Tendinopathy Not Tendonitis Now Is the Time for a.10

Medical Report
by Thomas Trojian, M.D., M.M.B., FACSM and Adae Amoako, M.D.
Tendinopathy Not Tendonitis
Now Is the Time for a Change
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INTRODUCTION
T
endon is a very organized fibrous connective tissue structure joining muscle to bone
(9). The regular densely arranged collagenous tissue is made up of collagen
fibers, sparse cells of various shapes,
and ground substance (Figure 1). This
arrangement of collagen fibers makes it
capable of resisting high tensile forces
while transmitting forces from muscle
to bone. Nearly 85% of the dry weight
of tendon is made up of collagen and
mostly type I collagen. The mechanical
and physiological characteristics of collagen dictate the qualities of tendon.
Tendon also shows a degree of extensibility. The tendon has a crimped pattern
like a mild zigzag. There is a flattening
of the tendon crimped pattern during
the first stage of tendon stretching and
with increasing stretch, other mechanisms such as an interfibrillar gliding
may be involved. The strain used to
stretch a tendon is partially regained on
return to normal architecture of the tendon, then a beneficial elastic effect
would be achieved. In the example of
the Achilles tendon, which can take
loads of 12 times the body’s weight, it
is stretched late in the stance phase as
the soleus and gastrocnemius muscles
contract and the ankle dorsiflexes. Before plantar flexion occurring, muscle activation ceases and stored energy helps
to initiate planter flexion (9).
When tendons are injured, it is often
called tendonitis (or tendinitis). This tendonitis, which literally means inflammation of the tendon, is labeled incorrectly.
Inflammation is not seen histologically
when the tendon is examined under the
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microscope. Tendinitis oftentimes
has been used interchangeably with
tendinopathy. To treat tendon injuries
properly, one must understand the pathology that is occurring; therefore, it is
inherent that these two terms are differentiated from each other. The term ‘‘tendinitis’’ has been used in sports medicine
for many years to describe the cycle of
damage, improper healing patterns, and
the subsequent reinjuries of tendons.
This cycle of tendon disordered degeneration secondary to abnormal, haphazard,
and poor healing response is actually a
tendinopathy (Figure 2) and not an inflammatory tendinitis. Authors have
been calling for an end to the term tendinitis for more than a decade. The term
‘‘tendonitis’’ has been so commonly
used in the medical vernacular that it is
often still used in the medical literature,
even as recent as 2014. Now, it is the
time to stop using ‘‘tendinitis’’ and start
using the correct term ‘‘tendinopathy.’’
The normal process for tendon
healing involves three different but
overlapping phases (Figure 3) (13).
There is an initial inflammatory phase
that lasts only 24 to 48 hours. At this
phase, erythrocytes, platelets, and inflammatory cells (e.g., neutrophils,
monocytes, and macrophages) migrate
to the site of damage and clean the site
of dead materials. Cells also release
factors that recruit tendon fibroblast to
begin collagen synthesis and deposition.
This phase is relatively short compared
with the other two phases; it fades quickly
and is replaced by the proliferative phase.
The inflammation stops at this time,
and after 48 hours, inflammatory cells
are replaced quickly. This second phase
usually takes place for the next 6 to 12
weeks. During this phase, the body
produces a different form of collagen,
called type III, which is not the normal
tendon collagen, which is type I collagen.
The type III collagen is used to protect the
tendon by developing a scar patch. New
blood vessels (neovessels) and nerve
endings are brought in to help supply
the repair. This leads to the third phase
(remodeling) where the type III collagen
and the new blood vessels and nerves
are removed and the normal type I collagen replaces the type III collagen to form
normal tendon (13). The disruption of
this normal process causes the tendon to
develop an abnormal thickened tendon
(Figure 4), leading to pain and a weakened tendon, hence tendinopathy.
ETIOLOGY
Tendon injuries can be caused by both intrinsic and extrinsic risk factors. Intrinsic
risk factors include age, genes, diabetes,
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Medical Report
Figure 1. Histological stain of normal densely arranged collagen tissue showing fibers, sparse cells of
various shapes, and ground substance.
thyroid disease, and elevated cholesterol.
Extrinsic factors include training errors,
biomechanics, and medications such as
fluoroquinolones, statins, and corticosteroids.
Age of participant and training errors seem
to be the two most influential factors
that predispose active individuals to
tendinopathy. Although tendinopathy
affects individuals regardless of age,
older individuals are more susceptible
than younger individuals and these older
athletes are likely to have severe forms of
tendinopathy. The loading of specific
tendons will often vary by the nature of
the sport played. For example, running
sports load the Achilles tendon and
jumping sports load the patellar tendons.
Tendons with different genetic alterations
to the collagen molecules that make up
tendon or the supporting extracellular
molecules have been shown to be more
common in tendinopathy compared with
the normal tendons. Studies on training
errors point to increased landing frequency
and substandard quadriceps extensibility as
risk factors for developing tendinopathy.
When training clients with certain medical conditions, be mindful that some may be
more prone to tendinopathy. The prevalence
of tendinopathy is increased in patients with
diabetes mellitus. The abnormal tendon
structure occurs because of abnormal healing
and the development of disorganized fibril
structure. Elevated cholesterol has been
associated with tendinopathy, and some
have recommended measuring cholesterol
levels in tendinopathy patients. The statins
used to treat hypercholesterolemia have
been associated with tendinopathy, but
whether this is caused by treatment of the
hypercholesterolemia or the medication
itself is unknown. For clients taking a
fluoroquinolone-type medication, used for
treating many infections, the risk of Achilles
tendon rupture is tripled; however, the overall incidence among users is low (È18 per
100,000 users within 30 days of medication).
Just like most injuries, tendinopathy
starts with an insult to the normal anatomy. This frequently follows a normal reparative process to return the tendon to
normal structure. But on occasion, the
normal healing pattern is disrupted and
tendinopathy occurs after a cascade of
events. Three theories have attempted to
explain how tendinopathy comes about.
In the mechanical theory, it is thought
that mechanical overload to the tendons
causes damages to collagen and other matrix components which, across time, can
accumulate during repeated stretch cycles
to the tendon (Figure 5). Tendons frequently have an area that is fed poorly
with blood supply. This area of the tendon
is called the watershed area. The vascular
theory proposes that these watershed
areas of the tendons are prone to vascular
insufficiency and therefore heal poorly
because the neovascularization is unable
to occur normally. An alteration to the homeostasis of tendon innervations is
thought to be responsible for tendinopathy according to the neural theory.
This is supported by the finding of increased Achilles tendon injuries in
patients with sciatica. The nerve supply
of tendons includes many autonomic
fibers, which are involved in regulating
tendon blood flow as well as local tendon
cell metabolism, collagen production, and
pain signaling. This would allow for
abnormal healing and dysfunction of
the tendon.
THREE THEORIES OF
TENDINOPATHY
Figure 2. Histological stain of tendinopathy showing discontinuous and disorganized collagen fibers.
38
Theory
Mechanism
Question
About Theory
Mechanical
Cause
damages
to collagen
Eccentric
training helps
tendon
Vascular
Watershed
area
Neovascularity
in damaged
tendon
Neural
Sciatica
highertendon
rupture
Substance
P fibers
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Figure 3. The normal process of tendon healing, which involves the overlapping phases of inflammation,
repairing, and remodeling.
DIAGNOSIS
The diagnosis of tendinopathy is based
on clinical examination assisted by imaging. The key feature in tendinopathy is
tenderness with activity. This is essential
when it comes to diagnosis because abnormal image findings can exist without
symptoms (7). Direct palpations of the
suspected injured tendon will elicit the
pain. However, this may not necessarily
indicate that tendinopathy is the source
of the pain (5). The positive predictive
value of tendon palpation tenderness
being tendinopathy is 68% for the patella
tendon (5). Those patients tender to palpation and with activity-related symptomatic tendons are more likely to have
ultrasound abnormality than those tender
to palpation alone. The level of tenderness
is more predictive of tendinopathy,
as moderate and severe tenderness
is more predictive than mild or no
tenderness (5).
In assessing tendinopathy, two
useful clinical tools have been developed. The Victorian Institute of
Sports Assessment-Achilles (VISA-A)
(Table 1) and the Victorian Institute of
Sports Assessment-Patella (VISA-P)
have been validated as measures of
Achilles and patella pathology. VISA-A
is a summed score with a maximum of
100 points if asymptomatic. The effectsize thresholds are 5 points for a small
effect and 15 points for a moderate effect. The VISA-P is scored similarly.
These can be found with any Web
search. It is helpful to assess client’s tendon health.
The imaging of choice for viewing of
tendons is either ultrasonography or magnetic resonance imaging (MRI). Ultrasonography has been shown for multiple different tendons to be more accurate in
the diagnosis of tendinopathy than MRI
(12, 15). It is the initial diagnostic tool of
choice because of its relative low cost,
easy accessibility of equipment, accuracy
of the test, and safety compared with
MRI. It is important to remember that tendon abnormalities without symptoms do
not predict future tendinopathy because
many of these tendon abnormalities will
resolve without treatment.
TREATMENT
In the past, tendon injuries have been treated
as an inflammatory process. Therefore,
Figure 4. Sonogrpahic findings of normal tendon (left) showing homogeneous, linear, and fibrillar pattern compared to tendinopathy (right) showing thickened area
with loss of fibrillar pattern represented by hypoechoic regions on ultrasound.
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Medical Report
Figure 5. In the mechanical theory of tendinopathy, tendons do not undergo adequate repair leading to tenocyte
disruption, which predisposes tendons to repeated injuries after the initial increase demands on the tendon.
nonsteroidal anti-inflammatory drugs like
naproxen or ibuprofen were prescribed or
an anti-inflammatory medication like corticosteroid was injected (10). However, it is
now known that these medications do not
help the healing process, and studies point
to them having a negative effect long-term,
although they help reduce short-term discomfort. The main goal of treatment of
tendinopathies should be alteration of the
abnormal healing pattern so that the body
can use its natural healing process to start
healing again (14).
Treatment of tendinopathy should start
with mechanotherapy (mechanical therapy).
Mechanotherapy (e.g., eccentric exercises or
heavy slow resistance exercises) is the employment of mechanotransduction for the
stimulation of tissue repair and remodeling
(8). These therapeutic exercises prescribed
to promote the repair or remodeling of
injured tissue should be done for at least
6 weeks, along with a relative reduction in
training load. Eccentric exercises should
be done multiple times a day but take a
shorter time to complete than heavy slow resistant training exercises. These exercises
stimulate the tendon repair by increasing
collagen synthesis rate to restore the tendon
structure. The heavy slow resistance
exercises are recommended to be done
three times a week with multiple sets during
each session. The load is then increased
weekly using the maximum lift for the
squat, hack squat, and leg press (4). The
heavy weight and slow repetitions load the
tendon, triggering signaling to produce observable structural change in the tendon.
Both eccentric exercises and heavy slow resistance training produce good results for
TABLE 1: VISA-A Components
Duration of morning stiffness
(0 = 100 minutes and 10 = 0 minutes)
Pain on stretching Achilles tendon
(0 = strong severe pain; 10 = no pain)
Pain on walking
(0 = strong severe pain; 10 = no pain)
Pain walking downstairs
(0 = strong severe pain; 10 = no pain)
Pain during/immediately after 10
single-leg heel raises from flat surface
(0 = strong severe pain; 10 = no pain)
Number of single-leg hops without pain
(0 = none; 10 = 10)
Current sport/physical activity
(0 = none; 4 = modified training and modified
competition; 7 = full training and modified
competition; 10 = competing at same or higher
level than when symptoms began)
Duration of training and practice
(maximum score 30 points for exercise
for 30 minutes with no pain)
40
Achilles tendinopathy, but heavy slow resistance has a slightly higher compliance rate
and patient satisfaction rate (4).
Stretching has been discussed across
the years to prevent hamstring injuries
and other tendon injuries. Despite the
change in the stiffness feeling after a
good massage and stretch, the studies
on the effects of stretches and prevention
of injuries to tendons are not favorable.
One review of the literature stated ‘‘No
evidence was found for a positive effect
of stretching exercises’’ (11). People like
the feeling after a good stretch and massage, but it is not going to protect against
tendon injury.
Despite the effectiveness of mechanotherapy, not everyone’s response to the
modality is positive and further treatment
is needed. It is important as a fitness professional to be aware of these further
treatment options to help guide clients
and not cause further injury. Treatments
can be divided intratendonous and
extratendonous. Procedures into the tendon can cause weakening, and tendon
rupture has been reported with intratendonous procedures in the first 6 weeks
postprocedure. Table 2 shows many of
the current procedures and treatments
with comments about their effectiveness
and current research. This information
can be useful when planning programs
for your clients.
In summary, ‘‘tendinitis’’ is not an appropriate term to describe the degenerative
chronic injuries to tendons. ‘‘Tendinopathy’’ is disruption of the normal healing
process developing an abnormal thickened
tendon. Treatments are geared at restarting
the normal healing process. Many treatments for tendinopathy have been recently
developed geared at restarting the healing process. We reviewed mechanotherapy, platelet-rich plasma, tenotomy,
sclerotherapy, shock wave, and topical
glycerol trinitrate. It is not known which
treatment is better, but mechanotherapy is
the recommended starting point for the
first 6 weeks, but these tendinopathy
treatments normally take 12 weeks for
full recovery.
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TABLE 2: Postmechanotherapy Treatments and Procedures
Procedure
Comments
Extratendinous procedures
Procedures outside the tendon
Glyceral trinitrate
It is the ‘‘nitro patch’’ for the heart. Off-label delivery of nitric oxide molecules to restart healing. Success in
double-blind, randomized, controlled trials. It can be a good next step because it has been shown effective
in well-controlled studies and the medicine results in minimal morbidity.
Grastoni and ASTyMi
Mechanical tools used to do a cross friction-type technique. One study on lateral epicondylosis that showed
promise. The study was not blinded, and it was a low-quality study.
Active release technique (ART)
A stretch-type therapy of the neurologic system. No randomized controlled trials to demonstrate its effectiveness.
Lots of anecdotal testimonials and very in vogue in 2015.
Extracorpeal shock wave therapy
Some positive results, not easy to find treatment centers in the United States. A study with lower energy levels and
higher number of pulses (equivalent to 0.18 mJ/mm2 energy flux density) to the affected knee at a single session
showed satisfactory results in 90% of patients. Consider the risk of rupture similar to the intratendinous procedure.
Acupuncture
Using traditional acupuncture points 5 sessions of 30 minutes each has been shown to be as effective as
other treatments and better than fake acupuncture. Not the end all to be all but an option in treating tendinopathy
after mechanotherapy.
Dry needling
Dry needling uses the tip of acupuncture-type needles to loosen the knot in the muscle and theoretically reducing
or eliminating pain caused by a trigger point. Not as scientifically studied as acupuncture and uses similar points.
Like ART, lots of anecdotal testimonials and very in vogue in 2015.
Sclerosing therapy
Sclerosing (destroying) the neovessels into chronic tendinopathy with polidocanol injections seem to provide
pain relief and support recovery. It has been shown to be effective in multiple studies, supporting its use (2,6).
But polidocanol is not readily available in the United States and it is used off-label.
High-volume image-guided
injection (HVIGI)
Uses ultrasound guidance of a high volume of fluid to destroy the neovessels like in sclerosing therapy. HVIGI
has been shown to significantly reduce pain and improve function in patients with chronic Achilles tendinopathy
in the short- and long-term follow-up. One thing to note about the treatment is the temporary deformation of
the tissue from the large volume of fluid.
Percutaneous scraping
Ultrasound and color Doppler-guided approach on the undersurface side of the Achilles tendon. The scraping
procedure is done percutaneously using a 14-gauge needle (with local anesthetic) to destroy the neovessels
entering the tendon; similar philosophy to sclerosing therapy. The results in studies have been successful with no
significant adverse events.
Intratendinous procedures
Procedures inside the tendon
Platelet-rich plasma
It seems to have a positive effect on attachment sites versus midtendon or watershed areas (1). Studies are needed
to determine how many platelet-rich plasma injections are ideal and the spacing between injections for maximum
results. It is an expensive out-of-pocket procedure with questionable results.
Stem cells
It may be very helpful, with animal studies showing beneficial results by restoring the natural healing process,
which in turn leads to regeneration of the damaged tissues. One concerning finding in animal testing is that
stem cells injected into tendons can turn to bone or cancer cells. Still very preliminary in 2015.
Percutaneous tenotomy
Uses ultrasound to see the damaged area of the tendon and helps guide a needle into the focus of tendinosis
using 30 to 40 passes of the needle to break up the damaged area. Studies show very good results.
Tenexi
Proprietary equipment that debrides damaged tendon but is not supposed to damage normal tendon.
Some effective results in studies.
Surgical debridement
Should be considered as last-resort treatment (3). Advantage is visualization of tissue directly and measured
debridement but prolonged healing and increased morbidity compared with other treatments. Results are similar
to sclerosing therapy with higher patient satisfaction.
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Medical Report
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Disclosure: The authors declare no conflict of interest and do not have any financial disclosures.
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Thomas H. Trojian,
M.D., M.M.B.,
FACSM, is a sports
medicine physician
practicing in
Philadelphia. He is
board certified in
sports medicine and family medicine,
with a special interest in injury prevention
(especially anterior cruciate ligament injuries), sports ultrasound use in the guided
treatment of tendon injuries, lower-leg injuries in runners, and concussion prevention
and treatment. He is the lead physician for
Drexel Athletics and the Sports Medicine
Fellowship director.
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Adae Amoako, M.D.,
is a fellow of sports
medicine at the
Drexel/Hahnemann
University Hospital
in Philadelphia. He
is a board certified
family physician clinical researcher
with special interest in soccer-related injuries and osteoarthritis in athletes.
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