FACT ...OR ...FICTION
SUSPENSORY LIGAMENT DESMITIS
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!
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.
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.
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.
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!
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.
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!
has been learned is that horses INJURED in the suspensory ligaments or flexor
tendons often have identical symptoms to those claimed to have DSLD.
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.
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.
newest study coming from UC Davis clearly states proteoglycan levels DOES NOT
provide symptoms or proof of DSLD.
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!
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
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
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.
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.
SYMPTOMS of DSLD
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.
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.
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.
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.
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!
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.
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.
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.
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
always affects legs in pairs. Both hind, both fore, or all four. It never manifests
in only one leg.
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.
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
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.
THE SYMPTOMS and CAUSES of SUSPENSORY
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.
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.
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
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.
that are not in condition when asked to perform strenuous movement are also at
risk for suspensory ligament injury.
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.
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!
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.
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.
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.
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.
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.
LIGAMENTS BREAK DOWN FROM INJURY
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.
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.
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.
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.
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.
WHAT ARE PROTEOGLYCANS
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!
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.
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.
these things can affect the proteoglycan count any averages that
do not include these variables may be out of context and less than accurate.
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.
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.
a similar yet more thorough study done at the University of California, Davis,
similar findings were found.
Article from UC Davis )
FACTS REGARDING DSLD
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?
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.
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.
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
What is being seen is that injury
to legs can become chronic and appear progressive due to re-injury.
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.
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.
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.
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
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
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" email@example.com
CC: "P.O. Eric Mueller" firstname.lastname@example.org
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
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.
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.
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.
mare these people are maligning is the 22 year old. The one injured in the Mustang
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.
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.
thank you for your reply.
Westvang Foxvangen Farm.
Here is the response
I received from the second letter to Dr. Halper.
Dear Mrs. Westvang,
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.
Halper, M.D. , PhD.
Professor and Graduate Coordinator
Department of Pathology
College of Veterinary Medicine
The University of Georgia
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!
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?
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?
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?
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
with extra flex in the limbs produce a softer motion at the same gaits. Why that
is so is likely molecular.
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:
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.
Halper, M.D., Ph.D.
Professor and Graduate Coordinator
Department of Pathology
College of Veterinary Medicine
The University of Georgia.
followed up this conversation with a letter to Dr. Mueller.
Halper said you performed a thorough examination on Captain Midnight, can you
explain what that actually means?
and full lameness evaluation (straight trot, canter, flexion tests, lunge)
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?
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:
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?
a horse has a dropped fetlock, what would be the next progression to look for
to distinguish injury from progression of DSLD?
physical examination findings, ultrasound, and the nuchal ligament biopsy findings.
and Serenade were put through all these tests and yet were found to not show symptoms
of DSLD therefore, THEY WERE SENT HOME.
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.
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.
a horse has clinical symptoms consistent with DSLD
Progressive lameness with out a traumatic
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
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.
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.
Diplomate, American College of Veterinary Surgeons
of Equine Programs
Department of Large Animal Medicine
College of Veterinary
University of Georgia
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,
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.
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
of Equine Veterinary Science
29, Issue 10, Pages 748-752 (October 2009)UC
9 of 12
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
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.
Equine, Desmitis, DSLD, Proteoglycan, Ligaments
a Pathobiological Sciences,
University of WisconsinMadison, School of Veterinary Medicine, Madison,
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
requests: Daniel Schenkman, DVM, PhD, Biomedxplor, LLC, 915 Martin Drive, Marshfield,
2009 Elsevier Inc. All rights reserved.
PROTOCOL FOR DEGENERATIVE SUSPENSORY LIGAMENT DESMITIS
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)
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
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
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.
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
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).
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.
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
Copyright 2002 DSLD Research Inc. All
Rights Reserved. (*Reprinting permitted for diagnostic purposes)
1. Young, JH. Degenerative Suspensory Ligament Desmitis. Hoofcare and Lameness.
2. Pryor, PB, Pool, RR, Wheat, JD. Failure of the suspensory
apparatus in Peruvian Paso horses, in Abstracts. ACVS meeting 1984; 56.
Dyson, S. Diagnosis and prognosis of suspensory desmitis. In: Proceedings of the
1st Dubai International Symposium, Ed:ML Hauser, Matthew R. Rantanen Design, USA,
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
7. Yeager, A. Ithaca, NY (personal communication) March 13,
8. Cuesta, IC, Riber, C, Pinedo, M, et al. Ultrasonographic measurement
of palmar metacarpal tendon and ligament structures in the horse. Vet Radiol Ultrasound
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
James Rooney, D.V. M.
taken the liberty of enlargint the print on some of the most significant points
in Dr. Rooney's report)