Hip Dysplasia and more - Page 2

SM, I don't know where you got your numbers, but according to Dr. Ron Schultz, after 12 weeks, close to 90% could be immunized. Any dog any age can be VACCINATED; the goal is IMMUNIZATION. :)

I do a parvo and distemper MLV (Nobivac DPv) at 8 and 12 weeks and all titered after that have been good. Distemper vaccine is quick- just hours after vaccination, many have shown protective antibodies according to Dr. Schultz.

Titer testing is always a good thing. Every dog I have owned I have done titer testing, it gives me a piece of mind since my dogs are exposed to the things I pick up at the vets office on a daily. My GSD comes to work with me almost daily therefor he is always vaccinated on schedule.

Since he was a puppy he has been at the clinic where parvo puppies come in daily. He was vaccinated at 12 weeks, and then continued a regular vaccine schedule, never once had parvo, distemper or kennel cough or canine influenza.

I believe in vaccinating, and maybe its cause I work for a vets office but even before then I have always vaccinated my animals.

If you're titering, why are you re-vaccinating?

I have to revaccinate for Rabies every year, unfortunately its a state law but I only vaccinated for Parvo and Distemperwhen he was a puppy, and he went though two boosters for influenza.

I should have specified which vaccines I was talking about, sorry.

How can anyone say environmental factors contribute more to occurence of Hip dyslasia than genetic factors do?

- Different breeds of dogs have HD incidence in varying percentages, this coupled with the fact that most breeds are exposed to similar environmental factors it makes sense to conclude that HD is largely a genetic issue.

- German shepherds have a higher incidence of HD and back issues than malinois and collies do. All three breeds are working breeds exposed to long bites, slippery floors, some owners over feed etc but still the Malinois and collies have a much lower incidence of HD and back problems. Even non sport breeds like Kelpies are exposed to harsh environmental conditions and have a much lower incidence HD and back issues.


Saying HD is an environmental issue is just an excuse by breeders who do not care about the breed and are more interested in making $$$$.
We need to tell ourselves the truth and try as much as possible to avoid breeding stock with a high propensity for developing HD and other sturctural issues and stop blaming owners who have to pay for overpriced GSDs that will incur health bills for the better part of their lives.

Gotcha, Shiros.

Tobi, think about what you just said. How is it that we have been x-raying since the 60's and still have the SAME percentage of dysplasia as when we started? Methinks that's enough to say we're barking up the wrong tree. ;)

You're stating info mostly correctly, but you're arriving at the wrong conclusion, imo. This is like what we were talking about yesterday in the 2-2 thread. Pet owners have all sorts of problems and enthusiasts don't have nearly as many. Pet owners therefore think breeders are lying about problems and the reality is, if breeders and trainers really had these problems, they likely wouldn't stay in the breed. I couldn't afford to keep all my dogs if they weren't healthy, strong, easy keepers.

Think about the lifestyle differences and environmental contrast between competition dogs and a pet GSD. Consider their diet, housing, training schedule, training activities,etc. Kelpies WORK and live in a pretty natural environment most of the time. Not at all surprising to me that they are quite hardy. Again, enthusiasts, trainers, breeders, etc. have fewer problems with GSDs than pet owners. Why? Why do you think that is?

I want to see these Collie long bite vids, too.

Oh, Mylanta. Someone took a deep belly breath.

Instead of acting like this: 

Read this :
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.


 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.

It might be hard to visualize what's going on, so here's a great video that shows how this can happen. It is about hip dysplasia in humans, but the anatomy is the same and the manual diagnostic techniques (Barlow and Ortolani tests) they demonstrate are used for dogs as well. The last 20 minutes or so are about examination of the human infant so you might want to skip that, and for some reason it's a 30 minute video that repeats, so it's not really an hour long.

Continued from above :
s 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'.