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Table of ContentsFlat-Coated Retriever Health Manual

Canine Hip Dysplasia

Canine hip dysplasia (CHD) is a mostly inherited disease involving abnormal development of the femoral head and acetabulum. All puppies are born with normal hips. The hips of dysplastic dogs will subsequently undergo progressive structural changes. Either the socket (acetabulum) will become too shallow or the ligaments and/or muscles do not exert enough control to keep the femoral head from slipping away from the socket. Recently, some authors have suggested that CHD is part of a systemic disease; that is, other joints in the body are affected, but not as severely as the hips. These may include elbows, shoulders and vertebral joints. The severity of radiographic changes in a particular dog can range from normal to mildly affected to severely affected. There is no correlation between radiographic findings and clinical signs. A dog whose x-rays show severe disease may not show any outward signs and a mildly affected dog may have difficulty even walking. Regardless of the symptoms, they are both dysplastic and they both carry the genes necessary to pass on the disease. The 1997 FCRSA Health Survey indicates that CHD affected 9.4% of Flat-Coated Retrievers reported.

Figure 1

Reproduced from Hill's Atlas of Veterinary Clinical Anatomy

The hip is a ball-and-socket joint. An excellent hip joint involves a femoral head (ball) that fits closely and tightly against the acetabulum (socket). In dogs there are four degrees of rotation that the hip can move through (humans have three). Full range of motion in the canine hip joint includes the ability of the femoral head to move outward and away from the acetabulum to a certain degree. Too much freedom of this movement indicates laxity in the joint which can lead to improper forces being applied to the joint. Changes in the joint structure then occur. The changes initially occur on a biochemical level. To better understand how this happens requires an understanding of the anatomy and physiology of the joint.

Between the femoral head and the acetabulum is a structure called the articular cartilage. It serves to cushion the force of the two bony structures against each other. Surrounding the entire joint (femoral head, acetabulum and articular cartilage) is the joint capsule. Synovial (joint) fluid is produced within the capsule and serves to lubricate the joint and transport nutrients to the joint from the bloodstream. The synovial fluid contains hyaluronic acid which is the actual lubricating substance in the capsule. When any part of the joint is injured, additional chemicals are released into the capsule which destroy the hyaluronic acid. Without the lubricant, the articular cartilage becomes damaged and its protective cushion is no longer functional. The femoral head and acetabulum then become injured and their bony structure changes. The rim of the acetabulum becomes misshapen and the femoral head becomes eroded and flattens out. The abnormal anatomy produces more trauma and a vicious cycle is perpetuated. Some believe that a hip joint with too much laxity can allow injury to the joint capsule producing the consequences as described.

There are a number of misconceptions regarding CHD that can be corrected by knowing the following facts provided by the Orthopedic Foundation For Animals (OFA):

  1. There are no environmental factors that cause CHD (however, early trauma such as pulling on the hind limbs has been shown to produce hip joint deformity in other species).
  2. There is no valid scientific evidence that megadoses of Vitamin C, or any other supplement, can reduce the effects of or prevent CHD.
  3. High caloric intake with resultant rapid growth and weight gain may worsen CHD, but will not cause it.
  4. Exercise, running, jumping, or a slick floor environment will not cause CHD.
  5. Prior injuries to the hip are taken into account when OFA radiographs are evaluated if they have produced radiographically visible changes (e.g. healed fractures). There is, however, no way to indicate that sprains or other soft tissue damage has occurred.


It is important to remember that a phenotypically normal-appearing dog with a normal gait can STILL be dysplastic. Do not rely on clinical signs to determine the presence of CHD. A diagnosis of CHD is based on radiographs.


Waddling/Swaying gait
"Bunny Hop" (both hind legs move together when the dog is running)
Acute episodes of lameness after exercise
Morning stiffness
Reluctance to move
Change in temperament
Obvious pain (some dogs are more stoic than others)
Overdevelopment of the fore-limb and shoulder musculature
Underdevelopment of the rear-limb musculature

The dog should be observed while at rest, then when walking and finally, while running. If possible, repeat this observation one day after the dog has engaged in vigorous exercise. Gait patterns that may indicate CHD include a shortened stride, bunny hopping, a left to right shift of the pelvis, or an elliptical swing to the leg and hip.

A veterinarian should examine hip joint range of motion. Forced extension of the hip joint in a dog with CHD may elicit a pain response. A dog with CHD may also offer little resistance, and will sit when downward pressure is applied to the rear limbs.

Because signs associated with CHD can mimic some neurological problems, a neurological exam to rule out the presence of spinal disease should be done. Spinal radiographs, myelography and other imaging techniques (CT scan) may be necessary.

There are 3 hip certification registries available in the United States. They differ in the radiographic techniques they use, what they look for on the radiographs and the certification process itself. The following is a summary of each of these registries:

OFA is probably the most familiar registry. A dog must be at least 24 months old at the time the x-rays are taken (preliminary radiographs can be done earlier, but the dog cannot be certified until two years of age even if the hips are deemed free of dysplasia). Sedation or general anesthesia is not a requirement, but is usually necessary for proper positioning. The radiographs are read by three separate board-certified radiologists and a consensus is determined among them as to the rating on the hips. Ratings include excellent, good, fair, borderline, mild dysplasia, moderate dysplasia and severe dysplasia. Certificates are issued only to those dogs that are considered to be dysplastic-free with ratings of excellent, good or fair (a confidential consensus report is issued on dogs found to be dysplastic).

An OFA number is assigned to the dog and the OFA reports this number to the AKC and to the appropriate breed club. The OFA will only forward certification numbers on dogs that are permanently identifiable by either a tattoo or microchip. OFA is a closed type of registry, that is the AKC and breed clubs are notified of only non-dysplastic dogs and therefore, owners who suspect their dogs are dysplastic do not always forward their radiographs to the OFA. This limits the data-collection process.

This is an open registry that evaluates for hip dysplasia and makes available all data obtained, including that on dysplastic dogs. The dog must be at least 12 months old to be certified. Two independent radiologists grade the hips as being EN (excellent normal), GN (good normal), AN (average normal), borderline, mild, moderate or severe.

This registry looks not just at bony conformation, but at the amount of laxity present in the joint. This amount of laxity is measured and a distraction index (DI) number is assigned based on a comparison of data collected on dogs of the same breed. A dog with a DI of less than 0.3 is considered to be at minimal risk of developing CHD or degenerative joint disease. A DI of more than 0.7 is at high risk. The dog must be anesthetized while a series of three views are taken. The first is a traditional extended view (like OFA requires), the second is a compression view and the third is a distraction view taken with the aid of a distraction device. The veterinarian taking these radiographs must be PennHIP-certified. All radiographs must be submitted without the veterinarian pre-screening them so that the managing company, Synbiotics, can collect a database of non-dysplastic and dysplastic animals for each breed.

A PennHIP report is sent to both the owner of the dog and the veterinarian. Dogs must be at least 16 weeks old.


Medical Management of CHD
CHD is a genetic disease. A dog is either born with it or not. Environmental factors cannot cause CHD. However, body weight and exercise can either hasten or delay the onset of clinical signs. An overweight dog will have additional forces on its hips. A recent experiment with Labrador Retrievers involved free-feeding one group while giving the other group of dogs 25% less food. The latter group had a lower incidence of CHD at two years of age. It is currently recommended that during the first nine months of life (when the greatest amount of bony changes are occurring) the dog should be kept slender. Better slightly underweight than overweight. Exercise must be individually tailored for each dog with CHD. Too much exercise, especially jumping and running, can stress the hips and promote further degeneration. Too little can lead to further atrophy of musculature. Each dog must be continually evaluated to determine the correct amount and type of exercise. Changes occur with time as arthritis tends to be progressive.

Medications: Always consult your veterinarian to determine the correct type and dosage of medication before treating your dog.

  1. Corticosteroids: These are useful only during acute stages of the disease as undesirable side effects occur with long-term use. The desired action of these drugs is anti-inflammation.
  2. Non-Steroidal Anti-inflammatory Drugs (NSAIDS).
    1. Aspirin: May cause stomach disorders (ulcers); interferes with blood clotting.
    2. Phenylbutazone: May cause bone marrow dysfunction, liver and kidney disease.
    3. Carprofen
  3. Glycosaminoglycans (GAGS). These are considered to be nutraceuticals rather than pharmaceuticals. They are believed to promote the synthesis of cartilage matrix components and slow the destruction of them. They also decrease inflammation, relieve pain and restore hyaluronic acid in the synovial fluid. The exact mechanism of these actions is not well understood. Of the three, only Adequan is FDA-FDA-approved for dogs at present and is only available in an injectable form. The other three are oral preparations.
    1. Polysulfated Glycosaminoglycan. © Adequan. Luitpold Pharmaceuticals.
    2. Perna Canaliculus Mussor. © Glyco-Flex. Vetri-Science Laboratories.
    3. Glucosamine, Chondroitin, Manganese Ascorbate. © Cosequin. Nutramax Laboratories.

Surgical Management of CHD.
There are several surgical techniques available to ameliorate the signs of CHD. Your veterinarian can assist you in determining which one would be most helpful to your dog depending on the dog's age, weight, expected activity level and extent of disease present in the joint. Several are listed below.

  1. Pectineal Myotomy: The pectineous muscle is cut. Early-stage procedure.
  2. Pectineal Myectomy: A portion of the pectineous muscle is cut out. Early-stage procedure.
  3. Three-Plane Intertrochanteric Osteotomy: Portions of the femoral head are cut in order to change the angle at which it fits into the acetabulum. Early-stage procedure.
  4. Triple Pelvic Osteotomy: Bones of the pelvis are cut in three different places, then realigned to create a more favorable angle between the femoral head and acetabulum. Early-stage procedure.
  5. Femoral Head and Neck Ostectomy: The femoral head and a portion of the femoral neck are removed. This is an affordable alternative to total hip replacement. Advanced-stage procedure.
  6. BOP Shelf Arthroplasty: The acetabulum is surgically remodeled to better fit the femoral head. Advanced-stage procedure.
  7. Total Hip Arthroplasty (Total Hip Replacement): This is the surgery of choice for advanced stage disease if affordable.


Research continues on this still little-understood disease. At present, it is considered to be a polygenic disorder with the possibility of "masked" or hidden genes that may not express themselves in every generation. This makes the elimination of this disease even more difficult because two normal dogs can still produce dyplastic progeny. In addition, a mixture of dominant, recessive and co-dominant genes may be involved. Research is being conducted to find a genetic marker for the disease so that in the future, a blood test can diagnose carriers. At present however, breeding decisions need to be made on the following basis as suggested by the OFA:

  1. Breed normals to normals.
  2. Breed normals with normal ancestry.
  3. Breed normals from litters with a low incidence of CHD.
  4. Select a sire that produces a low incidence of CHD.

Dogs diagnosed with hip dysplasia should be neutered and removed from the breeding pool. Know the hip status of as many dogs in a pedigree and their siblings and progeny as possible. Breeders should encourage all puppy buyers to screen for hip dysplasia at an appropriate age so that data on complete litters is available to use in the decision-making process.


Bowling, A. T. Congenital and inherited disorders. In: Siegal, M., ed. UC Davis book of dogs: a complete medical reference for dogs and puppies. New York: Harper Collins, 1995: 171.

Cargill, J., Thorpe-Vargas, S. Canine hip dysplasia part I: the normal canine hip. Dog World. 1995; Vol. No. 5.

Cargill, J, Thorpe-Vargas, S. Canine hip dysplasia part II: genetic, nutritional and environmental factors. Dog World. 1995; Vol. No. 6.

Cargill, J, Thorpe-Vargas, S. Canine hip dysplasia part III: methods for diagnosing the abnormal hip. Dog World. 1995;80:16-21.

Cargill, J, Thorpe-Vargas, S. Canine hip dysplasia part IV: the role of orthopedic registries in fighting canine hip dysplasia. Dog World. 1995;80:20-23.

Cargill, J, Thorpe-Vargas, S. Canine hip dysplasia part V: predicting the abnormal hip. Dog World. 1995; 80: 26-31.

Cargill, J, Thorpe-Vargas, S. Canine hip dysplasia part VI: medical management of canine hip dysplasia. Dog World. 1995;80: 24-27.

Cargill, J, Thorpe-Vargas, S. Canine hip dysplasia part VII: surgical management of canine hip dysplasia. Dog World. 1995;80: 20-25.

Cargill, J, Thorpe-Vargas, S. Canine hip dysplasia part VIII: surgical management of canine hip dysplasia part II. Dog World. 1995;80:22-25.

Corley E. A., Keller G. G. Hip dysplasia: a progress report and update. Columbia, MO: OFA, 1993:1-2.

Cornell University, James A. Baker Institute for Animal Health. Meeting on canine hip dysplasia." Press release. Ithaca, NY: Cornell University. 1996.

Ettinger, S, Feldman, E. Textbook of veterinary internal medicine: disease of the dog and cat, 4th ed. Philadelphia: W.B. Saunders Co.; 2047.

Graham, C. Methods of evaluating hips. Dogs in Canada. 1997,June:22-24. Hill's Pet Products. Hill's Atlas of Veterinary Clinical Anatomy. USA: Veterinary Medicine Publishing Co., Inc., 1989: 48.

Kealy, R. Effects of limited food consumption on the incidence of hip dysplasia in growing dogs. Paper presentation. AKC/CHF Canine Health Conference. St. Louis, MO. 1997, November.

Leighton, R.L. The skeleton and disorders. In: Siegal, M., ed. UC Davis book of dogs: a complete medical reference for dogs and puppies. New York: Harper Collins, 1995; 263.

Luitpold Pharmaceuticals, Inc. Animal Health Division. Adequan. Brochure. Shirley, NY. 1997,April.

Nutramax Laboratories, Inc. Cosamin DS. Brochure. Baltimore, MD. 1997, May.

Slater, M., Tomochek, J. A general health survey on Flat-Coated Retrievers. College Station, TX: Texas A&M University, 1997, April.

Veterinary Practice Publishing Co. Hip dysplasia in dogs. Client information series. Santa Barbara, CA.

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Last Revised: January 1, 1999
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