Diagnosing DSLD

Degenerative Suspensory Ligament Desmitis
Compiled by Rhonda Hart Poe

DSLD is a hot potato, misunderstood and feared. After two years of research, interviewing over 100 breeders, buyers, seller, vets, farriers, judges and researchers, none wanted to be named in an article. There were refusals to use e-mail, official "no comments" and warnings of threats and lawsuits. Just what puts this malady in such a maelstrom.

NOT MANY REALLY KNOW what DSLD is (or is not), and no one has yet proven how it is acquired. Thanks to the bulldog stick-to-it-ive-ness of a few dedicated professionals, the disease process is well documented. Diagnoses are easier to affirm, but then prognosis is bleak. So far, "successful" treatment only slows or postpones the progression of the disease, allowing afflicted horses to live out their lives comfortably, if not usefully. Most horses remain unsound to some degree for life. An extremely high percentage is put down.

Scenes of Suspicion

LET'S LOOK at what might be - or might not be - typical scenes of DSLD.

• The twelve-year-old mare delivered normally. The foal was healthy and active. They seemed to settle into a wonderful pattern of normal life. But the mare didn't move around the paddock as much as she used to. She laid down frequently. Her owner suspected colic.
• The stallion had kicked against the wall of his stall and injured his fetlock. But after six months of stall rest and treatment he hadn't totally recovered, and remained lame in his right hind leg.
• The eight-year-old gelding was in top form. He was a competitive show horse and none could rival the smoothness of his ride. There was an unmistakable springiness in his step, as the rider glided along. The only complaints were that the gelding leaned on the farrier and resisted stretching his leg out behind to be trimmed.
• The mare of unknown age and lineage resisted walking. She stood with first one hind foot drawn up beneath her, tipped up at the heel, then shifted onto the other. She resisted anyone touching her legs. Both hinds were hot, thick and oddly stiff to the touch.

What is it?

DEGENERATIVE SUSPENSORY LIGAMENT DESMITIS translates to progressive (degenerative) inflammation (desmitis) of the suspensory ligaments (of the legs). It is a rare and devastating lameness that seems to affect only a small percentage of the horse population.

Understanding that DSLD is progressive is essential.

Understanding that DSLD is progressive is essential. The differences between what is seen in a "full blown" case and at on?set can be extreme. Internal changes are reflected in a range of symptoms not always obvious at first to the owners, farriers and vets, so that early signs are usually missed, or mistaken for some other problem.

Another monkey wrench in diagnosing DSLD is that it doesn't always proceed the same way. One vet, who has treated scores of cases, cautions, "By it's very nature of being a chronic, progressive disease, it is slow and insidious, usually. What we don't know is what makes some horses's progression slow, sometimes very slow, and what makes some self-destruct in a matter of months." Just as confounding, classic symptoms don't develop in all cases. Experienced vets warn, "Many horses ultimately diagnosed with DSLD didn't develop classic symptoms."

Changes first occur at the cellular level. Normally, the suspensory ligaments, like other connective tissue in the horse's body, are in a state of continuous repair. In the first line of repair, cells called fibroblasts lay in a form of collagen known as TYPE III - a small, weak, not very pliable molecule. As damage increases, they progressively build up to installing stronger, larger, more elastic TYPE I collagen. But for some unknown reason, these cells change in DSLD horses. They fail to lay in the stronger type of collagen. As the suspensories become dominated by type III collagen, they weaken. Blood supply dwindles. Eventually, the malfunctioning fibroblasts change into chondrocytes, cells that weave in cartilage where collagen should go. The naturally springy tendons gradually thicken and stiffen, and are eventually disfigured by this rigid, unyielding material. When severe cases are dissected postmortem, some appear to have bone or pebbles in the ligament; others show unhealed tears in a "Swiss cheese" pattern.

As the makeup of the suspensories change, so does their character. They no longer support the horse's weight as the hooves impact the ground. As they lose the ability to stretch and rebound, they begin to tear. Each new tear continues the errant rebuilding process, causing more cartilage to be laid into the suspensories, making them even more susceptible to more injury, more cartilage, more injury, etc. They become hard and fibrous, and in severe cases may develop adhesions to the cannon or splint bones, or to the deep flexor tendon. Lack of support may cause the sesamoid bones to drop. Secondary conditions, such as founder, pain-induced colic, arthritis and ringbone may develop.

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