Page 888 - Adams and Stashak's Lameness in Horses, 7th Edition

854 Chapter 7

and microdamage, leading to degeneration. This also
predisposes the tendon to clinical tendinitis when an
VetBooks.ir that may predispose tendon to injury. Studies have deter­
acute supramaximal load is applied.
Hyperthermia during exercise is a physical influence
mined that temperatures up to 45 °C occur secondary to
galloping. These temperatures are high enough to
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Training damage most other tissue types; however, in vitro exper­
“window”
iments have revealed that tenocytes may resist these
increases. Nevertheless, the hyperemia that occurs in
28
tendon at high speeds may damage the tenocytes or even
the extracellular matrix.
Vascular disturbances are also hypothesized to con­
tribute to tendon damage. When tendon is maximally
loaded, blood flow is limited or abolished due to the com­
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Training level pressive forces generated. This may lead to a relative
hypoxic state of the tendon, predisposing the tissue to
lmmature adaptation Adult adaptation degeneration. Although certain areas of tendon have poor
lmmature injury risk Adult injury risk perfusion, there is histologic evidence of an adaptive state
to ischemia because fewer cells exist in these areas (i.e. the
Figure 7.59. A representation of the adaptive and injury risk for dorsal surface of the DDFT in the area of the fetlock) and
growing (immature) and adult (older than 2 years of age) equine matrix components in ischemic areas have compression‐
digital flexor tendons. Source: From Smith. Reproduced with resistant components. In addition, these areas may receive
32
permission of Elsevier.
nutrition from synovial fluid components.
Despite a reduction in blood flow to certain areas of
tendon such as the DDFT in the area of the fetlock, these
regions seem to be resistant to degeneration except in
the most severe cases of tendinitis. Furthermore, studies
Tendon strength Training metabolism does not lead to abnormal cell prolifera­
have shown that mechanically reducing oxidative
tion. Therefore, tenocytes, and tendons and ligaments
4
in general, may be resistant to hypoxia compared with
other tissues in the body. Although resistance may exist,
however, generation of toxic free radicals predisposes
the tendon to degeneration. This mechanism of injury
Tendinitis may occur as a result of reperfusion injury when perfu­
risk level sion is restored.
Finally, mechanical, vascular, and hyperthermic envi­
ronments may all lead to inflammation and release of
Racing career Age
Skeletal proteolytic enzymes such as collagenase or aggrecanase
maturity that promote tendon degeneration. While inflammation
and where it fits into tendon degeneration is yet to be
Figure 7.60. A diagram of an approach to tendinitis prevention. defined in tendinopathy, most of the literature suggests
The dotted line represents a horse with strong tendons, in contrast that fibrosis of tendons results from persistent inflam­
to the dashed line, which represents a horse that has poor‐quality mation and lack of tendon healing. Elevations in pro­
10
tendons at skeletal maturity (approximately 2 years old). The horse
with poor‐quality tendons sustains tendinitis during its racing career teolytic enzymes result in a slowed matrix synthesis and
due to cumulative fatigue damage to the tendon, whereas the horse an elevation in degradation, whereby overall degrada­
with strong tendons, although sustaining the same degeneration, tion is high. 11,15,30
begins at a stronger point and does not suffer from tendinitis. In summary, tendon degeneration results from many
Introduction of exercise throughout development improves tendon factors that contribute to matrix and cellular abnormal­
quality (arrow), potentially decreasing the incidence of tendinitis. ities. Ultimately, the resident cell population cannot
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Source: From Smith. Reproduced with permission of Elsevier. repair microdamage that is most likely due to deficient
or absent growth factor stimuli (such as TGF‐β) and cel­
17
tendon. Figure 7.60 illustrates a strategy for preventing lular senescence within the tendon. As loading contin­
tendinitis in the horse, focusing on tendinitis risk before ues and strain increases, failure of the fibrils occurs and
and after skeletal maturity. results in tendon damage.

MECHANISMS OF TENDON DEGENERATION RESPONSE OF TENDONS AND LIGAMENTS
Mechanisms of tendon degeneration may have several TO INJURY: PHASES OF HEALING
etiologies including mechanical, physical, vascular, and When tendons and ligaments are damaged, the pro­
inflammatory. Mechanical influences such as overexten­ cess of repair follows three stages of healing: the acute
sion or direct low‐grade repetitive forces cause fatigue inflammatory phase, the subacute reparative phase, and