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Canine
Hip Dysplasia
Hip dysplasia,
characterized by an abnormal formation of the hip joint, occurs in many
mammals. Both dogs and humans may fall victim to this disease, although
it is far more prevalent in dogs.
Who is affected?
Hip dysplasia
may affect any dog, whether it is male or female, small, medium or large
sized. It is estimated however that more than 50 percent of some large
breeds are affected, making it far more common in these animals than
in smaller dogs. The disease seems to strike certain breeds particularly
hard, including the Bernese Mountain Dog, Bloodhound, Boxer, Brittany
Spaniel, Chesapeake Bay Retriever, English Setter, English Springer
Spaniel, Golden Retriever, Gordon Setter, German Shepherd Dog, Labrador
Retriever, Old English Sheep Dog, Standard Poodle, Rottweiler, St. Bernard,
Welsh Springer Spaniel, and the Welsh Corgi. Large breeds with a low
incidence of hip dysplasia include the Borzoi, Doberman Pinscher, Great
Dane, Greyhound, Irish Wolfhound, and Siberian Husky.
What are the signs of hip dysplasia?
The earliest
symptoms of hip dysplasia often begin to manifest themselves between
the ages of four months and one year. This is not an “all or nothing”
type disease, and the spectrum of symptoms ranges from practically nonexistent
to severe crippling. Young dogs may have a wobbling, weaving, or waddling
and unsteady gait. An effort is often made to draw the hind legs forward,
placing more weight on the forelimbs and ultimately leading to an overdevelopment
of the forequarters and an underdevelopment of the hindquarters. When
running, afflicted dogs often move their hind legs together in a maneuver
commonly termed “bunny hopping.”
Dogs may
exhibit an aversion to strenuous exercise, or may be sore after such
activity. Stiffness is often at its worst in the morning, but dogs developing
hip dysplasia will consistently have difficulty navigating stairs and
rising from sitting or prone positions. A distinct clicking sound may
occasionally be heard when the dog is walking or running.
As is
the case in humans, dogs have a varying tolerance for pain, and some
animals may experience a change in temperament due to discomfort.
How is the disease diagnosed?
Though
physical examinations may be helpful, radiography and x-rays are the
only means of reaching a definitive diagnosis of CHD.
The goal
of a physical examination is to determine hip joint laxity, or the degree
of looseness in the joint. Looser hip joints are more likely to become
dysplastic than are stable ones. Palpation of the hip joint and surrounding
areas can provide an estimate of the laxity of the hip joint, but the
measurements are subjective and not as definitive as x-rays.
The traditional
radiographic method is regulated by the Orthopedic Foundation for Animals
(OFA). This organization upholds a standard based upon breed, age, and
conformation information. Dogs are not eligible to be registered with
the OFA until after 2 years of age. At this point they are examined
according to OFA guidelines and graded on a 7-point scale from excellent
conformation to severe hip dysplasia. Dogs with hip grades of excellent,
good, or fair are eligible for OFA certification of dysplasia-free status.
Positioning for the OFA test requires that the dog be sedated or anesthetized
and positioned on his back with hind legs extended together nearly parallel
to the tabletop.
Researchers
at Cornell University recently have developed a new test for canine
hip dysplasia. Termed the dorsolateral subluxation (DLS) test, the procedure
improves upon the OFA protocol by being more accurate at a younger age
than the traditional test. While the OFA test is not accurate before
2 years of age, studies have shown the DLS test to be accurate as early
as 8 months of age. The main difference between this new test and the
old OFA method is the way in which the dog is positioned while being
x-rayed. The OFA test places the hind limbs in a position that is not
natural and may hide symptoms of hip dysplasia. The DLS test relies
on a position much more similar to positioning normally found in a standing
dog.
Before
the DLS x-ray examination may take place, a dog must be anesthetized
or deeply sedated. It is then placed on its stomach on a foam rubber
pad. There is a hole cut in the pad for the dog’s hind legs. The
stifles (corresponding to a human knee joint) make contact with the
x-ray table, and the dog’s femurs are nearly perpendicular to
the table. Arranging the dog in a position that mimics its natural posture
allows the x-ray to show with a high level of accuracy what the position
of the hip joints is.
In a normal hip joint, the head of the femur fits snugly into the joint
socket, or acetabulum. In the dysplastic joint, the femoral head conforms
poorly to the acetabulum. More space is evident between the bones. Displacement
of the femoral head is the hallmark of the disease. Joints are evaluated
using the DLS score. This measurement, expressed as a percent, is calculated
from the radiograph and represents the percent of the femoral head covered
by the acetabular rim. The greater the coverage, the higher the DLS
score, and the healthier the hip joint. The DLS test, as with other
diagnostic procedures, is carried out by your veterinarian.
What is the nature of the disease in dogs?
Hip dysplasia
refers to the development of a poor fit between the femoral head and
the acetabulum that allows loose movement and altered pressure. These
changes result in joint damage, inflammation, and pain. The volume of
synovial fluid in the joint increases, and the round ligament that binds
the femoral head to the acetabulum becomes enlarged. The normally smooth
articular cartilage covering the end of the opposing femoral head and
acetabulum is abraded and weakened, and the joint capsule becomes inflamed
and thickened. Muscles in the region of the hip joint diminish in bulk
and may be affected in other ways as well. As the disease progresses,
the bones become damaged and spurs known as osteophytes develop at the
bone-cartilage interface. The whole joint is structurally weakened and
painful.
Hip dysplasia
was once thought to be an abnormality involving only the tissues in
the region of the hip joint. Evidence indicated however that the shoulder
and knee joints and the joints between vertebrae often show similar
changes. This suggests that hip dysplasia may be merely the most conspicuous
and serious manifestation of a more generalized abnormality affecting
all joints.
The disease is not readily observable in very young dogs. Joints of
newborn pups – even those destined to develop hip dysplasia –
seem to be structurally and functionally sound. Further, they do not
show the characteristic abnormalities revealed by x-ray photographs
in older dogs. There are no obvious anatomical abnormalities in the
shape of the bones of the joints of growing dogs that will eventually
develop hip dysplasia. For example, the disease is unrelated either
to the degree of inclination of the femoral head with reference to the
shaft of the femur or to the size of or the degree of rotation of the
femoral head about the femur.
Why is it painful?
The perceived
pain of hip dysplasia during its early stages is due to stretching of
nerve endings and inflammation in the joint capsule and ligament. In
its advanced stages the disease progresses to the painful condition
of osteoarthritis, or degenerative joint disease.
What
can genetics teach us about hip dysplasia?
It is
clear that hip dysplasia is an inherited, polygenic disorder, meaning
that more than one gene influences the development and transmission
of the disease. It is not yet clear however which genes are responsible,
and this is the subject of intense, ongoing research. Both genes and
environment have significant effects on the expression of hip dysplasia.
The disease has a heritability of between 0.25 and 0.48. This means
that 25 to 48 percent of the variability in hip dysplasia development
is due to additive genetic factors. We may interpret this to mean that
both genetic and environmental influences impact the progression of
the disease.
The knowledge that hip dysplasia has a genetic basis allows us to make
decisions about breeding. Dogs that are known to be dysplastic should
not be bred. The mating of two affected dogs produces an incidence of
75 percent in offspring – in other words, 3 out of 4 puppies produced
by two dysplastic dogs will themselves develop hip dysplasia. In contrast,
on average only 25 percent of offspring of a mating between two healthy
dogs will develop hip dysplasia. There is clearly an advantage to a
mating between normal dogs. By limiting the breeding population to only
those dogs with healthy hips, we can lower the number of new cases of
hip dysplasia that will appear in the coming generations.
Can the disease be prevented?
The time
of appearance and the rate of progression of hip dysplasia are influenced
by the growth rate of individual dogs. Studies at the Baker Institute
and elsewhere have shown that slowing growth during the early months
of life can lessen the severity of hip dysplasia and even prevent it.
One study followed two groups of susceptible pups from the time they
were eight weeks old until their death. One group of pups was fed nearly
25 percent less food than the second, which were permitted to eat all
they wanted of the same diet. Over the course of the 14 year study,
data was collected regarding general longevity and the development of
hip dysplasia. Not only did the dogs eating a restricted diet live significantly
longer than their well-fed counterparts, they developed hip dysplasia
at a much lower rate than did the second group. Further, for those dogs
on a restricted diet who did develop hip dysplasia, the risk of developing
osteoarthritis decreased by 57 percent. This study of course involved
a diet restriction that is difficult to enforce for many pet owners.
It would be desirable to use a less restrictive dietary regime that
would confer many of the same benefits this more severe diet did.
What are the treatment options?
Simple,
practical measures may be enough to give comfort to dysplastic animals.
Mild exercise such as walking, swimming, or slow running is beneficial,
but excessive activity such as jumping and prolonged running should
be avoided. Some analgesic and anti-inflammatory drugs can relieve the
pain. Such medications do not however halt or reverse the progression
of destructive changes in the joint. Injections and even oral administration
of carbohydrate polysulfates have shown promise in increasing clinical
use as a treatment for dysplastic dogs. These drugs can prevent pain
and aid in normal remodeling to improve the contour of the hip joint.
Although carbohydrate polysulfates do not cure hip dysplasia, many dogs
receive at least some benefit from this treatment. Similarly, nutritional
supplements have some proven benefits.
Surgical
procedures have been devised to treat dogs with chronic pain and lameness.
Operations that can be performed in dogs with severe hip dysplasia include
procedures that rearrange the bones of the pelvis or the femoral head
to improve joint function. Removing or cutting the pectineus muscle
near the pelvis often provides relief from pain. Creation of a false
joint by removing the femoral head can relieve pain and restore mobility
for a dog in some cases. Total replacement of the acetabulum and the
femoral head by prosthesis has succeeded in a number of active dogs.
What research is currently being done?
Researchers
have overcome one major hurdle by developing a test for hip dysplasia
that is more accurate at younger ages than traditional procedures. Taking
advantage of the wealth of information available from early detection,
the next step is to gather and study DNA sequences in an effort to locate
specific sequences that are markers for either normal or abnormal hip
joint development. This challenging task is made more difficult by the
fact that there are almost certainly a number of different genes that
trigger hip dysplasia, but the research team is confident that, by utilizing
ever-increasing molecular technologies, they will soon crack the genetic
code of hip dysplasia. Dr. Rory Todhunter, Professor of Surgery at the
Cornell University College of Veterinary Medicine, and his team of researchers
have successfully used an experimental breeding program of Labradors
(high risk for hip dysplasia) and Greyhounds (low risk) to identify
chromosomal regions harboring genes that confer susceptibility to and
protection against hip dysplasia.
Further,
though the DLS test is significant improvement upon traditional diagnostic
measures, there is a continuing search for the metabolic causes of hip
dysplasia that work in conjunction with genetics. It is noteworthy that
despite its genetic basis, the development of hip dysplasia is also
influenced by environments. Topics such as the possible metabolic abnormalities
are areas that Institute researchers continue to explore.
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