|Normal||Excellent||A-1||0-4 (no > 3/hip)||Normal|
|Normal||Good||A-2||5-10 (no > 6/hip)||Normal|
|Grade I||Borderline||B-2||19-25||Fast Normal|
|Grade II||Mild Dysplasia||C||26-35||Noch Zugelassen|
|Grade III||Moderate Dysplasia||D||36-50||Mittlere|
|Grade IV||Severe Dysplasia||E||51-106||Schwere|
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.
Additional resources on the web:
Orthopedic Foundation for
Information about hip dysplasia, as well as details on OFA testing and access to the OFA registry.
University of Pennsylvania Hip
Provides a description of the disease, answers to frequently asked questions, and detailed information on PennHIP testing.