertion of the supraspinatus tendon, which is

at or near the critical zone and the site of most tears, is composed of a complex
arrangement of proteins. The critical zone was defined by Codman [10] as a zone
of hypovascularity within the supraspinatus tendon, approximately 1 cm from the
insertion on to the greater tuberosity, which corresponded to the region where
most cuff tears were noted to occur. The purpose of the insertion is to serve as a
transition from hard, inextensible bone to the relatively soft, extensible tendon.
The tendon insertion is usually described as four regions: bone, calcified
fibrocartilage, fibrocartilage, and tendon midsubstance [9]. Although these
regions are helpful in classifying the tendon insertion, it should be noted that
there is a gradual transition from tendon to bone.
The midsubstance of the supraspinatus tendon is primarily composed of
Type I collagen, with relatively small amounts of Type III collagen, decorin,
and biglycan. The fibrocartilage portion of the insertion has a collagen and
proteoglycan content similar to that of tissues that have been subjected to
compressive loads. This is partly due to the wrapping of the tendon around the
humerus. Therefore, it mainly contains Type II collagen and larger proteogly-
794
Fig. 2. Five-layer structure of the cuff sectioned transversely at various sites in the supraspinatus (SP)
and infraspinatus (IS) tendons, coracohumeral ligament (chl), and capsule of the shoulder. (From
Soslowsky LJ, Carpenter JE, Bucchieri JS, et al. Biomechanics of the rotator cuff. Orthop Clin North
Am 1997;28(1):17 30; with permission.)
cans such as aggrecan. The histological organization, however, does not

resemble mature fibrocartilage [11]. In rotator cuff tendinopathy, an increase
in collagen Type III, a protein that plays a role in healing and repair [12,13],
and glycosaminoglycan and proteoglycan content has been observed. These
compositional changes may be adaptive, pathologic, or both, and are found to
be altered in the older population [11,12]. Furthermore, recent studies have
shown increased levels of smooth muscle actin (SMA) in torn rotator cuffs
[14]. SMA-positive cells have been shown to contract a collagen-glycosaminoglycan analog in vitro. SMA-containing cells in rotator cuff tears may react
with the high levels of GAG and proteoglycan resulting in retraction of the
ruptured rotator cuff and inhibition of potential healing.
795
Clinical background
Typically, patients with rotator cuff disease represent a wide range of ages and
occupations. The incidence of shoulder complaints ranges from 10 to 20/1000/
year; the greatest proportions of complaints are reported during the fifth to
seventh decades of life, with a slight majority of female patients. Occupations
having a predilection for rotator cuff tendinopathy include athletes (especially
throwing) and heavy laborers. Most patients who present, however, do not have a
known cause for their pathology [15].
A variety of terms have been used to describe tendon injuries. Descriptions of
complete or partial tendon tears from mechanical overload are well accepted;
however, the correct terminology for describing and classifying tendon injuries is
unclear. This difficulty stems from a lack of routine histologic evaluation of tissue
from such patients, as they are generally treated nonoperatively. Clinically, these
disorders are commonly identified as tendinitis, and this term has become
accepted by patients and other nonmedical people. Tendinitis has been a catchall
phrase used to define a symptom complex consisting of acute or chronic pain,
with our without swelling, located in or about a tendon. In reality, tendinosis is
usually the term best suited to describe the pathologic condition that occurs
within tendinous tissue in these circumstances [16]. Strictly speaking, tendinitis is
a misnomer, because inflammatory infiltrates within tendon are not a predominant feature. Although the etiology of tendinosis is multifactorial, a number of
observations are characteristic. These observations are based on histopathology
of biopsy material from tissues adjacent to tendon ruptures taken during surgical
repair, as well as from samples of tissue from a number of tendon disorders that
required surgical treatment [16]. Khan and colleagues confirmed that the
histopathological findings in athletes with overuse tendinopathies are consistent
with those in tendinosisa degenerative condition of unknown etiology [17]. In
fact, inflammatory changes are more commonly seen in the peritendinous tissues,
which has led some to describe these conditions as paratendonitis or tenosynovitis when a tendon sheath is present [18]. Because the topic of this article is
rotator cuff tendinopathy, tendinopathy will be used to describe the overall
condition, and more specific terms will only be used when needed.
Despite the specific nomenclature, most symptomatic patients usually have a
painful arc of motion between 60 and 120 of elevation [19]. Strength is generally preserved on clinical examination; however, pain inhibition may result in
both apparent loss of strength and a decrease in active range of motion. The
impingement signs described by Neer and Hawkins are positive in nearly all
patients with symptomatic rotator cuff tendinopathy or a partial rotator cuff tear
[20]. A laxity examination should also be performed, especially in younger
individuals and athletes, as increased anterior translation has been associated with
rotator cuff lesions [21].
Because of the considerable overlap in clinical presentation, other conditions
may mimic a rotator cuff tendinopathy, such as subacromial bursitis, bicipital
tendinitis, and mild cases of frozen shoulder.
796
Although conventional radiographic films assist in the evaluation of the painful

shoulder, there are no specific plain-radiographic diagnostic features of rotator cuff
tendinopathy or tears. Plain radiographic examination should include an anteroposterior view in the plane of the scapula and an axillary view of the shoulder.
Specialized views, such as the supraspinatus outlet view, can help delineate
acromioclavicular arthritis or supraspinatus outlet narrowing. When properly
obtained, these views can define the anterior extension of the acromion beyond
the clavicle, the presence of a spur, or cystic changes in the acromioclavicular (AC)
joint [1].
Arthrography and bursography, although considered the standard studies, play
a small role in defining rotator cuff tendinopathy. Clinical studies have found
arthrography to play a limited role in partial-thickness rotator cuff tears and a
greater role in full-thickness cuff tears. Although these procedures are inexpensive and relatively easy to perform, they are invasive, resulting in a transient
synovitis and the possibility of infection [1].
Ultrasound evaluation of the shoulder has been reported to be an accurate and
cost-effective noninvasive screening tool for the diagnosis of full-thickness
rotator cuff tears, but its use in partial tears and tendinopathy is limited [22].
Furthermore, accuracy of ultrasonography is highly dependent on the experience
of the ultrasonographer and the type of equipment used.
Magnetic resonance imaging (MRI) has become an established technique for
diagnoses of shoulder pathology. In addition to its noninvasiveness, MR imaging
has the advantages of defining tendinitis by increased signal and loss of anatomic
definition, and of accurately measuring the size of cuff defects, the magnitude of
tendon retraction, and the degree of supraspinatus and infraspinatus muscular
atrophy (Fig. 3). The presence of AC joint arthritis, acromial spur formation,
Fig. 3. Proton-density (A) and T2-weighted (B) coronal oblique MR images show tendon thickening
and extensive intrasubstance tendon degeneration (black arrows), indicated by hyperintensity of the
signal in the tendon. (From McConville OR, Iannotti JP. Partial-thickness tears of the rotator cuff:
evaluation and management. J Am Acad Orthop Surg 1999;7:32 43; with permission.)
797
glenohumeral arthritis, capsular and labral pathology, rupture of the long head of
the biceps, and ganglion cysts can also be visualized.
Initial treatment includes relative rest with a decrease in overhead activities,
nonsteroidal anti-inflammatory agents, and a stretching and strengthening program for the rotator cuff and scapular stabilizers. If no improvement is seen in
2 to 3 months, a subacromial injection of corticosteroids can be tried. If nonoperative treatment fails for a period of 6 to 9 months, surgical options can be
considered [21].
The indications for surgical intervention must be individualized, and patient
factors such as age, physical demands, size of tear, and mechanism of injury,
should be taken into consideration during preoperative planning. Surgical
treatment for rotator cuff tendinopathy and tears generally fall into three
categories: debridement, acromioplasty with debridement, or cuff repair in addition to acromioplasty. Surgery may be performed arthroscopically, openly, or
arthroscopically assisted.
Results are generally quite encouraging for all three categories of surgical
treatment if patients fail conservative therapy [21]. Furthermore, recent studies
have revealed favorable results with arthroscopic procedures. It is difficult to
compare the outcomes of this group with that of the open group, however, as the
open group includes a large number of patients who have chronic disease.
Etiology
Although the precise pathogenesis of rotator cuff disease is unknown, it is
generally accepted that the etiology of rotator cuff tendinopathy is multifactoriala combination of intrinsic and extrinsic factors. Which of these mechanisms
are the primary and secondary factors in a particular patient, however, is a
controversial topic. The intrinsic mechanism is defined as a tendon injury that
originates within the tendon from intrinsic inferior tissue mechanical properties,
direct tendon overload, intrinsic degeneration, or other insult. On the other hand,
the extrinsic mechanism is associated with damage to the tendon through
compression against surrounding structures [8,9].
Intrinsic conditions include traumatic, reactive, or degenerative changes
originating in the substance of the supraspinatus. Specifically, the proposed
causes of intrinsic degeneration are primarily the microvascular supply, aging,
and tensile overload. The microvascular supply of the rotator cuff tendon in
the pathogenesis of tendinopathy of the supraspinatus tendon has been the focus
of much of the debate over the last several decades. Many researchers have
suggested that hypovascularity within the area of greatest impingement
(ie, Codmans critical zone) is a primary reason that tendinopathy and rotator
cuff tears originate from that region. There is evidence to both support and refute
this suggestion, however. The major vascular supply to the rotator cuff is derived
from the ascending branch of the anterior circumflex humeral artery, the acromial
branch of thoracoacromial artery, as well as the suprascapular and posterior
798
humeral circumflex arteries [23]. Cadaveric studies have demonstrated a hypovascular area within the critical zone of the supraspinatus tendon. More recent
studies of the microvasculature have shown that the critical zone is actually
hypervascular in those with impingement syndrome. In contrast to the cadaveric
model, these studies imply that hypervascularity or angiogenesis is associated
with symptomatic rotator cuff disease secondary to mechanical impingement
[23 27].
The negative effect that age has on tendon mechanical properties is less
controversial. Histologic studies have shown degenerative changes characterized
by calcification, fibrovascular proliferation, and microtears in elderly individuals
but not in younger subjects [28]. Age has also been shown to have a great
influence on the mechanical properties of tendons. The significantly higher
mechanical properties of mature tendon versus immature tendon may be in part
due to the improved organization of the proteoglycan filaments and collagen
fibrils in mature tendon [29 31]. Furthermore, the healing potential of elderly
individuals is thought to be decreased in tendons and would therefore make
elderly individuals more susceptible to a tensile overload mechanism of injury.
Although it is generally accepted that younger tissues heal better and faster, there
appear to be no studies that specifically correlate age with a reduced healing
potential for tendons. Although aging is clearly a factor in tendinopathy, it is
unclear whether or not the degenerative changes to tendon structure and function
that result from aging are a primary or secondary factor. Aging may simply make
the tendons more susceptible to macroscopic or microscopic damage associated
with extrinsic compression or tension overload.
Tension overload is another intrinsic injury mechanism that can result in
damage to the supraspinatus tendon. Several studies have been conducted to
delineate the mechanisms that may be responsible for the different types of tension
overload tears. For instance, the bursal and articular portions of the supraspinatus
tendon have been separately tested in vitro to determine if the mechanical
properties are inhomogenous. It was found that the modulus of elasticity is lower
and the ultimate strain and stress is greater on the bursal side rather than the
articular side [32]. This suggests that if the joint and the bursal sides of the
supraspinatus tendon are subjected to the same loads, the joint-side will be more
susceptible to failure. These studies are limited, however, in that the supraspinatus
tendon must be divided to obtain the properties, which does not take into account
the interactions between the two sides. To address this limitation, a novel,
nondestructive method to measure intratendinous strain using MRI has been
developed. Using this method, it was found that intratendinous strain fields
increased with increasing glenohumeral joint angle, but that the strain did not
vary between the articular and bursal sides (Fig. 4) [33]. Taken together, these
findings may indicate that individuals who are involved in overhead activities may
be susceptible to articular side tears due to tendon overload because the joint side
of the supraspinatus tendon may be closer to its failure strain during these
activities [34]. Because experimental studies are difficult to conduct and it is
difficult to control the myriad of factors that may be associated with the
799
Fig. 4. Representative specimen demonstrating a map of maximum principal strain throughout the
intact supraspinatus tendon at four glenohumeral joint positions. (From Bey MJ, Song HK, Wherli
FW, et al. Intratendinous strain fields of the intact supraspinatus tendon: the effect of glenohumeral
joint position and tendon region. J Orthop Res 2002;20:869 74; with permission.)
progression of rotator cuff tears, mathematical models have been used. For
example, a two-dimensional, linear elastic finite element model of the shoulder
was created and used to compare the mechanical environment of the shoulder with
varying degrees of acromial impingement (Fig. 5). Results of this preliminary
study revealed high stress concentrations about the critical zone, with tears
potentiating on the bursal side, articular side, or within the tendon [35]. More
complicated models will undoubtedly be developed for further analysis.
Extrinsic causes of rotator cuff tendinopathy can best be summarized as
subacromial impingement lesions. Compression of the tendons can occur through
bony impingement or direct pressure through surrounding soft tissues [36].
Numerous studies have been conducted that have attempted to correlate the
incidence of rotator cuff tendinopathy and tears with the soft tissue and bony
anatomy that surrounds the supraspinatus tendon. Cotton and Rideout [23]
qualitatively noted that a decrease in the acromiohumeral interval was associated
with rotator cuff tears. In 1972, Neer [8] proposed that 95% of rotator cuff
injuries resulted from mechanical compression of the tendons under the coracoacromial arch. Neers studies revealed that the anterior third of the acromion was
responsible for impingement on the structures of the subacromial space. As a
result of this observation, acromioplasties are now routinely performed and have
been very successful in relieving shoulder pain associated with tendinopathy.
In 1986, Bigliani and Morrison [37]studied the relationship of the shape of the
acromion to the incidence of full-thickness tears in cadavers. The overall
incidence of full-thickness tears in the elderly was 34%. Three acromial types
were defined in their cadaveric study: Type I, which were flat, had an incidence
of 17%; Type II, which were curved, had an incidence of 43%; and Type III,
800
801
which were hooked, had an incidence of 39%. The Type III acromion was present
in the majority of rotator cuff tears. Subsequent clinical studies revealed a
correlation between Type III acromions seen on radiographs and rotator cuff
tears, with treatment being directed at increasing the space between the coracoacromial arch [4,38,39].
A limitation of all these previous studies is that they attempted to describe the
shape of the acromion and supraspinatus outlet in two dimensions. Although this
can be appropriate in some cases, a two-dimensional description of a threedimensional structure can be misleading and difficult to interpret. Furthermore,
findings in some of these studies must be considered carefully because interobserver reliability in describing acromial morphology using radiographs has
been questioned [40]. More recent three-dimensional reconstruction studies have
revealed a significant decrease in the width of the subacromial space with muscle
activity and arm position in individuals with impingement syndrome compared
with those without impingement syndrome [41].
Osteoarthritis of the acromioclavicular joint, which may be traumatic or
atraumatic, can result in impingement and mechanical irritation to the rotator cuff
tendons through osteophyte formation. Cuomo et al [42] revealed that the position
of the acromioclavicular joint is constant within the supraspinatus outlet, and
therefore the acromioclavicular joint itself does not predispose to rotator cuff
tendinopathy. Fractures of the distal clavicle and acromioclavicular dislocations
may, however, predispose this joint to osteoarthritis. Repetitive upper-extremity
activity can cause mechanical wear of the articular cartilage. Also, age-related
deterioration of the articular disk has been associated with osteophyte development
at the acromion and bony changes of the distal clavicle [43].
No studies to date have conclusively proven that extrinsic compression is the
primary factor in rotator cuff tendinopathy. It has recently been shown, however,
that the percentage of Type I, II, and III acromions remained constant with age
[44]. This indicates that acromial morphology may not be acquired but instead
may be a native anatomical feature. Other studies have found, however, that
acromioclavicular joint morphology seemed to be acquired in nature rather than
inherent in its location within the outlet [42,45 47], indicating that intrinsic
injury may be the primary initiating factor. This topic remains controversial.
Aside from bony changes to the acromion, the coracoacromial ligament has
been implicated as a possible cause of impingement on the rotator cuff [48]. The
ligament consists of a predominant lateral band and a more variable medial band.
The lateral band is shorter and has been shown to have a larger cross-sectional area
in individuals with rotator cuff tears. A lower load to failure, a lower stiffness, and a
lower failure stress were seen in specimens with rotator cuff disease, and this
Fig. 5. Distortional strain distribution in model with subacromial impingement at humeroscapular
angles of (A) 0, (B) 30, and (C) 60. Circled letters a, b, c, and d represent sites of maximal mechanical stresses: a = insertion at articular side; b = middle portion of articular side; c = insertion at bursal side;
d = impingement site. (From Luo Z, Horng-Chaung H, Grabowski JJ, et al. Mechanical environment
associated with rotator cuff tears. J Shoulder Elbow Surg 1998;7:616 20; with permission.)
802
may be attributable to ultrastructural organizational changes present in the ligament due to an altered loading environment [48 50]. Clinical studies have revealed that a persistent coracoacromial ligament in light of normal bony anatomy
may account for a rotator cuff tendinopathy [51,52]. The unyielding nature of the
coracoacromial ligament combined with increased volume of soft tissue in the
subacromial space exerts an abnormal pressure on the tendon.
Internal impingement, also known as throwers shoulder, is a recently defined
entity that can lead to rotator cuff pathology (Fig. 6). Impingement of the
posterior labrum and cuff can occur in throwing athletes with external rotation
and anterior translation (secondary impingement) [53,54]. The hyperextension
phase of throwing may be the most important component of internal impingement. The late cocking position (abduction, external rotation, extension) may
cause the posterosuperior edge of the glenoid to become caught between the
humeral head and the rotator cuff. With anterior instability, the humeral head can
then anteriorly translate on the glenoid, accentuating the impingement of the
rotator cuff against the posterosuperior glenoid rim. The primary problem in
internal impingement is often instability [53]. This may result in articular tears.
Glenohumeral instability is another form of extrinsic injury that can lead to
damage of the rotator cuff. For example, derangement of the inferior glenohumeral ligament, a significant restraint against anterior glenohumeral instability,
can alter the kinematics of the shoulder and could lead to rotator cuff tendinopathy
[55,56]. Disruption of the inferior glenohumeral complex most often appears at
the glenoid insertion, as opposed to the ligament substance or humeral insertion
[55,57]. Three-dimensional analysis of shoulder girdle and supraspinatus motion
has shown that only a small subset of patients with impingement syndrome have
an abnormality of shoulder girdle and supraspinatus motion [58]. Subacromial
contact studies, however, have shown that altered excursion of the greater tuberosity may play a role in damage to the rotator cuff [4]. Significant pressure has
Fig. 6. Schematic representation of posterosuperior glenoid impingement between posterior edge

of glenoid and deep surface of supraspinatus and infraspinatus tendon. (From Walch G, Boileau P,
Noel E, et al. Impingement of the deep surface of the supraspinatus tendon on the posterosuperior
glenoid rim: an arthroscopic study. J Shoulder Elbow Surg 1992; 1:238 45; with permission.)
803
also been noted beneath the coracoid, suggesting that the coracoid plays a role in
impingement syndrome with the arm in certain positions [9].
Scapulothoracic motionshoulder motion occurring between the scapula
and posterior thoracic wallmay also play a role in the development of rotator
cuff tendinopathy. When the arm is abducted to 180, there is approximately 1 of
scapulothoracic motion for every 2 of glenohumeral motion. This 2:1 ratio
of glenohumeral to scapulothoracic motion may vary normally, depending on
arm elevation in the scapular plane. Warner et als topographic analysis [59] of
asymptomatic shoulders and shoulders with instability or impingement revealed
that scapulothoracic dysfunction is common with both instability and impingement
syndrome. Whether this dysfunction is a primary or secondary phenomenon of
rotator cuff pathology has yet to be determined.
Vicious cycle and tear progression

The progression of rotator cuff tendinopathy to either partial-thickness bursal or
articular or full-thickness tears also likely has a multifactorial etiology (Fig. 7).
Fig. 7. Photomicrographs of rotator cuff tears. (A) Bursal-side partial thickness cuff tear. (B)
Intratendinous tear of the supraspinatus tendon. (C) Articular-side tear. (From Fukuda H, Craig EV,
Yamanaka K, et al. Partial-thickness cuff tears. In: Burkhead WZ, editor. Rotator cuff disorders.
Baltimore: Lippincott Williams & Wilkins; 1996. p. 174 81; with permission).
804
Tears most commonly occur in and around the critical zone of the supraspinatus
tendon, which lies in the region between the bony insertion of the tendon and the
nearest musculotendinous junction [24]. Degenerative changes caused by intrinsic
or extrinsic mechanisms result in changes to the mechanical environment surrounding and within the tendon, resulting in the initiation of the vicious cycle. The
initial degeneration will alter the mechanical environment, and mechanical attrition
of the tendon due to extrinsic or intrinsic factors will increase, which will in turn
alter the mechanical environment, increasing mechanical attrition, and the cycle
continues, initiating a tear. Bursal, articular, and intratendinous tears are often
found at the time of surgical repair and the causes for these tears are unknown.
It is likely that a combination of factors is related to the propagation of
bursal side, articular side, and intratendinous tears. More research must be done
to delineate the precise factors related to each type of tear to develop specific therapies.
Animal model
Although both intrinsic and extrinsic factors have been implicated in the cause
of rotator cuff disease, studies, for the most part, have not been designed to test
hypotheses concerning the etiology or pathogenesis of the disease. Many of these
mechanistically based hypotheses cannot be addressed in retrospective clinical
studies or in cadaveric experiments. Although these studies continue to provide
important longitudinal information, a reliable animal model allows for repeatable
and controllable prescribed initiating alterations (both intrinsic and extrinsic),
which can be quantitatively monitored and evaluated over time [60].
Because animal models must be appropriate for the condition being studied, no
single model exists that is appropriate for all investigations [60]. Criteria for
evaluation of a rotator cuff tendon model include size of the animal, intrasynovial
versus extrasynovial presence, ease of manipulation, and available analysis
techniques. Anatomic considerations include shoulder musculature, bony anatomy
(acromion, coracoid, clavicle, humerus), articulations, and planes of motion [61].
Based on a series of studies, the rat was determined to be an appropriate
animal model, aside from several nonhuman primates, for the study of rotator cuff
tendinopathy, based on anatomic and functional similarities [61]. For example,
the rat has a supraspinatus tendon that passes through an enclosed arch, much as
in humans. In addition, the rat supraspinatus tendon passes repetitively under the
acromion (during ambulation) similar to the manner in which the tendon passes
under the acromion in the human (during overhead activities). Histologic analysis
of the supraspinatus tendon revealed changes in the rat model with prescribed
intrinsic, extrinsic, or a combination (intrinsic and extrinsic) injury factor. The
histologic changes seen in the rat supraspinatus mimic those seen in other sites of
tendinosis in humans. It should be noted, however, that the rat model does hold
some limitations, such as its small size and some differences in function. If one
believes that the acromion plays either a primary or secondary role in rotator cuff
805
disease pathogenesis, then there are no commonly used animal model alternatives
to date, excluding primates, that provide certain critical features comparable to
the human [34]. The rat has been used to study the effects of intrinsic degeneration, extrinsic compression, and overuse.
Intrinsic degeneration has been modeled in the rat through the use of carrageenan. Carrageenan, a polysaccharide with increased viscosity at room temperature, has been used in the past to study the effects of inflammation on tendons
and joints. Tillander and colleagues [62] were the first group to use carrageenan to
induce inflammation within the subacromial space in a rat model. Although
injection of the compound did not cause any direct damage, the subacromial
bursitis induced by the carrageenan resulted in fibrocartilaginous and bony
metaplasia in the supraspinatus tendon [62].
Previous studies by Soslowsky et al [61] used collagenase injections in the
supraspinatus tendon of the rat as a model for intrinsic degeneration. They also
used the Achilles tendon wrapped around the acromion as a model to test
the extrinsic theory. Although Soslowskys group found disruption of collagen
organization in the tendons and inflammatory changes in the peritendinous
region, they did not find any inflammatory changes in the tendon itself, unlike
in the carrageenan study. It should also be noted that injuries in the Soslowsky
model began to heal by 12 weeks, with the exception of the group that had a
combination of intrinsic and extrinsic injury, where no healing was observed.
Schneeberger et al [34] also did not find any signs of inflammatory reaction in
the bursa or the tendon in a study in which they applied a constant compressive
load to the infraspinatus tendon in a rat, mimicking extrinsic injury by fixing
bony plates to the undersurface of the acromion. Their group did find chondrocytes adjacent to the tendon rupture, however. They noted that primary subacromial impingement always caused bursal side tears in the rat (Fig. 8). This
was consistent with a cadaveric study published by Ozaki et al [63] revealing that
partial rotator cuff lesions on the articular side or within the tendon were not
associated with acromial undersurface changes or with signs of subacromial
impingement, whereas bursal side lesions were associated with attritional changes
of the acromion. Thus the rat model has revealed that subacromial impingement
may be a primary cause for bursal side degeneration in some situations and an
important secondary factor in the pathogenesis of rotator cuff tears.
In addition to intrinsic and extrinsic mechanisms, overuse activity, especially
when overhead motion is involved, has also been implicated as an etiologic agent in
tendon injuries. In the human, overhead activity causes the supraspinatus tendon to
translate repetitively under the acromion. This dynamic anatomic process may be
partially responsible for the pathology related to overhead activity in the human. To
test this mechanism independently, a model was created using an overuse activity
protocol with rat treadmill running [64]. This model causes the rat supraspinatus
tendon to repeatedly pass under the acromion, mimicking the overhead condition in
the human.
Molecular analysis of the overuse model in rats, seen on Northern blot
analysis, revealed significant changes within 4 weeks of overuse, before overt
806
Fig. 8. Shoulder of rat with subacromial impingement killed 2 weeks after surgery. (1) Humeral
head. (2) Glenoid. (3) Area of intact infraspinatus tendon at articular side and large partial defect on
bursal side with more than 50% of tendon thickness ruptured (black arrows). (4) Area of tendon
destruction with amorphous areactive tissue with loss of collagen fiber bundles and dead cells. (5)
Area of infraspinatus tendon with intact collagen fiber bundles but increased distance between fiber
bundles and increased number of fibroblasts. (6) Bony transplant. (7) Acromion. (8) Thickened
subacromial bursa. (From Schneeberger AG, Nyffeler RW, Gerber C. Structural changes of the
rotator cuff caused by experimental subacromial impingement in the rat. J Shoulder Elbow Surg
1998;7:375 80; with permission.)
histologic changes occurred. Clear evidence of increases in cell number, changes

in cell shape, and disorganization and damage in collagen fibers was seen at the
8 weeks. The extracellular matrix gene products also correlated with tendon
degeneration [65]. These molecular data are consistent with previous biomechanical and histologic data [64]. Collagen fibers were less aligned with
respect to the longitudinal axis in the overuse rat population. Cross-sectional area
increased significantly and maximum stress decreased significantly in the overuse
population. Based on these data, tendons are damaged early in the course of
overuse and fail to regain the material properties and gene expression profile of
the original tissue over an extended period (Fig. 9).
Clinically, though, each of the individual factors (intrinsic, extrinsic, overuse)
cannot predict the full range of injuries seen. Patients may have a multifactorial
etiology of their shoulder pain. Comparing overuse alone to overuse combined
with intrinsic or extrinsic injuries demonstrated several significant differences in
the rat model [66]. Specifically, the overuse/extrinsic combination injury shoulders had greater injuries than those caused by overuse or extrinsic compression
alone. This work demonstrated that extrinsic compression did not cause injury
until overuse activity was introduced as a confounding factor. Some of this work
may help explain the variability encountered in the clinical setting.
Future directions
Further understanding of the etiology of rotator cuff tendinopathy is needed.
There are multiple cellular factors that may play a role in both the pathogenesis
807
and natural history of rotator cuff disease. Some of these factors include
pluripotent cells, transcription factors, and morophogenetic proteins. Based on
the mechanical data, there is an obvious role of extrinsic factors in inciting rotator
cuff tendinopathy. Further evaluation of normal and pathologic shoulder biomechanics needs to be addressed through in vivo human and animal studies, as
Fig. 9. (A) Northern blot analysis of control, 4-, and 13-week rat supraspinatus tendon showing
significant downregulation of gene expression in collagen Type I, collagen Type III, and TGF-b1 in
rats run for only 4 weeks. (B) Histologic section of rat control supraspinatus tendon demonstrating
normal cellularity, long, spindle-shaped cells, and well-aligned collagen fibers. (C ) Histologic section
of tendon from 8-week overuse rat supraspinatus tendon demonstrating slight to moderate increases in
cellularity and collagen disorganization and change in cell shape to more round, plump, metabolically
active cells. (D) Injury created by overuse plus extrinsic compression is greater than the injuries
created by overuse or extrinsic compression alone. OV/E = overuse plus extrinsic compression;
OV = overuse alone; E = extrinsic compression alone; significant differences relative to control are
indicated by * inside each bar (average standard deviation); significant differences between singe
factors (E, OV) and multiple factors (OV/E) are indicated by * above each pair of bars. (From Soslowsky
LJ, Thomopoulos MS, Tun S, et al. Overuse activity injures the supraspinatus tendon in an animal
model: a histologic and biomechanical study. J Shoulder Elbow Surg 2000;9:79 84; with permission
[Fig. 9A,B]; and Soslowsky LJ, Thomopoulos S, Esmail A, et al. Rotator cuff tendinosis in an animal
model: role of extrinsic and overuse factors. Annals of Biomedical Engineering 2002; 30:1057 63;
with permission [Fig 9C].)
808
Fig. 9 (continued).
well as through mathematical modeling approaches. Improvement and refinement

of the animal models are underway, with increased emphasis on a model of
chronic disease and evaluation of the entire bone-tendon-muscle complex.
Treatment for this tendinopathy can be improved as the underlying mechanism
is better appreciated. Some groups have started to use fascial autografts in an
attempt to repair supraspinatus tendon defects [67]. Their preliminary work in a
rabbit model has revealed histologic remodeling of the autografted tissue. Studies
involving porcine small intestine submucosa are under way for massive rotator
cuff defects. Cartilage-derived morphogenetic protein-1, one of the known
essential factors for tendon formation, has been identified specifically at the site
of the torn rotator cuff tendon [68]. Delivery or increasing upregulation of this
protein may help in tendon healing or regeneration. Also, patterns of localized
gene expression have been studied in the rat model [13]. By understanding the
regulation of tendon healing and tissue formation at the genetic level, gene
therapy may provide an avenue for treatment.
809
The emphasis on further study at the basic science level needs to be coupled
with a continued stress on clinical understanding of the disease. As future basic
science studies elucidate the pathogenesis of rotator cuff tendinopathy, treatment
strategies, timing of intervention, and prevention of disease will be impacted.
Summary
Etiologic and pathogenetic factors for rotator cuff tendinopathy, although often
compartmentalized to intrinsic or extrinsic causes, have multifactorial roots. The
development of animal models for the study of rotator cuff disease has increased
the fund of knowledge regarding this disease and has paved the way for future
studies. Further multidisciplinary studies at molecular, biomechanical, and
clinical levels should be undertaken to enhance the understanding of this
common disorder. Ultimately, the goals of improved care, increased comprehension, and prevention of rotator cuff tendinopathy are attainable.
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Clin Sports Med 22 (2003) 813 836
Elbow tendinopathy: tennis elbow

Robert P. Nirschl, MD, MSa,b,*, Edward S. Ashman, MDb
a
Georgetown University Medical Center, 4000 Reservoir Road, Washington, DC 20057, USA
b
Nirschl Orthopedic and Sportsmedicine Clinic, Virginia Hospital Center,
1715 N George Mason Drive, Suite 504, Arlington, VA 22203, USA
Tennis elbow, which was originally coined as lawn tennis elbow in 1883
[1], is a popular term. Over the years, it has been used to describe a variety of
maladies that occur in and about the elbow [2 5]. To eliminate confusion, it is
important to define terms accurately. The malady as currently understood is
reflective of tendon overuse and failed tendon healing. The evolution of current
treatment is dependent upon the understanding of the true pathoanatomy of all
tendon failure in addition to specific reference to that of the elbow.
Initial surgical approaches were developed to lateral tennis elbow essentially
by trial and error as published by Hohman [6] and subsequently, Bosworth [7].
The focus of these historical surgical interventions was on releasing the extensor
digitorum communis origin, in essence weakening the force generator and
thereby decreasing potentially abusive forces. It is clear that these authors did
not understand the pathology or the mechanisms by which some pain relief might
occur with the release technique. In 1936, Cyriax [8,9] theorized by clinical
evaluation that the extensor brevis was the key anatomic structure in lateral tennis
elbow but did not publish confirmatory surgical data. Goldie (1964) [10] and
Coonrad and Hooper (1973) [11] published evidence of pathologic tissue without
precise anatomic location. In 1979, Nirschl et al [12] published specific information identifying lateral tennis elbow as primarily a pathologic alteration of the
extensor carpi radialis brevis (ECRB). The histology of the abnormality was
identified and the term angiofibroblastic hyperplasia was introduced. The term
was subsequently modified to angiofibroblastic tendinosis and the etiology has
been theorized to be a degenerative process, as no inflammatory cells are
identified histologically.
In 1980, Nirschl reported the anatomic site of medial tennis elbow to be
primarily in the pronator teres and the flexor carpi radialis [13], and in 1981
* Corresponding author. Nirschl Orthopedic and Sportsmedicine Clinic, 1715 N George Mason
Drive, Suite 504, Arlington, VA 22203.
E-mail address: nirschl@erols.com (R.P. Nirschl).
doi:10.1016/S0278-5919(03)00051-6
814
R.P. Nirschl, E.S. Ashman / Clin Sports Med 22 (2003) 813836
reported the triceps tendon as the primary site of posterior tennis elbow [14]. The
histologic changes in medial and posterior tennis elbow are identical to lateral
tennis elbow, and again show no evidence of inflammatory cells [15].
Our present and continuing surgical experience (more than 1000 cases of lateral
elbow and 300 cases of medial elbow) continues to confirm our earlier observations in defining the pathoanatomy of tennis elbow as angiofibroblastic tendinosis in the following areas: (1) lateral tennis elbow tendinosis (primary: extensor
carpi radialis brevis; secondary: extensor digitorum communis); (2) medial tennis
elbow tendinosis (primary: pronator teres, flexor carpi radialis, palmaris longus;
secondary: flexor carpi ulnaris, flexor sublimis); and (3) posterior tennis elbow
tendinosis (primary: triceps).
Companion pathologic problems can and do occur. These associated problems
are independent of the primary tendinosis, but they often have some relationship
to the etiologic mechanisms of repetitive overuse. The most typical problems
include the following: (1) medial elbowneuropraxia at the ulnar nerve zone 3
of medial epicondylar groove; (2) lateral or medial elbowchondromalacia, synovitis, osteophytic spurs, and loose fragments (olecranon compartment, lateral
compartment); and (3) medial elbowmedial collateral ligament attritional strain/
rupture (valgus instability of the elbow).
Of these companion problems, neuropraxia of the ulnar nerve in association
with medial tennis elbow is the most common (40% of cases overall in our
experience). Symptom-producing chondromalacia and synovitis of the anterolateral compartment as secondary issues to lateral tennis elbow are relatively
uncommon in our experience (5% of cases). Posterior osteophyte and collateral
ligament issues are most commonly primary rather than secondary when combined with medial or lateral tennis elbow.
Etiologic factors
The common denominator of all tendinosis (eg, rotator cuff, patellar tendon,
Achilles tendon, and plantar fascia) is overuse, with focus on the elbow in this
article. The characteristics most likely to result in elbow tendon overuse are:
Over 35 years of age
High activity level (sports or occupational)
3 times per week or greater
30 minutes or greater per session
Demanding activity technique
The characteristic patient age for onset of classical uncomplicated tennis
elbow is between 35 and 50 years old, with a median of 41 years old. Although
the condition is most common in the third, fourth, and fifth decades, we have
diagnosed in patients as young as 12 and as old as 80. Depending on a given
patient population, the overall male/female ratio is usually equal.
815
The overall intensity and duration of arm use is the ultimate symptom incitement and major cause of this tendinosis. In this regard, younger patients such as
competitive tennis players or professional baseball athletes characteristically place
high demands on the upper extremities. An inadequate, marginal, or compromised
musculoskeletal condition also appears to play a role in the etiology of medial or
lateral elbow tendinosis.
Multiple sites of tendon pain (mesenchymal syndrome)

In certain patients, the existence of multiple painful tendon sites can be
explained by mechanical overuse. Some patients merely compensate by switching the activity from one extremity to the other; in others, the activity is bilateral.
For example, in golf, the leading elbow is susceptible to lateral tennis elbow and
the trailing arm is subject to medial tennis elbow. In these situations, overuse
trauma is probably the key etiologic factor. We have observed, however, that the
etiologic factors of tennis elbow also involve a distinct, albeit small, subgroup of
patients who have a tendency to develop generalized tendinosis. This observation
was initially reported by the senior author in 1969 and termed the mesenchymal
syndrome [16]. In the extreme case, the mesenchymal abnormalities may
include bilateral rotator cuff tendinosis, medial and lateral tennis elbow, carpal
tunnel syndrome, triggering tenovaginitis of the finger flexors, and DeQuervains
syndrome, all in the same patient. In almost all instances, routine rheumatologic
work-up is normal. These observations have led to the conclusion that some
individuals have a heritable constitutional factor that predisposes to profuse or
generalized tendinosis.
Pathology (angiofibroblastic tendinosis)

The term tendinosis is used rather than tendinitis because it more accurately
defines the histopathological presentation of the degenerative process. The term
tendinitis has been used to describe the theoretical chronic inflammatory
changes in the overused tendon. Histologic examination of excised pathological
tendons has consistently failed to reveal the presence of inflammatory cells,
however. If chronic inflammatory cells are evident in the tendon, they are those of
traumatic repair, and include granulation tissue and scar [12,15].
The characteristic appearance of this tissue consists of invasion of immature
fibroblasts and disorganized, nonfunctional vascular elements. Electron microscopy has demonstrated that these vascular buds do not possess a lumen [15].
This granulation-like tissue has been termed angiofibroblastic hyperplasia by
Nirschl. As tendinitis is now known to be a misnomer, it should be replaced
by the term tendinosis.
Angiofibroblastic hyperplasia is intrinsically abnormal, and insinuates itself
through the adjacent normal-appearing tendon fibers, disrupting them. The
816
adjacent tendon appears hypercellular, degenerated, and microfragmented. In

advanced lesions, the characteristic reaction occurs in the supportive tissue as
well as in the tendon itself. Although acute inflammatory cells are almost always
absent in these supportive tissues, a mild sprinkling of chronic inflammatory cells
may be noted.
It is theorized that this angiofibroblastic hyperplasia may be the result of an
aborted healing response to microtears, combined with vascular deprivation in the
tendon origin. Healing may not occur, due to the poor vascularity of the tendon
origins well as the normal anatomic absence of a periosteal lining over the lateral
and medial epicondyles. In addition, the normal fibroblastic repair response may
be disrupted by continuing injury, and the degenerative tendinosis itself may act
as a detriment to the process of tissue repair [15].
The characteristic gross appearance of chronic tendinosis (angiofibroblastic
tendinosis) differs from that of normal tendon in that it is dull, gray, friable, and
often edematous. Microscopically, the normally orderly tendon fibers are dis-
Fig. 1. (A) Angiofibroblastic tendinosis. (B) Normal tendon.
817
rupted by a characteristic invasion pattern of fibroblasts and vascular, atypical,

granulation-like tissue that may be called angiofibroblastic tendinosis (Fig. 1). The
adjacent tendon appears to be hypercellular, degenerated, and microfragmented.
The angiofibroblastic tissue insinuates itself throughout the abnormal hypercellular regions and extends focally into adjacent normal appearing tendinous
fibers. In advanced lesions, the characteristic reaction occurs in supportive tissue
as well as in the tendon itself. Acute inflammatory cells may be noted in the
supportive fibroadipose, connective, and even skeletal muscle tissues. If chronic
inflammatory cells are evident in the tendon, they are those of traumatic repair
rather than tendinosis, and include either new or organizing granulation tissue and
early-to-late scar tissue. The degree of angiofibroblastic infiltration appears to
correlate with the clinical phases of pain and the duration of symptoms.
Diagnostic evaluation
The keys to diagnosis of elbow tendinosis are initial signs and symptoms of
activity-related pain followed by rest pain once pathologic change becomes more
extensive. Palpable tenderness in the typical anatomic areas, whether lateral,
medial, or posterior, is present in the early stages. Pain with provocative manual
stress testing in the usual pathologic area confirms the site of the lesion.
Functional strength losses are common, and can be measured with objective
dynamometer testing. Range-of-motion is generally within normal limits, with
the exception of the occasional loss of terminal extension (up to 15) with chronic
medial elbow tendinosis.
Radiographic evaluation may be helpful, as in our experience 20% of patients
will demonstrate tendon calcification or reactive exostosis at the tip of the
epicondyle. The radiograph is also important to rule out other pathologic problems
(especially noted in patients with medial and posterior elbow problems).
Phases of pain and pathological staging
In the senior authors experience, an accurate diagnosis of tendinosis best
includes an assessment of the magnitude of pathologic change. This is helpful for
prognosis as well as for treatment. Although it is not always possible to precisely
quantify the degree of pathologic change, we have developed a pathological
staging system that has proved helpful in estimating the amount of pathology
present. The staging has three components; the first is based on the observed
histology at the time of surgery and offers no preoperative predictive value, but
adds value when combined with the other components. The other two are derived
from the patients description of the duration and intensity of pain. The staging
systems and pain phase systems are outlined in Box 1. Pathological stages III and
IV generally require surgical treatment. Since 1981, the senior author has used an
expanded and modified pain phasing system, as first described by Blazina et al
for patellar tendon overuse [17]. A standard pain intensity analog scale is used to
818
Box 1. Staging systems and pain phase systems of tendinosis

Pathologic stages
Stage I: Temporary irritation (chemical inflammation?)
Stage II: Permanent tendinosisless than 50% tendon crosssection
Stage III: Permanent tendinosisgreater 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 disturbs sleep
further quantify each pain phase in common practice; this is a 10-point scale in
which no pain is represented by zero and severe pain is represented by 10. In
general, persistent pain phases IV and V with a pain intensity 5 or greater are
indicative of stage II or III pathology; and persistent pain phases VI and VII again
with a pain intensity of 5 or greater, are indicative of pathologic stages III or IV.
Differential diagnosis
Pain about the lateral, medial, and posterior aspects of the elbow does not
always imply tendinosis, even though it is the most common elbow problem.
Other maladies do occur, and must be addressed in the differential diagnosis.
The following is a brief and by no means all-inclusive, description of some of
the more common problems that may present with elbow pain that may mimic
elbow tendinosis.
The most commonly cited diagnosis in the differential for lateral tennis elbow
is posterior interosseus nerve entrapment (eg, motor component of radial nerve in
the forearm). The clinical signs suggesting radial nerve neuropraxia include
diffuse pain and tenderness along the track of the radial nerve in the extensor
mass of the proximal forearm and pain with provocative supinator stress testing.
Confirmation of the diagnosis may require positive electromyography (EMG)
testing changes of the posterior interosseus nerve-innervated distal muscle
groups. Aggressive nerve block injection (which includes temporary wrist drop)
819
with pain relief may also be considered as a confirmatory test. The confirmed
diagnosis of a Posterior Interosseus Nerve (PIN) lesion is rare in the senior
authors experience.
The lateral elbow may have associated lesions including synovitis, plica,
chondromalacia, and adolescent Osteochondral Defect (OCD). Careful history,
clinical examination, and diagnostic imaging should identify these intra-articular
abnormalities. Medial elbow issues include attritional degeneration or rupture of
the superior segment of the medial collateral ligament at its attachment to the
distal underside of the medial epicondyle. This malady is not common except in
the throwing sports (especially baseball and javelin). Tenderness is specific to the
distal underside of the medial epicondyle, and pain in this area is noted with
valgus stress. In full collateral ligament rupture, instability will also be noted with
valgus stress.
The ulnar nerve is quite vulnerable to compression because it penetrates through
the flexor ulnaris arcade or under the retinaculum of zone 3 of the medial
epicondylar groove (Fig. 2). Tenderness and a positive Tinels sign to ulnar nerve
distribution are specific to direct palpation over these zone 3 areas. Motor
dysfunction of the ulnar muscle innervation is a late finding. Congenital subluxation of the ulnar nerve may also occur as an independent issue but in combination
with medial tennis elbow. Under these circumstances, a positive Tinels sign will
occur in epicondylar zone I, or II, especially with the elbow in flexion.
The differential diagnosis for posterior tennis elbow includes extra-articular
olecranon exostosis and bursitis. Intra-articular issues included olecranon fossa
synovitis, chondromalacia, exostosis, and loose fragments. These maladies may
occur independently or associated with posterior elbow (triceps) tendinosis.
Fig. 2. Ulnar nerve zones at medial elbow (medial epicondylar ulnar nerve zones). The most common
clinical problem in the ulnar nerve is compression neuropraxia in zone 3. In this clinical circumstance,
surgical decompression is the treatment of choice. (From Nirschl RP. Muscle and tendon trauma:
tennis elbow. In: Morrey BF, editor. The elbow and its disorders. Philadelphia: WB Saunders; 1985;
with permission.)
820
Treatment concepts
The basic concepts of the treatment of elbow tendinosis are designed to work
with and enhance the natural biologic healing response. The healing response
after injury follows a natural sequence: (1) inflammatory exudation; (2) cellular
invasion; (3) collagen and ground substance production; and (4) maturation
and strengthening.
To achieve these concepts, implementation of treatment takes the following
form: (1) relief of pain with control of exudation or hemorrhage; (2) promotion of
specific tissue healing; (3) promotion of general fitness; (4) control of force loads;
and (5) removal of abnormal pain-producing pathological tissue surgically if nonoperative measures fail.
Relief of pain and control of inflammatory exudation
It has been our experience that approximately 95% of patients with tennis
elbow will improve with conservative therapy. Because overuse and subsequent
degenerative tendinosis occur when the repetitive forces applied to the tendon
exceeds its stress tolerance, there are two factors conservative therapy can address:
(1) lowering the stresses the tissue is exposed to, and (2) improving the quality of
the patients tissue by re-establishing its strength, flexibility, and endurance.
Initially, efforts may be directed toward making the patient more comfortable.
This includes the standard principles of PRICEMM: Protection, Rest, Ice,
Compression, Elevation, Medication (nonsteroidal anti-inflammatory drugs)
and Modalities. It is critical that the treating physician distinguish between
comfort and cure. Comfort is the relief of pain, but does not necessarily imply
enhancement of healing, or improvement in the quality of the patients tissue.
Rest and medication may result in temporary comfort, but at the expense of
further deconditioning and further delay of the rehabilitative process.
Rest should be understood as the absence from abuse, not as absence from
activity. Only activities that aggravate the condition should be eliminated. This
does not necessarily mean abstaining from work or play, if the injured tissue can
be protected through a reduction in playing time or intensity. Grasping or lifting
with the forearm pronated (palms down) should be avoided, and the patient
should be shown how to lift with the forearm supinated [14].
Likewise, cortisone injections and the comfort modalities of physical therapy
(eg, standard ultrasound and heat/cold modalities) do not directly or specifically
induce fibroblastic proliferation or improve the quality of the tendons collagen,
or bring in new vascularity to promote tissue healing, and therefore must be used
in the perspective of a broader treatment plan. With reference to the physical
modalities, heat and electrical stimulation followed by cold are helpful. We have
recently [18] published a placebo-controlled, double-blinded study using iontophoresis of dexamethasone sodium phosphate in patients with severe lateral
epicondylitis in which enhanced effectiveness in reducing the symptoms of elbow
tendinosis was noted. Recently reports have surfaced concerning pain control
821
with high intensity shock (sound wave) therapy. We have no experience with this
modality but conflicting reports suggest that further study is indicated to better
establish its effectiveness [19,20].
Promotion of healing
The goal in this category is to enhance the proliferative invasion of vascular
elements and fibroblasts, followed by collagen deposition and ultimate maturation. This is accomplished by (1) rehabilitative exercise, (2) high-voltage electrical stimulation, (3) central aerobics and general conditioning exercise, and
(4) absence from abuse.
The initiation of these programs occurs after adverse inflammation and pain
control are secure (usually 1 to 2 weeks for tennis elbow and shoulder tendinosis). Rehabilitative exercise often uses multiple resistance systems in proper
sequence. The concepts of endurance training are used (high repetitions and low
resistance). The resistance systems include water, calisthenics, isometrics, isotonics (weight resistance), isoflex (elastic-band resistance), and isokinetics
(hydraulic resistance).
General body conditioning
General body conditioning offers many advantages in enhancing rehabilitation
for specific body-part injury, including the following: (1) central and peripheral
aerobics provide increased regional perfusion, (2) neurophysiologic synergy and
overflow provide neurologic stimulus to injured tissue, (3) minimization of loss
of strength of adjacent tissue, (4) minimization of negative perceptions by patient,
and (5) fat weight control.
Control of force loads
In addition to improvement in the quality of tissues, it is highly appropriate to
minimize or eliminate excessive loading during rehabilitation, at the time of
sports return, and during activities of daily living. We have identified specific
methods to control excessive loading of tendon:
(1) Bracing. Counterforce control of intrinsic overload of the elbow tendons is
appropriate. The counterforce concept of diffusing overuse forces over a
broader area while maintaining muscle balance has proved quite helpful in
pain control, especially with forearm activities that surpass those of normal
daily living. Elbow counterforce bracing has been noted by Groppel and
Nirschl to decrease elbow angular acceleration and decrease EMG activity
[21] (Fig. 3).
(2) Improved performance technique. Certain performance activities such as
sport and occupation allow a variety of techniques to accomplish certain
goals. In tennis, for example, inadequate techniques serve to concentrate
increased force loads to the upper extremity (especially medial and lateral
elbow). Those tennis techniques that place priority on lower body
822
Fig. 3. CountR Force elbow braces. CountR Force bracing is used to decrease pain and control
abusive force overloads. Proper design includes multiple tension straps, wide dimensions, and curved
contours to accurately fit conically shaped extremities. Local pressure points through solid materials or
air cells are avoided to prevent muscle imbalances. (A) Lateral elbow brace. (B) Medial elbow brace.
(Courtesy of Medial Sports, Inc., Arlington, VA.)
participation have proved to be extremely effective in decreasing the

potential for upper body injury. Each sport or activity requires similar
individual analysis.
(3) Control of intensity and duration of activity.
4) Equipment. In tennis, for example, the racquet plays a large role in abusive
force loads. Much work continues to be needed in this area of research. A
present clinical observation is that a midsized (90 to 100 square inches of
hitting zone), medium-flex racquet of lightweight materials offers some
protection. Grip size is also an important element (Fig. 4). Anecdotally,
good quality gut string strung at the racquet manufacturers low-range
recommendations for string tension seems best as well.
Each sport or occupational activity has similar opportunities to diminish the
potential for overuse, and it is recommended that each activity be investigated
thoroughly for treatment recommendations.
Indications for surgery
The features of persistent pain warranting surgery include: pain intensity that
limits function, such as interference with daily or sports/occupational activities;
823
Fig. 4. Hand-size measurement to determine proper grip handle sizeNirschl technique. Measure
length of ring finger along the radial border from the proximal palmar crease to the ring finger tip.
Measurement indicates working length of hand. (From Nirschl RP. Elbow tendinosis/tennis elbow.
Clin Sports Med 1992;11(4):851 70; with permission.)
and clear localization of pain in association with tenderness to the focused anatomic
areas of the extensor carpi radialis brevis (ECRB), and extensor digitorum
communis (EDC). Recalcitrance of such pain after an appropriate period of
nonoperative management of 6 months or more is the usual indication.
The contraindications to surgical intervention include an inadequate nonoperative program, noncompliant patients (especially in reference to activity
modification), and presenting symptoms and examination that are not localized. Individuals on workers compensation disability should be assessed on
several occasions to assure that the above noted surgical indications have been
clearly met.
Principles of tendon surgery

The principles of surgery are: (1) identification of the pathology which is
symptom producing, (2) resection of the pathologic symptom-causing tissue,
(3) protection of normal tissues and their attachments, and (4) quality postoperative rehabilitation.
824
Lateral tennis elbow surgery

Historically, surgical release or a slide of the extensor aponeurosis, often
combined with release of the orbicular ligament has been advocated [7]. The
concept of release has never been adequately articulated by prior authors but our
presumption has been that the force generators are weakened, thereby decreasing
stress to the sensitized tissues. With release of the extensor aponeurosis and the
orbicular ligament, the origin of the ECRB is also undoubtedly released or
altered. Garden advocated lengthening of the ECRB tendon in the distal forearm
to reduce transmitted forces [22]. All of these release techniques have high
incidences of complications, such as injury to the lateral ligament complex
(occasionally even leading to posterolateral rotational elbow instability), weakness and persistent pain, and the less predictable results. None are recommended
by the authors of this article.
Our technique involves identification and excision of any pain-producing
tendinosis tissue. In lateral tennis elbow, the tissue most commonly involved,
based on the experience of the senior author, is the origin of the ECRB (100% of the
time), the anterior edge of the EDC (50% of the time), and occasionally the
underside of the extensor carpi radialis longus. Radiographic identification of bony
exostosis of the lateral epicondyle occurs in 20% of cases, but has no significance
regarding indications for tendon surgery per se. If, however, the exostosis is
prominent, or tender to palpation, removal of the exostosis is recommended as
adjunctive treatment at the time of surgery. In this instance it should be noted that
the majority of the lateral epicondyle and the origin of the extensor aponeurosis is
not resected, only the exostosis. The surgeon should be aware, however, that
excision of the exostosis adds to the patients postoperative pain and morbidity, and
postoperative soreness may be extended for 1 to 2 months.
Because the origin of the ECRB is extensive (from the distal lateral humeral
supracondylar ridge, the anterior ridge of the lateral epicondyle, the underside of
the anterior medial edge of the extensor aponeurosis distal to the lateral epicondyle,
the undersurface of the extensor carpi radialis longus [ECRL], the distal extensor
aponeurosis, and the annular ligament), the tendon does not retract more than 1 mm
to 2 mm even when the majority of the tendon is excised. It is therefore not
necessary to reattach the remaining tendon to the surrounding tissue or bone and
doing so risks the creation of an iatrogenic flexion contracture.
In our approach, care is taken to spare the origin of the other tendons, including
the extensor aponeurosis. The focus of surgery is the ECRB tendon attachment to
the antero-medial aspect of the extensor aponeurosis, and all abnormal tendinosis
tissue is debrided. The cortex of this aspect of the lateral condylar triangular recess
is then drilled one to two times to enhance vascular supply, improve the biological
environment, and stimulate healing and the formation of healthy fibro-tendon scar
to replace the resected tendinous tissue. The lateral epicondyle itself is not altered
or drilled. The normal tissues (ECRL and EDC) are then anatomically repaired.
Symptomatic intra-articular synovitis and effusion are usually stress induced
and may be associated with chronic and long-standing tennis elbow. In the senior
825
authors experience this occurs in 5% of cases. In the majority of tennis elbow

cases, however, it is unnecessary to address the joint intra-articularly unless clear
clinical or imagining evidence suggests that additional intra-articular pathology
is present.
Recently Baker and Brooks have advanced an arthroscopic technique in the
surgical care of lateral tennis elbow [23]. Their approach is also predicated upon
identification and removal of pathological tendinosis tissue. Conceptually this
approach attempts to reduplicate our open technique. The disadvantage of the
arthroscopic approach is to violate the joint for an extra-articular problem, thereby
increasing cost and risk (such as potential neurovascular complications) for little or
no short- or long-term benefit. In addition, it is questionable that the entire spectrum
of extra-articular tendinosis pathology can be accurately identified.
One benefit of the development of arthroscopic treatment of lateral tennis elbow
is that it has encouraged us to minimize our surgical incision. We now have
developed a mini-incision for lateral tennis elbow that is approximately 2.5 cm
long. The mini-incision has become our standard approach, and we have had no
difficulty performing our technique through it. With practice, this approach may be
used to easily identify all relevant anatomic structures. The mini-incision minimizes postoperative pain and enhances the speed of rehabilitation, one of the
proposed advantages of the arthroscopic technique. The mini-open approach can be
easily modified to include a mini-arthrotomy if necessary (for example, for
synovial plica resection or even loose body removal). Given the ability to perform
an open technique through this mini-incision, the limited benefit to an arthroscopic approach with its much higher cost and potential morbidity makes it difficult
to justify.
Lateral tennis elbow surgery (Nirschl mini-open technique)
The initial version of the described surgical technique was originally published
in 1979 [12] and as noted has been refined over time with enhanced experience.
One such modification has been the development of the mini-incision, through
which all relevant anatomic structures may be easily visualized if our described
technique is adequately performed (Fig. 5).
The patient is positioned supine, with the arm on an arm board. A bolster or
three towels are placed under the elbow to internally rotate the shoulder, and
better position the elbow.
1) A 2.5 cm straight lateral incision is made, centered over the epicondyle, and
passing just anteromedial to the lateral epicondyle. Care is taken not to
place it too distally (a common error). It is angled approximately 30
anteromedially to the axis of the humerus.
2) The interface between the extensor carpi radialis longus (ECRL) and the
extensor aponeurosis is identified and incised. The ECRL tendon is
palpably softer, and the combined origin of the extensor aponeurosis
palpably firmer tissue. The interface is approximately 3 mm posterior to the
826
Fig. 5. Mini-open technique (Nirschl) for lateral tennis elbow surgery. Solid delta, lateral epicondyle;
open delta, tendinosis tissue; solid arrow, extensor carpi radialis longus (ECRL); open arrow, extensor
aponeurosis. (A,B) Incision is 2.5 cm long, passing just anteromedial to lateral epicondyle. (C,D)
Interface between ECRL and extensor aponeurosis (extensor digiti communis [EDC]) is identified.
(E,F) Incision is made 2 3 cm deep and ECRL is retracted as extensor carpi radialis brevis (ECRB)
comes into view. The typical grayish edematous changes of tendinosis should be visible. (G,H)
Removal of degenerated ECRB. (I,J) To enhance vascular supply, 2 or 3 holes are drilled through
cortical bone of anterior lateral condyle to cancellous bone level. (K,L) ECRL is firmly repaired to
anterior margin of extensor aponeurosis. Because the ECRB is still attached to the underside of the
ECRL, it is unnecessary to suture the distal brevis. (From Nirschl RP. Elbow tendinosis/tennis elbow.
Clin Sports Med 1992;11(4):851 70; with permission.)
Fig. 5 (continued ).
827
828
3)
4)
5)
6)
posterior border of the muscle of the ECRL. The goal is to lift the ECRL off
of the extensor carpi radialis brevis (ECRB) without harming the ECRB
origin. The depth of the cut should be only 2 3 mm (the ECRL is thin). Do
not cut too deeply, as this distorts the proximal origin of the ECRB, and
makes it difficult to identify. Scalpel dissection proceeds horizontally
(coronally) with elevation of the thin muscle of the ECRL. Retract it
anteromedially to bring the ECRB into view. The EDC (firm diagonallyoriented tissue posteriorly) is untouched.
The pathologic tissue (grayish edematous tendon) often encompasses the
entire origin of the ECRB to the level of the joint line. All unhealthy
tendinosus tissue is excised in elliptical triangular fashion. Tendinosis is
identified as degenerative, edematous, and dull tissue. Normal tendon is
bright and shiny. Any questionable tissue is challenged with the scratch
test: the broad blade of the scalpel is used to scrape the tissue in question.
Healthy tissue will remain firmly behind, whereas unhealthy tendinosis
tissue will scratch off. This is analogous to peeling paint, where the bad
paint easily scrapes off, whereas the good paint is left behind. The bone is
also scraped to be sure no tendinosis is left.
In 35% of cases, changes are present in the anterior underside of the
extensor aponeurosis, and this area is also removed; it is unusual to have
more than 20% of its area involved. Calcific exostosis of the lateral epicondyle is present in 20%; if present, the anterior aspect of the
extensor aponeurosis is partially peeled off the lateral epicondyle and the
exostosis is removed with a rongeur (warn patient that this adds to postoperative pain).
If intra-articular pathology is suspected, a small longitudinal opening is made
in the synovium anterior to the Lateral Collateral Ligament (LCL), by cutting
along the lateral supracondylar ridge, and the lateral compartment is
inspected. In the standard lateral tennis elbow case it is rare to have intraarticular pathology, and arthrotomy is not routinely performed unless clearcut intra-articular signs are noted preoperatively.
If a small rent is inadvertently made in the elbow joints synovium, an
opportunity to inspect the joint occurs. Flex the elbow to 90; if more than a
drop or two of synovial fluid is expressed through this opening, examine
the joint further by incising the synovium in line with the incision.
Two drill holes are placed through the exposed cortical bone of the anterior
lateral condyle to cancellous depth to enhance the vascular supply. Because
the distal attachments of the ECRB are intact, and a firm attachment of the
extensor aponeurosis has been maintained at all times, minimal retraction
takes place. It is, therefore, unnecessary to suture the remaining ECRB to
obtain proper mechanical length.
If an arthrotomy was made, synovial repair is performed. (Our preference is
with a running 2-0 chromic suture). Firmly repair the ECRL to the anterior
margin of the extensor aponeurosis with a running suture (our preference is
#1 PDS). Take care to bury the knots. The tissue quality is better in the
829
middle of the incision; this is where the initial anchoring knot should be
placed. The suture may then be run proximal then distal. Close
subcutaneous tissue, then skin.
Failed surgery (lateral)
The most common reason for continued pain after lateral elbow surgery is
failure to adequately address the tendinosis pathoanatomy at the time of the
primary operation. This occurs most commonly with the original Hohman
concept of release operations, as this historical technique is designed to weaken
the force generator rather than resect the pain producing pathological tissue.
Salvage surgery is dedicated to the principles and technique as described for the
primary procedure in this text and has an 83% opportunity of success as in our
1995 report [24]. If need be, iatrogenic harm from the initial release operation,
such as lack of EDC attachment or instability of the collateral or annular
ligament, is also corrected.
Medial tennis elbow surgery (Nirschl mini-open technique)

The surgical concepts for medial tennis elbow are the same as those for the
lateral (Fig. 6). In addition, ulnar nerve dysfunction may be an associated
problem, and surgical decompression may be required. Medial collateral ligament
attrition or rupture has also been observed on occasion, and surgical repair or
reconstruction is indicated in these circumstances.
In the typical medial elbow tendinosis, the majority of pathologic changes are
present in the origin of the pronator teres, palmaris longus, and flexor carpi
radialis close to their attachment to the medial epicondyle. Pathologic change in
the flexor carpi ulnaris also occurs occasionally. On rare occasions, flexor
sublimis degeneration and rupture into the medial joint with secondary pseudobursal formation has been observed.
The skin incision is longitudinal, approximately 4 cm to 5 cm in length, and
parallels the medial epicondylar groove, starting approximately 1 cm proximal
and just posterior to the medial epicondyle and proceeding distally. Placement of
the incision posteriorly avoids sensory branches of the medial antebrachial
cutaneous nerve anterior and distal to the epicondyle. The subcutaneous tissue
and skin are retracted en bloc over the medial epicondyle, exposing the common
flexor origin. A thin fascial layer may mask the pathologic changes underneath,
and so it is important to have a clear understanding of the patients primary area
of tenderness before the anesthetic is given, as this area of tenderness precisely
locates the area of pathologic change.
A longitudinal incision is made in the tendon origins at the prime area of
patient tenderness, extending from the tip of the medial epicondyle distally for
3 cm to 4 cm. The tendons are spread, and the tendinosis tissue will come clearly
into view if the surgical indications are correct. All excision of pathologic tissue
830
831
Fig. 6. Mini-open technique (Nirschl) for medial tennis elbow surgery. Solid delta, medial epicondyle;
open delta, tendinosis tissue. (A,B) Incision is made from tip of medial epicondyle distally for 3 4 cm.
Care is taken to avoid harm to the sensory cutaneous nerve (medial antebrachial) just anterior to the
medial epicondyle. (C,D) Resection of angiofibroblastic tendinosis. The angiofibroblastic changes are
usually in the origin of the pronator teres and flexor carpi radialis. The pathologic tissue is removed in
longitudinal and elliptical fashion, leaving attachments of normal tissue intact. In 60% of cases, ulnar
nerve dysfunction has been noted clinically; decompression of the ulnar nerve in zone 3 is performed.
(E,F) Repair of medial tennis elbow. Repair of the common flexor origin is undertaken. Note that the
medial epicondylar attachments of normal tissue are not disturbed. (From Nirschl RP. Elbow
tendinosis/tennis elbow. Clin Sports Med 1992;11(4):851 870; with permission.)
832
is done longitudinally and elliptically, including resection to the joint in the rarely
indicated case. All normal tissue attachments to the medial epicondyle are
left intact (caution: the common flexor origin is a key medial stabilizer, and
indiscriminate release of normal tendon attachment can lead to medial instability). The resulting elliptic dead space is then closed with absorbable suture (our
preference is number 1 PDS suture).
If the patient had preoperative ulnar nerve symptoms this is also addressed. So
that a logical treatment sequence is established, the anatomy of the medial
epicondylar groove is described as three zones: zone 1, proximal to medial
epicondyle; zone 2, at medial epicondyle; and zone 3, distal to medial epicondyle
(see Fig. 2). Overall, nerve dysfunction usually occurs by either compression or
tension forces. The majority of ulnar nerve symptoms in association with medial
tennis elbow occur by compression in zone 3. Compression issues usually not
associated with tennis elbow can occur from osteophytic spurs, loose bodies, or
rheumatoid synovitis can occur in zone 2, and zone 1 compression may be caused
by a tight medial intermuscular septum.
In contradistinction to compression forces, tension forces can occur with a
subluxating nerve (congenital, traumatic, or iatrogenic), skeletal valgus (usually
from fracture malunion), or medial ligament rupture with secondary dynamic
valgus instability (fairly common in throwers). A hostile scar environment from
prior disease, trauma, or surgery may result in combination of compression
and tension.
In the senior authors experience, 60% of those patients operated on for medial
tennis elbow will have symptoms reflective of ulnar nerve dysfunction. In most
instances, the offending problem is compression dysfunction in zone 3 of the
medial epicondylar groove. Decompression of this zone by release of the
epicondylar ulnar or retinaculum of the flexor ulnaris arcade or both will
generally resolve the symptoms (eg, ulnar nerve transfer is not indicated).
Present indications for anterior nerve transfer are persistent dysfunctions,
primarily secondary to tension problems, and include the following: (1) nerve
subluxation or dislocation from the epicondylar groove; (2) skeletal valgus;
(3) dynamic valgus secondary to ligamentous instability; (4) unresolvable hostile
environment; and (5) necessity of surgical exposure to the medial elbow
compartment. These indications are not usually present in association with
medial tennis elbow. If anterior transfer is indicated, our preference is subcutaneous, but attention to specific and correct detail including fascial buttress
development and nerve position are critical to success.
Failed medial elbow surgery

As with failed lateral elbow surgery, the most common reason for unsuccessful
medial elbow surgery is failure to identify and resect the offending tendinosis
tissue. This usually occurs when an ill-advised release technique or epicondylectomy has been used. Release of the common flexor origin also invites
833
iatrogenic instability. With the technique of elliptical excision of pathologic tissue

these issues of failure are eliminated. An additional factor that leads to a lack of
surgical success is failure to address the ulnar nerve.
Triceps tendinosissurgical considerations

Isolated triceps tendinosis is uncommon. The histopathology is the same as
with lateral and medial tendinosis. A small longitudinal posterior incision
centered over the palpably sensitive area with elliptical excision is the recommended approach. If a spur at the tip of the olecranon is present, this should be
removed as well. More commonly, especially in the throwing athlete, triceps
tendinosis is associated with olecranon fossa synovitis, chondromalacia, ostephytes, or loose bodies. Appropriate surgical care in this instance should address
these issues as well, and an arthroscopic approach may be considered. Triceps
tendinosis is commonly seen in cases of repetitive overuse of aggressive elbow
extension, as occurs in pitching, football line play, track and field events (shot
put, javelin throw), bowling, and heavy weight lifting. Triceps tendinosis is
uncommon as an isolated entity, and usually occurs in combination with other
posterior pathology (olecranon osteophytes, posterior ulnotrochlear, chondromalacia, and so on). These should be addressed as well, either by arthrotomy or
arthroscopy. Triceps tendinosis may also be encountered in association with
lateral or medial tennis elbow. All symptomatic pathologies are addressed at the
same surgical sitting.
1) A longitudinal incision is made just lateral to the midline over the triceps
insertion.
2) The triceps is incised, its fibers spread, and the pathologic tissue identified.
3) Elliptically excise all pathologic tissue, as in the medial tennis elbow
resection and repair procedure. If olecranon fossa pathology is present,
exposure and treatment is performed at this time.
4) Close the triceps with a running suture (our preference is #1 PDS), then
close the subcutaneous tissue and skin closure.
Postoperative management
Postoperative management is similar for lateral, medial, and posterior tennis
elbow. The surgery is with few exceptions done on an outpatient basis. A light
adaptable elbow immobilizer holding the elbow at 90 with the forearm in
neutral position wrist and hand free is used for 48 hours (Fig. 7). Wrist and
hand movement is encouraged in the immediate postoperative period. Active
motion exercises are started at 48 hours. The immobilizer is used intermittently
for protection for another 3 to 5 days, and normal activities of daily living are
usually instituted within 7 days. Active wrist extension, flexion, radial and ulnar
834
Fig. 7. Elbow immobilizer. Lightweight elbow immobilizer provides marked improvement over
plastic splint in patient comfort and rehabilitative enhancement. (Courtesy Medical Sports, Inc.,
Arlington, VA).
deviation, pronation, and supination exercise without resistance are started,

usually within 5 to 6 days, dependent upon patient comfort. Neck and shoulder
exercises are started at this time as well. At 3 weeks, wrist resistance exercises
with 1 pound weights are started. A CountR Force brace (Medial Sports, Inc.,
Arlington, VA) is used during resistance exercises over the next 2 months.
Thereafter the brace use is at patient discretion. Gradual return to high demand
activities such as tennis starts on average between 6 and 8 weeks, and chipping and putting in golf often starts at 3 to 4 weeks. Full unrestricted competitive sport and occupational activity return is in large part dependent upon
patient rehabilitation diligence but usually is complete within 4 to 6 months.
High-demand patients may continue to use the CountR Force brace as a prophylactic measure.
Surgical results
The senior authors experience with the described surgical techniques now
exceeds 1300 cases (1000 lateral and 300 medial). Of the lateral group, 85%
experience complete pain relief and full-strength return. An additional 12%
experience significant pain relief and strength return but not total normalcy.
Of the 12% group, the relief usually allows return to vigorous sports. The remaining 3% (including workmans compensation patients) have experienced no
pain relief or strength improvements. Of this 3% group, the senior author has
observed no patient who experienced an increase in symptoms over the preoperative situation. The medial group is similar, but has a slightly higher rate of
no improvement (5%).
835
Complications have been minimal. Wound closure is subcuticular and on a

few occasions a temporary superficial wound infection has been noted. In cases
that undergo arthrotomy and partial synovectomy, temporary subcutaneous
synovial fluid collection has been observed on rare occasions. Partial neuropraxia
of median nerve function secondary to anesthesia axillary block was noted on
one occasion.
Summary
The pathoanatomy of overuse tendinopathy is noninflammatory angiofibroblastic tendinosis. The areas of elbow abnormality are specific, including the
ECRB-EDC complex laterally, the pronator teres, flexor carpi radialis medially,
and triceps posteriorly. The goals of nonoperative treatment are to revitalize the
unhealthy pain-producing tendinosis tissue. The key to nonoperative treatment is
rehabilitative resistance exercise with progression of the exercise program. If
rehabilitation fails, the surgical interventions as described are highly successful.
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Clin Sports Med 22 (2003) 837 847
Rehabilitation of rotator cuff tendinopathy

W. Ben Kibler, MD*
Lexington Clinic Sports Medicine Center, 700 Bob-O-Link Drive, Lexington, KY 40504, USA
Rehabilitation of the dysfunction associated with rotator cuff tendinopathy

rests on several bases that have been discovered as part of the investigations into
the pathoetiology of the clinical injury, and on observations into the clinical
presentation associated with the dysfunction. The first base is that the tendinopathy is the result of a process of injury [1,2]. This implies a failed healing
response to a set of still incompletely characterized tensile or compressive stress
loads, and that the failure occurred over a period of time, rather than as an acute
event. The second base is that at the time of clinical presentation, alterations in
physiology and biomechanics of the rotator cuff and associated structures exist
and can be clinically evaluated [1]. These alterations are in flexibility, motion,
strength, or strength balance, and may be causative in the rotator cuff dysfunction, or may be the result of the rotator cuff injury and increase the dysfunction.
The third base is that due to these alterations, symptoms of external or classical
rotator cuff impingement under the coraco-acromial arch are common, but are
most frequently secondary to the underlying alterations. Fourth, rehabilitation
should start with optimized anatomy of the rotator cuff and then seek to restore
the altered physiology and biomechanics to allow optimal rotator cuff function.
Finally, rehabilitation should shade into prehabilitation, or functional exercises
designed to minimize reinjury risk. This article addresses each of these bases to
develop a scientifically-based rehabilitation program.
Physiological and biomechanical alterations in patients with rotator cuff

tendinopathy
Flexibility
Glenohumeral internal rotation deficit (GIRD) is the most commonly associated alteration in flexibility [3 5]. This alteration creates an anterior/superior
humeral translation with arm forward flexion [3] that has been associated with
* 1221 S. Broadway, Lexington, KY 40504.
E-mail address: Wkibler@aol.com
doi:10.1016/S0278-5919(03)00048-6
838
W.B. Kibler / Clin Sports Med 22 (2003) 837847
external impingement-based rotator cuff tendinopathy [4]. In addition, GIRD

creates a posterior/superiorly-directed, humeral-head translation in arm-externalrotation at 90 of abduction, which can cause internal impingement-based
undersurface rotator cuff tendinopathy [5]. Also, tightness of internal rotation
at the glenohumeral joint results in excessive scapular protraction in arm-forward
flexion or the follow-through motion to allow the arm a complete arc of motion in
throwing or serving. The excessive protraction may result in external impingement due to decreased acromial elevation [4 7].
Inflexibility of the muscles that insert on the coracoid process, the pectoralis
minor, and the short head of the biceps is also common. Tightness in these muscles
also leads to scapular protraction, decrease in scapular posterior tilt, and a decrease
in the subacromial space height, which is associated with external impingement
[6,7].
These alterations may be evaluated in the clinical examination. GIRD should be
evaluated measuring true glenohumeral rotation by goniometric means in both
shoulders with the scapulae stabilized. Side-to-side differences greater than 25
are considered significant for GIRD [5]. The spinal level estimation technique
for arm internal rotation has at least 6 of freedom, only one of which is glenohumeral motion, and does not correlate with goniometric measurements [8]. Coracoid-based tightness is more difficult to quantitate, but can be established by
palpating the tight muscles and feeling the tautness along the course of the tendons.
This test is usually painful due to the tightness.
Strength
One of the clinical hallmarks of rotator cuff tendinopathy is alteration in rotator
cuff strength, especially in empty can isolated supraspinatus testing, or in
resisted external rotation, either at the side or at 90 abduction. Isolated testing of
each of the individual rotator cuff muscles by the standard techniques is used
diagnostically in the clinical examination, and they invariably demonstrate the
weakness. Some of the demonstrated weakness may be more apparent than real.
Rotator cuff muscle activation, and the resultant force production, may be
decreased up to 23% in the presence of excessive scapular protraction [9]. Rotator
cuff strength will often test normal or improved if the scapula is positioned in
retraction [9]. It is best to test isolated rotator cuff strength with the scapula in a
stabilized retracted position.
Rotator cuff strength balance is also frequently altered in tendinopathy.
External rotation strength deficit, both at 0 and at 90 of abduction, is the most
common finding [4,5]. This alters the force couple for humeral head stabilization
and depression.
Scapular position and motion
Weakness in the muscles that stabilize scapular motion and position is also a
common finding in rotator cuff tendinopathy. The serratus anterior and lower
839
trapezius are the most commonly altered [10 12]. This may result from a true
deficit in strength [9], an inhibition of activation [11], and an alteration in activation
sequencing [10,12,13]. These muscles are particularly involved with horizontal
and vertical stabilization of the scapula [13 15]. Deficiencies in activation in these
muscles decrease posterior tilting and elevation of the acromion, contributing to
external impingement [7,10,14], and increase scapular protraction.
The combination of glenohumeral rotation inflexibility, coracoid based anterior
muscle tightness, and posterior muscle weakness results in alterations in scapular
position at rest and motion-upon-arm motion that are collectively called scapular
dyskinesis [14]. These alterations can be evaluated by observing scapular posture
from behind with the patient in a resting position, and then by having the patient
elevate his arms in the scapular planes three to five times. Attention should be paid
to the symmetry of the medial scapular border to look for unilateral prominence
along the border. Specific patterns of dyskinesis in single planes have been
described [16]. Excessive acromial anterior tilt and protraction producing inferior
medial border prominencetype I, and excessive superior scapular translation
producing superior medial border prominencetype III, are both associated with
external impingement and rotator cuff tendinopathy. Occasionally, these patterns
may be seen in combination, and create an extra degree of acromial depression.
Clinical applicationanatomically intact rotator cuff tendinopathy

Flexibility
Tight coracoid based muscles may be stretched by the open book stretch
(Fig. 1). Arms should be placed at the side to reduce the risk of provoking
thoracic outlet symptoms. Internal rotation deficit should be corrected by specific
rotation exercises with the scapula stabilized (Fig. 2). The classical horizontal
Fig. 1. The open book stretch for tight anterior coracoid muscles.
840
Fig. 2. Stretch to specifically address internal rotation deficit.
adduction stretch creates an impingement position, does not stretch rotation, and
increases scapular protraction.
Scapular control
Improvement in strength of the lower trapezius and serratus anterior is based not
only on increasing strength production, but also on decreasing inhibition and
restoring normal muscle activation patterns. Early exercises should be prescribed at
submaximal activation levels with the arm below 90 abduction, to avoid
impingement-related pain and inhibition, and should use facilitation of activation
by trunk-muscle activation [17]. Examples of exercises include scapular pinches,
low rows (an isometric exercise combining hip/trunk extension), scapular
retraction, and arm extension (Fig. 3), and integrated diagonal trunk rotation/
scapular retraction (Fig. 4) or trunk extension/scapular retraction. As the arm can be
moved toward 90 elevation, closed chain exercises like the scapular clock may
be added (Fig. 5). Further progressions in scapular control exercises will involve
integration with rotator cuff activation.
Rotator cuff activation
Rotator cuff rehabilitation should be emphasized when the cuff is anatomically
intact or strong enough to withstand the applied loads, and when a stable scapular
base has been established for activation and for acromial clearance. The clinical
evidence for scapular stability includes resolution of scapular dyskinesis, with
control of scapular retraction. Rotator cuff activation is most efficient when it is
done in an integrated manner with other potent facilitators of rotator cuff
activation such as the lower trapezius and latissimus dorsi [17].
Rotator cuff rehabilitation must be graded in intensity of activation and position
of activation, so as to not place undue strains on the injured cuff and thus to avoid
reinjury. One method of estimating the strain load is to evaluate the percentage of
841
Fig. 3. The low row exercise to activate the serratus anterior and the lower trapezius.
maximal voluntary contraction (MVC) that a muscle is generating in an exercise. A

spectrum of activation can then be demonstrated (Table 1). Early passive and active
assisted range-of-motion exercises develop only 5% MVC [18]. These exercises
include supported positions of the hand and emphasized humeral head depressions.
The transition to more challenging types of exercises is a crucial part of the
rehabilitation protocol. Studies in our lab (Wise et al, submitted for publication)
show that changing type of exercise (closed- versus open-chain), hand position
(horizontal versus vertical versus diagonal), and arm velocity (slow versus fast) can
affect percent MVC activation. This study documented a progressive increase in
MVC activation from 11% to 18% in horizontal closed-chain exercises (Fig. 6)
through vertical closed-chain exercises (Fig. 7), horizontal open-chain exercises,
and diagonal closed-chain exercises (Fig. 8). Horizontal closed- or open-chain
842
Fig. 4. Integrated diagonal trunk rotation/scapular retraction.
exercises at faster speeds increased the activation to 27% and 34% MVC
respectively. This progression may be used as a template to structure exercises
that gradually increase the demand on the healing cuff. Final progressions can be
open-chain plyometric type exercises. Isolated rotator cuff exercises using rubber
tubing or other resistance in specific arm positions may be done at the end of the
rehabilitation sequence.
Clinical applicationsurgically repaired rotator cuff tendinopathy

Protection of the healing tendon from excessive tensile or shear load is the
prominent factor in the early rehabilitation stages. The length of time for
843
Fig. 5. Scapular clock exercises. The hand is stabilized and the scapula may be moved in a closed
chain fashion to the points of the clock. (A) Elevation to 12:00. (B) Retraction to 9:00.
protection varies with the underlying tissue and the type of repair, but usually
takes 6 to 10 weeks. Rehabilitation may be performed during this time, however.
Emphasis is placed on proximal kinetic chain and scapular rehabilitation, and
development of shoulder motion in safe planes.
Most of the kinetic chain and scapular exercises can be performed without
inducing shear at the repair. All of the integrated trunk extension/scapular
retraction or trunk rotation/scapular retraction exercises can be done while the
arm is still in a sling.
Passive and active assisted range-of-motion can be started in the planes below
60 abduction/flexion early in the rehabilitation stages. Closed-chain based
rotations, with the hand supported on a ball, allow motion without inducing shear
(Fig. 9). An alternative method to achieve rotation is to move the body around the
supported hand. The effect at the shoulder to increase motion is the same. Within
844
Table 1
Range-of-muscle activations for common exercises
Exercise
Activation % MVC (SD)
Self-assisted elevation
Open-chain pendulum
Horizontal closed-chain, 45/sec
Stick assisted vertical
Vertical closed-chain
Horizontal open-chain, 45/sec
Diagonal closed-chain
Diagonal open-chain
Horizontal closed-chain, 100/sec
Horizontal open-chain, 100/sec
Scaptionweights
3 (4)
9 (12)
11 (6)
13 (17)
13 (7)
15 (9)
18 (12)
22 (11)
27 (17)
34 (18)
74 (33)
Abbreviations: MVC, maximal voluntary contractions; SD, standard deviation.
2 or 3 weeks, the same supported position at low levels of abduction/flexion can be

used to initiate humeral head depression exercises, starting the rotator cuff
progressions as previously outlined. Care must be maintained to keep the rotator
cuff activation and strain load within the limits imposed by the healing tissue.
Using the progression framework outlined in Table 1 can increase the margin
of safety.
Prehabilitation
Completion of rehabilitation of rotator cuff tendinopathy requires fulfillment
of specific criteria regarding healing, range-of-motion, strength, and kinetic chain
restoration [15,19]. Frequently the patient will then return to the same activity or
Fig. 6. Horizontal closed-chain exercise. The arm slides along a board or other support.
845
Fig. 7. Vertical closed-chain exercise.
sport that created the injurious stresses, however, thereby placing himself at some
increased risk for repeat injury. Because the exact nature of the stresses operating
in rotator cuff tendinopathy is not completely known, the best strategies for
prevention are based on empirical protocols that attempt to understand the
inherent demands of the sport or activity, and then devise a maintenance exercise
program to maximize the bodys ability to withstand those demands [20]. The
specific flexibility, strength, power, anaerobic, and aerobic demands can then be
matched with specific exercise programs. Examples include trunk/hip strengthening and continued rotational flexibility exercises for baseball pitchers and
tennis players, scapular stabilization exercises in workers who continually use
Fig. 8. Diagonal closed-chain exercise.
846
Fig. 9. Closed-chain Codman exercises, rotations with the hand supported.
their arms extended in front or overhead, and isolated mild rotator-cuff strength
exercises in older patients.
Summary
Rehabilitation of the dysfunction that is associated with rotator cuff tendinopathy should be based on the evidence known about the pathoetiology of the
tendinopathy, what is known about the extent of the local anatomic injury,
the local and distant physiological and biomechanical alterations, and on the
knowledge developed regarding progressive loading of the injured or altered
structures. Prehabilitation, or prospective exercises to minimize future rotator cuff
loading stresses, should be included at the end of rehabilitation as part of the
return to function.
References
[1] Kibler WB, Chandler TJ, Pace BK. Principles of rehabilitation after chronic tendon injuries. Clin
Sports Med 1992;11:661 73.
[2] Leadbetter WB. Cell matrix response in tendon injury. Clin Sports Med 1992;11:533 78.
[3] Harryman DT, Sidles JA, Clark JM. Translation of the humeral head on the glenoid with passive
glenohumeral motions. J Bone Joint Surg 1990;72:1334 43.
[4] Tyler TF, Nicholas SJ. Quantification of posterior capsular tightness and motion loss in patients
with shoulder impingement. Am J Sports Med 2000;28:668 73.
[5] Burkhart SS, Morgan CD, Kibler WB. Shoulder injuries in the throwing athlete: the dead arm
revisited. Clin Sports Med 2000;19:125 69.
[6] Lukasiewicz AC, McClure P, Michener L. Comparison of three dimensional scapular position
and orientation between subjects with and without impingement. J Orthop Sports Phys Ther
1999;29:574 86.
[7] Bertoft ES, Thomas KA, Westerburg CE. The influence of scapular retraction and protraction on
the width of the subacromial space: an MRI study. Clin Orthop Rel Res 1993;296:99 103.
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[8] Mallon WJ, Herring CL, Sallay PI, et al. Use of vertebral levels to measure presumed internal
rotation at the shoulder: a radiographic analysis. J Shoulder Elb Surg 1996;5:299 306.
[9] Kebatse M, McClure P, Pratt N. Thoracic position effect on shoulder range of motion, strength,
and three dimensional scapular kinetics. Arch Phys Med Rehabil 1999;80:945 50.
[10] McQuade KJ, Wei SH, Smidt GL. Effects of local muscle fatigue on three dimensional scapulohumeral rhythm. Clin Biomech 1995;10:144 8.
[11] Glousman R, Jobe FW, Tibone JE, et al. Dynamic EMG analysis of the throwing shoulder with
glenohumeral instability. J Bone Joint Surg 1988;70:220 6.
[12] Cools AM, Witvroux EE, Deeclerq GA, et al. Scapular muscle recruitment pattern: trapezius
muscle latency in overhead athletes with and without impingement symptoms. Am J Sports Med
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[13] Bagg SD, Forrest WJ. EMG study of the scapular rotators during arm abduction in the scapular
plane. Am J Phys Med 1986;65:111 24.
[14] Kibler WB, McMullen J. Scapular dyskinesis and its relation to shoulder pain. J Am Acad
Orthop Surg 2003;11:142 51.
[15] Johnson G, Bogduk N, Nowitze A, et al. Anatomy and actions of the trapezius muscle. Clin
Biomech 1994;9:44 50.
[16] Kibler WB, Uhl TL, Maddux JWQ, et al. Qualitative clinical evaluation of scapular dysfunction:
a reliability study. J Should Elb Surg 2002;11:550 6.
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[18] McCann PD, Wootten ME, Kadaba MP, et al. A kinematic and EMG study of shoulder rehabilitation exercises. Clin Orthop 1993;288:179 88.
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2003, Vol.22, Issues 4, Current Concepts in Tendinopathy

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2003, Vol.22, Issues 4, Current Concepts in Tendinopathy

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Clin Sports Med 22 (2003) xi

Current concepts in tendinopathy

Tendinopathy? How can we devote an entire issue to tendinopathy? What ever

Clin Sports Med 22 (2003) xiii

Current concepts in tendinopathy

Clin Sports Med 22 (2003) 675 692

Types and epidemiology of tendinopathy

Department of Trauma and Orthopaedic Surgery, Keele University School of Medicine,

N. Maffulli et al / Clin Sports Med 22 (2003) 675692

Basic pathology of overuse tendon conditions

Achilles tendinopathy, Achilles paratendinopathy,

Supraspinatus syndrome (impingement syndrome,

N. Maffulli et al / Clin Sports Med 22 (2003) 675692

N. Maffulli et al / Clin Sports Med 22 (2003) 675692

Several subcategories have been identified by electron microscopy: (1) hypoxic

N. Maffulli et al / Clin Sports Med 22 (2003) 675692

Tendinopathies: new definitions

Epidemiologic approach to sports injuries

N. Maffulli et al / Clin Sports Med 22 (2003) 675692

specialist sports centers. Often studies cannot be compared, due to lack of

N. Maffulli et al / Clin Sports Med 22 (2003) 675692

Injury risk factors

N. Maffulli et al / Clin Sports Med 22 (2003) 675692

N. Maffulli et al / Clin Sports Med 22 (2003) 675692

injuries) [43,44]. Calcaneal apophysitis (Severs disease) is another common

Blood group distribution

N. Maffulli et al / Clin Sports Med 22 (2003) 675692

N. Maffulli et al / Clin Sports Med 22 (2003) 675692

N. Maffulli et al / Clin Sports Med 22 (2003) 675692

N. Maffulli et al / Clin Sports Med 22 (2003) 675692

N. Maffulli et al / Clin Sports Med 22 (2003) 675692

Paratendinopathy of flexor carpi radialis

N. Maffulli et al / Clin Sports Med 22 (2003) 675692

N. Maffulli et al / Clin Sports Med 22 (2003) 675692

N. Maffulli et al / Clin Sports Med 22 (2003) 675692

N. Maffulli et al / Clin Sports Med 22 (2003) 675692

Clin Sports Med 22 (2003) 693 701

Cell death and tendinopathy

Apoptosis is an active, often physiological, process distinguished from necrosis,

Modes of cell death

* Corresponding author. Orthopaedic Research Institute, St George Hospital Campus, University

J. Yuan et al / Clin Sports Med 22 (2003) 693701

Toxins, hypoxia, trauma

Physiological and pathological conditions

J. Yuan et al / Clin Sports Med 22 (2003) 693701

Biological significance of apoptosis

J. Yuan et al / Clin Sports Med 22 (2003) 693701

Apoptosis also plays a critical role in removing unwanted, injured, or potentially

Apoptosis in degenerative diseases

J. Yuan et al / Clin Sports Med 22 (2003) 693701

J. Yuan et al / Clin Sports Med 22 (2003) 693701

Fig. 6. Immunohistochemical identification of fibroblast-like cells and macrophages. (a) In

J. Yuan et al / Clin Sports Med 22 (2003) 693701

Mechanisms involved in apoptosis in tendinopathy

J. Yuan et al / Clin Sports Med 22 (2003) 693701

J. Yuan et al / Clin Sports Med 22 (2003) 693701

Clin Sports Med 22 (2003) 703 710

Compression etiology in tendinopathy

Chronic tendon problems or tendinopathies remain a common problem for

L.C. Almekinders et al / Clin Sports Med 22 (2003) 703710

L.C. Almekinders et al / Clin Sports Med 22 (2003) 703710

Regardless of the factors involved in the development of a chronic tendon

Clinical challenges to the traditional concept

L.C. Almekinders et al / Clin Sports Med 22 (2003) 703710