Page 887 - Adams and Stashak's Lameness in Horses, 7th Edition

Principles of Musculoskeletal Disease 853

evident nor produces any reparative responses, but EFFECT OF AGING AND EXERCISE
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instead progressively weakens the structure. Detection ON TENDON INJURY
VetBooks.ir normal horses is consistent with this observation. and adult horses have elucidated the effect of exercise
of asymptomatic lesions in postmortem studies of
Recently, a number of controlled studies in young
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Furthermore, many strain‐induced tendinopathies are
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bilateral. Large studies analyzing epidemiologic data on developing and mature tendons. 5,13,23 Subjects used in
in both horses and humans have shown strong correla­ these studies had no evidence of previous tendinitis nor
tions between age and injury rate. Experimental stud­ any evidence of tendinitis induced by the exercise
22
ies and postmortem analyses of normal tendons have protocols.
indicated that increasing age and exercise may induce Histological analysis revealed that local differences
tendon matrix degeneration instead of adaptation in the occurred in collagen fiber diameter of older but not
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adult horse. 12,33 younger exercised horses. In adult tendon, a reduction
Tendinopathies often begin with degeneration. Minor in crimp occurred with aging and exercise. Exercise also
changes in the structural integrity predispose an already induced a greater number of smaller fibrils within the
high‐risk structure to injury. When the structural central region of the SDFT. This change did not correlate
integrity is overwhelmed, irreversible damage ensues. with new collagen formation, indicating that an adap­
12
Palmar structures, especially at the heel, sustain load tive response occurred rather than an elevation in
increases during heel strike, quickly placing the SDFT collagen.
and suspensory ligament at risk. Conversely, load of Molecular composition changes also occurred with
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the DDFT rises during stance. exercise. A reduction in GAG content and loss of COMP
Physical disruption occurs within the tendon matrix occurred in the center of the tendon with long‐term exer­
4
when structural strength is overcome. Various struc­ cise. This is in contrast to an increase in GAG and type
tural breakdowns may occur, including fibrillar III collagen found in the SDFT of exercising horses
stretching with breakage of cross‐links, fibrillar rup­ whose tendons were collected postmortem. Because
ture, or, in severe cases, separation of tendon tissue. damage to these tendons was thought to result from sub­
12
Once this occurs, the damage signals repair processes clinical tendon degeneration, these molecular changes
that are common throughout the body such as inflam­ most likely reflect a response to injury (or a reparative
mation followed by repair mechanisms (see phases of response) rather than a degenerative change associated
healing). with age and/or exercise.
The risk of strain‐induced injury is increased by fac­ Similar to cartilage, a lack of load to tendon results in
tors such as the horse’s speed, track surface (the harder a deficit of COMP levels within the tendon. However,
the track, the higher the risk of injury), the horse’s once adequate COMP has accumulated within tendons,
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weight, fatigue level, and shoeing. Increased heel eleva­ loading does not appear to affect the COMP levels.
tion has been demonstrated to be protective for the Clinically, this implies that a deficit of exercise in the
DDFT, but it increases the extension of the MCP joint. developing tendon may likely result in a tendon prone to
3
Although low heels have been viewed as protective of injury due to a poorer quality of matrix since COMP
SDFT tendinitis, epidemiologic studies have correlated levels are directly correlated to tendon strength. In con­
an increased risk of tendon and ligament injuries with a trast, too much exercise may also result in tendon injury
low heel and long toe conformation. 12 if the strain levels of the tendon are exceeded. 5
Tearing of the tendon also occurs, although with Exercise studies suggest that as tendon ages, degen­
much less frequency than tendon degeneration. The erative changes associated with exercise accelerate.
most common site is the DDFT of the forelimb and Cellular activity decreases and most likely collagen turn­
occasionally the manica flexoria of the hindlimb. The over slows. Growth factors such as TGF‐β also decrease,
mechanism of injury is not clear; however, it has been which may lead to a reduced ability of the tendon to
hypothesized that hyperextension of the fetlock canal undergo a reparative response. Furthermore, less adap­
combined with compression of the DDFT as it passes tive changes may occur following maturity, as evidenced
over the palmar aspect of the joint may predispose the by epidemiological data in horses and humans that draw
structure to injury. The hindlimb manica tears may be a strong correlation between age and exercise and the
12
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a result of ongoing tenosynovitis that frequently occurs incidence of tendon injury. A recent study proved that
in the tendon sheath of the hindlimb combined with as tendons age, there is an increase in stiffness in the
hyperextension in that region. interfascicular matrix that may result in tendon fascicles
The third common mechanism for tendon and liga­ being loaded at an earlier point in the stress–strain
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ment injury is percutaneous trauma. The distal limbs curve, which leads to increased risk of damage.
have minimal soft tissue coverage and commonly sus­ Additionally, there is significantly less sliding at the fas­
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tain contusion. Injuries resulting from wire, kicks, blunt cicular interface in aged tendons. Conversely, young
trauma, and overreaching contribute to most of the per­ growing tendon appears to be much more adaptive and
cutaneous injuries seen. The most serious include those responsive to loading and exercise, especially during the
to the palmar/plantar region of the limb and tendon lac­ early stages of growth.
erations that are from wire. Common locations of ten­ Among the unknown factors are the level and amount
don lacerations are the mid‐cannon area of the hindlimb of work necessary to initiate the response. The natural
and the pastern region (including the tendon sheath) of exercise intensity of foals at play may be ideal to allow
both the front limb and hindlimb. These injuries often strain rates that boost tendon matrix production.
result in moderate to severe adhesion formation and a Figure 7.59 is a hypothesized schematic representation
poor return to athleticism. of adaptive responses to injury in mature and immature