Posted by on 1. January 2021

Tendon injuries are the most common injuries in our sport horses, accounting for 46%. 97-99% affect the superficial flexor tendon. Oftentimes the horse has injured itself on the pasture by stepping in a whole, or has landed badly after a jump.

Are sudden symptoms really always acute injuries?

Osteotherapy demonstrates to me on a daily basis that many injuries that seem acute are really not.

Perhaps an example from last week:
A client calls me to treat her horse. The problem is an acute right front lameness. Acute as it appeared quite suddenly 6 weeks ago.
On palpation of the foreleg, a hard circumferential increase is noticeable craniomedially at the pastern joint. At the same time the lateral rotation is restricted.
X-ray control confirms my diagnosis: ringbone in the pastern joint.
The client’s first question was whether the injury could have occurred acutely 6 weeks ago.

Clear answer: no.

The problem must have been present for longer than 6 weeks. Otherwise, no bony change could be seen on the radiograph.

Now her horse is an Andalusian. And unfortunately a large number of these horses don’t see proper hoof care when they are young.
In this horse, in addition to the anomaly of toe narrowness and ground width, there is also a faulty hoof treatment. With a lateral and medial hoof imbalance.

In the left frontleg – radiographically still inconspicuous – the joint space medially is smaller than laterlly.
The radiographs of the right forehand reveal the whole problem:

Krongelenkschale lateral
Krongelenkschale ap

Joint space laterally slightly narrower than medially, still present after attempted correction by farrier. In the red circle: Structural changes at the medial collateral ligament due to increased tensile forces caused by widening of the joint space.

The lateral joint space is narrower than the medial joint space. So exactly the other way around than in the left forehand. On the medial side, there are ossifications of the capsule at the craniomedial edge of the joint as well as at the insertions of the medial collateral ligament.
These changes are due to a permanent overstretching of the structures of the medial side of the joint. And this not only since yesterday or last month or the month before but at least over the last half year.

This case clearly shows that a continuous incorrect loading leads to a gradual change of capsule, ligaments and other load-bearing structures. The symptom of lameness may appear suddenly or acutely, while the actual cause of the symptom has been acting for a long time. Thus creating the conditions for an injury.

What does it look like now with tendon injuries?

The superficial flexor tendon works at a maximum stretch of 16% during canter. This is close to the stress limit. They belong to the “energy storing tendons”, like achilles tendon in humans, and release the absorbed momentum when landing back into the movement at lift of.
Thus, microlesions and molecular changes are preprogrammed, especially due to repetitive loading cycles. Studies show that chronic pre-damage is already present in 97% of all tendon ruptures.

Chronic damage more common than thought


Chronic tendopathy

Image from: Tendon and Ligament Injury; Roger K. W. Smith, MA, VetMB, PhD, DEO, Diplomate ECVS, MRCVS; The Royal Veterinary College, University of London, United Kingdom

(Left) Tranverse and (right) longitudinal ultrasonographs taken from the proximal metacarpal region of a horse with chronic
superficial digital flexor tendinopathy. Note the enlarged SDFT with heterogeneous echogenicity and a poor longitudinal striated
pattern. This is similar to the appearance of the tendon in the transverse image, which suggests the absence of normally aligned
collagen fibers.

More interestingly, even in healthy animals without symptoms, chronic changes in the superficial flexor tendon are found in 34% of the animals studied.
This indicates that age- and strain-related changes are likely to be the cause of injury to this tendon much more frequently than acute injury.

Microlesions and poor perfusion cause “molecular inflammation” that cannot be detected by ultrasound. Metalloproteases change their activity, tenocytes their function. This alters the histological composition of the tendon, especially in the middle region of the superficial flexor tendon, as well as its elasticity and stability.
If a momentary strong overload then occurs, for example if the shoulder girdle can no longer absorb shock, or a blow to the tendon under load (kicking its own tendon), severe tendon damage can occur.
However, the trauma is then only the trigger, not the cause.

By the way: lateral and medial hoof imbalances are also often the cause of microtrauma of the superficial flexor tendons.

So: prevention through regular osteotherapeutic treatment (shoulder girdle, passive standing apparatus, Os carpi accessorium), sensible training and good shoeing pay off.

For those who really want in-depth information:

Age-related changes of tendon fibril micro-morphology and gene expression.
Iris Ribitsch, Sinan Gueltekin, Marlies Franziska Keith, Kristina Minichmair, Christian Peham, Florien Jenner and Monika Egerbacher.

Department for Companion Animals and Horses, Veterm, University Equine Hospital, Vetmeduni Vienna, Vienna, Austria
Department of Pathobiology, Unit of Histology and Embryology, Vetmeduni Vienna, Vienna, Austria