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In t e r n a t I o n a l Jo u r n a l o f th e r a p e u t I c Ma s s a g e a n d Bo d y w o r k —Vo l u M e 5, nu M B e r 1, Ma r c h 2012
EdUcatioN
Tendinopathy: Why the
Difference Between Tendinitis
and Tendinosis Matters
Think tendinitis and you think pain and burning in
the affected area, decreased strength and flexibility,
and pain caused by everyday activities. As it turns
out, tendinosis is far more often responsible for
these symptoms than tendinitis(1,2,3). It is important
for health care practitioners to distinguish between
these disorders in order to apply the most appropri-
ate treatment.
Tendinitis is the inflammation of the tendon and
results from micro-tears that happen when the muscu-
lotendinous unit is acutely overloaded with a tensile
force that is too heavy and/or too sudden. Tendinitis
is still a very common diagnosis, though research
increasingly documents that what is thought to be
tendinitis is usually tendinosis(1,2,3,4,5).
Tendinosis is a degeneration of the tendon’s col-
lagen in response to chronic overuse; when overuse is
continued without giving the tendon time to heal and
rest, such as with repetitive strain injury, tendinosis
results. even tiny movements, such as clicking a
mouse, can cause tendinosis, when done repeatedly.
The confusion about the difference between ten-
dinitis and tendinosis is widespread. Many injuries
commonly presumed to be tendinitis are actually
tendinosis. For example, tennis elbow is usually de-
scribed as tendinitis of extensor carpi radialis brevis;
however, “signs of either acute or chronic inflamma-
tion have not been found in any surgical pathologic
specimens in patients with clinically diagnosed lateral
tennis elbow syndrome,” proving that tennis elbow is
not tendinitis(4). The histology of tennis elbow shows
that it is actually tendinosis(5).
A microscopic view of tendinosis reveals an in-
crease of immature type III collagen fibers (mature
type I fibers dominate in healthy tendon tissue); loss
of collagen continuity so that collagen fibers are
no longer aligned with each other and sometimes
fail to link together to facilitate load-bearing; an
increase in ground substance (the material between
the body’s cells); and a haphazard increase of
vascularization(2,3,5). These vascular structures “do
not function as blood vessels” and “are not associ-
ated with increased healing(2).” The appearance of the
tendon shifts from a reflective, “white, glistening and
firm” surface to a “dull-appearing, slightly brown and
soft” surface (mucoid degeneration)(2,3).
These changes result in a loss of strength in the
tendon and increase the bulk of the tendon, both of
which contribute to the cycle of injury and can set the
stage for secondary conditions, such as tendinitis and
nerve impingement. My study leads me to believe
that, in the forearm and wrist, tendinosis can result
in secondary carpal tunnel syndrome; this is because
the thickening of the tendons with excess ground
substance and the swelling of the surrounding tissue
crowds and compresses the median nerve.
There is a prevalent supposition that tendinosis
begins with tendinitis, which then instigates a healing
process that changes the collagen and weakens the
tendon, becoming tendinosis. Perhaps this supposition
exists because the stages of soft-tissue healing are
generally listed as, in short: inflammation response,
regeneration (collagen production), and remodeling
(strengthening the collagen in the direction of the
forces placed upon it). In one article, tendinitis is cited
as the first stage of a tendinopathy; tendinosis is cited
as the second stage and rupture as the third stage. The
fourth stage is described as a combination of stages 2
and 3, along with fibrosis and calcification(2).
The suggestion that tendinitis precedes tendinosis
is at odds with the fact that a healthy tendon is up to
twice as strong as the muscle, making the body of
the tendon unlikely to tear before the muscle unless
the tendon has already been weakened by degenera-
tive changes(6).
The idea that tendinitis is the first stage of tendinosis
seems to presume that micro-tears and inflammation
are a precursor to collagen degeneration. Histopatho-
logic analyses show that torn fibers, scar tissue, and
calcification are only found in conjunction with ten-
dinosis some of the time, and inflammatory cells are
rarely found in conjunction with tendinosis, support-
ing the hypothesis that tendinitis occurs secondarily to
tendinosis(1,2,3,5,7). excessive and/or repetitive tensile
forces on the tendon are likely what instigate the
chemistry of degenerative changes associated with
tendinosis(8). Arnoczky et al. have reportedly shown
that tensile forces placed on the tendon are directly
related to persistent activation of a stress activated
protein kinase (c-Jun N-terminal kinase (JNK)); the
persistent activation of JNK has been related to the
initiation of programmed cell death(8).
evelyn Bass, LMT
Massage Department, Southeast Medical Clinic, Juneau, Alaska, USA
we often
mistake
tendinosis for
tendinitis
microscopi
c
characteris
tics
tendinosis:
-immature
collagen
(type III)
-Loss of
collagen
continuity,
increased
ground
substance,
vasculariza
tion
prevalent
continum
model:
tendinitis —>
eventually
tendinosis
reverse
hypothesis:
maybe tendinosis
comes before
tendinitis
