I have only seen two cases of it. Both were mares; one an AQHA and the other a Trakehner.
[QUOTE=JB;8835787]
Definitely get a biopsy to confirm. Iām suspicious itās not, given the other hind leg isnāt showing all the same issues. Itās nearly always bilateral - not sure Iāve even heard of a confirmed case that was unilateral. The reason being, itās a systemic connective tissue disease, not simply a suspensory
issue.[/QUOTE]
What I can gather is that most horses that are diagnosed are quite further into the degeneration process. If he does conclusively have it, I think we just caught it a bit earlier than usual. But that being said, my primary question is, āhow long until the other legs and tissue are affected?ā and so far no one has a great guess. His legs straightened within about six months time so it seems like a fairly quick timetable. Iāve also been in contact with Dr Halper at UGA who does the biopsy testing and hope to get a little more information.
Iām holding out a little bit of hope that there is a chance itās not DSLD, but even if itās not Iāve been cautioned that he wonāt be a performance horse with his new confirmation and that the typical treatments for suspensory injuries wonāt be life changing.
Iām definitely moving forward with the biopsy. Dr Halper prefers fresh samples so we just have to schedule. My vet has assured me that while it will leave an indentation in his neck because they go through the muscle, it isnāt terribly traumatic to my pony.
Iām happy to share what I can. When I search for information, the posts are typically very outdated, the horses very aged. So I would love to help anyone else going through what I am. I havenāt taken a photo of his hind end this week, I will shortly. The photos below will be much more helpful with a current comparison
He was born April, 2011. His main confirmation ācomplaintā when I purchased him was the lower fetlocks, which obviously turned out to be very unhelpful. His hocks didnāt look like Valegro before but they definitely had an acceptable angle. I donāt have a lot of whole body photos, but going back through them, his hocks look ok to me in the shots I have. Iām fairly upset that I didnāt notice sooner, I always tack him in his stall since I ride early and I feel like I didnāt step back and look at the whole picture soon enough. But then I searched my phone and even through the photos in April, I donāt know if I would have called the vet crying that his hocks were posts. What I did notice in my pictures though is what Beowulf mentions, the soft pasterns. In some action photos the angle of his pastern seems extreme. I havenāt had the time to compare regularly built horses at the exact stride yet so Iām going to do that tonight.
May 30, 2014:
https://themodernblonde.files.wordpress.com/2016/02/img_0397-1.jpg?w=620
March 2015:
https://themodernblonde.files.wordpress.com/2015/08/img_0247.jpg?w=620
March 26, 2016:
https://themodernblonde.files.wordpress.com/2016/04/12321430_10102646196388039_4183754834373194472_n.jpg?w=616&h=616&crop=1
April 20, 2016:
https://themodernblonde.files.wordpress.com/2016/07/11140352_10102690367014749_6276360947541294545_n.jpg?w=620
Sales video, March 2015:
https://www.youtube.com/watch?v=tJi6tXO2HuE
His dam with a foal by Dr Watson:
https://youtu.be/iJRJoKisNyE
Sidenote: They are tracing bloodlines so if anyone reading this has a confirmed DSLD horse, please contribute your information to the study. Hopefully they can find the genetic marker one day. It is anonymous.
PPS: Sorry I just hijacked this thread :\
1 Like
[QUOTE=The Blonde & The Bay;8836583]
What I can gather is that most horses that are diagnosed are quite further into the degeneration process. If he does conclusively have it, I think we just caught it a bit earlier than usual. But that being said, my primary question is, āhow long until the other legs and tissue are affected?ā and so far no one has a great guess. His legs straightened within about six months time so it seems like a fairly quick timetable. Iāve also been in contact with Dr Halper at UGA who does the biopsy testing and hope to get a little more information.
Iām holding out a little bit of hope that there is a chance itās not DSLD, but even if itās not Iāve been cautioned that he wonāt be a performance horse with his new confirmation and that the typical treatments for suspensory injuries wonāt be life changing.
Iām definitely moving forward with the biopsy. Dr Halper prefers fresh samples so we just have to schedule. My vet has assured me that while it will leave an indentation in his neck because they go through the muscle, it isnāt terribly traumatic to my pony.
Iām happy to share what I can. When I search for information, the posts are typically very outdated, the horses very aged. So I would love to help anyone else going through what I am. I havenāt taken a photo of his hind end this week, I will shortly. The photos below will be much more helpful with a current comparison
He was born April, 2011. His main confirmation ācomplaintā when I purchased him was the lower fetlocks, which obviously turned out to be very unhelpful. His hocks didnāt look like Valegro before but they definitely had an acceptable angle. I donāt have a lot of whole body photos, but going back through them, his hocks look ok to me in the shots I have. Iām fairly upset that I didnāt notice sooner, I always tack him in his stall since I ride early and I feel like I didnāt step back and look at the whole picture soon enough. But then I searched my phone and even through the photos in April, I donāt know if I would have called the vet crying that his hocks were posts. What I did notice in my pictures though is what Beowulf mentions, the soft pasterns. In some action photos the angle of his pastern seems extreme. I havenāt had the time to compare regularly built horses at the exact stride yet so Iām going to do that tonight.
May 30, 2014:
https://themodernblonde.files.wordpress.com/2016/02/img_0397-1.jpg?w=620
March 2015:
https://themodernblonde.files.wordpress.com/2015/08/img_0247.jpg?w=620
March 26, 2016:
https://themodernblonde.files.wordpress.com/2016/04/12321430_10102646196388039_4183754834373194472_n.jpg?w=616&h=616&crop=1
April 20, 2016:
https://themodernblonde.files.wordpress.com/2016/07/11140352_10102690367014749_6276360947541294545_n.jpg?w=620
Sales video, March 2015:
https://www.youtube.com/watch?v=tJi6tXO2HuE
His dam with a foal by Dr Watson:
https://youtu.be/iJRJoKisNyE
Sidenote: They are tracing bloodlines so if anyone reading this has a confirmed DSLD horse, please contribute your information to the study. Hopefully they can find the genetic marker one day. It is anonymous.
PPS: Sorry I just hijacked this thread :[/QUOTE]
What a gorgeous, beautiful horse. I am so very sorry. Jingling that it is something elseā¦ like JB said, it is almost always bilateral so maybe thereās hope. His dam looks lame in that video, but nice foal.
Where/who is conducting the study?
You are not hi-jacking the thread; youāre providing first hand experience with suspected DSLD in warmbloods. Have you contacted the breeders yet? That is something Iād be doing once you got a confirmation that it was indeed DSLD.
The other thing to consider, and I am not sure if it has been mentioned, but angles behind in my experience do tend to change slightly as they get older. My suspicion is itās the growth plates closing. That and work will change the way a horse stands significantly - IE some horses with very sore hocks and SI will stand way under themselves and it makes them look cow-hocked or makes them look like their hind cannons are too long and sloped ā sometimes the inverse happens when it is SI and stifle issues, where they start to stand very straight. Typically, horses that are conformationally straighter behind do tend to start to get ādroppedā pasterns as they age and the tendons/ligaments lose their elasticity.
1 Like
[QUOTE=beowulf;8836382]
DSLD is definitely genetic. I think the when it happens might possibly be environmental/circumstantial, but you are either born with the predilection for it or youāre not.[/QUOTE]
āGenetic conditions are those that are related to our genes, at least in some part. Changes in our genes, like mutations, can cause medical problems. Some medical problems are hereditary, meaning they are caused by a gene mutation (or mutations) that are inherited (or passed on) from a parent.ā
Wikipedia
'When we examine a trait strongly linked to a family, statistically related to a lineage of several generations, we tend to define the trait as hereditary or genetic, using either term, treating them as perfectly interchangeable synonyms. Because the feature in question is transmitted along that lineage, we deduce that the feature is related to the genetic makeup of those organisms, being directly dependent on a gene or on group of genes. And I believe that, doing this, we make a mistake. Genetic and hereditary are not synonymous. What is the difference?
The adjective genetic refers to a trait or a feature determined, directly or indirectly, by the organismās genes, and phenotypically perceptible because of the occurrence of those geneās protein products or the activity of these protein products in a given environmentā¦ā
https://evolutionarybio.wordpress.com/2014/09/15/the-difference-between-genetic-and-hereditary/
āGenetic: A medical condition or a trait that is related to our genes
Hereditary: A medical condition caused by a change in our genes that is passed down in a family. Sometimes this happens for the first time in someone, and they can pass it on to their children.ā
http://patients.ambrygen.com/general-genetics/know-the-basics/genetics-101/inherited-vs-genetic
I lean towards believing it is inherited.
So far none of the research has found a gene for it [I donāt think there is the funding for the research] and their claim that it is āgeneticā is mostly based on certain lines of breeding having itā¦ for example Northern Dancer lines.
Yes there are some TBs from that line who end up diagnosed, but that doesnāt mean itās genetic.
.
ā What I did notice in my pictures though is what Beowulf mentions, the soft pasterns. In some action photos the angle of his pastern seems extreme. I havenāt had the time to compare regularly built horses at the exact stride yet so Iām going to do that tonight.ā
Yes. Yo had fetlock/pasterns that articulated very low in motion. He was never unsound/lame, jumped like anything and loved to do it.
His hock angle was always ānormalā.
[QUOTE=beowulf;8836610]
What a gorgeous, beautiful horse. I am so very sorry. Jingling that it is something elseā¦ like JB said, it is almost always bilateral so maybe thereās hope. His dam looks lame in that video, but nice foal.
Where/who is conducting the study? .[/QUOTE]
Dr Halper, Dr Mero and Dr Kellon have all done research of one kind or another.
You can see some of the info available here:
http://www.angelfire.com/bc/curlygait/DSLD.html
ETA the above probably contains the research info ladyj refers to on page one [regarding effected breeds] as well, as it is/was the main clearinghouse for all info years ago when Yo was diagnosed.
āThe genetic aspect is being studied by Dr Gus Cothran. He has studied over 200 samples from affected horses and has found a number of markers to date which he is following up.ā
Phone: (979) 845-0229
1 Like
Iām not sure I understand saying itās not genetic since thereās no identified gene for it. It may not be a single gene responsible - it might be 2 or more that need to be activated.
We knew the colors black and red, and the dun markings, were inherited traits, a set of genetics, long before their genes were discovered. We know gaiting is an inherited trait, and now we have at least one identified gene for it - there is a genetic factor in a horse who gaits.
Genes are inherited, therefore anything that is inherited is genetic. Yes, that form of that gene might have been a novel mutation with one of those parents, but at that point it becomes a gene that is heritable.
The fact that there have been markers identified as interesting is pointing towards the future (hopefully sooner rather than later) location of the gene, or genes responsible for ESPA.
The horse is just lovely! So very lovely. And yes, very soft in his pasterns in the video 
I also noticed, or at least think I do without knowing how to slo-mo the video, that he seems to be landing slightly toe-first behind almost all the time, instead of a very definitive flipping up of the feet right before they land. What I donāt know is if that was a precursor to whatās going on now, or if something else was going on with him and that continued movement has led to this?
4 Likes
[QUOTE=JB;8837136]
Iām not sure I understand saying itās not genetic since thereās no identified gene for it. It may not be a single gene responsible - it might be 2 or more that need to be activated.
We knew the colors black and red, and the dun markings, were inherited traits, a set of genetics, long before their genes were discovered. We know gaiting is an inherited trait, and now we have at least one identified gene for it - there is a genetic factor in a horse who gaits.
Genes are inherited, therefore anything that is inherited is genetic. Yes, that form of that gene might have been a novel mutation with one of those parents, but at that point it becomes a gene that is heritable. [/QUOTE]
Yes I get all thatā¦ but what the people involved [not the DVMs but the people behind the Delphi page and the Yahoo group, who also make and sell the herbs to treat it] have been saying [understand Yo was diagnosed at 23, lived 6 years with this, and then died about 30 months ago] going back 8 years-ish was that because these affected TBs had this stallion in common, it was āgeneticā. That the shared lineage of affected TBs was the evidence that it was inherited from that common stallion/line.
The group is one that ascribes causation to correlation without any more study.
I am not saying it isnāt genetic, I am saying that the info available at present hasnāt proven that it is. And personally I think thereās a hereditary component as well as, in some cases, environmental influences that lead an animal to exhibit the symptoms [fetlocks drop, skin gets sensitive, etc] that may have otherwise stayed latent/dormant sans environmental influence.
In Yos case had he never suffered the stress that lead to the ulcersā¦ would he have dropped? I believe thereās a good chance he may not have.
That a DVM is researching the genetics of it is great to hear, and news to me.
If anyone has any links to more about that I would love to learn more.
But information available DOES prove itās genetic. Heredity is genetics. You canāt inherit something that doesnāt have a gene to produce it.
There may be environmental factors that active the gene(s) for sure. Iāve seen several people on this board state that it wasnāt until their older mare had a foal that ESPA became apparent, and that makes sense - the ligament-relaxing hormones for birth may well have triggered the DLSD/ESPA. But you canāt trigger a latent disease without the genetics for that disease being present.
Itās like cribbing - itās proven to have a genetic component, but also known to have environmental/management triggers.
4 Likes
[QUOTE=JB;8837230]
Itās like cribbing - itās proven to have a genetic component, but also known to have environmental/management triggers.[/QUOTE]
Not to take this thread off-track, but I would love to see the proof that cribbing has been proven to be genetic.
2 Likes
I think DSLD is related to the horse using itself incorrectly, and it is repetitive strain injury most likely due to a tight and locked back which causes abnormal stresses on the limbs. Therefore, breeds that tend to drop and lock their backs either because they have been selected for a certain type of movement (Saddlebreds, Arabians, gaited horses) or due to being worked incorrectly with respect to use of their backs. Also long pasterns I believe are contributory. Since it therefore may appear more in those particular breeds people tend to believe it is āgeneticā. How do you separate conformation and way of moving from genetics??I think whatās genetic/inherited is conformation and body mechanics that leads to DSLD.
I donāt know whether this means anything, but Furstenball has received criticism for being soft in his hind pasterns. He has, at this point, many many offspring, among them quite a few approved stallions, so the feeling must be that he isnāt passing this along. However, a good friend of mine thinks that the problem is Furstenball is very obvious. That said, he has a performance career.
[QUOTE=clint;8837235]
Not to take this thread off-track, but I would love to see the proof that cribbing has been proven to be genetic.[/QUOTE]
http://www.thehorse.com/articles/23939/cribbing-not-a-learned-behavior-researchers-say
2 Likes
I read that article long ago. I donāt take a possible genetic predisposition in TBs to be conclusive that cribbing is genetic.
30% higher incidence of cribbing in relateed horses vs the standard population
http://www.sciencedirect.com/science/article/pii/0301622686900989
Perhaps āall but provenā is a better way to state it.
Itās certain not learned, and that really only leaves inherited.
https://equineink.com/2009/03/24/cribbing-presumed-causes/
Research conducted in Japan by Hosada in the 1950s showed that while cribbing rates across the equine population was less than 1%, in some lines of thoroughbreds the cribbing rate was as high 7%. For example 8.3% of the offspring and 6.4% of the next generation of the stallion Ryopan (a cribber) also cribbed. It appears that 25% of offspring of one cribbing parent and 50% of offspring of two cribbing parents cribbed. Similar results were discovered by Italian researchers Vecchioti and Galanti in 1986. They found that in a population of 1035 thoroughbred horses the incidence of cribbing overall was 2.4%. However, among certain āfamilyā lines the incidence was as high as 44%.
4 Likes
This also points strongly towards genetics:
http://horse-journal.com/article/the-cribbing-controversy-6251
There seems to be little doubt among researchers that cribbing has a heritable component. Among breeds, Thoroughbreds hold the distinction of having the largest population of cribbers (8.3 to 10%). However, donāt blame racing. Standardbreds, which undergo similar training, feeding and housing regimen, have a much lower incidence.
1 Like
[QUOTE=rebecca yount;8837248]
I think DSLD is related to the horse using itself incorrectly, and it is repetitive strain injury most likely due to a tight and locked back which causes abnormal stresses on the limbs.[/QUOTE]
You do realize that DSLD is a systemic disease that doesnāt just effect hind limbs, rather all of an animalās connective tissue, right? If a horse has DSLD, no amount of āworking correctlyā will fix the problem.
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Albion, you are correct.
Thereās a difference between suspensory desmitis resulting from over-work, or poor conformation, or both, and ESPA (renamed from DSLD because it was discovered to affect more connective tissue than just the suspensory ligament).
You cannot prevent it. You cannot cure it. At best you manage it. It IS progressive, and it ends up resulting in PTS.
2 Likes
[QUOTE=JB;8838381]
30% higher incidence of cribbing in relateed horses vs the standard population
http://www.sciencedirect.com/science/article/pii/0301622686900989
Perhaps āall but provenā is a better way to state it.
Itās certain not learned, and that really only leaves inherited.
https://equineink.com/2009/03/24/cribbing-presumed-causes/[/QUOTE]
It certainly IS learned in some instances - if the factors are right (and assuming they are referring to wind sucking not wood chewing).
In 40 years of breeding horses with the same mare lines we have had a total of 2 foals become windsuckers. Different bloodlines, different environmental situations - the ONLY constant between the 2 was that we had a couple of mares (not related to the foals) but in the same paddock and they sucked wind.
Since then (18 years ago) I have not allowed a wind sucker near my young horses and I have not had another foal learn to suck wind. Iām not saying that there isnāt an inherited predilection to the behaviour but Iāve definitely not had a foal become a wind sucker (and we bred full siblings to both the foals that learned to suck wind) without first seeing another horse doing it. If it was only inherited then we should have witnessed a young horse taking it up when the environmental factors were right but we have not.
