Normal Hips, Early Dysplasia,
Moderate Dysplasia, Severe Dysplasia
Hip dysplasia is a common and potentially debilitating joint disease in dogs. Although occurring in many canine lines, hip dysplasia most often affects large dog breeds. The Golden and Labrador Retrievers, German Shepherd Dogs, Rottweilers, and Chow Chows are particularly susceptible to hip dysplasia. Fortunately, there are a number of treatment options available for dogs afflicted with this painful and degenerative disease. Normal, healthy hip joint with a deep acetabular cup and healthy cartilage in the cup and on the ball of the femur.
Note how the head of the femur sits tightly within the acetabulum. Early/Mild dysplastic hip with no degenerative changes. Note how joint laxity allows the head of the femur to subluxate. The acetabular cup may be abnormally shallow and the joint may exhibit laxity. This stage of hip dysplasia can often be treated with corrective surgery (see TPO in this brochure) before the disease progresses requiring more invasive and costly surgery. Moderate/ Severe hip dysplasia is recognized by the cartilage fibrillation and erosion on the ball of the femur and the acetabular cup. There is also a buildup of osteophytes (bone spurs and calcium deposits) around the rim of the acetabular cup.
This is a very painful joint that requires corrective surgery to alleviate the pain and return the joint to normal function. If corrective action is not taken then the dysplasia will inevitably progress to severe. Severe dysplasia is common in older dogs whose hip dysplasia has gone untreated for an extended period of time. This hip joint has severe arthritis. Note the flattening of the head of the femur and added bone fillings around the neck of the femur and within the acetabulum This dog's joint requires a total hip replacement to restore his quality of life and provide him with a pain-free, normal functional hip joint.
What is hip dysplasia?
Hip dysplasia is a developmental disorder affecting the coxofemoral (hip) joints in dogs. The problems associated with hip dysplasia stem from an imbalance in the muscle mass and mechanical forces which are centered on the hip joint. This imbalance is associated with excessive laxity (looseness) which is usually the result of a shallow acetabulum (cup).
When the hip joints exhibit laxity (looseness), the ball of the femur rides on the edge of the socket rather than gliding smoothly in the socket. This results in pain and eventually to the formation of abnormal calcium deposits, bone spurs and/or arthritis. Eventually, some hip joints will suffer either a partial or complete luxation.
Continued use of the affected joint causes abnormal wear on the joint's cartilage surfaces leading to further damage and a self-perpetuating degenerative process ensues.
Abnormal bony development of the hip joint often results, and inflammation and irritation (arthritis) ultimately cause mild to severe lameness. The joint capsule becomes inflamed and a subsequent increase in synovial fluid in the joint exacerbates the laxity.
These physiological changes should be dealt with early (between 4 and 8 months) to attempt to reduce the progress toward degenerative joint disease. The hallmark sign of degenerative joint disease is articular cartilage damage.
This results in the exposure of subchondral bone and pain nerve fibers resulting in significant joint pain. Once degenerative joint disease is present, there a fewer treatment options available.
Breeds Commonly Affected by Canine Hip Dysplasia
The Genetics of Hip Dysplasia
The heritability of hip dysplasia has been firmly established. Several genes have been found to contribute to the ultimate size, shape, strength and growth potential of the hip joint. Furthermore, hip dysplasia is a genetically additive disease; the severity of the affliction is largely the result of a number of disease-related genes present in a particular animal.
The multitude of genetic and environmental factors that influence the transmission and development of hip dysplasia make it difficult to predict how the disease will be expressed. It is safe to say that breeding dogs between phenotypically normal dogs will generally result in more normal puppies than will breeding a dysplastic and normal dog or two dysplastic dogs to each other. However, studies have shown that even when both parents are phenotypically normal they can still produce offspring that are phenotypically dysplastic . In spite of careful breeding efforts and the use of classifications from the Orthopedic Foundation for Animals (OFA), such as breeding animals whose parents and grandparents were normal, the progress toward eradication of this disease has been frustratingly slow.
The OFA Hip Registry
The Orthopedic Foundation for Animal's Hip Registry is designed to provide a standardized criterion for evaluation of CHD and develop a multi-breed database. This database is used to develop selective breeding programs that reduce the prevalence of CHD. The OFA requires symmetrical radiographs of the pelvis. These radiographs are evaluated by three board certified radiologists and classified as excellent, good, fair, borderline, mild, moderate or severe. Excellent or good classifications on individuals older than 24 months receive a breed registry number. A preliminary evaluation may be performed as early as 4-5 months with 90% accuracy.
Environmental Factors and Hip Dysplasia
Environmental factors do not cause hip dysplasia but can significantly affect whether or not the condition will eventually manifest itself and to what degree. Environmental influences help explain the fact that only animals with a hip dysplasia genotype can develop the condition while not all animals with the genotype will exhibit the disease.
Nutrition in the young dog is one of the most studied exogenous elements affecting the development of hip dysplasia and may have a profound influence on the development of the disease. One study noted that only 33% of dogs that were fed ad libitum developed normal hips, whereas 70% of the dogs that were fed one quarter of the same diet developed normal hips. Another study in German Shepherds showed that 63% of the dogs weighing more than the mean, developed dysplastic hips.
In contrast, 37% of the dogs that weighed less than the mean developed dysplastic hips . Puppies that are genotypically susceptible to canine hip dysplasia will exhibit an increased incidence and severity if placed on a high caloric diet. These studies strongly suggest that limiting caloric intake in young, growing dogs (especially the larger at risk breeds) is beneficial in preventing the development of canine hip dysplasia.
Clinical Signs of Hip Dysplasia
Dogs suffering from hip dysplasia are often reluctant to jump or rise from the rear legs, exhibit abnormal locomotion and may hesitate to climb and descend stairs. Young dogs in the age range of five to ten months may exhibit pain when the hips are extended. In addition, there may be evidence of decreased muscle mass and a reduced range of motion. Many of these young dogs have a torn round ligament and a significantly stretched joint capsule. Clinical signs often do not correlate well with radiographic changes in young dogs.
Hip dysplasia literally means an abnormality in the development of the hip joint. It is characterized by a shallow acetabulum (the "cup" of the hip joint) and changes in the shape of the femoral head (the "ball" of the hip joint). These changes may occur due to excessive laxity in the hip joint.
Hip dysplasia can exist with or without clinical signs. When dogs exhibit clinical signs of this problem they usually are lame on one or both rear limbs. Severe arthritis can develop as a result of the malformation of the hip joint and this results in pain as the disease progresses. Many young dogs exhibit pain during or shortly after the growth period, often before arthritic changes appear to be present. It is not unusual for this pain to appear to disappear for several years and then to return when arthritic changes become obvious.
Dogs with hip dysplasia appear to be born with normal hips and then to develop the disease later. This has led to a lot of speculation as to the contributing factors which may be involved with this disease. This is an inherited condition, but not all dogs with the genetic tendency will develop clinical signs and the degree of hip dysplasia which develops does not always seem to correlate well with expectations based on the parent's condition. Multiple genetic factors are involved and environmental factors also play a role in determining the degree of hip dysplasia. Dogs with no genetic predisposition do not develop hip dysplasia.
At present, the strongest link to contributing factors other than genetic predisposition appears to be to rapid growth and weight gain. In a recent study done in Labrador retrievers a significant reduction in the development of clinical hip dysplasia occurred in a group of puppies fed 25% less than a control group which was allowed to eat free choice. It is likely that the laxity in the hip joints is irritated by the rapid weight gain. If feeding practices are altered to reduce hip dysplasia in a litter of puppies, it is probably best to use a puppy food and feed smaller quantities than to switch to an adult dog food. The calcium/phosphorous to calorie ratios in adult dog food are such that the puppy will usually end up with higher than desired total calcium or phosphorous intake by eating an adult food. This occurs because more of these foods are necessary to meet the caloric needs of puppies, even when feeding to keep the puppy thin.
If clinical signs of hip dysplasia occur in young dogs, such as lameness, difficulty standing or walking after getting up, decreased activity or a bunny-hop gait, it is often possible to help them medically or surgically. X-ray confirmation of the presence of hip dysplasia prior to treatment is necessary. There are two techniques currently used to detect hip dysplasia, the standard view used in Orthopedic Foundation for Animals (OFA) testing and X-rays (radiographs) utilizing a device to exaggerate joint laxity developed by the University of Pennsylvania Hip Improvement Program (PennHIP). The PennHIP radiographs appear to be a better method for judging hip dysplasia early in puppies, with one study showing good predictability for hip dysplasia in puppies exhibiting joint laxity at four months of age, based on PennHIP radiographs.
Once a determination is made that hip dysplasia is present, a treatment plan is necessary. For dogs that exhibit clinical signs at less than a year of age, aggressive treatment may help alleviate later suffering. In the past a surgery known as a pectineal myotomy was advocated but more recent evidence suggests that it is an ineffective surgical procedure. However, administration of glycosaminoglycans (Adequan Rx) may help to decrease the severity of arthritis that develops later in life. Surgical reconstruction of the hip joint (triple pelvic osteotomy) is helpful if done during the growth stages. For puppies with clinical signs at a young age, this surgery should be strongly considered. It has a high success rate when done at the proper time.
Dogs that exhibit clinical signs after the growth phase require a different approach to treatment. It is necessary to determine if the disorder can be managed by medical treatment enough to keep the dog comfortable. If so, aspirin is probably the best choice for initial medical treatment. Aspirin/codeine combinations, phenylbutazone, glycosaminoglycosans and corticosteroids may be more beneficial or necessary for some dogs. It is important to use appropriate dosages and to monitor the progress of any dog on non-steroidal or steroidal anti-inflammatory medications due to the increased risk of side effects to these medications in dogs.
If medical treatment is insufficient then surgical repair is possible. The best surgical treatment for hip dypslasia is total hip replacement. By removing the damaged acetabulum and femoral head and replacing them with artificial joint components, pain is nearly eliminated. This procedure is expensive but it is very effective and should be the first choice for treatment of severe hip dyplasia whenever possible. In some cases, this surgery may be beyond a pet owner's financial resources. An alternative surgery is femoral head ostectomy. In this procedure, the femoral head (ball part of the hip joint) is simply removed. This eliminates most of the bone to bone contact and can reduce the pain substantially. Not all dogs do well following FHO surgery and it should be considered a clear "second choice".