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

quite so often!

Mark D. Miller, MD

Department of Orthopedic Surgery

University of Virginia

Charlottesville, VA 22903-0753, USAjust 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 roomsForeword

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

Clin Sports Med 22 (2003) xiE-mail address: [email protected]

0278-5919/03/$ see front matter D 2003 Elsevier Inc. All rights reserved.

doi:10.1016/S0278-5919(03)00050-4

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; site-

specific 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 theseefforts will come a better understanding and more efficacious treatment for

tendon injuries.Preface

Current concepts in tendinopathy

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

W. Ben Kibler, MD

Guest Editor

Clin Sports Med 22 (2003) xiiiW. Ben Kibler, MD

Lexington Clinic Sports Medicine Center

1221 S. Broadway

Lexington, KY 40504, USA

E-mail address: [email protected]


doi:10.1016/S0278-5919(03)00069-3

Clin Sports Med 22 (2003) 675692Types and epidemiology of tendinopathy

Nicola Maffulli, MD, MS, PhD, FRCS(Orth)a,*,Jason Wong, MRCSb, Louis C. Almekinders, MDc

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

North Staffordshire Hospital, Thornburrow Drive, Hartshill, Stoke on Trent,

Staffordshire, ST4 7QB, UKbDepartment of Orthopaedic Surgery, University of Aberdeen Medical School, Polwarth Building,

Foresterhill, Aberdeen AB25 2ZD, UKcDepartment 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 repre-sentative, are only a small cross-section of clinically relevant tendinopathies


doi:10.1016/S0278-5919(03)00004-8

* 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: [email protected] (N. Maffulli).

(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

semimembranosus

N. Maffulli et al / Clin Sports Med 22 (2003) 675692676Supraspinatus Supraspinatus syndrome (impingement syndrome,

swimmers shoulder)

Other rotator cuff tendons (infraspinatus, Rotator cuff tendinopathy or tearbased on the work of several authors [68] (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)

Patella Patellar tendinopathy, patellar peritendinopathy, patellar

apicitis (jumpers knee), Osgood-Schlatter lesion,

Sinding-Larsen-Johansson lesion

Posterior tibial Medial tibial syndrome

Iliotibial tract Iliotibial tract syndrome

Biceps femoris, semitendinosus, Hamstring syndromesubscapularis, teres minor)

Common wrist extensors Lateral epicondylitis (tennis elbow)

Common wrist flexors Medial epicondylitis (throwers elbow,

golfers elbow, little league elbow)

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)

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

Tendinitis Symptomatic degeneration

of the tendon with vascular

disruption and inflammatory

repair response

Degenerative changes as noted

above with superimposed evidence

of tear, including fibroblastic and

myofibroblastic proliferation,

hemorrhage and organizing

granulation tissue.

Paratenonitis Inflammation of the

outer layer of the tendon

(paratenon) alone, whether

Mucoid degeneration if the areolar

tissue is seen. A scattered mild

mononuclear infiltrate with or

N. Maffulli et al / Clin Sports Med 22 (2003) 675692 677athletes 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 infiltra-

tion 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.

or not the paratenon is

lined by synovium

without focal fibrin deposition and

fibrinous exudate

Paratenonitis

with tendinosis

Paratenonitis associated with

intratendinous degeneration

Degenerative changes as noted in

tendinosis with mucoid degeneration

with or without fibrous and scattered

inflammatory cells in the paratenon

alveolar tissue

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) fibrocar-

tilaginous 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 ultrasono-

graphic 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 inflam-

mation. 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 con-

dition. Hence, we recommend that the use of the misnomer tendinitis in the

context of overuse tendon conditions be abandoned [5,21].

Paratenonitis

N. Maffulli et al / Clin Sports Med 22 (2003) 675692678Paratenonitis 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

sheath). Examples include paratenonitis of the abductor pollicis longus and exten-

sor pollicis longus (de Quervains disease), and of the flexor hallucis longus as it

mostly with tendon ruptures [2426]. Tendinosis implies tendon degeneration

without clinical or histological signs of intratendinous inflammation, and is notnecessarily 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.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 associatedN. Maffulli et al / Clin Sports Med 22 (2003) 675692 679Epidemiologic 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

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 [2729].

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 denom-

inator-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

N. Maffulli et al / Clin Sports Med 22 (2003) 675692680rugby are played more in Europe, cricket has the maximum number of

participants in the Commonwealth countries, and many countries have their

indigenous sports.

an overuse injury as an injury which arose because the limits of tolerance of themusculo-skeletal system had been exceeded by repetitive submaximal loading

[34]. Prospective and retrospective studies are a good source of injury character-

istics. 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 compli-

cated 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: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

N. Maffulli et al / Clin Sports Med 22 (2003) 675692 681Malalignment (ie, excessive pronation, femoral neck anteversion, etc)

Limb length discrepancy

Footwear and equipment

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].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 injuryMuscular imbalance

Muscular insufficiency

Extrinsic risk factors:

Training errors (ie, distance, intensity, hill work, technique, fatigue, etc)

Training surfaces

Environmental conditions

N. Maffulli et al / Clin Sports Med 22 (2003) 675692682Injuries 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

Josza et al [50] reported a significant association between the increased risk

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 withthat 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 0.68of 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 peritendinop-

athy (A/O ratio, 0.70) when compared with the blood group distribution of the

Finnish population (A/O ratio, 1.42) [51].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

N. Maffulli et al / Clin Sports Med 22 (2003) 675692 683for 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.

Specific tendinopathies

Achilles tendinopathy

The etiology of Achilles tendon overuse injuries is multifactorial [53]. Train-

ing 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

N. Maffulli et al / Clin Sports Med 22 (2003) 67569268483 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

to suffer from Achilles tendinopathy in the initially uninvolved contralateral ten-

don [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 Osgood-

Schlatter 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].

N. Maffulli et al / Clin Sports Med 22 (2003) 675692 685Iliotibial 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

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 asso-

ciated with hard running [76]. At 20 to 30 of knee flexion, the ITB rubs againstthe 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. Amore 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 tendinop-

athy, 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].

N. Maffulli et al / Clin Sports Med 22 (2003) 675692686Hamstring 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

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

N. Maffulli et al / Clin Sports Med 22 (2003) 675692 687may 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].

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 carpometa-

carpal 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 postpartumwomen and 30 nonpregnant women. Conserv-

ative 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

N. Maffulli et al / Clin Sports Med 22 (2003) 675692688patients [91]. This suggests that hormonal status may play a role in the etiopatho-

genesis of the condition.

findings in 40 patients. Acta Orthop Scand 1997;68:1705.

[13] Movin T, Kristoffersen-Wiberg M, Shalabi A, et al. Intratendinous alterations as imaged byultrasound and contrast medium enhanced magnetic resonance in chronic achillodynia. Foot

Ankle Int 1998;19:3117.

[14] Cook JL, Khan KM, Kiss ZS, et al. Asymptomatic hypoechoic regions on patellar tendon ultra-

sound: a 4-year clinical and ultrasound followup of 46 tendons. Scand J Med Sci Sports 2001;

11(6):3217.

[15] Cook JL, Khan KM, Kiss ZS, et al. Prospective imaging study of asymptomatic patellar tendi-

nopathy in elite junior basketball players. J Ultrasound Med 2000;19(7):4739.

[16] Cook JL, Khan KM, Kiss ZS, et al. Patellar tendinopathy in junior basketball players: a con-

trolled clinical and ultrasonographic study of 268 patellar tendons in players aged 1418 years.

Scand J Med Sci Sports 2000;10(4):21620.

[17] Cook JL, Khan KM, Harcourt PR, et al. Victorian Institute of Sport Tendon Study Group.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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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 [36].

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 nuclearCell 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

Clin Sports Med 22 (2003) 693701contents into the intercellular milieu with an inflammatory response and secondary

damage [7,10].


doi:10.1016/S0278-5919(03)00049-8

* 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: [email protected] (G.A.C. Murrell).

Table 1

Criteria distinguishing apoptosis from necrosis

Features Necrosis Apoptosis

Stimuli Toxins, hypoxia, trauma Physiological and pathological conditions

without ATP depletion

Energy requirement None ATP-dependent

Histology Cellular swelling,

disruption of organelles,

death of patches of tissue

Chromatin condensation, apoptotic bodies,

death of single isolated cells

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):3007; with permission.

J. Yuan et al / Clin Sports Med 22 (2003) 693701694Apoptosis

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 shrinkFig. 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):13729;

with permission.)

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.

J. Yuan et al / Clin Sports Med 22 (2003) 693701 695Fig. 2. Apoptosis in rotator cuff tendon was assessed by in-situ DNA end labeling assay. (a) Sub-

scapularis tendon from a rotator cuff-normal patient showing only a few apoptotic cells. (b) A largenumber 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):13729; with permission.)

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 [1820], 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].

J. Yuan et al / Clin Sports Med 22 (2003) 693701696Fig. 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, andthe 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):13729;

with permission.)

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):13729; 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). (FromYuan J,

Murrell GA, Wei AQ, et al. Apoptosis in rotator cuff tendonopathy. J Orthop Res 2002;20(6):13729;

with permission.)

J. Yuan et al / Clin Sports Med 22 (2003) 693701 697

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).

J. Yuan et al / Clin Sports Med 22 (2003) 693701698Fig. 6. Immunohistochemical identification of fibroblast-like cells and macrophages. (a) Indegenerative 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. (FromYuan J, Murrell GA, Wei

AQ, et al. Apoptosis in rotator cuff tendonopathy. J Orthop Res 2002;20(6):13729; with permission.)

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,

J. Yuan et al / Clin Sports Med 22 (2003) 693701 699including 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;36:3923; with permission.)

Hospital and NiCox Corporation.

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[8] Lockshin RA, Zakeri ZF. Physiology and protein synthesis in programmed cell death. Early

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[1] Kanduc D, Mittelman A, Serpico R, et al. Cell death: apoptosis versus necrosis [review]. Int JSummary

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

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20:13729.

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[27] Yuan J, Murrell GAC, Trickett A, et al. Involvement of cytochrome c release and caspase-3

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[29] Murrell GA. Understanding tendinopathies. Br J Sports Med 2002;36:3923.

Compression etiology in tendinopathy

Louis C. Almekinders, MDa,*, Paul S. Weinhold, PhDb,Nicola Maffulli, MD, PhD, MS, FRCS(Orth)c

aDivision of Orthopaedic Surgery, North Carolina Orthopaedic Clinic, 4309 Medical Park Drive,

Suite 100B, Durham, NC 27704, USAbDepartment of Orthopedic Surgery, Sports Medicine Section,

University of North Carolina School of Medicine, Chapel Hill, NC 27599, USAcDepartment 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 [35]. 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 tendino-

pathy have been described. At this point, the anatomic location of the tendino-

pathy 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

Clin Sports Med 22 (2003) 703710[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;


doi:10.1016/S0278-5919(03)00067-X

* Corresponding author.

E-mail address: [email protected] (L.C. Almekinders).

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 isnot 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 musclehowever, 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

L.C. Almekinders et al / Clin Sports Med 22 (2003) 703710704imbalances 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.

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 withRegardless 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 signifi-

cant 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, inflexi-

bility, 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 patella

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

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