via Alaskan Malamute Email List -- Reprinted Verbatim
Author Unknown
(if you know the original source of this article, please tell us!)
Canine
Hip Dysplasia (CHD) is a complicated and often misunderstood disease. The
purpose of this article is to provide a basic understanding of Canine Hip
Dysplasia (CHD), particularly concentrating on its causes. Hopefully, this
information will be helpful in reducing the incidence of this disease.
The
clinical signs listed above are not diagnostic, as they may also be caused by
other conditions. The only way to correctly diagnose CHD is to have a
radiographic (X-ray) examination performed by your veterinarian. The classic way
of determining if a dog has CHD is to have the animal radiographed with the hips
extended outward. In other words, the dog lying on its back with its legs
extended straight back. This position is required for the Orthopedic Foundation
for Animals (OFA) to correctly evaluate the dog's hips. This is often an
uncomfortable position for the dog and sometimes an anesthetic or tranquilizer
is required for the animal to remain in this position long enough for the
radiograph to be taken. Some veterinarians believe that placing the dog under
anesthesia gives a better evaluation of the hip, as the muscles around the hip
joint are relaxed, while other veterinarians do not believe that the anesthetic
enhances the evaluation process. OFA will evaluate hips regardless of whether an
anesthetic was used or not. OFA is a non-profit organization that consists of
several veterinarians specially trained to evaluate the canine hip for CHD. The
OFA is the oldest and best known registry in the
PennHip
is a new organization for evaluating dogs for CHD. Their technique requires that
the dog be radiographically examined with the hips flexed (frog like position).
They also require that the animal must be anesthetized during the procedure. One
of the advantages of PennHip evaluation over OFA is that animals as young as 16
weeks can be evaluated. Currently, there is no prevailing evidence as to which
system is better. There are only a few veterinarians that advocate the PennHip
system, but it does appear to be gaining in popularity.
As
with people, dogs appear to differ in their ability to adapt to a disease. Some
dogs may have severe radiographic evidence of the disease and show little in the
way of clinical signs, while others may only have mild radiographic changes yet
show severe clinical disease. This may be due to differences in the ability of
individual dogs to adapt to the presence of chronic pain. If a dog develops CHD
it is not necessarily a death sentence as most cases, with the exception of the
severest forms, symptoms can be relieved by the use of pain medication. However,
even in its mildest forms this disease may limit the canine athlete from
attaining his full potential.
Both
heredity and environmental factors are important in the development of CHD. CHD
has an estimated inheritability that ranges from 0.2 to 0.6, with 0.0 being
non-inherited condition and 1.0 meaning that a condition is completely under
genetic control. Thus, demonstrating that CHD is a condition where both the
environment and the genetics of the dog play a role in the development of this
disease.
The
interaction between the dog's genetic makeup and environment determine whether
an individual dog will develop CHD. The genetics of the dog, to a large part,
determine if a given dog has the potential to allow the environmental factors to
act in such a way that CHD is produced. However, even dogs that are not
genetically predisposed to develop CHD can contract the disease if they are
pushed too hard when young by hyper-nutrition and excessive exercise.
During
puppyhood, diets that are low in protein combined with low activity levels
markedly reduced the severity of CHD in animals that were genetically
predisposed to developing this condition. However, even dogs that are not at a
genetic risk of developing CHD, if exercised too strongly early in life and/or
are fed diets that are too high in calories and protein can develop CHD, since
hyper-nutrition and excessive exercise may interfere with proper joint growth
and development. Thus, it is best to prevent a puppy from jumping or undergoing
sustained exercise until at least a year old. Also, the premium dog foods that
are so often recommended may also contribute to CHD development by increasing
the growth rate. A protein percentage of 22% (dry food) is generally all that is
required for normal growth. However, we all want our dogs to reach their full
potential, so premium dog foods are often fed. Here in lies the problem -
consider this information as food for thought (sorry to say).
In
addition to the environmental influences that confound our understanding of CHD,
the genetics of this condition are very complicated and not completely
understood. CHD is inherited as a polygenetic trait. In other words, many genes
are involved. This makes sense when we consider that that the hip joint is
composed not only of bone but also of muscles, tendons, ligaments, and a joint
capsule which together hold the bones in the proper position for a normally
functioning hip. Coordinating all of these parts into a normal functioning joint
requires many different genes. But it is even more complicated, if we consider
that this joint during the first year of life is continuing to change and adjust
to the tremendous growth of the dog. If the parts of the joint grow at different
rates or are out of synchrony with each other, then this will lead to a joint
that is loose which predisposes the dog to develop CHD. Additionally, other
seemingly unrelated factors such as rear leg angulation could also exacerbate or
alleviate CHD. Dogs that have straight rear legs have less shock absorption,
while well angulated dogs would not transmit as much of the movement stress to
the hip joint, as more of the trauma is absorbed by the hock and knee. When all
other factors are equal, the dog with well angulated rear legs is less likely to
develop CHD than a dog with straight rear legs. Thus, it is easy to see that the
genetic control of CHD is complicated and difficult to understand.
Selective
breeding is the only way we can reduced the incidence of CHD. However, knowing
which animals to breed is not a simple question. Both environmental factors and
genetics determine whether an individual dog will develop CHD. Genetics alone is
not the only cause of CHD. Therefore we will never be able to completely
eliminate CHD from the breed by selective breeding. However, we can
realistically reduce the incidence of CHD through appropriately selecting the
correct dogs to breed. Obviously a dysplastic dog should not be bred even if
there is reason to think that environmental factors may have contributed to the
animal developing CHD, such as trauma to the rear end when the dog was young. In
such an animal, it is impossible to determine the exact role genetics played in
CHD development, and it is far too easy to make excuses for breeding a
dysplastic animal once one starts down this road. Thus, only breed animals that
do not have CHD and all should be fine - right? Unfortunately this is not the
case. The polygenetic control of the hip joint structure greatly complicates the
situation. It is entirely possible for a dog with an OFA rating of excellent to
produce puppies that develop CHD. How can this occur?
Without
going too deeply into the genetics, some basic genetic background is needed to
explain how an OFA certified animal can produce off-spring that develop CHD. The
following is a gross over simplification of the genetics of the CHD; but does
provide a framework for understanding a problem with multiple gene control over
a single trait. Dogs have two copies of each gene that controls CHD (the total
number of genes that control or contribute to the development of CHD is unknown;
but it is believed that many are involved). They get one gene from their mother
and the other from their father. Some of the "good genes" can mask the
presence of a "bad gene". In other words some of the "good
genes" are dominant over the recessive "bad genes". Thus, the
physical expression of the "good genes" will be result in good hips,
even though the animal is carrying a number of hidden (recessive) "bad
genes". When the sperm or egg is formed the two copies of each gene are
separated so that sperm and the egg end up with only one copy of each gene. In a
case where an animal had a copy of one good gene and one copy of the bad gene,
50% of the eggs or sperm would get the "good gene" and 50% will get
the "bad gene". Now recall that many genes are involved in the
development of CHD, so this separation occurs for each of the genes that control
hip joint development. Thus, a very few of the eggs and sperm will get all of
the "good genes" and a very few will get all of the "bad
genes" but most will get a mixture of both "good" and
"bad" genes that control CHD. The outcome of a particular mating will
be determined by the match up between the genetic make -up of the parents. If
the bad recessive genes line up incorrectly then more of the puppies could have
hip dysplasia. However, if the good dominate genes line up well then many of the
pups will have good hips, but may still carry the hidden bad genes. Complicating
the situation even further is that some genes may be good when combined with one
set of genes and bad when combined with different set of genes. It is also
possible for some genes to have a greater or lesser influence on CHD than
others, adding to the complexity of the problem. Thus, one can see that the
genetics of CHD is very complicated.
Some
puppies will have the same genetic combination as the parents. Some may have a
more desirable genetic make-up than either parent; and others may have a less
desirable genotype. Predictions of a specific CHD outcome from a particular
mating is currently very difficult if not impossible.
However,
it is OFA's opinion that a dog with fair hips and less than 25% of its
littermates exhibiting dysplasia is a better breeding prospect than a dog with
excellent hips having more than 25% of its brothers and sisters affected by hip
dysplasia. In other words, less of the bad genes are likely to be present where
a smaller percentage of the littermates have CHD. Ideally, we would want to
achieve a homogeneous gene pool composition where the dogs carry two copies of
the good genes for each gene that controls CHD. In other words eliminate the bad
hidden (recessive) genes from the pool. This could be achieved by careful line
breeding, making good hips part of that line's type. However, to accomplish this
it is important to look beyond the individual animals of the proposed mating and
consider the OFA status of the littermates as well as other relatives on both
sides of the mating before proceeding. It is also important to point out that a
good dog is more than just good hips. Care must be taken that the breeding of
dogs is not based only on one trait. Otherwise we may end up with dogs that have
excellent hips but have poor temperaments, bad coats, no herding instincts, or
other genetically related health problems. The whole animal should be considered
with hips status being important but not the only consideration.
From
this article, it is easy to see why CHD is such a difficult problem to control.
However, through careful breeding selections of OFA certified animals that have
a low incidence of CHD in their littermates and in their pedigrees, we should be
able to reduce, although not eliminate, CHD as a problem in certain breeds.