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Tendon function and failure: Recent advances

VETERINARYWeb Master
Tendon injuries continue to be one of the most problematic injuries that affect racehorses. One of major issues facing veterinarians and trainers is that we have little understanding of why tendons become injured in the first place, how such the SDFT in the horse acts like the spring of a pogo stick, stretching and storing energy as a horse lands, and releasing energy to aid a horse’s locomotion as the limb pushes off.   There is a lot of clinical and research focus on these “energy-storing” tendons (such as the equine SDFT), as it is these tendons which are most prone to injury, and it appears to be a property of the function of such high strain, elastic tendons which result in these significant injuries will lead to so much economic loss and welfare issues for the affected horses. Under such extreme mechanical demands, it is not surprising the SDFT is prone to overuse injury, particularly amongst racehorses. SDFT injuries are highly debilitating, requiring considerable rehabilitation periods and are often career-limiting.   There is little convincing evidence of efficacy for any current treatment, and even after extensive periods of rest and rehabilitation, re-injury rates are extremely high, with little knowledge of how best to safely reintroduce training.  In the horse, tendons are also extremely long, due to the length of a horse’s leg. In the horse’s forelimb, there is no muscle lower in the leg than the level of the knee (carpal) joints, and tendons mainly extend from the level of the knee down to the hoof.   To understand why tendons, such as the equine SDFT, become injured and how we may develop methods to allow better treatments, we and other researchers, have been developing an understanding of how elastic “energy-storing” tendons function and how do they fail. We have recent, exciting data which leads us to believe that tendon injury occurs because of ageing or damage within a specific part of the tendon structure called the interfascicular matrix (IFM). The IFM is also known by some people as “the endotenon”. Tendon is like braided rope, with the IFM connecting the rope strands laterally. Our evidence shows that the IFM is both stretchy and lubricating to allow the rope strands to slide around relative to each other, but as a tendon ages or becomes damaged, this mechanism does not work as well. Separately, we have shown that tendon overuse causes damage and inflammation in the IFM. Combining these results, leads us to think that the changes in the IFM with age cause damage to occur more easily to this region and this leads to tendinopathy. The main molecule which makes up tendons are long rope-like proteins called collagens. In particular, in tendons, a specific collagen (Collagen-I) is bundled together into ropes of many thousands of collagen fibres and fibrils to ultimately form tendon structures known as fascicles. Fascicles are like individual strands or threads which make up a rope and are approximately half a millimetre in diameter. If a cut tendon is examined at post-mortem, it has a honeycombed liked appearance which are the individual fascicles, with the IFM surrounding each fascicle (Fig 1). Interestingly, when we use ultrasound to examine a tendon as part of a clinical examination, the fascicle is the smallest part of the tendon which we define ultrasonographically, and the presence of ordered fascicles is a good sign for tendon health (Fig 2) Historically, the collagen which makes up the majority of a tendon has been the major focus of interest when it has come to trying to understand why tendons are so commonly injured, and why they never heal particularly well following injury. However, the central role of collagen to tendon function has been recently questioned. Undoubtedly, this molecule is important to tendons, but whilst the collagen material in a tendon has a major role in providing structural strength to a tendon, it has only a minor role in allowing a tendon to perform as an elastic structure. The collagen molecules which make up most of the tendon are like large metal reinforcing rods which are used when constructing large buildings. They give a lot of the strength to the material, but don’t fully effect the functional properties of a tendon. Another aspect of the collagen in tendon is that it is an extremely long-lived molecule and through life is hardly turned-over, so the body has very little capacity to repair and early damage. Research has shown that the half-life of a collagen molecule in a horse tendon is probably well over two hundred years, meaning that most horses will not repair or replace most of the collagen in their tendons between the time they stop growing, to the point that they die. The unique properties of the equine SDFT, which in part makes the horse such a superb athlete, are due to its elastic structure.   These elastic properties of tendon derive almost entirely from the IFM, which contains a lot of specialised molecules which both allow low-friction sliding between the collagen fascicles (proteoglycans) as well as specialized molecules, which allow elastic recoil. In the horse, this part of the tendon is uniquely adapted to both allow tendon extension and recoil, as well as withstanding multiple cycles of loading which would occur with fast galloping exercise over considerable distances.   Interestingly, it has been shown in a number of different studies that older horses are at increased risk of tendon injury. Coupled with this finding is the discovery that the IFM in older horses loses its ability to slide and extend as easily, and also loses its elasticity to some extent. Also this part of the tendon in older horses becomes less able to withstand the repeated loading which comes with fast galloping exercise, and as a consequence, is more likely to become damaged with repeated loading. Overall the IFM in older horses is stiffer, meaning that the collagenous tissue in tendons is likely to become loaded at an earlier part of weight bearing at the gallop, leading to a greater likelihood of overall tendon injury.   Another recent research finding is that when a tendon is subjected to repeated loading, analogous to the loading a tendon may receive during galloping exercise, is that early damage is seen to occur specifically in the IFM, and as a consequence the cells present in the IFM respond and produce an inflammatory response (like a local bruise) as a consequence of this damage. Thus the IFM tendon is not only important for the elastic function of the tendon, but there is now evidence that the earliest stage of injury probably starts in this part of the tendon. As mentioned earlier, one of the problems with tendon injuries is that the tendon does not heal appropriately post-injury. The tendon heals by forming a scar tissue, which whilst often very mechanically strong, is a much stiffer and much less elastic than normal tissue. Hence an injured tendon is often mechanically very different from a normal tendon, even once healing is complete. There is often a marked discrepancy in the elastic properties of the normal tendon and the scarred tendon tissue, and it is at the interface between the two different tissues that re-injury occurs during a horse’s future racing career. We have observed that one of the major issues with the scarred tendon repair tissue is that it totally fails to reform any structure which is like an IFM (Fig 3); hence repair tissue in tendon is unable to extend and work elastically, and this is probably one of the main reasons why tendon repair is currently inadequate. Through understanding these mechanisms of tendon function and failure, it opens up the possibilities in the future to make progress in both preventing and treating tendon injuries in a more optimal manner. Using current imaging technology, this understanding identifies the importance of the fascicular and IFM structure, which can be currently imaged using ultrasound, and emphasises the importance of identification of reformation of this structural appearance in injured horses before they are allowed to undergo fast work again after injury (Fig 2 & 4). It also identifies the need to develop better imaging methodologies which could be used to assist diagnosis and management of tendon injuries. An example of this is high-field MRI, which currently in the research laboratory allows exquisitely detailed imaging of the key tendon structure (Fig 5). There is also the potential for development of novel ultrasound imaging technologies which will allow dynamic measurement of sliding of the fascicles and potentially both identify tendons at altered risk of injury, as well as assisting with the rehabilitation of injured horses whilst they return to work. Such technology is being developed in our laboratories at the moment through generous support from the Horserace Betting Levy Board in the UK. Regenerative therapies need to be developed which specifically target regeneration of the IFM, as we think recreation of the IFM organisation is key to long term healthy tendon function following injury. Finally, we need to understand how the properties of tendons develop as a foal grows to discover  whether we can intervene at this stage to allow formation of a healthier, less injury-prone tendon. We have evidence that the IFM undergoes considerable adaptation during the initial development and weanling stage of growth. It is an exciting time for understanding tendon injury, its treatment and its prevention in the horse. We are now much closer to understanding the biological causes of this frustrating condition, and this gives us the potential to really make major advances in the next 5-10 years, which will be of substantial benefit to the horse.
 

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Tendon injuries continue to be one of the most problematic injuries that affect racehorses. One of major issues facing veterinarians and trainers is that we have little understanding of why tendons become injured in the first place, how such the SDFT in the horse acts like the spring of a pogo stick, stretching and storing energy as a horse lands, and releasing energy to aid a horse’s locomotion as the limb pushes off.

There is a lot of clinical and research focus on these “energy-storing” tendons (such as the equine SDFT), as it is these tendons which are most prone to injury, and it appears to be a property of the function of such high strain, elastic tendons which result in these significant injuries will lead to so much economic loss and welfare issues for the affected horses. Under such extreme mechanical demands, it is not surprising the SDFT is prone to overuse injury, particularly amongst racehorses. SDFT injuries are highly debilitating, requiring considerable rehabilitation periods and are often career-limiting.

There is little convincing evidence of efficacy for any current treatment, and even after extensive periods of rest and rehabilitation, re-injury rates are extremely high, with little knowledge of how best to safely reintroduce training.  In the horse, tendons are also extremely long, due to the length of a horse’s leg. In the horse’s forelimb, there is no muscle lower in the leg than the level of the knee (carpal) joints, and tendons mainly extend from the level of the knee down to the hoof.

To understand why tendons, such as the equine SDFT, become injured and how we may develop methods to allow better treatments, we and other researchers, have been developing an understanding of how elastic “energy-storing” tendons function and how do they fail.

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