Narrative Review

Shoulder tendinopathy
Daniel Lorenz1,2, John C. Walker3, Dennis Burke4
1
Providence Medical Center, Kansas City, KS, USA, 2Rockhurst University, Kansas City, MO, USA, 3Beacon
Orthopedics, Sharonville, OH, USA, 4TMI Sports Medicine, Arlington, TX, USA

Background: Shoulder tendinopathy is a common condition in physical therapy, and the term tendinopathy
covers a broad spectrum of pathology. Additionally, there is a lack of consensus on proper terminology for
shoulder disorders. Nomenclature for shoulder disorders includes such terms as impingement, tendinitis,
tendinosis, and tendinopathy. The continuum of physiologic changes with tendinopathy, as well as the
various causes of tendinopathy are complex and require a detailed physical examination to discover the
source of pain and extent of pathology to determine appropriate course of treatment.
Objectives: The purpose of this review is three fold. First, the physiology of shoulder tendinopathy will be
discussed. Second, the various mechanisms for shoulder tendinopathy will be explored. Finally, a review of
the proposed interventions for shoulder tendinopathy will be highlighted, citing the best available evidence
for each intervention.
Major findings: Both the causes and the physiology of shoulder tendinopathy require a multi-faceted
approach to maximize outcomes. There is a paucity of data supporting modalities in the management of
shoulder tendinopathy, but high-energy extracorporeal shock wave therapy has shown some effectiveness
in calcifying tendinitis. Therapeutic exercise is generally accepted as a beneficial intervention, but definitive
conclusions cannot be made at this time. Furthermore, eccentric training for management of tendinopathies
in general is gaining more support in the literature, but evidence for its utilization in shoulder tendinopathy is
scarce.
Conclusions: A host of causes and physiologic changes exist for shoulder tendinopathy, in addition to
multiple treatment options. However, no definitive conclusions can be made regarding the best treatment
for shoulder tendinopathy. Current evidence is largely anecdotal and speculative. More randomized,
controlled trials are needed that compare modalities, manual therapy, and therapeutic exercise.
Keywords: Rotator cuff, Shoulder pain, Tendinitis, Tendinopathy, Tendinosis

Introduction overhead tasks. In a survey of 644 elderly people over

Musculoskeletal disorders of the shoulder are extre- age 70, prevalence of shoulder disorders was 21, and
mely common, with reports of prevalence ranging 70% of cases involved the rotator cuff.7 From a
from one in three people experiencing shoulder pain demographic perspective, rotator cuff disorders have
at some stage of their lives to approximately half been found to be more frequent in women,7 but
the population experiencing at least one episode overweight and obese men also had a high prevalence
annually.1 Shoulder pain is only second to that of of chronic rotator cuff tendinitis.7 Odds ratios
complaints stemming from low back pain in the determined that statistically significant increased risk
general population,2 and the rotator cuff and for shoulder disorders was also found in those with
surrounding tissues are the most common sources increased waist circumference and waist-to-hip ratios,
of shoulder pain.3,4 Over the course of one-year in as well as a history of smoking.9 Additionally, odds
eleven general practices, rotator cuff tendinitis was ratios revealed that diabetes was associated with
the most frequently recorded disorder, constituting chronic rotator cuff tendinitis.9
29% of cases.5 Silverstein et al.6 evaluated prevalence, Shoulder tendinopathies are not exclusive to the
incidence, and persistence of non-traumatic rotator rotator cuff. In a prospective study of 200 shoulders
cuff tendinitis over a one-year period in a working undergoing arthroscopic subacromial decompression
population and found prevalence at baseline was for impingement syndrome,10 the incidence of chro-
7.6% but 18.6% at a year due to increased exposure to nic biceps tendon inflammation was 63%. Addi-
tionally, degenerative changes were found in 13%.
The study found a high incidence of chronic infla-
Correspondence to: Daniel Lorenz, Providence Medical Center, 8929 mmation of the long head of biceps in patients with
Parallel Parkway, Kansas City, KS 66112, USA. Email: danielslorenz@
gmail.com painful rotator cuff disease and arthritic shoulder

ß W. S. Maney & Son Ltd 2011

DOI 10.1179/1743288X11Y.0000000042 Physical Therapy Reviews 2011 VOL . 16 NO . 5 365
Lorenz et al. Shoulder tendinopathy

conditions.10 The long head of biceps is a humeral are significant differences in the physiological heal-
head depressor11 and it has been found to be more ing responses of acutely and chronically diseased
important than any other rotator cuff muscle in tendons.19 The reader is referred to Table 1 outlining
stabilizing the glenohumeral joint against anteri- the stages of tendon injury as previously proposed
or translation with an artificial Bankart lesion.12 by Nirschl.20
Therefore, it is plausible to conclude that the pro-
ximal bicep may be a primary or secondary source
Anatomy and physiology of tendinopathy
Tendons transmit force generated by muscle to bone,
of shoulder dysfunction or pain in rotator cuff
and act as a buffer by absorbing external forces to limit
disorders.
muscle damage.21 The structure of tendons reveals that
The purpose of this review is to discuss the anatomy
they have a wavelike appearance at rest making them
and physiology of tendinopathy as well as to clearly
available to stretch for functional demands. Tendons
define the often ambiguous terminology. Finally, va-
are composed of 30% Type I collagen, glycosami-
rious interventions to treat shoulder tendinopathy will
noglycans, elastin, and 68% water.22 Collagen’s role
be highlighted.
is to resist tensile forces, while elastin functions to
Terminology increase the flexibility of tendons. Glycosami-
Nomenclature for tendinopathy is often confusing noglycans and water are the primary components
and inappropriately described. Rotator cuff disease of ground substance.23 Ground substance contains a
has been described by Neer13 as a progressive disorder high portion of water, thereby allowing diffusion of
of the rotator cuff tendons which begins with an nutrients and waste products.23 Ground substance
acute tendinitis. It then progresses to tendinosis with also serves as a mechanical barrier against invading
degeneration and partial thickness tears, ultimately bacteria and microorganisms.23 Finally, ground
resulting in full thickness rupture.13 Rotator cuff substance serves to help maintain interfiber distance
tendinopathy is used to signify a combination of pain to prevent adhesions.23 Ground substance content
and impaired performance associated with rotator cuff seems to decrease in age, likely contributing to
tendons.4,14 The term ‘tendonitis’ is often used as a decreased flexibility in aging. Tendon injuries can
catch-all label for tendon injuries, but histological happen essentially at three locations. Tendon injury
studies have shown that frequently, no actual inflam- can be midsubstance, or in the body of the tendon
mation exists.15,16 Leadbetter17 previously defined proper. There is also potential for injury at the
tendonitis as a symptomatic degeneration of a tendon enthesis, which is the attachment of a tendon,
with vascular disruption and inflammatory repair. ligament, or joint capsule to the bone.24 Injury at
Evidence for inflammatory cell infiltrate in early mild/ the enthesis is commonly referred to ‘insertional’
moderate human tendinopathy exists, particularly tendinopathy. Lastly, tendon injury can occur at the
mast cells and macrophages, suggesting role of im- musculotendinous junction.
mune pathways in early tendinopathy.18 Leadbetter17 Tendons are prone to injury because of a ‘tendon
has also defined tendinosis to be a focal area of non- paradox’ that exists. Oxygen consumption is seven
inflammatory degeneration that may be asympto- and a half times lower in tendons and ligaments than
matic. Complicating this matter further is that there skeletal muscle.25 Previously, there has been evidence

Table 1 Nirschl’s stages of tendinopathy

Stage Diagnosis Macroscopic pathology Histologic findings Clinical signs

0 Healthy No inflammation Organized collagen, Firm tendon, not painful, absent

absent blood cells swelling, normal temperature
I Acute Symptomatic tendon Degenerative changes Acute swelling, pain, local
tendinitis degeneration, increased w/microtears, inflammatory tenderness, warmth, dysfunction
cellularity; vascular disruption; cells in paratenon; focal
inflammation of paratenon collagen disorientation
II Chronic Increased tendon degeneration Greater evidence of Chronic pain w/tenderness,
tendinitis and vascularity microtears, increased increased dysfunction, person
levels of collagen voluntarily unloads structure
disorientation in tissue
hypercellularity
III Tendinosis Intratendinous degeneration Increased celluarity, Palpable tendon enlargement,
due to microtrauma, cellular/tissue neovascularization, focal swelling of tissues, increased
aging; vascular compromise necrosis, collagen dysfunction w/or w/o pain, tendon
disorganization and sheath may be swollen
disorientation
IV Rupture Tendon failure Complete disruption Weak and painful muscle testing,
of fibers inability to move affected joint,
zclinical tests for tendon disruption

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 Lorenz et al. Shoulder tendinopathy

showing hypoxic damage throughout the spectrum of influence tendon structure as well as performance.
rotator cuff disease, which may contribute to loss of These factors result in degeneration or breakdown of
cells by apoptosis.26 Apoptosis is programmed cell the tendon due the natural process of aging, poor
death to maintain health in tissues by eliminating old vascularity, altered biology, and inferior mechanical
cells, unnecessary cells, or unhealthy cells.27 A low properties resulting in damage when the tendon is
metabolic rate and anaerobic generating capacity are stressed.4
needed in tendons to carry loads and maintain Age-related degenerative changes include de-
tension for long periods. Risk of inadequate or creased cellularity, thinning or disruption of the
deficient blood supply is reduced because of the lower fascia surrounding the tissue, and calcification.30 All
metabolic rate in tendinous tissue. The lower meta- of these changes are irreversible. There is an area on
bolic rate requires less oxygen for tendons during the articular surface of the rotator cuff that is a zone
functional tasks. However, the low metabolic rate in of relative poor vascularity which is worsened with
tendons results in slow healing after injuries. Thus, age as well.30 Additionally, the articular surface of
this may explain why tendon injuries persist or the rotator cuff has an ultimate stress to failure that is
develop chronic issues.25 If the aggravating stimulus approximately half that of the bursal surface, with
is not removed, or the rehabilitation specialist does thinner and less uniformly arranged collagen bundles.
not provide the appropriate environment for regen- The changes in vascularity of the rotator cuff and
eration, the tendon will be in a perpetual state of age-related degenerative changes may be responsible
breakdown and attempted but failed healing. The end for articular-surface tears in patients older than
result is pain, dysfunction, and potentially, disability. 40 years without other clear mechanisms. This has
been supported in the literature by both cadaveric
Causes of Tendon Injuries and clinical studies.30 Potentially, another intrinsic
Pathoetiology of cuff failure results from a combina- mechanism for rotator cuff tendinopathy is differential
tion of factors.1 The shoulder is a joint with high shear stress within the tendons. Loading the tendon in
range of motion (ROM) and long lever arm. There- various arm positions may result in strain differentials
fore, the shoulder is liable to injuries that may only between the articular and bursal side of the supraspi-
heal partially and have residual symptoms.9 natus. Greater strain has been shown on the supras-
Occupational demands have previously been re- pinatus tendon articular side with the arm positioned
ported to cause shoulder tendinopathy. In a study28 at the beginning of elevation ,30u.4 A progressive
consisting of 1961 workers, 787 were referred for increase in strain is also seen as elevation increases to
shoulder pain. Neither frequency of movements or 120u. Greater bursal side strain was seen at about 90u
lack of pauses in shoulder flexion was related to of elevation or in the mid-range. Biomechanical conse-
disease prevalence, but increased force requirements quences of intrinsic complex tendon properties are
increased risk slightly.28 Determinants of chronic only exacerbated in combination with extrinsic factors
shoulder tendinitis in a sample of 8028 persons aged such as over use or repetitive strain associated with
30 years or more revealed that work-related cumula- daily activities as well as sports.4
tive loading on the shoulder, increased age, and Other relevant examples of anatomical factors
insulin-dependent diabetes.8 include presence of subacromial spurs, ossification
Tendons respond to repetitive overload beyond the of the coracoacromial ligament, arthritis of the
physiological threshold by either inflammation of their acromioclavicular joint, and the subacromial space
sheath, degeneration of their body, or a combination itself.13,31 The shape, orientation, slope of the
of both.21 There are a host of reasons that tendon acromion, as well as osseous changes in the acro-
injuries occur, but the etiology remains unclear, and mioclavicular joint all play a role in the function of
many causes have been theorized.21 Typically, there the rotator cuff tendons.31,32 The shape of the
are two main types of injury mechanisms that have acromion, as described by Bigliani et al.,32 may
several potential sources in each category.29 Intrinsic include Type 1 (flat), Type 2 (curved), or Type 3
causes are factors contributed to a patient’s make-up. (hooked) and shape of the acromion has been linked
Intrinsic risk factors include but are not limited to such to rotator cuff tendinopathy. It is still controversial
things as anatomical abnormalities or malalignments whether or not acromion shape is congenital or
(i.e. acromial abnormalities), age, gender, joint laxity, acquired with age.4 Multiple studies have shown that
muscle weakness, biomechanics/sport technique, fati- the association of shape and severity of the acromion
gue, and psychological factors. Intrinsic causes may or and rotator cuff pathology show trends of greater
may not be adjusted or changed and may be something prevalence of hooked acromions in patients with
that the subject must learn to live with, or possibly impingement and rotator cuff tears.33–35 Finally, the
make modifications in lifestyle or occupation.4 In- slope of the acromion can also cause rotator cuff
trinsic mechanisms of rotator cuff tendinopathy tendon compression in the subacromial space.36 The

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Lorenz et al. Shoulder tendinopathy

flatter or more horizontal the slope is associated with humeral head translation and decreased abduction
subacromial impingement, changes of the rotator torque.
cuff, and a greater loss of function in patients with A discussion on shoulder tendinopathy would not
tendinopathy.36 be complete without highlighting the proximal bicep
Unlike intrinsic factors, extrinsic mechanisms can tendon as it is intimately involved in shoulder
usually be easily changed and modified to help the function and pathology. Although its role in shoulder
patient. In the athletic population, the two main function has not been clearly defined, the proximal
extrinsic causes of injury to tendons are overuse and long head of biceps tendon (LHBT) is an area of
training errors.29,37–41 In general, alterations in scap- dysfunction in the shoulder that affects people of all
ular or humeral kinematics, postural abnormalities, ages and activity levels.45 The biceps stretch from
rotator cuff and scapular muscle performance deficits, scapula to forearm aiding in both shoulder and elbow
and decreased extensibility of pectoralis minor or pos- function. The LHBT attachment sites are both intra
terior shoulder are a few other examples of modifiable and extra-capsular with half to the superior glenoid
extrinsic causes.4 tubercle and half to the superior glenoid labrum
The reasons for altered scapular kinematics in making it a very dynamic structure.46 LHBT tendi-
patients with rotator cuff tendinopathy are also not nopathy can be broken down into three categories:
clearly defined, but in theory, include shortening of degeneration, instability, and SLAP lesions. These
the pectoralis minor muscle, posterior shoulder categories are not exclusive and have been shown to
tightness, poor scapular and rotator cuff muscle contribute to each other.45
performance, and increased thoracic spine flexion or Degeneration of the LHBT has been shown to be
kyphosis.4,42,43 Poor scapular muscle performance either a factor of an acute inflammation and the
has been identified in patients with rotator cuff associated natural histological response or change
tendinopathy.42 Patients with rotator cuff tendino- over time secondary to faulty mechanics.47 Neer48
pathy have been shown to have decreased perfor- reported that biceps inflammation was due to LHBT
mance of the serratus anterior and lower trapezius impingement under the subacromial arch. Murthi
and increased activity of the upper trapezius.42 and others10 similarly correlated most LHBT dys-
Potentially, poor performances of scapular muscles functions with rotator cuff disease in the elderly
can alter the position of the scapula and affect the population secondary to degeneration over time from
length tension relationship of the rotator cuff muscles subacromial impingement. Although the Murthi
and alter the subacromial space.4 Additionally, et al.10 study correlated LHBT tendinopathies to
thoracic kyphosis has been directly linked to a rotator cuff disease, Petersons’ dissection of over 150
decrease in subacromial space and a decrease in shoulders over the age 60 showed no such signs of
scapular posterior tilt, both of which have been LHBT tendinopathy.49 Also, two electromyography
linked to rotator cuff tendinopathy.43 (EMG) studies showed no LHBT activity in active
Biomechanical compensations exist as well. Patients movements in the shoulder in those without rotator
with rotator cuff tendinopathy demonstrate a great- cuff pathology.50,51
er superior and anterior translation of the humeral More recent studies have focused on athletes and
head with active elevation than patients who are the biomechanical factors that are linked with LHBT
asymptomatic.44 Scapular kinematic abnormalities have degeneration/inflammation. Baseball has had various
been identified in patients with rotator cuff tendino- studies link the throwing motion to impingement
pathy compared to healthy patients.42,43 Decreased and possibly biceps tendinopathy.52–54 The throwing
scapular posterior tilting, decreased upward rotation, motion is normally broken down into phases with
and increased internal rotation are all characteristics one being the follow through. During the follow
shown in patients with subacromial impingement.42,43 through the arm is placed in a position of horizontal
Altered biomechanics can result in a reduction of adduction and internal rotation. The follow through
subacromial space with arm elevation causing more phase brings the LHBT in close proximity and in
rotator cuff compression. some cases, contact with the coracoacromial arch. It
Posterior shoulder tightness can be due to adapta- has been shown LHBT strain is greatest in humeral
tions of the infraspinatus, teres minor, and or posterior horizontal adduction.55 This position may cause
deltoid musculature, osseous changes of the humeral biceps impingement over time due to the cumulative
head or glenoid retroversion.4 Deficits in rotator cuff effect of throwing on the shoulder, especially in
muscle performance contribute to rotator cuff ten- pitchers.56
dinopathy by leading to proximal migration and One common objective measurement found in the
subsequent rotator cuff compression in the subacro- overhead athlete, especially in baseball pitchers is
mial space.4 Decreased force particularly in the in- glenohumeral internal rotation deficit.53 Glenohumeral
fraspinatus muscle has resulted in increased superior internal rotation deficit is defined as any loss of internal

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 Lorenz et al. Shoulder tendinopathy

rotation in the glenohumeral joint greater than 20u as present in the throwing shoulder when examined
measured from the opposite side.57 Harryman et al.52 arthroscopically.65
found that any capsular tightness on the posterior side
of the glenohumeral joint will cause anterior transla- Interventions
tion of the humeral head which in turn places more Therapeutic Exercise
stress on the LHBT. The combination of these stresses, In a systematic review by Ainsworth and Lewis,68
coupled with the biomechanics of the follow through there is some evidence to support the use of exercise
may be a reason why baseball pitchers highest injury in the management of full thickness rotator cuff tears.
rate occurs at the shoulder.54 A recent Cochrane database review revealed that
Instability of the LHBT refers to the tendon and its exercise was demonstrated to be effective in terms of
articulation with the bicipital groove. This type of short-term recovery in rotator cuff disease and longer
tendinopathy occurs when there is a disruption of the term with respect to function.69 In addition, combin-
stabilizing structures that result in a subluxation or ing mobilization with exercise resulted in additional
dislocation of the LHBT.45 Since the LHBT is part of benefit when compared to exercise alone for rotator
the anterior stability complex of the shoulder, any cuff disease.69 Likewise, Crawshaw et al.70 found
factor that causes the humeral head to migrate similar results when it was combined with manual
forward could be a cause of biceps tendinopathy (i.e. therapy to a combined treatment of corticosteroid
posterior cuff tightness, repetitive maximal external injection plus exercise and manual therapy in patients
rotation, trauma, etc.).52 Most LHBT instabilities are with shoulder pain due to subacromial impingement
associated with another pathology, most commonly syndrome at twelve weeks. Recent reviews of
rotator cuff dysfunction58 with the demographic for literature revealed that therapeutic exercise and joint
most instabilities being young throwers.59 mobilizations had limited effectiveness for treatment
Superior labrum anterior to posterior (SLAP) of subacromial impingement syndrome.2,71 Compar-
lesions refer to a type of injury to the LHBT insertion ing surgical intervention to conservative treatment
into the superior glenoid tubercle and superior via exercise, surgery (arthroscopic subacromial de-
glenoid labrum.46,60 Snyder made the first classifica- compression) or supervised exercise significantly and
tion system of ‘SLAP’ lesions by separating them into equally improved rotator cuff disease (Stage II
four primary categories based on the extent and impingement) and treatment costs were higher for
location of the lesion. The reader is referred to those having surgery.72 In a shoulder case study,73 a
Snyder’s work60 for a more detailed description of 73-year-old patient with one year of shoulder pain
various types of SLAP lesions as it is beyond the and diagnosed with chronic supraspinatus tendinitis
scope of this article to provide an analysis of SLAP showed improvements in regeneration of the sup-
lesions.60 raspinatus tendon via diagnostic ultrasound. Re-
One potential mechanism of SLAP lesions is due to searchers proposed that tendons may repair with
the eccentric load of the biceps at both the elbow and biomechanical stresses from exercises and that low
shoulder. Because the internal rotation velocity has metabolic structure can regenerate with exercises
been found to approach speeds of 7000u per second61 only.73 Resting pain was reduced and improved
at the shoulder and elbow extension velocity is MVIC after a program of supervised exercises to
around 2300u per second,62 the eccentric forces on the level of the unaffected side in patients with
the bicep are readily apparent. Once the phase of unilateral rotator cuff tendinosis and more than
deceleration begins, the biceps works to eccentrically 3 months of pain.74 In summary, there is a lack of
control this velocity of elbow extension.61,63–65 Using definitive evidence for therapeutic exercise in the
EMG analysis of professional pitchers during the treatment of shoulder pain, but multiple interven-
throwing motion, Jobe et al.64 discovered the biceps tions (i.e. various modalities, injections) have similar
to be most active in the deceleration phase of issues with efficacy.75
throwing with contractions reaching up to 44% of There is currently a paradigm shift in favor of
maximal.63,64 Shepard et al.66 concluded that the high utilizing therapeutic exercises with an eccentric em-
level of biceps activity in the deceleration phase of phasis in the treatment of tendinopathies,76–83 al-
throwing may be indicative of the prevalence of though evidence for the use of eccentric exercise for the
SLAP lesions in throwing athletes. Additionally, shoulder is lacking. Even though evidence supporting
adolescent and amateur pitchers have been shown eccentric exercise for tendionpathies in the shoulder is
to have greater EMG activity of the biceps during non-existent, the rehabilitation professional can con-
throwing compared to professional pitchers.67 These sider utilizing the concepts for the shoulder. It is
loads placed on the biceps and biceps anchor at the beyond the scope of this article to discuss the physi-
supraglenoid tubercle over long periods of time may ologic mechanisms and proposed benefits of eccentric
contribute to the high prevalence of SLAP lesions exercise in tendinopathies. The reader is directed to

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Lorenz et al. Shoulder tendinopathy

other a host of references for information on this with calcific tendinitis, ultrasound was shown to
topic.14,26,83–92 improve pain and function at six weeks. However, at
nine months, there were no differences.99 There are
Therapeutic modalities very few controlled studies using ultrasound that are
A Cochrane Database Review69 of the literature on of methodological quality. Further research is needed
effectiveness of various therapeutic modalities in the to determine its effectiveness in shoulder tendino-
rehabilitation of rotator cuff tendinopathy showed no pathy/pathology.
definitive evidence substantiating the use of modalities To the author’s knowledge, only two studies used
with rotator cuff tendinopathy. There is a paucity of acetic acid iontophoresis for the treatment of calcific
quality trials that demonstrate the effectiveness of tendinitis and both found minimal to no positive
therapeutic modalities including ultrasound, acupunc- benefit from treatment. In a double-blind, randomized
ture, acetic acid iontophoresis, extracorporal shock controlled trial, Leduc and others98 found that acetic
wave therapy (ESWT), and laser. Clearly, more acid iontophoresis and physical therapy was no better
clinical trials are needed on this topic. than physical therapy alone for treatment of calcific
Berry et al.93 compared patients treated with acu- tendinitis. Perron and Maloulin100 reported similar
puncture with those treated with placebo, ultrasound, findings when comparing a control group to an acetic
steroid injection, or non-steroidal anti-inflammatory acid and continuous ultrasound experimental group in
drugs. They found no differences between groups with a cohort of subjects with calcific tendinitis.
regard to pain, function, or shoulder ROM immediately
ESWT has been found to have some effectiveness
at four weeks post-treatment. Kleinhenz and others,94
for calcifying rotator cuff tendinitis. In a randomized
using the same variables, found that there were short-
controlled trial, Gerdesmeyer et al.101 found that
term benefits shown with acupuncture, but in the long-
both high and low-energy ESWT provided a bene-
term at four months, positive benefits were no longer
ficial effect on shoulder function as well as on self-
demonstrated. Acupuncture has been shown to have
rated pain and diminished size of calcifying lesions in
little or no long-term benefits but rather short-term
self-rated pain scale at six months and in the size of
benefits in regards to pain.2
calcium deposits. In non-calcifying rotator cuff
Low-level laser therapy is becoming more popular tendinosis, Huisstede and colleagues102 found no
as a physical agent in the United States. Theo- evidence that ESWT was more effective than placebo
retically, it is designed to deliver laser energy to in a systematic review. However, there was strong
induce cell proliferation. England et al.95 revealed a evidence that high-energy ESWT was effective for
short-term benefit on pain, function, active range of calcific rotator cuff tendinosis. In a randomized
shoulder motion, stiffness, and restriction after two controlled trial, Albert et al.103 also found that
weeks of treatment compared with a placebo. It was high-energy ESWT significantly improved symptoms
also demonstrated that better pain relief and shoulder in calcifying tendinitis of the shoulder at three
ROM was shown with laser treatments than that months follow-up in patients with at least a three
of non-steroidal anti-inflammatory drugs. Another
month history, but the size of the lesion remained
study by Saunders96 demonstrated improvements in
unchanged. Similar findings were discovered by
function, pain, and strength using laser therapy after
Harniman et al.104 in another systematic review.
three weeks of treatment. Evidence exists on the
They found that moderate evidence exists for high-
contrary as well. Vecchio et al.97 compared laser
energy ESWT in the treatment of chronic calcific
therapy and ROM exercises to a placebo laser and
tendinitis. However, moderate evidence exists that
ROM exercises. There were no significant differences
low-energy ESWT is not effective for chronic non-
between groups at four and eight weeks with regard to
calcific rotator cuff tendinitis.104
pain, strength, and ROM, and function. In the
Cochrane Database Review by Green et al.,69 laser Manual therapy
therapy was found to be more effective than placebo for Tendinopathy of the shoulder results in various forms
adhesive capsulitis but not for rotator cuff tendinitis. of dysfunction, one being decreased ROM. Muscular
Ultrasound has been shown to have no effectiveness and capsular tightness, both limiting factors for
in the treatment of patients with subacromial impinge- ROM, have been linked to impingement in the
ment syndrome. Multiple studies have shown no shoulder.57,105,106 Manual therapy has been shown
significant differences in people treated with ultra- to increase ROM and decrease pain in subjects with a
sound and a placebo both short term as well as long shoulder dysfunction in various studies.107,108 Both
term.98 In the Cochrane Database Review by Green studies looked at the effectiveness of anterior and
and colleagues,69 ultrasound showed no evidence of posterior glenohumeral joint glides to improve
effect on shoulder pain, adhesive capsulitis, or rotator shoulder ROM in patients with shoulder dysfunction.
cuff tendinitis. On the contrary, in a group of patients Also, thoracic manipulation has been shown to

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 Lorenz et al. Shoulder tendinopathy

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