Overuse Tendinosis, Not

Tendinitis
Part 1: A New Paradigm for a Difficult Clinical Problem

Karim M. Khan, MD, PhD; Jill L. Cook, B App Sci, PT; Jack E. Taunton, MD; Fiona Bonar, MBBS, BAO
THE PHYSICIAN AND SPORTSMEDICINE - VOL 28 - NO. 5 - MAY 2000
This is the first of two articles on tendinopathies by Dr Khan and colleagues; the second, on patellar
tendinopathy, will appear in a subsequent issue.
In Brief: Overuse tendinopathies are common in primary care. Numerous investigators worldwide have
shown that the pathology underlying these conditions is tendinosis or collagen degeneration. This applies
equally in the Achilles, patellar, medial and lateral elbow, and rotator cuff tendons. If physicians
acknowledge that overuse tendinopathies are due to tendinosis, as distinct from tendinitis, they must
modify patient management in at least eight areas. These include adaptation of advice given when
counseling, interaction with the physical therapist and athletic trainer, interpretation of imaging, choice of
conservative management, and consideration of whether surgery is an option.

Physicians in primary care, sports medicine, and orthopedics see patients with overuse tendon conditions
nearly every day. Tendon conditions are not restricted to competitive athletes but affect recreational sports
participants and many working people, particularly those doing manual labor (1). Unfortunately, these
disorders are not only common, they can also be recalcitrant to treatment.
One factor that may interfere with optimal treatment is that common tendinopathies may be mislabeled as
tendinitis. Advances in the understanding of tendon pathology indicate that conditions that have been
traditionally labeled as Achilles tendinitis, patellar tendinitis, lateral epicondylitis, and rotator cuff tendinitis
are in fact tendinosis. An increasing body of evidence supports the notion that these overuse tendon
conditions do not involve inflammation.
If this is correct, then the traditional approach to treating tendinopathies as an inflammatory "tendinitis" is
likely flawed. The recommendations presented here reflect the current scientific data and will help
physicians avoid common misconceptions about tendinopathies and their management (table 1) (2-11).

TABLE 1. Common Misconceptions About Tendinopathies and Their Management

Misconception Evidence-Based Finding

Tendinopathies are self-limiting conditions Tendinopathies often prove recalcitrant to treatment and may
that take only a few weeks resolve (2) take months to resolve

Imaging appearance can predict prognosis Imaging does not predict prognosis; it adds to the likelihood
of a diagnosis of tendinopathy but does not prove it (3-5)

Cyst-like ultrasonographic abnormalities in Surgery should be based on clinical grounds; cyst-like

tendons are indications for surgery ultrasonographic findings can be found in asymptomatic
athletes (5)

Surgery provides rapid relief of symptoms in After surgery, return to sport takes a minimum of 4-6 mo (6-
almost all subjects 11); not all patients do well (8,9)

Tendinosis: A Noninflammatory Disorder

Pathology. The pathology of the major tendinopathies has been well described and is based on
examination of surgical specimens. In studies of the Achilles (11), patellar (12), lateral elbow (9,13),
medial elbow (14), and rotator cuff tendons (15), tissue appeared remarkably consistent. Macroscopically,
abnormal tissue examined at surgery shows the tendon to be dull-appearing, slightly brown, and soft.
Normal tendon tissue is white, glistening, and firm.
When examined under a light microscope, abnormal tendon from patients with chronic tendinopathies
differs from normal tendon in several key ways. It has a loss of collagen continuity (figure 1) and an
increase in ground substance, vascularity, and cellularity (figure 2: not shown). Cellularity results from the
presence of fibroblasts and myofibroblasts (figure 3: not shown), not inflammatory cells. Thus, in patients
who have chronic overuse tendinopathies, inflammatory cells are absent.

Tendinosis vs tendinitis. Key features of tendinosis are described in table 2. Tendinitis is a rather rare
condition but may occur occasionally in the Achilles tendon in conjunction with a primary tendinosis.
Paratenonitis, one of the disorders in the differential diagnosis, is a condition of inflammation of the outer
layer of the tendon (paratenon) alone, whether or not the paratenon is lined by synovium. It is commonly
associated with intratendinous degeneration (16) and produces the "crepitus" that is easily felt in some
cases of Achilles paratenonitis. Unfortunately, distinguishing tendinosis from the rare tendinitis is difficult
clinically. But because tendinosis is far more likely, our advice is to treat patients initially as if tendinosis
were the diagnosis.

TABLE 2. Bonar's Classification of Overuse Tendon Conditions (17)

Pathologic Macroscopic Pathology Histologic Finding

Diagnosis

Tendinosis Intratendinous degeneration Collagen disorientation, disorganization, and fiber

commonly due to aging, separation by increased mucoid ground substance,
microtrauma, or vascular increased prominence of cells and vascular spaces with
compromise or without neovascularization, and focal necrosis or
calcification

Partial rupture Symptomatic degeneration of Degenerative changes as noted above with

or tendinitis the tendon with vascular superimposed evidence of tear, including fibroblastic
disruption, inflammatory repair and myofibroblastic proliferation, hemorrhage, and
response organizing granulation tissue

Paratenonitis Inflammation of the outer layer Mucoid degeneration is seen in the areolar tissue: a
of the tendon (paratenon) alone scattered mild mononuclear infiltrate with or without
whether or not the paratenon is focal fibrin deposition and fibrinous exudate
lined by synovium

Paratenonitis Paratenonitis associated with Degenerative changes as noted in tendinosis with

with tendinosis intratendinous degeneration mucoid degeneration with or without fibrosis and
 scattered inflammatory cells in the paratenon alveolar
tissue

Tendinosis as a concept. Although recent research has clearly demonstrated the presence of tendinosis
in chronically injured tendon tissue, this is not a new discovery (17). The term tendinosis was first used by
German researchers in the 1940s; the term's recent usage results from Puddu et al (18) and Nirschl and
Pettrone (9). Writing about tendinopathies in 1986, Perugia et al (19) noted the "remarkable discrepancy
between the terminology generally adopted for these conditions (which are obviously inflammatory since
the ending 'itis' is used) and their histopathologic substratum, which is largely degenerative."
Thus, physicians must shift their perspective and acknowledge that tendinosis is the pathology being
treated in most cases and that treatment needs to combat collagen breakdown rather than inflammation.
Tendinosis may require a reasonable period of relative rest and attention to strengthening with the aim of
first breaking the tendinosis cycle. Once this is done, the patient uses modalities that optimize collagen
production and maturation so that the tendon achieves the necessary tensile strength for normal function.

Clinical Significance of the Diagnosis of Tendinosis

If we accept that a patient with overuse tendinopathy has an injury that is due to collagen degeneration,
then the diagnosis has repercussions (table 3) on at least eight aspects of our practice.

TABLE 3. Implications of the Diagnosis of Tendinosis Compared With Tendinitis

Trait Overuse Tendinosis Overuse Tendinitis

Prevalence Common Rare

Time for recovery, early presentation 6-10 wk Several days to 2 wk

Time for full recovery, chronic 3-6 mo 4-6 wk

presentation

Likelihood of full recovery to sport ~80% 99%

from chronic symptoms

Focus of conservative therapy Encouragement of collagen-synthesis Anti-inflammatory

maturation and strength modalities and drugs

Role of surgery Excise abnormal tissue Not known

Prognosis for surgery 70%-85% 95%

Time to recover from surgery 4-6 mo 3-4 wk

1. Imaging. Tendinopathies are very well visualized with both magnetic resonance imaging (MRI) and
diagnostic ultrasound (2). Histopathologic studies prove that the characteristic imaging appearances (see
figure 1) are due to tendinosis (12,20,21). We use MRI to confirm our clinical diagnosis and to
demonstrate to the patient that in tendinosis, tendon collagen has lost continuity.
2. Patient education. The physician should take the time to explain and illustrate the pathology of
tendinosis, especially since textbooks and Web sites have yet to embrace this pathology and its clinical
implications. We find that patients with chronic tendinopathy need no convincing of the veracity of
tendinosis. They are generally relieved to find a scientific rationale behind their prolonged symptoms.
Patients who have symptoms of short duration but are still able to "warm up" the injury and engage in
sports are the ones who need the most education. They are likely to try to continue playing without
undergoing appropriate treatment, and thus worsen the tendinosis.
3. Biomechanical deloading. Because tendinosis results from collagen degeneration and, generally,
mechanical overload, it is vital that the physician establish why this occurred. Training errors are a
common cause (22), but in some instances a more subtle mechanism underlies tendinosis. Thus, it is
important to assess any equipment being used (eg, running shoes, tennis racket), examine movement
biomechanics (eg, running, throwing motion, stroke pattern), and diagnose and treat any muscle
imbalances (23). The details of biomechanical correction are outside the scope of this paper, but their
importance cannot be overemphasized in treatment.
4. Anti-inflammatory strategies. Common strategies to reduce inflammation include cryotherapy,
electrotherapeutic modalities, nonsteroidal anti-inflammatory drugs (NSAIDs), and corticosteroid
injections.
Patients with tendinosis may benefit from cryotherapy because ice has a vasoconstrictive role, and
abnormal neovascularization is a feature of the pathology (see figure 2A: not shown). Because a strong
clinical impression exists that icing is helpful in tendinopathies, this modality should not be discarded.
Physical therapies that purport to reduce inflammation would not help treat tendinosis if that were their
only role. Enwemeka and others (24,25), however, have shown that electrotherapy (eg, laser, high-voltage
galvanic stimulation) can stimulate collagen synthesis in the laboratory setting. Clearly this effect would
be favorable to the treatment of tendinosis.
Almekinders and Temple (26) have published a thorough review of the role of NSAIDs and corticosteroids
in treating tendinopathy and found little evidence that they were helpful. It is not known whether the
antiprostaglandin action of NSAIDs and cyclooxygenase-2 inhibitors helps or hinders tendon repair through
mechanisms other than the pathways associated with inflammation.
The role of corticosteroid injection or iontophoresis in tendinosis remains controversial (27). In brief,
because tendinosis is not an inflammatory condition, the same arguments as those for NSAIDs apply.
Further, given the known deleterious effect of corticosteroid injection into tendon and inhibition of collagen
repair when the drug is injected around tendon, this treatment has lost favor. Astrom (28) found that
corticosteroid injection was the only predictor of partial tendon tears in a large series of cases of chronic
Achilles tendinosis that eventually required surgery. This being stated, it is clear that in some cases,
corticosteroid injection provides short-term but rapid symptom relief.
5. Load-decreasing devices. Because tendinosis results from excessive load on collagen, braces and
supports that attenuate load through the tendon may benefit the patient. Braces have gained clinical
support to unload the tendon at both the elbow and the knee. Heel lifts unload the Achilles tendon, and
orthoses serve to control pronation and whip at both Achilles and patellar tendons. Further research into
the efficacy of these devices is required because they have not yet undergone randomized, controlled
trials. They do, however, have a solid biomechanical rationale for therapy.
6. Interaction with the physical therapist. It is important that the physical therapist and physician
have a similar understanding of the pathology of tendinopathies and a parallel approach to management.
When referring a patient for physical therapy, it is essential that both therapist and patient have a realistic
time frame for rehabilitation. A randomized, controlled trial of strengthening treatment in Achilles
tendinopathy (29) and data from other cases (1) suggest that for patients who first present with short-
duration tendon symptoms, return to full sporting competition takes, on average, 2 to 3 months. A patient
with chronic symptoms may require 4 to 6 months to achieve a similar outcome. Clearly, these guidelines
will vary for individual patients, but they are supported strongly by the literature (1,8).
7. Appropriate strengthening. Eccentric strengthening programs have a long track record of clinical
effectiveness (22,29,30), and recent research adds further scientific support (31,32). It is likely that
specific eccentric training drills result in tendon strengthening by stimulating mechanoreceptors in
tenocytes to produce collagen, and thus help reverse the tendinosis cycle (figure 4: not shown) (33).
Collagen production is probably the key cellular phenomenon that determines recovery from tendinosis.
Animal experiments have revealed that loading the tendon improves collagen alignment and stimulates
collagen cross-linkage formation, both of which improve tensile strength (34). Therefore, the clinical
success of tendon strengthening programs has a demonstrable biological basis that is supported by clinical
(32) and laboratory evidence (35).
8. Surgery as a last resort. Surgery has been considered the treatment of last resort for tendinopathies,
and this certainly applies, if not more so, for a confirmed case of tendinosis. Surgery can be used to excise
tissue affected by tendinosis, but surgery has not been proven to stimulate collagen synthesis or
maturation. Thus, the tendon that has had surgery requires time for repair and strengthening. Reviews
suggest that surgery in tendinosis has a 75% to 85% success rate, and for some tendons this figure may
well be a very-best-case estimate (7,8).
Therefore, an important implication of tendinopathy's underlying pathology being tendinosis is that
conservative management must progress slowly. If the initial prognosis the patient receives is realistic, it
is less likely that the patient will attempt to return to sport prematurely, suffer re-injury, and thus, "fail"
conservative management. Because surgical treatment of tendinosis is not without failure, and recovery
takes a minimum of 4 to 6 months, this treatment should be reserved for failure of a high-quality program
of conservative management.

The New Paradigm

Tendinopathies have provided long-lasting frustration for both patients and physicians, and attributing the
pathology to tendinitis rather than tendinosis may have contributed to this problem. Physicians must
acknowledge that the cause is most often due to tendinosis, rather than tendinitis, and treat the problem
using a fundamentally different paradigm. Advice and suggestions for patients along these lines of clinical
thought can help them recover more quickly and avoid surgery.
References

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exercise in the management of Achilles tendonitis. Clin J Sport Med 1992;2(2):109-113
30. Curwin SL, Stanish WD: Tendinitis: Its Etiology and Treatment. Toronto, Collamore Press, 1984
31. Hölmich P, Uhrskou P, Ulnits L, et al: Effectiveness of active physical training as treatment for
long-standing adductor-related groin pain in athletes: randomised trial. Lancet
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of chronic Achilles tendinosis. Am J Sports Med 1998;26(3):360-366
33. Leadbetter WB: Cell-matrix response in tendon injury. Clin Sports Med 1992;11(3):533-578
34. Vilarta R, Vidal B de C: Anisotropic and biomechanical properties of tendons modified by exercise
and denervation: aggregation and macromolecular order in collagen bundles. Matrix
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408

Dr Khan is a sports physician at the Allan McGavin Sports Medicine Centre at the University of British
Columbia. Ms Cook is a physical therapist at the Victorian Institute of Sport, Melbourne, Australia, and a
doctoral candidate at Griffiths University in Gold Coast, Queensland, Australia; Dr Taunton is a professor in
the department of family medicine and School of Human Kinetics at the University of British Columbia,
Vancouver, Canada; and Dr Bonar is a pathologist at Douglass-Hanly Moir Pathology in North Ryde,
Australia. Address correspondence to Karim Khan, MD, PhD, School of Human Kinetics, 210 War Memorial
Gym, 6081 University Blvd, Vancouver, British Columbia V6T 1Z1; e-mail to kkhan@interchange.ubc.ca.

Science of Sport: Do You Really Have Tendonitis - Or Is It Tendonosis?

By Owen Anderson, Ph. D. (copyright © 2003-2005)

The Two Conditions Have Quite-Different Recovery Processes

Tendonitis has a tenacious grip on the sports world. At least 25 percent of athletes treated for knee
problems at major sports clinics are typically diagnosed with tendonitis (1), and 40 percent of competitive
tennis players are thought to suffer from some form of elbow tendonitis (2). In the world of running, as
many as 30 to 50 percent of all endurance runners experience tendonitis during a typical training year (3).
Tendon injuries are among the most common "overuse" injuries - maladies which occur when an athlete's
body is unable to adequately repair the insults it receives during strenuous or prolonged workouts (4).

Why are tendons such easy prey for the injury bug? Because tendons are constructed of strong, parallel,
tightly packed bundles of a unique protein called collagen, tendons are rather stout structures, but they
must transmit forces from muscle to bone and are thus subject to powerful tensile stresses. In addition,
the linear arrangement of collagen fibers means that tendons resist shearing (side-to-side and/or
rotational) forces rather poorly; such forces are a natural part of sporting activity, even during such
"linear" sports as endurance running. Tendons are also not noted for their recovery prowess; although not
as balky as the cartilage covers on the ends of bones or the cartilaginous pads which cushion the knees,
tendons can take several days to mobilize the repair process fully after a damaging workout - days during
which another red-hot training session may further aggravate the collagen bundles.

Of course, the majority of athletes who are part of the tendonitis plague take what are considered to be
the appropriate steps to alleviate their problems. They ice, they stretch, they take their anti-inflammatory
medications, and they attempt to strengthen the hurting areas; some athletes are even daring enough to
take a short rest from their usual activities! There is just one little problem, however: There is strong
evidence that the majority of athletes diagnosed with tendonitis are not really suffering from
the disorder. In effect, they are treating something which does not exist.

Tendonitis, you see, is an inflammation of a tendon and/or the tendon's attachment point with
a muscle, with characteristic white blood cells swarming through the red-hot tendon and leaky
blood vessels infiltrating the tendonous area. And that's the problem: Most athletes diagnosed
with tendonitis do not have these inflammatory reactions going on.

We know this because there have been 14 different studies carried out with human subjects in which the
pathology of apparent "tendonitis" injuries was investigated by means of examination of biopsied tendon
material. As Drs. Louis Almekinders and John Temple point out in a fascinating review article (5), almost
all of these investigations have failed to find any inflammatory processes taking place in the examined
tendons; what have been found instead are tendons undergoing degeneration (actual breakdowns and
increased disorder of the collagen fibers), without inflammation. In other words, the "tendonitis plague"
may actually be a severe outbreak of tendonosis, not tendonitis. Tendonosis is a degenerative
problem in a tendon, not an inflammatory disorder.

So what, you might say? Why does the name we attach to a tendon problem make a difference, if the
treatment is the same? And there is the hitch: The treatments for tendonitis and tendonosis are quite
different. For example, a reasonable course of therapy for tendonitis, an inflammatory condition, would
involve the use of anti-inflammatory drugs; in fact, non-steroidal anti-inflammatory medications have
become the mainstay of treatment for so-called "overuse" injuries to tendons. The trouble is that there
is evidence that anti-inflammatory drugs can actually have a negative impact on the progress
of tendonosis, in effect retarding the healing process.

In ingenious research carried out at the University of North Carolina School of Medicine, Dr. Almekinders,
along with Lynette Bracey and Dr. Albert Baynes, extracted human-tendon fibroblasts (the cells which
actually produce collagen fibers) from the cores of normal tendons of individuals who were about to
undergo surgery (6). These fibroblasts were then cultured in the laboratory and divided into four groups:
(I) Control fibroblasts, which were not treated with anti-inflammatory medication and which were not
subject to any repetitive strain, (II) Strain fibroblasts, subject to repetitive motion at 25 percent of
maximal strain but exposed to no anti-inflammatory meds, (III) Strain-Med fibroblasts, subject to the
same strain as group 2, along with 25 micromoles per liter of an anti-inflammatory medication called
indomethacin, and (IV) Med fibroblasts, under no strain but getting the indomethacin. After 72 hours, the
medium surrounding about 60 percent of the fibroblasts from each group was transferred and mixed with
human macrophages (large white blood cells which are present in inflamed tissues). This transfer was
accomplished to determine whether the presence of inflammatory cells (such as the macrophages) would
alter the response of the fibroblasts to repetitive motion and strain. After 24 hours of macrophage contact,
the medium was transferred back to the tendon fibroblasts for 12 final hours.

Interestingly enough, the synthesis of DNA (the chemical from which genes are made) was
significantly elevated in Group-II fibroblasts (compared with the beginning of the experiment),
and it was higher still in the Group-II fibroblasts which had been in contact with the
macrophage medium. In other words, there was something about repetitive motion and strain
which stimulated fibroblasts to begin making significant quantities of new DNA, presumably to
provide genetic material for the new fibroblasts which would be created as part of a tendon-
strengthening process. It seems clear that new-DNA creation is an adaptive response to physical stress
and repeated motion. In contrast, DNA synthesis was suppressed in both of the anti-inflammatory-treated
groups (III and IV from above), compared with group II. The anti-inflammatory medication acted to
stop the creation of new genetic material - and presumably new tendon cells, potentially
thwarting healing.

As it turned out, anti-inflammatory treatment did enhance protein synthesis in groups III & IV, compared
with I & II. This would seem to be a good thing, since the protein could be used to form new collagen
fibers (a process called matrix formation). However, matrix creation often occurs somewhat late in
the healing process of a tendon injury, after the worst pain has subsided. In effect, an athlete
using anti-inflammatory medication to control tendon pain might be likely to stop taking the
medicament before its potentially positive effect (augmented protein synthesis) could be
exhibited.

In addition to the directly negative effect mentioned above (the blocking of DNA production), anti-
inflammatory medications have a variety of unpleasant side effects; they can be very hard on
the digestive system and can increase the risk of abnormal bleeding, for example. Anti-
inflammatory meds can produce a centrally induced analgesia which can make many injured
athletes feel more comfortable, but they have not been proven to be effective for the treatment
of tendonosis (remember that tendonosis does not involve inflammation, the condition for
which anti-inflammatory drugs have been designed). Tendonosis has its own unique treatment
modalities (which we will describe in a moment).
Let's return to our original contention that most tendon injuries probably represent tendonosis, rather
than tendonitis. If this is really the case, it raises a legitimate question: How could so many athletes be
misdiagnosed? As Almekinders and Temple point out in their review article (5), exercise scientists and
physicians may not have a very good understanding of what produces tendon maladies in the first place.
The traditional view in endurance sports is that tendons become injured because of "overuse" (i. e., due to
repetitive, damaging strain on a tendon which exceeds its capacity for repair), leading to the development
of tendonitis. To put it another way, the conventional belief is that cumulative microtrauma leads to an
inflammatory reaction.

The trouble is that this reasonable-sounding scenario remains absolutely unproven, because
very few prospective scientific studies have been able to demonstrate that this is what really
happens. Most research concerning tendon injury is retrospective, with sports scientists looking back in
time to try to figure out why the members of their study group have so many tendon problems. After
gazing into the past, the researchers attribute the "tendonitis" to training errors, inappropriate shoes,
anatomic predispositions, inflexibility, and so on, but there is no real evidence to back up these claims
(without control subjects in these retrospective analyses, the "evidence" is very hard to interpret). In
addition, the subjects in these studies may be suffering from a variety of tendon disorders, including
tendonitis, tendonosis, and tenosynovitis (a distinct disorder in which the connective-tissue sheath around
a tendon becomes inflamed), and the etiologies of these difficulties may be quite different.

Unfortunately, animal studies are not much help; in fact, there is no reliable animal "model" available. A
difficulty which bedevils researchers is that most animals, aside from race horses, do not seem to develop
tendonitis; investigations carried out with animals have failed to show that even extraordinarily repetitive
use of a tendon will produce true tendon inflammation. In a classic study conducted at the
Neurobiological Research Unit in Marseille, France, researchers dramatically overloaded the
plantaris muscles in the legs of experimental rats by removing both the soleus and gastrocnemius
muscles in both posterior appendages, leaving only the plantaris muscles to plantar-flex the poor-rats'
ankles (7). Within one week after the surgery, the rats' plantaris tendons began undergoing
major changes. The fibroblasts (tendon cells) increased their activity dramatically and became
much larger than usual, while arranging themselves in linear columns in between existing
collagen fibers (they were getting ready to "lay down" new collagen tendrils). In the junction between
the tendon and muscle, the fibroblasts began to project thick processes directly into the muscle tissue. In
effect, the plantaris tendons were undergoing remodeling, with old collagen fibers breaking down
and new collagen being created to strengthen the tendons. There was no trace of inflammatory cells
or the inflammation process in general.

The Marseille study was a good one. It helped to explain why athletes often are weaker after a very
severe workout or following a period of very strenuous training (for one thing, their affected tendons may
be breaking down as part of the process of tendon renewal; during this breakdown period, the tendons are
less strong and less resistant to stretch). It also showed that - at least in the rat - overuse of a muscle
and a tendon does not lead to tendonitis but rather to something which looks much more like
tendonosis.

In yet another piece of interesting research, investigators repeatedly overloaded the Achilles tendons of
rabbits. The experimental bunnies developed significant cases of tenosynovitis (inflammation in the
sheaths surrounding the tendons), but there was virtually no inflammation within the Achilles
tendons, i. e., there was no sign of tendonitis (8). Overall, there is little experimental evidence to support
the idea that tendonitis is truly a repetitive-load, "overuse" tendon injury.

True, the real-world experiences of many endurance athletes seem to suggest that repetitive loads can
induce tendonitis. Almost any runner who has developed Achilles pain, ITB syndrome, or patellar-tendon
discomfort, for example, after he/she has expanded training mileage significantly can attest to that.
However, in these cases it is possible that the hurting athletes are like the overworked bunnies and the
French rats; there may be no tendonitis present at all, and tendonosis, tenosynovitis, or some other
abnormality may be the real problem.

Almekinders also likes to point out one other unsettling fact: Although the rate of tendon malady appears
to be high in athletes, many studies have shown that it is not much different from the frequency of tendon
disorder in the completely sedentary population (5). If overuse is the key cause of tendon problems, why
do underused tendons have about the same rate of injury as their overused cousins?

Of course, understanding what is really happening to tendons when they suddenly become painful during
training is extremely important; as mentioned earlier, the appropriate course of treatment depends
entirely on whether the problem is really tendonitis, tenosynovitis, or tendonosis. Ice and anti-
inflammatory medications would seem to be appropriate treatments for tendonitis, although solid scientific
support for these therapies is weaker than one would think. For example, there have been over 30 studies
published in English in the scientific literature concerning the effects of non-steroidal anti-inflammatory
medications on the outcome of tendon injuries; however, only nine of these studies included a placebo
group and were prospective in nature (5). In addition, the true nature of the tendon problems was
unknown; in most cases, researchers simply assumed that tendonitis was present. In effect, the anti-
inflammatory medications may have been used to treat a plethora of problems. Five of the nine
prospective, placebo-controlled investigations documented improved pain scores at the final follow-up in
individuals taking an anti-inflammatory medication, but (and it's a big "but") the duration of the follow-up
periods ranged from just seven to 28 days, and so it is unclear if there were long-term benefits associated
with use of the anti-inflammatory medication. It is possible that the anti-inflammatory medicines provide
some pain relief but have no positive impact (and may indeed have a negative impact) on the long-term
healing process.

Physical therapy is often prescribed for tendon discomfort, and there is evidence in the scientific literature
that physical therapy can be helpful in the treatment of tendon problems (physical therapists will be
relieved to know this). Bear in mind, though, that there are lots of reports of the positive effects of
physical therapy, but few of these accounts are prospective and actually include control groups. One
controlled study found that physical therapy was useful for the treatment of supraspinatus "tendonitis"
(9), compared with a laser placebo, and another investigation detected upgraded range of motion in
patients suffering from shoulder tendonitis who were treated with physical therapy (10). However, note
that no proof was offered that tendonitis was the real problem in either of these studies; as mentioned, an
entirely different disorder may have been the primarily malady. It's possible that everyone in these
investigations had not a trace of tendonitis - and that tendonosis was the aggravator.

As noted, there is no point in treating a tendonosis with anti-inflammatory medication

(especially since such medication might block DNA synthesis and harm tendon healing, as in
Almekinders' fibroblast study). To be on the safe side, it would seem to make sense to take a
simple analgesic such as acetaminophen to control tendon pain, if necessary.

So, what should you do if one of your tendons suddenly flares up? Ice the darned thing, take
acetaminophen if necessary, and reduce your activity for awhile. If the problem persists for more than
two weeks, it's a reasonable bet that you have tendonosis. That's the bad news: The good news is
that there are three solid treatments for tendonosis. Dr. Almekinders is in the forefront of the first
treatment; he cultures blood platelets in his laboratory, extracts growth factors from the platelets, and
then injects the growth factors into the damaged tendon. The growth compounds then seem to block
further degeneration and appear to spur the reconstruction of the tendon. Dr. Almekinders' e-mail address
is almek002@mc.duke.edu

Noted Swedish researcher H. Alfredson and his colleagues at the University of Umea have been
experimenting with a very interesting, second technique for treating tendonosis, also with excellent
success. The Swedes noticed that troubled tendons seem to be excessively vascularized, i. e.,
they have an abnormally large number of blood vessels leading into them. At first, this was
thought to be a good thing; it was felt that the extra capillaries could bring supplemental nutrients, growth
factors, and oxygen to a damaged tendon, spurring recovery. However, the Swedes gradually began to
realize that the expansive blood supply might in fact be stimulating too much "turnover" within the
harmed tendons, in effect causing the breakdown portion of the remodeling process to be occurring at too
high a rate, ultimately preventing repair of the tendon. So, the Swedes have been chemically
destroying a large percentage of the blood vessels leading into hurting, damaged tendons, and
the results have been outstanding. Pain relief is dramatic, and athletes treated with the technique
return to close-to-normal training with surprising rapidity. The technique is called Swedish
sclerotization.

The third method of treating tendonosis is a tried-and-true one, described on several occasions in the
pages of Running Research News (http://www.rrnews.com). This therapy involves the deliberate,
eccentric loading of a painful tendon and its muscle, a process which seems to accelerate
strengthening of both the tendon and its associated sinew. A runner with Achilles tendonosis, for
example, would rely on heel-drop exercises, in which the balls of the feet were placed at the edge of a
step or bench and the heels were allowed to drop down suddenly to below the level of the step, with the
Achilles tendons and calf muscles attempting to control such plummeting.
How about rest? Shouldn't you always treat a tendon problem with rest - until the symptoms go away?
Strangely, the scientific literature is almost completely silent on this issue. While it might seem that rest
would give an injured tendon an opportunity to heal, it might also give a tendon suffering from tendonosis
a chance to degenerate further. In fact, it is clear that a tendon needs to be mechanically
stimulated in order to begin the process of activating its fibroblasts and synthesizing
significant quantities of new collagen fibers; complete rest would prevent this from happening
(recall Almekinders' study in which the fibroblasts which were subject to strain were the ones
which hiked DNA synthesis, as long as they were not exposed to anti-inflammatory
medication). Thus, it is probably good to carry out reasonable numbers of eccentric exercises for a
calling-out tendon, pain permitting, as soon as it is possible to do so.

Of course, before you get too carried away and start booking your flights to Raleigh-Durham or Umea,
make sure that you really do have a tendon problem; bear in mind that other conditions may masquerade
as tendon difficulties. An arch strain, for example, might disguise itself as a case of tibialis posterior
tendonitis, and what appears to be a chronic, non-tractable Achilles-tendon problem might actually be
nothing more than retrocalcaneal bursitis. If you are a serious athlete, it is important to have an
extremely wise, skilled, sports-medicine physician who can make the right diagnosis and recommend the
proper treatment.

It's now time for our final apothegm? Have you been plagued by "tendonitis" for a long time? One reason
that your plague might be continuing is that your malady might not be tendonitis - you could have
tendonosis, which is not well treated by the conventional therapies for tendonitis. Almekinders' growth
factors, the Swedes' blood-vessel sclerosis, or systematic eccentric exercise might be what you really need
to remove yourself from the ranks of "tendonitis" victims. ©

References

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