For countless centuries there have been horses who have broken down in the suspensory ligaments. These horses were usually older animals that had served a hard service life or horses that had been overworked, or in some cases older brood mares who had produced a number of foals.

In more modern times horses also break down but often times at a far younger age. Of course in more modern times we also put horses into service at much younger ages, tend to over work them between times of idleness and feed them for rapid growth!

In the past, horses that broke down were not started young, had very limited access food additives or grains, and were used on a daily basis which kept them conditioned to their tasks without a lot of repetitious work involving collection, circling, fast starts and stops etc.

More recently there is a sort of overblown craze to declare animals with suspensory breakdown as genetically defective. The problem with such a blanket assertion is that there are those animals who break down from minute injuries that compound over periods of time, and some that break down from sudden trauma. There are those who break down over time due to hard use, lack of care or nutrition, or just plain old age or in some cases conformational aspects that make them more predisposed to the problem.

So far, all the studies done on the breakdown of suspensory ligaments do not take into account how the horse was raised, fed, how young it was put under saddle, how hard it was used, or how much weight it was carrying or a host of other external situations that in the past have caused such breakdowns.

Recently two of the horses I bred were accused of having DSLD. That assertion was put on the internet by someone angry with me personally over a totally unrelated issue. This person at no time contacted me mentioning problems with the horses but instead blasted the internet lists with accusations and untruths regarding them and their mother who is one of the matriarchs of our breeding program. Whether the assertions regarding the horses was due to misinformation or a deliberate act to discredit the animals and me personally is anyone's guess.

On a personal level I have forgiven these people for the things they have done and said because to do otherwise would not be living up to my beliefs. At the same time, it is important to me to seek truthful information and learn more about this disorder with the hope of sorting truth from fiction about things posted on the Internet. To get a more clear perspective of what truly is known about the condition one needs to do a thorough search for ALL things printed on the subject. If a negative situation can be turned into a positive learning experience that is a good thing.

During the time when such erroneous posts were being sent out to the world, there were claims made that are not true. For instance a particular vet was claimed to have examined my old mare and reached a conclusion via photographic evidence that she had DSLD. To that I must state that any vet who would breach legal boundaries to do such a thing on any animal belonging to someone she has never met, puts herself liable to lose her veterinary license. Since DSLD can only be diagnosed by a post mortem, comprehensive necropsy, it would be interesting to know just how a person who has never physically SEEN the horse in question could come to such conclusions. If that were possible to be done, then the millions of dollars being spent on the research of this disease would certainly not be necessary!

All the same, for the sake of learning the truth and educating myself further with regard to DSLD I pursued my own investigation in the hope of finding answers. The deliberate maligning of my horses caused me to want to know more about the disease and to more fully understand how it affects the horse.

What I found in my research was interesting. To begin with there is precious little actually known about the disorder yet there are countless pages devoted to it on the internet presenting information as fact that simply has not been borne up with actual research.

In point of fact, to date no one has even been able to prove there is such a thing as DSLD as a disease much less as a heritable disease! There are theories and there are educated hunches but after 7 years of comprehensive study and research done in several different universities, no one has yet been able to identify a genetic marker or exclusive specific clinical symptoms that separate injury from "DSLD" indicating there truly is such a disease!

What has been learned is that horses INJURED in the suspensory ligaments or flexor tendons often have identical symptoms to those claimed to have DSLD.

Further, biochemical evidence shows that some horses do not repair damage to tendons and ligaments to the same degree others do because the collagen in those horses never solidifies. To date that appears to be the one, single noted difference between injury and healing that may indicate a disease is at play. That disease may simply be a damaged immune system for all that is known. None of the studies and none of the researchers has been able to identify any other abnormality separating injured horses from those thought to be DSLD.

This is not what is being touted on the media however. The current theory is that an over abundance of proteoglycans of unknown identity cause DSLD. In 7 years of research by the very researchers making these claims, however, has not identified such proteoglycans. What HAS been found is the proteoglycan level in unaffected horses is frequently higher than that in affected horses.

The newest study coming from UC Davis clearly states proteoglycan levels DOES NOT provide symptoms or proof of DSLD.

It seems there are countless armchair experts touting bits of information out of context and yet with authority enough to make uninformed people accept such incorrect information as fact!

Scientific theory or hunches are being posted to the net as scientific law and that is simply not responsible nor helpful and may cause a large number of horses to suffer needlessly or to even be put down.

Because I am a stickler for knowledge and truth, I decided to post an article on the subject in order to bring some actual and factual information out to anyone truly interested in learning about this disease and how to determine whether a horse may have it, or simply have a suspensory ligament injury!

If one really researches all the published works on DSLD and reads each paper carefully, a more rounded and informative picture begins to unveil. The more one learns on the subject the more questionable it becomes as to whether there truly is such a disease or whether there are just some unfortunate animals who are predisposed to injuries that compound and fail to heal. This could give the impression of a degenerating condition when in fact it may well be a case of multiple and continuous injury.

Supposedly horses with DSLD have more than the suspensory ligaments involved. Organs such as the heart, lungs, even the skin are said to break down in the connective tissues. Therefore the progression of the disease gradually includes much of the horse's body. It is not limited to only the legs. AND if these assumptions by the experts are to be believed, the "disease" is progressive though some horses progress faster than others.

IF a horse with suspensory ligament injury is not treated properly long term and with the utmost of care it continues to suffer repeated injuries from those of microscopic nature to visual injuries.

If there truly is such a thing as DSLD then it is considered a degenerative disease whereby the outcome is always the same. The horse progresses in lameness and pain until nothing can be done to make it comfortable. At that point the horse is generally humanely euthanized. NO horse with this disease ever improves or gets better.

In order to make it simpler and less time consuming for horse owners to do their own research, I have attached many of the articles and patented papers from many different researchers, vets and Universities to this page and in separate articles in the "Articles" files in the hope of educating people to the real facts of Suspensory Ligament injuries and DSLD.




First and foremost the most obvious symptom of DSLD is a dropping of the fetlock accompanied by lameness. That is what most people see but it is also normally where they stop looking before they declare the horse has DSLD. That is not only imprudent but does a disservice to the horse. MANY horses can have dropped fetlocks due to injury, overwork, advancing age, or in some cases merely from carrying too much weight on the hind quarters.

In the past brood mares were often noted as having dropped fetlocks during late-term gestation. Some of those mares would spring back up to normal ranges when they were open or in early gestation only to drop again during late term. Over time, some of those mares as they aged and carried more foals lost the ability to bring their fetlocks back up. Think of it as elastic that has been over stretched. The spring wears out and eventually the elastic becomes rather limp and lifeless. (See attached article on this subject) It is unclear as to why that occurs but most observers realize an over abundance of weight distribution to the hind quarters plays a significant role. Over time and many pregnancies some of these mares never regain the normal fetlock position even though many of them walk sound and are in no particular pain.


DSLD is thought to be a PROGRESSIVE and PAINFUL condition. Horses thought to have DSLD progressively get worse over time. Some degenerate slower than others, but none the less all will eventually get worse and worse. Horses with suspensory ligament injury though they may never fully recover from the dropped fetlock, will heal and move without abject pain. However once a horse has suffered a serious ligament injury or tendon injury the leg will never be as strong as it once was. Therefore it is subject to re-injury at a far greater risk than a horse that has never suffered injury.

When horses are re-injured the damage done to the ligaments or tendons never fully regains original strength and therefore the results is a degeneration of the affected tendon or ligament. That makes it highly questionable as to just what the difference is between horses with repeated injury and those thought to have DSLD.



DSLD is thought to affect more than just the suspensories. Though the most common visual symptom of DSLD is the dropped fetlock, horses that truly have DSLD break down in ALL their ligaments and soft tissue. That means the progressiveness of the disorder has an affect on the entire body of the horse, not simply it's legs. DSLD affects organs such as the heart as well. But does it truly?

In all the papers published there is no mention of other organs or parts of the body being affected other than to report a build up of proteoglycans in certain areas of the body. Proteoglycans are the building blocks for soft tissue. It would stand to reason that minuscule injures or damage to the body that occurs in the act of simply living, would need to be repaired. That in itself could account for specific areas of the horse having higher levels of proteoglycans than others. If the body is functioning properly it would produce higher levels of proteoglycans specifically to do the maintenance and repair to such areas!


There is pain involved with DSLD. As the disease progresses the animal becomes lame and develops to a pain level that is extremely difficult to manage. They require special care such as soft bedding, stall rest, pain therapy and other medications just to keep them able to be on their feet. The pain is so severe at times the horse will be reluctant to move and in some cases will not want to stand. Most of these horses are eventually humanely euthanized.

This is not inconsistent with injured horses who have either not received sufficient care for their injuries or for those who have inadvertently sustained repeated subsequent injury even while housed in a stall.

The famous race horse Barbaro was humanely euthanized when he became so pain ridden and lame he could no longer stand yet it was not the broken leg that was causing the problem! It was the opposite leg that had been holding him up all through his therapy and confinement without additional support! The constant extra weight and stress to the sound leg eventually broke it down to the point he could no longer support himself.

In horses claimed to have DSLD it is claimed that injury always happens in two legs or four legs with one perhaps showing symptoms first and then gradually the other limb succumbs. Point of fact however, indicates the second limbs wear out the same way as Barbaro's did, simply by having to carry too much of the load stress constantly without support or relief! Barbaro did not have DSLD yet his symptoms were he a less famous horse would have likely been identified or diagnosed as such!



DSLD can and does affect all legs but most commonly is first seen in the hind fetlocks. Onset is most generally gradual in nature and progressive once it has manifested. The nature of the disease does not allow for horses to heal or improve. The disease progresses and affects more than simply the legs. Other organs can be involved such as skin, heart, etc.

THESE symptoms describe DSLD. It is a very painful, progressive ailment that most generally results in a horse having to be put down or dying on it's own accord. It is a chronic ailment that may have flare ups and times of remission from the pain but over time decidedly gets worse…and never gets better.

What this is really saying is if a horse is suffering ligament or tendon injury and is not supported sufficiently it will eventually worsen as repeat injuries degenerate the tendons of BOTH legs from being forced to carry a disproportionate amount of the weight load stress continually for an extended period of time.

Anyone who has had leg surgery and had to rely upon the "good' leg for weeks while the other healed can relate to how sore and tired the "good" leg becomes and likely they had support of a cane. walker or crutch while a horse has no support whatever!


DSLD always affects legs in pairs. Both hind, both fore, or all four. It never manifests in only one leg.

That does not mean all horses with two legs involved with dropped fetlock have DSLD. If the same degree of trauma is inflicted upon more than one limb, then the resultant damage can and most likely will be similar. The fact is in most cases injury only occurs in one leg unless there is an unusual cause for the initial injury.

As mentioned before, it is logical both legs would eventually succumb to injury when the horse becomes out of balance and can no longer distribute the weight load stress evenly.

As you will read in one of the studies posted to this site, one veterinary school highly recommends wrapping the UNinjured leg as well as the injured leg in order to help supply additional support to the tendons and ligaments of the sound leg.





First of all an injury may be of an acute type via an accident or incident that suddenly occurs causing severe noticeable pain and/or lameness. Horses prone to poor stall behavior such as kicking walls, or spinning, or horses that hyper-extend the hind legs kicking can suffer such injury and breakdown of the suspensory ligaments.

Injury may also be less acute or noticeable and may occur over time particularly in the case of animals expected to carry great weight on the hind quarters which was seen in pack horses and freight carriers in past centuries, older broodmares that carry larger foals causing heavy weight to be carried on the hind quarters, broodmares that have had many pregnancies, or horses required to do repetitious work during training or work that stresses and places torque on the suspensory ligaments can cause suspensory breakdown.

There is a very good article attached to this page illustrating how the ligaments and tendons are built and how they can be damaged as well as how they attempt to heal themselves.

Activities such as racing, cutting, jumping, dressage, or any other activity that causes a horse to have to push off repeatedly at speed with the hind legs or over stress the legs by being worked in fully rounded frame, can cause suspensory break down.

Suspensory ligament injury can also occur from humans riding horses using poor equitation skills. ANY time a horse is caused to carry more weight on the hind quarters than is normal the suspensory ligaments are placed into a stressed situation. Surprisingly that includes horses that are ridden in full collection for extended periods of time!

Poorly fitted or poorly placed saddles can cause suspensory ligament damage. If the front end of the horse or it's shoulders becomes sore enough a horse will shift it's weight to the hind quarters. It is unnatural for a horse to carry that much weight on the hind quarters so the ligaments over time have potential to break down from over use. Horses in training when a trainer is not prudent in tack fit or the amount of time used in repetitive motion are at risk for suspensory ligament injury.

Horses that are not in condition when asked to perform strenuous movement are also at risk for suspensory ligament injury.

Old age can also lead to suspensory ligament break down. In all horses the tendons and ligaments wear out as the horse ages, just as they do in humans. They become weaker and more subject to injury and can break down simply due to the normal aging process. Such injury may be accelerated if a horse has also been used hard or in the case of brood mares have produced many foals. It may also be that lack of nutritional care may limit the service life of such ligaments and tendons. Assuredly certain conformational flaws can contribute to such break down.


Suspensory Ligament INJURY is generally noticed first when the horse becomes lame on one or more legs. Most generally this will be a hind leg and often it will only be in one hind leg. It may well be the horse has been suffering quiet injuries all along but it only becomes noticed when it reaches the point of lameness. If equal stress or injury occurs to more than one leg then breakdown can also occur in both hind legs.

As mentioned before, if one legs is injured and shifting it's load to the other, that second leg will also tend to break down, however there are times when trauma simply injures two or more legs equally!


Suspensory ligament injury can be anywhere from mild to severe but will almost always result in lameness, heat, swelling and other signs of injury. In the case of severe injury the damage is never fully correctable even though the horse may eventually no longer have pain or signs of injury other than a dropped fetlock.

There are surgical techniques to correct these situations however they are rarely very successful. Recently there is a new therapy being explored that includes the use of stem cells in the hope of repairing the damaged tendons. So far this is experimental and highly costly but shows promise.


Horses with suspensory ligament injury that results in chronic dropped fetlocks often heal to a point there is no longer pain and can function without lameness or discomfort at moderate activities. THIS is one of the biggest differences between DSLD horses and those with suspensory ligament injury. Though some horses may take time to heal and improve from an injury to the suspensories the key difference is they do improve while DSLD horses progressively worsen. It is quite likely the failure of the collagen to solidify the natural patches in the ligaments or tendons is what causes some horses to progressively worsen while others improve.


Horses with mild damage to suspensory ligaments may heal and improve to a state of soundness while those with severe damage may never function at the same level they did prior to injury. Many race horses have been retired due to this sort of injury. Few ever regain the ability to race after suspensory ligament injury though they may be sound for use as a normal riding horse.

This is very similar to torn or pulled tendons in humans. Anyone who has ever suffered torn tendons knows the leg involved always tends to be a little weaker than it was prior to injury. They also know those involved legs are prone to reinjury more than the uninjured leg. In short, once the tendon has been over stretched or torn it is never quite the same again. It is the same in horses.


Horses have both flexor tendons and suspensory ligaments in their legs. Flexor tendons are connected to one another with strong, fibrous tissue that helps support each tendon by sharing the load. Flexor tendons are also connected to muscle tissue for additional support.

Suspensory ligaments are actually part muscle and part tendon. This unique construction makes them vulnerable to tears, ruptures and sprains similar to other muscles but can also make them vulnerable to stresses and stretching much like what happens to tendons.

The suspensory ligaments act on their own. They are not connected to other tissues for support and have no shared support with other ligaments or tendons.

Because the flexor tendons DO have support any strain placed upon the leg causes a disproportionate amount of that stress or load to fall upon the suspensory ligaments because they are more flexible due to lack of support than are the flexor tendons.

This sounds simplistic but really think about it. The flexor tendons are stiffer due to having much more support so if stress is stronger and the flexors peak out in their stretch ability, the suspensory ligament suddenly bears the full brunt of the stress and can tear, over stretch and therefore break down.


In short proteoglycans are proteins that build and repair soft tissues such as tendons, ligaments and cartilage. When a horse is placed on joint compounds that contain glucosamine their proteoglycan count can increase as much as 150%. THAT is what allows the compounds to actually work to repair damage to joints, tendons, ligaments and cartilage. Having more proteoglycans can speed up the healing process!

Proteoglycans may increase naturally in horses that have suffered injury or those who are growing and developing in the joints or ligamenture. Since it is impossible to tell whether horses have small injuries occurring and therefore needing repair there is no real measure as to what a proper level for these proteins should be.

The current research on this issue is in my personal opinion rather flawed. In the research the proteoglycan count is tested in a number of horses in order to draw conclusions as to what an average count should be. HOWEVER in this study no attention was given to the type of activity and use the horse was subjected to, the diet or nutritional quality of the horse, the age or condition of the horse. The study also did not take into account individual conformation even though certain conformational weaknesses have proven to be more likely to produce suspensory issues. Furthermore the study did not take into account at what age the horse was placed under saddle. Until such measures are compared there is no way to fully understand what an excess of Proteoglycans may indicate.

Since ALL these things can affect the proteoglycan count any averages that do not include these variables may be out of context and less than accurate.

In most living things auto-immune systems work with varied success. In humans for instance a very healthy person can safely be acknowledged as having a very strong immune system. A person with a compromised or stressed immune system often suffers illness of some sort whether it be a common cold or some chronic disease.

A person with a strong immune system will heal faster from injury than a person with a damaged immune system.

In horses surely the same holds true. Therefore a horse with a strong immune system may well produce a higher proteoglycan count while healing than a horse with a weaker immune system.

So far the researchers themselves are unsure just what a "normal" proteoglycan count ought to be and by their own admissions cannot even say whether a proteoglycan count will ever make a good and reliable diagnostic for DSLD.

In at least two independent studies for DSLD in which the proteoglycan counts were taken, the results were erratic and unreliable as a diagnostic. In the study paid for by the Peruvian Paso Association, (Please read the article on misdiagnosis DSLD in the Peruvian Horse)of the proteoglycan count of DSLD affected horses was at times LOWER than the count taken on none DSLD control group horses.

In a similar yet more thorough study done at the University of California, Davis, similar findings were found.

(See Article from UC Davis )




All the research on DSLD is in it's infancy. To date there are no hard facts known about it. There are theories and hunches being voiced and explored by the researchers but so far no hard evidence has been found to verify or substantiate theory.


Researchers have NOT, even after more than seven years of searching, located a genetic marker that causes DSLD, therefore it is still uncertain whether this condition is genetic in origin. One school of thought claims the only genetic link between DSLD and genetic transmission comes in the fact certain horses are bred with conformational weaknesses that make them predisposed to suspensory break down. Conformation such as steep croups coupled with sickle hocks much like we see in many modern Quarter Horses is suspect…because the weight shifts to the hind quarters with such conformational weaknesses.


Some researchers theorize that horses with DSLD have a super abundance of proteoglycans in their nuchal ligaments. This so far is only theory and has not been borne out because some horses known to have DSLD do not have an over abundance of proteoglycans while horses that do not have DSLD can have an over abundance of proteoglycans. This makes it very impractical to use the proteoglycan level of a horse alone as an indicator. Researchers at UC Davis, very clearly concur with this as well in fact they have published a paper clearly stating Proteoglycans are not a diagnostic for DSLD detection.


To date in the current study being conducted on DSLD at the University of Georgia, only 28 horses have been studied. Of those 22 were PasoFino horses. Paso's have long been accused of having a higher level of DSLD than many other breeds. Interestingly clinical research done by some of the very same authorities, showed that STANDARDBREDS were more likely to suffer the disorder than were Pasos yet they are not publicly sited as having a tendency for the disorder..why?

28 horses from a small group of similar animals is by far not a broad enough range of equine from which to draw any conclusions. Clearly this is a premature time to voice opinions based upon such limited research and the researchers themselves admit to this.

It can be assumed the 22 horses studied from the Paso group would have fairly similar conformation yet the conformational aspect is not being included in the study, only measurable things such as proteoglycan counts which could be totally misleading in such a case are being measured.


One of the purposes for the current study on DSLD is to try to locate a genetic marker for the disorder by which to develop a test for the disease. To date the ONLY DEFINITIVE proof of DSLD being in a horse has to be done by a COMPREHENSIVE NECROPSY. That is a significant bit of information because unless a horse dies, no one can really tell whether or not it has DSLD!! Yet there are those willing to condemn any horse that happens to have dropped fetlocks as being a genetic defect? That would seem to be rather unintelligent and less than accurate way to label things.

In point of fact, if the research being amassed is to be believed, there is a strong indication there is no such thing as DSLD or a genetic disorder that breaks down horses legs.

What is being seen is that injury to legs can become chronic and appear progressive due to re-injury.





No one can tell if a horse has DSLD by simply looking at the horse or a photo. Were it possible to do such a thing there would be no need for ongoing, expensive research.


People claiming that a veterinarian has made diagnosis of a horse belonging to a third party without the consent of the owner are either dealing with a very poor representative of the veterinary community, or are distorting fact. It is against the law for a vet to examine a horse without owner consent unless there is a legal order to do so. NO vet would attempt to diagnose a horse from a photo only and no vet worthy of being a vet would hazard to make a statement regarding a third party's horse publicly. To do so could place such a vet in a tenuous legal position liable for censure and/or legal actions such as suit for slander or liable.


Claims that DSLD is a hereditary ailment are premature and unsupported by scientific evidence. To date, no gene or genetic marker has been located for the disorder. While the disorder may be genetic, until evidence is found to support such a theory there is no way of really knowing whether it is a heritable ailment or simply a result of similar breeding.


The presence of a dropped fetlock is not proof of DSLD being present. The presence of proteoglycan build up has been proven to beUNreliable evidence of DSLD.



In recent months the internet ran rampant for some days with accusations regarding my own horses claiming them to have DSLD. I took it upon myself to contact the very researchers being misquoted on the internet as having claimed my horses and those I bred, had DSLD. The responses from those researchers are being posted here as clear evidence that those statements against my horses were not only incorrect but totally unfounded.

Also posted here are a number of published papers regarding DSLD research and what false information is being placed out in the public eye. In order to truly inform yourself regarding this possible disorder and to help anyone with an injured or lame horse identify the possible cause, I urge you to read these articles. They are very informative and come straight from the researchers themselves.

In October of 2009, I wrote a letter to Dr. Halper at the University of Georgia asking specific questions with regard to her examination of biopsy tissue from Captain Midnight. Captain Midnight was bred by me from our old mare Chief's Magic Ribbon who has also been touted on the internet as having DSLD even though repeatedly I have informed those parties she is the result of a severe trauma to her suspensory ligaments.

That initial letter led to subsequent emails between Dr. Halper and myself as well as emails from Dr. Mueller. These are the two primary researchers (Dr. Halper is a pathologist, Dr. Mueller is the clinician who examines the horse physically) responsible for the current research project on DSLD at the University of Georgia. Below are the emails with the significant parts underlined.

It is very important that people do not go around accusing horses of having diseases and spreading rumors that have no basis in truth.

My first letter was addressed to Dr. Halper in which I asked if she actually did an examination on Captain and if so whether he had been diagnosed with DSLD. Her response to that letter came by way of email. Here it is:

Captain and Serenade
From: "Jaroslava Halper" jhalper@uga.edu
To: foxvangen@yahoo.com
CC: "P.O. Eric Mueller" emueller@uga.edu

Dear Ms. Westvang:

I received your letter in today's mail. I did look at the nuchal tissues obtained by biopsies from Captain and Serenade, and yes the tissues, in my opinion, did contain some excess of proteoglycans. However, as a rule the nuchal biopsy does not provide definitive diagnosis, and should be used together with clinical and ultrasonic examination, never on it's own, to make diagnosis.

You are right that only a comprehensive necropsy could give us definitive diagnosis. As a matter of fact, Captain underwent thorough and careful examination by Dr. Mueller, a clinician and my collaborator. Dr. Mueller did not think Captain has DSLD. As a result, Captain went back home. Both Captain and Serenade will be followed up clinically and with nuchal biopsies. This provides us with an opportunity to study what is going on with the nuchal tissues, and to correlate with clinical exams. By the way, I was told Serenade is 8 years old, the mare you are describing in your letters is 22, so this is a different horse then? I hope that this provides you with some answers.
With regards,

Jaraslava Halper, M.D., Ph.D.
Professor and Graduate Coordinator
Department of Pathology
College of Veterinary Medicine
The University of Georgia

This letter from Dr. Halper expressly states the examination of Captain Midnight indicated he DOES NOT have DSLD. We now know that proteoglycans are totally unreliable for indicating DSLD is present in horses and that has been borne out in more than one study posted to this page. Clearly there is no connection between DSLD and Captain Midnight nor to his sister Moonlight Serenade and their dam Chief's Magic Ribbon.

I followed up that letter with a second letter to Dr. Halper.

Dear Dr. Halper,
I truly appreciate you taking the time to respond to my letter. No, the mare you speak off, Serenade is the 8 years old DAUGHTER of the 22 year old and Captain is the son of the 22 year old.

The mare these people are maligning is the 22 year old. The one injured in the Mustang attack.
I would like to ask you in the case of DSLD do the joints flex normally? Other than the dropped fetlock that is? I'm asking because my old mare has full use of her joints, the fetlocks are just dropped due to the extreme damage done to her ligaments and tendons. I'm really surprised she is able to move as readily and does after so long with this injury.

My vets have told me repeatedly that she is a trauma result not DSLD and therefore that is what makes the difference. I have never seen an actual case of DSLD other than in still pictures which never show action.

Again, thank you for your reply.

Dyan Westvang Foxvangen Farm.

Here is the response I received from the second letter to Dr. Halper.

Dear Mrs. Westvang,

We are at the beginning of research into DSLD, the 28 horses studied on our paper are meant as one group on which to build. There is a spectrum of excess and accumulation, this happens in most diseases. You need to look at the whole picture, pathological examination is just one part. Clinical and ultrasonic examination are others. We are looking for biochemical markers so we can better diagnose it. We do not know much about proteoglycans and tendons in horses that's why we need to study more animals.

Jaroslava Halper, M.D. , PhD.
Professor and Graduate Coordinator
Department of Pathology
College of Veterinary Medicine
The University of Georgia
Athens, Georgia 30602-7388

In the above letter, Dr. Halper clearly explains they, as the top and primary researchers on the subject, do not understand DSLD as a disease as yet. That is the reason for the study. The study is just beginning, therefore they have no hard, fast rules to apply to the disease. Nor do they have any firm conclusions regarding DSLD or for that matter even proved there is such a disease. Dr. Halper clearly states that having a rise in proteoglycans does not on it's own indicate DSLD! In fact to date no one truly knows what a good or "normal" proteoglycan count should be! In additional information that will be added to this page you will note that that proteoglycans are not well understood but can vary due to growth, injury, disease or even from a horse being fed additives with glucosamine in them!

To the above letter I followed up with yet another correspondence.

Dear Dr. Halper,
I understand and thank you. Two more questions if I may? When you say these horses have "some" excess in the proteoglycans how much excess are we speaking of and can that indicate something else? How is the average determined between acceptable levels and excess?

I have been reading your papers that are on line and was interested in learning more so I can better understand what all this means. It was mentioned that 28 horses were studied and of those 22 were Pasos. Do you feel that is a broad enough spectrum from which to gather data?

The reason I ask this is that if only that group was studied how do we know that other groups may not factor differently according to genetic make up?

Though I am not a credentialed researcher I have an avidly curious mind and have been studying motion in horses for several decades. I have studied various groups of animals performing the same motion yet each group moves differently. Some groups are more supple and flexible in the limbs and some are more rigid and stiff in the limbs.

Those with extra flex in the limbs produce a softer motion at the same gaits. Why that is so is likely molecular.

If that is so, then it could be that those types would have a higher degree of proteoglycans than those who move differently. Could that not be so?

Dr. Halpers reply:

Dear Ms. Westvang:
I cannot answer your question about the joints because I am not an equine clinician. I am a pathologist doing research, and hopefully helping people and horses.

Jaroslava Halper, M.D., Ph.D.
Professor and Graduate Coordinator
Department of Pathology
College of Veterinary Medicine
The University of Georgia.

I followed up this conversation with a letter to Dr. Mueller.

Dear Dr. Mueller,

Dr. Halper said you performed a thorough examination on Captain Midnight, can you explain what that actually means?

Dr. Mueller's response:

Palpation, and full lameness evaluation (straight trot, canter, flexion tests, lunge)

My next question:

I have read articles on Suspensory ligament injury and the chronic result of having a dropped fetlock. If a horse can get a dropped fetlock from injury how does one identify or distinguish that from a horse with DSLD?

Dr. Mueller's response:

There is no definitive anti-mortem test. Examination of the affected tissues under a microscope is the only reliable method. Otherwise we use the clinical history, physical examination findings, ultrasound, and the nuchal ligament biopsy findings to assess each horse individually. Currently, we are not making any recommendations on breeding or euthanasia based upon results of the test alone, because of it's lack of specificity.

My next question:

One article I read mentioned over worked horses and those with conformational flaws that place too much stress on the suspensory ligaments can cause dropped fetlocks and injury to suspensory ligaments. It also mentions injuries that rupture the ligament and the fact that surgery is not often successful to bring the horses back to the same degree of service. Is that what you find as well?

Dr. Mueller's response:


My next question:

If a horse has a dropped fetlock, what would be the next progression to look for to distinguish injury from progression of DSLD?

Dr. Mueller's response:

History, physical examination findings, ultrasound, and the nuchal ligament biopsy findings.


Captain and Serenade were put through all these tests and yet were found to not show symptoms of DSLD therefore, THEY WERE SENT HOME.

Because of the confab on the internet many people who had been considered friends began to question. One of these friends went straight to the source and also contacted Dr. Mueller. Here is a copy of Dr. Muellers response to that correspondence.

Dear Ms. …….

Thank you for your e-mail. At this point in time, the evaluation of nuchal ligament biopsy tissues in horses may only support or not support the clinical diagnosis of the disease, but it is not a definitive test. We are currently performing research in which we are trying to develop a sensitive and specific test for DSLD.

If a horse has clinical symptoms consistent with DSLD

( Progressive lameness with out a traumatic cause, dropped fetlocks, ultrasound findings consistent with DSLD) and the nuchal ligament biopsy contains large amounts of proteoglycan, without signs of chronic fibrosis or inflammation, we can be fairly confident that the horse has the disease. However, we have seen small accumulations of proteoglycan in horses without clinical symptoms. Therefore, the test is not specific. Currently we are not making any recommendations on breeding or final disposition of horses that have proteoglycan accumulation consistent with DSLD but no clinical symptoms.

If your horse is asymptomatic, and has had no other problems, I would not recommend performing the test at this time, because it is difficult to interpret the significance of the results.

It is believed DSLD may have a genetic basis. If we can identify a specific gene marker for the disease, hopefully we will be ale to develop a reliable and accurate test for the disease that will identify predisposed horses before they develop clinical signs. At present, we have not identified a definitive heritable trait nor a specific test.

Hope this helps.

Eric Mueller, DVM, Ph.D.
Diplomate, American College of Veterinary Surgeons
Director of Equine Programs
Department of Large Animal Medicine
College of Veterinary Medicine
University of Georgia

Perhaps the most significant part to this email is the statement marked in red. In the case of our old mare, Chief's Magic Ribbon, by these qualifications she is ruled out of DSLD because her dropped fetlocks were the result of severe trauma. She has not progressed in lameness, she does have scar tissue from her trauma. She is not sore to palpate, she runs and gaits with her foals and frequently bucks and kicks and moves like any of our other horses. Her condition has improved, not degenerated.

She is more than 8 years post trauma with no progression to lameness and no signs of other degeneration to skin, other limbs, organs and is not in pain. She is 23 years old as of March 2010. Since her injury she has produced an additional six healthy foals and readily keeps up with them, running and playing with them at times. She has no trouble standing for farriers, and she rarely lays down. She has a healthy appetite and can still outrun most of the horses on our farm even at her advanced age.

These emails along with accurate data on the disease fairly and clearly rule out DSLD in our horses.

The remainder of the information on this page supports these findings and brings into question some of the former research done on DSLD. It is very lengthy and detailed, however anyone truly interested in understanding this disease and this issue should read all of it in order to have a better and more complete understanding of the disease and how information about it is being commonly distorted by various people on the internet. Though many of these people may be well intentioned it is very destructive and counter productive to continue to voice distortions of fact.

Attached here are a number of articles regarding the subject.





Journal of Equine Veterinary Science

Volume 29, Issue 10, Pages 748-752 (October 2009)

9 of 12

Systemic Proteoglycan Deposition Is Not a Characteristic of Equine Degenerative Suspensory Ligament Desmitis (DSLD)


Daniel Schenkman, DVM, PhDa, Anibal Armien, DVM, PhDb, Roy Pool Jr., DVM, PhDc, James M. Williams, PhDd, Ronald D. Schultz, PhDa, Jorge O. Galante, MDd

Recently Degenerative Suspensory Ligament Desmitis (DSLD) has been proposed to be a disease characterized by systemic deposition of proteoglycan (PG) in connective tissues. To investigate this hypothesis, 6 clinically affected Peruvian Paso horses were compared to 2 unaffected quarterhorses and one unaffected standardbred. Histological sections of limb ligaments and tendons, nuchal ligaments, aortas, hearts, eyes, visceral organs and brains from both groups were stained with H&E as well as special stains for PG. Safranin-O stained sections were found to be optimal for elucidating the presence of PG. Although lesions characteristic of DSLD were present in suspensory ligaments of each clinically affected horse, including foci of chondroid metaplasia with abundant PG, a similar but less pronounced pattern of PG deposition was present in control horses. In contrast to findings of the previous study, PG deposition was not unique to DSLD horses, and PG deposition in aortas and nuchal ligaments of some control horses exceeded levels of PG present in similar tissue of DSLD horses. Furthermore, the “vascular lesion” described in the media of arteries as cellular separation and intercellular amorphous matrix deposition was within the spectrum of changes recognized in both affected and unaffected horses. We found no evidence that DSLD is a systemic PG deposition disease.

Keywords: Equine, Desmitis, DSLD, Proteoglycan, Ligaments
a Pathobiological Sciences, University of Wisconsin–Madison, School of Veterinary Medicine, Madison, WI

b Veterinary Population Medicine, University of Minnesota, College of Veterinary Medicine, St. Paul, MN

c Department of Veterinary Pathobiology, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX

d Departments of Orthopedic Surgery and Anatomy and Cell Biology, Rush University Medical Center, Chicago, IL

Reprint requests: Daniel Schenkman, DVM, PhD, Biomedxplor, LLC, 915 Martin Drive, Marshfield, WI 54449.

PII: S0737-0806(09)00573-5


© 2009 Elsevier Inc. All rights reserved.



By Dr. Mero ~ Revised March 12, 2006

1. SIGNALMENT- Breeds such as Warmbloods, Arabians, Quarter Horses and race horses tend to contract DSLD at ages older than 15 years.3,4,5 Exceptions to this occur in broodmares, horses that are subjected to intense work loads, or have sustained a prior suspensory desmitis (injury).3,4,5 In breeds other than Peruvians DSLD occurs usually in the rear limbs only. Peruvian Pasos appear to develop DSLD differently than other breeds. They most commonly develop DSLD in all four limbs, with a widespread age range from weanlings to over 20 years of age.6,9 Average age of onset in Peruvians is between 4-10 years with both sexes roughly affected in equal numbers.9 And unlike other breeds, Peruvians Pasos can develop disease regardless of athletic function, i.e. no work is needed for disease to occur..9 (*Note- latest research has found other breeds also develop DSLD in all limbs and at early ages without work or injury)

2. MEDICAL HISTORY- This is always a quadrilateral (4 limb) or bilateral (2 limb) disease. Early cases can develop obscure signs such as generalized stiffness, changes in attitude, reluctance to work and back pain.9 As disease progresses horses often are painful for the farrier. Others can appear extremely stiff and unwilling to move after inactivity and then seem to work out of it with exercise. Obscure, intermittent or chronic lameness is common. End stage cases become reluctant to move about, spend much of their time lying down and often dig holes to stand in to relieve pressure off of their sore limbs.

A. Conformation changes: Over 90% of the time DSLD starts and predominantly affects the suspensory ligament (SL) branches.9 Similar lesions can occur in other soft tissues structures such as the flexor tendons.2,6 The classic signs of swollen, dropped fetlocks, with coon shaped hooves and straight leg angles occur in less than 1/2 of cases ? even with advanced disease.9 Early onset cases usually have no visual abnormalities. As disease progresses diffuse swelling and wind puffs about the fetlocks sometimes are noticed.1,2,5,6,9 Visible enlargements specifically involving the branches of the suspensory can also be seen.

B. Palpation of Suspensory Ligaments: Initially cases may or may not exhibit pain response and will have no thickening on palpation. By early to mid stage a marked pain response occurs to SL branch palpation.6,9 Usually a palpable thickening and enlargement of the SL branches will occur by mid to late stages.6,9

C. Baseline Lameness: In early stages lameness is often not apparent. Even advanced cases may not be obviously lame due to more than one limb being painful.9 Front limb cases can look tight and appear reluctant to move out and extend their gait. Hind and four limb cases move stiffly, will not drive in the rear and will have a marked widening of their hocks and lower limbs during gaiting as viewed from the rear. Many rear limb cases stab their toes into the ground and appear reluctant to load their heel regions. Tight circles will usually exacerbate lameness.

D. Flexion Tests: In all cases, even initial cases, flexion tests are ALWAYS positive.9 Early onset cases may show only a mild response of 1-2/5. By mid to late stage disease responses to flexion tests are usually dramatic with horses being crippled after the test with responses of 4-5/5 for several minutes.9 It can often be difficult to flex contralateral limbs as pain can be residual for some time post flexion test.

4. ULTRASOUND EXAMINATION of Suspensory Ligaments- What distinguishes DSLD apart from just an injury is the progressive, continual enlargement of the suspensory ligaments, primarily in the branches, over time, in more than one limb.1,7,9 Early onset cases often are only slightly enlarged and may warrant a second exam in 3-6 months to document continual enlargement. Typically, the SL branches at their largest are no more than 1.1cm2 on area, or 1.1cm in the lateral to medial, or the palmar/plantar to dorsal plane.8,9 The SL body can range up to 2cm just below the hock or the knee. Views of the individual SL branches in the lateral to medial plane are best for accurate measurements.
In Peruvians 0.7cm squared for the suspensory ligament branches in zones 3A or 4A and up to 1.3 cm for the suspensory ligament body at midcannon are considered the cut offs or high normal sizes for the suspensory ligaments in these areas, according to Dr. Mero's paper (10).

Other ultrasound lesions present can be a diffuse loss of fiber patterns both in the cross sectional and the longitudinal plane.1,3,5,9 An overall increase in the hyperehocogenicity (whiteness) of the affected tissues is typical.1,3,5,9 Most commonly in zones 3A/4A to 3B/4B the SL branches will appear enlarged and often are bright white on the distal ultrasound screen in cross section. Less commonly will discrete hypoechoic (black) lesions, often thought of as tears, be noted in the SL branches and/or the SL body.9 On post mortem these represent areas of degeneration and widespread tissue destruction.

5. SUMMARY- Consistent clinical findings: Pain on palpation of suspensory branches, lameness of some kind though often subtle and seen as only stiffness, and positive fetlock flexion tests. The presence of positive flexion tests in more than one fetlock, especially severe responses in horses with seemingly no visual abnormalities and only mild palpation findings, should raise the examiner's index of suspicion for DSLD. Some of the worst affected cases have not had any appreciable ankle swellings, no obvious lameness and no ankles that dropped below the horizontal. Four limb cases in Peruvians seems to be more common, and routine scanning of all four limbs of any Peruvian suspected of having DSLD is recommended. Four limb cases usually are more painful and often deteriorate faster. Some bilateral cases can remain at least pasture sound for several years. Re-exams 3-6 months from the initial exam will usually distinguish DSLD from a healing injury, by the presence of worsening clinical signs and progressive enlargements of the suspensory ligaments on ultrasound.

Copyright 2002 DSLD Research Inc. All Rights Reserved. (*Reprinting permitted for diagnostic purposes)

1. Young, JH. Degenerative Suspensory Ligament Desmitis. Hoofcare and Lameness. 1993;(61)6-19.
2. Pryor, PB, Pool, RR, Wheat, JD. Failure of the suspensory apparatus in Peruvian Paso horses, in Abstracts. ACVS meeting 1984; 56.
3. Dyson, S. Diagnosis and prognosis of suspensory desmitis. In: Proceedings of the 1st Dubai International Symposium, Ed:ML Hauser, Matthew R. Rantanen Design, USA, 1996: 207-225
4. Dyson, S, Arthur, RM, Palmer, DE, et al. Suspensory ligament desmitis. Vet Clin. N. Am: Equine Pract. 1995;11: 177-215
5. Gibson, KT, Steel, CM. Conditions of the suspensory ligament causing lameness in horses. Equine Vet Ed 2002;4: 50-64
6. Pryor, PB, Pool, RR, Wheat, JD. Clinical and pathological characterization of suspensory apparatus failure in Peruvian Paso horses. Unpublished paper. 1984.
7. Yeager, A. Ithaca, NY (personal communication) March 13, 2002.
8. Cuesta, IC, Riber, C, Pinedo, M, et al. Ultrasonographic measurement of palmar metacarpal tendon and ligament structures in the horse. Vet Radiol Ultrasound 1995: 131-136.
9. Mero, JL, Pool, RR. 20 Cases of Degenerative Suspensory Ligament Desmitis in Peruvian Paso Horses, in Proceedings. American Association of Equine Practitioners Mtg.2002;48:329-334
10. Mero, JL, Scarlett, JM. Diagnostic Criteria for Degenerative Suspensory Ligament Desmitis in Peruvian Paso horses. Journal of Equine Veterinary Science 2005;5





By James Rooney, D.V. M.

(I have taken the liberty of enlargint the print on some of the most significant points in Dr. Rooney's report)


Gradual loss of function of the suspensory ligament of the hind leg of the horse has been recognized for many years. In earlier times it was most often seen in older horses, particularly older, multiparous mares. The sinking of the hind fetlocks became more apparent late in pregnancy. It often, but not always, seemed to disappear-return to normal-after parturition. In recent years such loss of function has been seen in younger performance horses, particularly the Paso Fino and particularly the Peruvian Paso Fino. While egg bar shoes seem to help some of these horses, the condition appears to be essentially irreparable.

By loss of function I mean loss of strength of the suspensory, loss of the ability to maintain the fetlock joint in it's usual, normal position.

It should be noted that the suspensory ligaments, both fore and hind, are really highly modified muscles, the mm. interossei. While they are largely composed of tendinous tissue, there is muscle present.

It is also noted that there are histological features of the tendinous tissue which are somewhat different from that seen in other tendons. The nuclei of the tenocytes have the characteristics of chondroid cells. while that suggests an adaptation to frequent and/or continuous movement, the significance of these differences remains to be determined.


To my knowledge there has been no serious study of the suspensory ligaments of older mares. I regret that I did not get around to that while still active in the postmortem room. Perhaps some younger pathologis will undertake the task. Since many of these older mares "recover" normal fetlock angulation after parturition, there may not be obvious structural, anatomical changes in all cases. Tendons and ligaments lose strength to varying degrees with age and in vitro tests of suspensory strength in affected and normal older mares would be of interest.

What is apparent is that the weight of the foal in utero, is directly related to the sinking of the hind fetlocks late in gestation. That will be of importance later in our discussion.



I know that damaged suspensories from Paso Fino horses have been examined pathologically. Unfortunately, threats of legal action apparently caused a prominent university ( which should have done better) to stop publication of the results. There are, also, specimens of damaged suspensories in fixative in various people's hands, but I have been unable to obtain any for examination. What I suggest for pathogenesis, therefore, cannot address all the possibilities which thorough pathological study might raise.


Pathogenesis is the study of the development of a disease process. Often, and certainly in the case of suspensory dysfunction, we do not have complete information and, so, cannot completely develop the natural history of the disease process. What we can do is take the information we have and try to construct a reasonable and coherent history as far as possible. Once that is done, the gaps which have to be filled will be more readily apparent.

As already mentioned old mares show evidence of at least temporary suspensory dysfunction during the latter stages of gestation. This may be related immediately to the increasing weight of the fetus, shifting the center of mass of the horse toward the hind quarters, and thereby increasing the static loading of the hind legs. An equally efficient way to increase the static loading of the hind legs is to move the feet forward beneath the body.

The shifting of the hind feet under the body is one of the principal features of the process of collection. As discussed in some detail in Rooney, 1998, ( The Lame Horse) collection is a normal response of the horse to a scary situation. Collection renders the animal alert: head and neck raised, feet under the body and ready to perceive, analyze and react immediately by flight to a dangerous situation. As riders know, collection is a reflex chain process which can be elicited and maintained by the appropriate use of the reins and leg aids. Collection is induced in this way because the horse is more alert and ready to move in a coordinated, graceful manner.

If a horse, performing as required, works in the collected manner, the hind legs are carrying more weight (load) than if not collected. If the work period is prolonged, obviously the horse is carrying that additional weight on the hind legs for a considerable period of time. Such rather prolonged periods of collected work seem to be characteristic for the Paso Fino horse, for example. In an unforced situation such as free in field or paddock the horse only collects itself when a suddenly interesting or threatening situation occurs. The collected condition is maintained only briefly and not for the prolonged periods enforced by trainer/rider.

If, in addition, the rider sits back in the saddle, in back of he line of action of the center of mass of the horse, additional load is added to the hindlegs. This style of riding is adopted, I presume, in order to reduce the load on the forelegs thereby allowing flashier, higher-going movement of the forelegs. This strategy seems to be one employed by saddle horse riders as well, particularly with three-gaited saddle horses.


A reasonable question is why the suspensory is affected and not the superficial or deep flexor tendons. The answer is a bit complicated, particularly if you are not too familiar with anatomy. With increasing loading of the leg, the fetlock dorsiflexes, and tension increases in all three tendons. The fetlock dorsiflexion, however is accompanied by coffin joint plantar flexion, and the flexion decreases the tension in the deep flexor tendon. The superficial and deep flexor tendons-but not the supspensoy..are tied together through the metatarsus ( from hock to fetlock) by heavy deep fascia. As the load on the leg increases, then the suspensory undergoes greater strain ( becomes tenser). The tension in the superficial flexor and deep flexors increases the amount of tensile increase experienced by the independent suspensory. In other words the increasing tension in the superficial and deep flexor tendons caused by fetlock dorsiflexion is countered in part by the decrease in tension caused by coffin plantar flexion.


Is what I have said all there is to it? Is it all environment-the way the horse is ridden and worked? The straight-out answer is that the answer is not known. The greater frequency of the problem in the Peruvian Paso Fino suggests, but certainly does not prove, that there is an hereditary component. Experience indicates that most abnormal conditions in all animals are not a function of environment alone but of the variable interaction of environment and heredity.

The genetic part COULD be as follows. The Paso Fino works collected. If one selects for the breeding of the most successful animals, they will be the ones who either collect "best" or who are already, built (by confomation; e.g., heredity) in a more collected fashion: that is, the short-coupled individual with a strongly sloping croup and a tendency to sickle hocks. The story here is not unlike that for swayback in American Saddlebreds which I shall address in another piece.

Pedigree information on horses affected and not affected with suspensory dysfunction certaily exists. Such data could be placed in the hands of a geneticist for careful analysis. ( I hasten to note that I am not a geneticist and not qualified to undertake such an analysis)

POSTERIOR TIBIAL TENDON DYSFUNCTION is a condition in the human which may be analogous to suspensory dysfuncton in the horse. Unfortunately, the cause of that condition in man is not known either.



It would be nice to ofer an easy solution for suspensory dysfunction in the young horse. Obviously, with the information presently available that is not possible. I do not intend to preach on this subject ( or any other, for that matter!), but the solution-easy or otherwise- is in the hands of horse owners and their breed organizations. What has been done here is to show the rold mechanice can or might play in the pathogenesis of the condition. There is obviously more to be learned.

Mosier et al. Pathoanatomy and Eiology of Posterior Tibial Tendon Dysfunction. Clincal Orthopaedics and Related Research. 365:12-22. 1999







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