Bob Fox wants me to breed a dog with SEVERE hip dysplasia - Page 7

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by Rik on 17 December 2018 - 01:12

well, since it seems a personal debate.

"No, it's not good luck, it's excellent musculature and no loose ligaments, dry ...complete opposite of the gsd showlines from USA and Germany."

so, are you saying only S/L have HD? pretty sure SV has stringent requirements for breeding and GSDCA has strong recommendations, though everyone is free to do their own thing in the U.S.

"Look at the racing grey hound that is devoid of developmental hd when raised as a whelp on good footing, and compare it with the neopolitan mastif that is almost 100% with hd no matter where it's raised."

I really don't understand what you are saying here, the mastiff is 100% genetic HD, but somehow, the same rules don't apply to the GSD?

"Show the proof that 99.9% of gsd hd is " genetic" ....point to the " hd gene marker"....you can't because there are none. Hip development is mechanical...not a gene trigger."

I really don't know how to respond to this statement. if it was true, it would be true for 100% of all breeds. same % all breeds.

shallow sockets are in no way mechanical and please, if you believe this, then you provide the studies.

 

Rik

 

 

 

by joanro on 17 December 2018 - 02:12

@Rik...

Let's start with a point made in a previous blog (The 10 most important things to know about canine hip dysplasia), that puppies are born with "perfect", normal hips. Of course, they're puppy hips and not adult hips, but they are quite remarkable.

A newborn puppy looks like it has no joints at all on an x-ray. This is because the ends of the long bones and many parts of the pelvis are soft cartilage at birth. Because cartilage doesn't show up on x-rays, a radiograph of a newborn puppy can look like an apparition of a spooky, disarticulated body. But this is just nature's way of providing enough support to be able to move around while the skeletal grows rapidly in the first few months of life.
The hip joints are also formed of cartilage at birth and are little more than a round ball at the end of the femur that sits in a depression in the pelvis where the hip socket will be.

An image
As the puppy grows, the formation of the bony structures that will become the hip joint is not programmed by genes. Instead, the forces on the joint stimulate the deposition of bone in the right places to form an articulating ball and socket joint. As long as the head of the femur stays seated where it belongs in the developing hip socket, the hip joint should form perfectly.

This seems truly magical, but there's a catch. If, for some reason, the head of the femur is not tightly held in the hip socket, development will go awry. What results is "developmental hip dysplasia"; a malformed hip socket. In dogs, this is canine hip dysplasia.

​Wayne Riser, who studied hip dysplasia in dogs for many years and was also the founder and first director of the Orthopedic Foundation for Animals, explained it this way (1975):
"In all mammalian embryos, the hip is laid down as a single unit from mesenchymal tissue, and it develops normally as long as the components are left in full congruity. The hip is normal at some time in the development of the mammal, and abnormal development occurs only when stresses pull the components apart.

In the dog, the hip is normal at birth. Intrauterine stresses are not sufficient to produce incongruity of the hip. The first time such forces are great enough is when the pup begins to take its position to nurse.

​Observations of the disease in man, dog, and a number of other mammals for many years have culminated in the conviction that the bony changes of hip dysplasia, regardless of species, occur because the soft tissues do not have sufficient strength to maintain congruity between the articular surfaces of the femoral head and the acetabulum."
Riser is saying here that muscles, ligaments, and tendons ("soft tissues") normally keep the head of the femur properly seated in the developing socket. But if there are abnormal forces on the joint, the soft tissues might be inadequate to stabilize the joint, and malformation of the socket - hip dysplasia - will occur.

As Riser described, looseness or laxity of the hip joint is the prerequisite for the development of hip dysplasia. If the head of the femur is not positioned properly in the hip socket during development, the mechanical forces that stimulate bone deposition in the joint will be abnormal and the result will be a dysplastic hip.

In breeds like the Greyhound, which very rarely suffer from hip dysplasia, the muscles that support the hip are exceptionally well developed. Riser found that less pelvic muscle mass was associated with higher risk of dysplasia. This even held within a breed: in both German Shepherds and July Hounds, dogs with a higher pelvic mass index had better hips on average.


Unfortunately, most breeds of dogs don't have the exceptional pelvic muscles of the Greyhound at birth, which are the result of selection over hundreds of generations to produce a dog with exceptional speed. The Bernese Mountain Dog, on the other hand, was bred to have the size, strength, and substance necessary for drafting (cart hauling). In fact, anatomical differences among breeds are reflected in propensity to develop hip dysplasia.

After studying radiographs of tens of thousands of dogs in dozens of breeds, Riser (1975) found that a pattern began to emerge.
There was...a strong correlation between body form, size, growth rate, quantity of subcutaneous fat, type of connective tissue, pelvic muscle mass, and the general body type of the different breeds and the prevalence of hip dysplasia. Recently, we have identified certain general characteristics of a breed that increase the risk of hip dysplasia.

Body Size
The breeds with the lowest percentage of hip dysplasia were near the size of the ancestral dog. The bones were small in diameter and smooth, the feet were small and well arched, and the shape of the head was long and narrow. The giant breeds with a high percentage of hip dysplasia were two to three times larger than the ancestral dog. Their bones were coarse and large in diameter, with prominent protrusions and depressions. The feet were large and splayed, and the head was wide and oversized.

Body Type​
In general, the body conformation of the breeds with the lowest percentage of hip dysplasia was slender and trim. The skin was thin, smooth, and stretched tightly over the underlying tissues. The muscles were prominent, hard, and full-bellied. At dissection in these breeds, the skin and subcutaneous tissues and fascia rarely contained over 1-2% fat by weight. The joint ligaments were well developed; the fibers were coarse, closely packed, and relatively free of fat. The well-formed pelvic and thigh muscles were attached to broad, coarse tendons that were securely attached to the bones. This group of dogs is fleet-footed and well-coordinated in their movements. Of the high-risk group, the four breeds of the giant type were not only two to three times the size of the ancestral dog, but their body conformation was heavy, round, and stocky. Acromegalic characteristics were present to some extent in all four breeds. The skin was thicker than that in the other group; it lay in folds over the head and neck. At dissection, the thickened skin was infiltrated with fat. Fat was also abundant in the subcutaneous and fascia spaces and commonly accounted for 5-10% of the weight of the soft tissues of the hindquarters. In comparison with the other group, the muscles were less prominent and less developed. Fat also was infiltrated into the tendons and ligaments. The fibers of these two structures were smaller in diameter than those of the low-risk group. The gait of the giant breeds was less graceful and slower than that of the smaller breeds.

Growth Pattern
The group of breeds with the highest percentage of hip dysplasia grew and matured more rapidly than did those in the low-risk group. We have observed this in several studies. Starting at birth, this group gained rapidly. The pups of these breeds were aggressive eaters, both as they nursed and as they began to take supplemental food.

The 38 breeds, when ranked according to the highest prevalence for hip dysplasia, with few exceptions exhibited a gradual shift from the poorly muscled and poorly coordinated, acromegalic type giants at the top, to the lowest percentage of hip dysplasia at the bottom, characterized by the breeds that were sleek, tight skinned, highly coordinated and well muscled. These correlations and observations support previous findings that the poorly muscled and coordinated breeds have a high percentage of hip dysplasia, whereas the well-muscled and highly coordinated types are relatively free of the disease.

Selection for acceleration in growth created dogs with excessive fat and weight at an early age. This has resulted in lowered dynamic and biomechanical efficiency of the hip joint. The young dog that carries excessive weight runs the risk of over-extending the supporting soft tissues, and injury to these tissues results in pulling apart (subluxation) of the joint components. This results in changes that have been recognized as hip dysplasia. This is not a new concept. It was pointed out as long ago as 3 centuries that 'Muscles and bone are inseparably associated and connected, between muscle and bone there can be no change in one but it is correlated with changes within the other'.

Riser summarized these findings in a table:

An image



 

by Rik on 17 December 2018 - 02:12

well, that's a lot of words I'm not going to read.

but like I said, regardless of what Riser said, if it's not the same across all breeds, 100%, then it's something genetic.

and it really doesn't take a Rocket Surgeon to figure that out.

and, also, just for the record, in 40 years of GSD, I have only seen/heard breeders/sellers blame it on the buyer/environment.

present company excepted, of course.

Rik

by joanro on 17 December 2018 - 02:12

You will recognize that many of these traits are features of breed type, and of course most are under direct genetic selection or are secondary to some other trait under selection. As it seems to go in the competitive show world, many of the traits on the "High Prevalence" list have become progressively more exaggerated through artificial selection - the large size gets larger, heavy bone gets heavier, a broader head gets broader. And to make matters worse, the desire for dogs that "finish" (become champions) at ever younger ages drives selection for rapid growth, which overloads the immature skeleton and muscle systems. It seems that we are trying to select against hip dysplasia at the same time as we select for many traits that increase the risk.

The factors that cause hip laxity and the development of dysplasia occur in the first few months of the puppy's life. Sometime between birth, when the cartilagenous tissues of the hip joint have the capacity to become a perfectly constructed ball and socket joint, and when the puppy is four or five months old, the soft tissues of the pelvis fail to provide the support necessary to keep the femoral head properly seated in the hip socket. As a result, the joint doesn't develop properly, then abnormal biomechanical forces exacerbated by environmental factors such as weight and inappropriate exercise begin the cycle of damage and inflammation that result in dysplasia and osteoarthritis.
Wayne Riser showed 40 years ago that ​
In very young human and canine subjects with unstable coxofemoral joints, hip dysplasia can be prevented and the instability corrected if the congruity of the components of the hip joint is maintained and if femoral subluxation does not occur. If proper congruity cannot be maintained, the hip joint becomes malformed in a relatively short time. The changes in the bones and cartilage of the hip are thus the indirect result of failure of the soft tissues to support full congruity of the bony components of the hip.

Few genes so far analyzed directly affect osseous structures. [This is still true.] The shape of bones reflects changes by biomechanical stresses.

The spread of hip dysplasia centers around the genetic transmission and heritability of certain body size, type, conformation, movement, growth pattern, and temperament. This conclusion is based on the facts that the prevalence of hip dysplasia is approximately the same in a number of breeds with similar body characteristics and there is no gene flow between these purebred breeds. Since these facts must be respected, biomechanical and environmental factors associated with certain body conformation and size must be considered as the causes.

You will recognize that many of these traits are features of breed type, and of course most are under direct genetic selection or are secondary to some other trait under selection. As it seems to go in the competitive show world, many of the traits on the "High Prevalence" list have become progressively more exaggerated through artificial selection - the large size gets larger, heavy bone gets heavier, a broader head gets broader. And to make matters worse, the desire for dogs that "finish" (become champions) at ever younger ages drives selection for rapid growth, which overloads the immature skeleton and muscle systems. It seems that we are trying to select against hip dysplasia at the same time as we select for many traits that increase the risk.

The factors that cause hip laxity and the development of dysplasia occur in the first few months of the puppy's life. Sometime between birth, when the cartilagenous tissues of the hip joint have the capacity to become a perfectly constructed ball and socket joint, and when the puppy is four or five months old, the soft tissues of the pelvis fail to provide the support necessary to keep the femoral head properly seated in the hip socket. As a result, the joint doesn't develop properly, then abnormal biomechanical forces exacerbated by environmental factors such as weight and inappropriate exercise begin the cycle of damage and inflammation that result in dysplasia and osteoarthritis.
Wayne Riser showed 40 years ago that ​
In very young human and canine subjects with unstable coxofemoral joints, hip dysplasia can be prevented and the instability corrected if the congruity of the components of the hip joint is maintained and if femoral subluxation does not occur. If proper congruity cannot be maintained, the hip joint becomes malformed in a relatively short time. The changes in the bones and cartilage of the hip are thus the indirect result of failure of the soft tissues to support full congruity of the bony components of the hip.

***Few genes so far analyzed directly affect osseous structures. [This is still true.] The shape of bones reflects changes by biomechanical stresses.*****


##### The spread of hip dysplasia centers around the genetic transmission and heritability of certain body size, type, conformation, movement, growth pattern, and temperament. This conclusion is based on the facts that the prevalence of hip dysplasia is approximately the same in a number of breeds with similar body characteristics and there is no gene flow between these purebred breeds. Since these facts must be respected, biomechanical and environmental factors associated with certain body conformation and size must be considered as the causes. #####

##### According to Riser, the risk factors for hip dysplasia are related to the features of a dog and its breed that result in a mismatch between the forces necessary to maintain congruency of the hip joint and the support the soft tissues are able to provide during the critical first few months of life. By the time the puppy is 6 months old, the strength of the supporting tissues and ossification of the bones should be adequate to prevent the development of hip dysplasia under normal circumstances. Prevention of hip dysplasia will come both from reducing the genetic risk factors through selection and from avoiding situations that could result in joint instability or incongruity.

The literature review and report of our work presented here have revealed a basis for optimism in controlling and reducing the prevalence of hip dysplasia in both man and animals...In children, it is basically the test for hip laxity at birth, and for the dog it is restriction of breeding only those animals with radiographically normal hips. Both in children and dogs, hip dysplasia is, for the most part, a ‘man-made’ problem and can be controlled if man will use the tools at his disposal.

These findings uphold the validity of our two premises that (1) hip dysplasia occurs only if hip joint instability and joint incongruity are present in the young child or animal; and (2) the disease can be prevented if hip joint congruity can be maintained until ossification makes the acetabulum less plastic and the abductor muscles and supporting soft tissues become sufficiently strong and functional to prevent femoral head subluxation.

Genetic selection and management of environmental risks are both necessary to lower the frequency of hip dysplasia. For selection to be effective, we need to recognize that some of the traits that are valued as part of breed type are themselves risk factors for development of hip dysplasia. Selecting for faster growth and ever increasing size will confound efforts to produce dogs with better hips. Likewise, inadequate weight management of both puppies and adults is an environmental factor that dramatically increases the risk of developing dysplastic hips. Finally, we should use a little common sense about activities that are appropriate for puppies...


by joanro on 17 December 2018 - 02:12

Rik, educate yourself and read ....yes!!! It is across ALL breeds as to cause, and why it is absent or present.. Open your mind and stop being so thick headed. You are believing old unproven crap! Spewed by so called breeders who will claim that hd in so many of their pups aint their fault by golly, because it's in the GENES and it's going to be there no matter how good the pedigree looks with all those hd clear on paper.
emoryg

by emoryg on 17 December 2018 - 03:12

Duke, if I remember correctly this is a small sample of GSD.  I never followed up on additional research. 

   https://helda.helsinki.fi/bitstream/handle/10138/135177/grundstr%C3%B6m.pdf?sequence=1

by Rik on 17 December 2018 - 03:12

joan, you don't even make sense.

are you saying HD in GSD is genetic or environment.

Are you saying that it's environment, that thousands of GSD breeders across several continents and a 100 years haven't been able to figure this out, but you have?

who is "thick headed" here?

hd is not the same across all breeds. my claim is not that bad breeders say it's genetic, but that it's the buyers fault.

any responsible breeder would replace with no issue if they claimed "genetic".

you are the one saying it's "environmental", otherwords, it's all on the buyer, no fault on the breeding.

as far as being "thick headed", well I have no argument there. but,, I don't try to ride both sides of the fence, as I don't sell GSD.

so, since there seems to be a disconnect in what I post and what you read, here is my belief and experience.

1. HD is a prevalent genetic condition in the GSD. From my experience, it can be improved by careful choice of HD free breeding. not 100% eliminated, or it would already have been done so.

2. Some, less than honest breeders, often try to blame HD on the buyer. I call bullshit on this unless there is an obvious injury.

3. I don't mean anything else and really don't know how to put it any more clear.

Rik

 

Prager

by Prager on 17 December 2018 - 04:12

@ Hundmutter you say that
Joan was right to ask: "what desirable traits would also be eliminated ?"
Prager: The point is that no traits regardless of how excellent they are are worth crap if the dog is dysplastic. As I have said before one must evaluate the whole dog. But the hips are limiting condition. In another word, I will not breed a dog who has lesser hips and has many lesser hips in the pedigree in the last 5 generations regardless of how good he is. There always is a dog with the same excellent traits who has the good hip background. To say that by breeding only good hips will eliminate other desirable traits from the GSD is a silly notion or excuse of someone who is kennel blind and thinks that his dog is so super and must be bred even though it will pass down bad hips gene.

Prager

by Prager on 17 December 2018 - 04:12

Joan that article looks familiar. From where did you tape and paste it? 

by Rik on 17 December 2018 - 06:12

prager, I am just amazed that someone who started wit GSD digs from you, only 15 years ago, is now the end all, be all authority on thr GSD in thre U.S., on every thread on this forum.

Riik


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