Speaking with clients about hip dysplasia (Proceedings)

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Speaking with clients about hip dysplasia (Proceedings)

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Aug 01, 2008

When we diagnose hip dysplasia owners want to know why their dog has it and what it means for their dog's future. Therapeutically, we need to explain both conservative and surgical options to our clients and help them decide which is best for them. Conservative therapy is multimodal and consists of dietary modification, provision of regular moderate exercise, chondroprotectants, and judicious use of nonsteroidal anti-inflammatory drugs (NSAIDS). One of the goals of multimodal therapy is to lower the dose of NSAID required to control joint pain. Surgical options include triple pelvic osteotomy, pubic symphysiodesis, femoral head and neck ostectomy and total hip replacement. The best time to diagnose hip dysplasia is when puppies are presented for examination and vaccination. The full range of surgical options are available when dogs are young and initiating conservative management at this phase may confer more benefit than when osteoarthritis is already well established. Hip dysplasia is diagnosed by evaluating the Ortolani sign followed by radiographs. A positive Ortolani sign indicates hip dysplasia even if there is not yet evidence of osteoarthritic change or obvious subluxation on pelvic radiographs. If dogs do not have an obvious lameness, owners may not be aware of a problem. The veterinarian can inquire about certain types of behavior that indicate joint pain. Common behaviors associated with joint pain are slowness to rise, difficulty with stairs or getting into a car, increased time of inactivity, abrupt cessation of play activity and difficulty posturing to void.

Etiology of hip dysplasia

Hip dysplasia results from a combination of genetic predisposition and environmental triggers. We know that dogs that have the genetic basis for hip dysplasia and undergo rapid growth are at high risk for physical symptoms of hip dysplasia. The genetic profile for hip dysplasia is polygenic and therefore unpredictable. The heritability for hip dysplasia varies widely in that heritability scores range from a high of 0.6 to a low of 0.1. A heritability score of 1.0 signifies complete genetic control of disease expression whereas a score of 0.0 signifies complete lack of genetic contribution. Because of the heritability scores, environmental influences have a significant impact on the phenotypic expression of hip dysplasia. The influence of growth rate on bone development is an active area of study. Excess intake of energy alters bone development through changes in hormones that have a powerful impact on endochondral ossification. Specifically, increased energy alters levels of growth hormone (GH), insulin-like growth factor 1 (IGF-1) and thyroid hormones (T3 and T4). High levels of GH and IGF-1 alter the normal balance of vitamin D metabolites. There is an excess of 1,25(OH)2 D3 and a deficiency of 24,25(OH)2 D3. At the growth plate level this is thought to be responsible for retarded maturation of chondrocytes. There is evidence that endochondral ossification is abnormal in dogs with hip dysplasia. Onset of mineralization of the femoral head occurred significantly later in dysplastic than in normal Labrador retriever pups in one study. In another study, 100 % of German shepherd pups that did not have radiographic evidence of femoral head ossification by 15 days of age developed hip dysplasia by one year whereas less than half of those that did have femoral head ossification by this time developed hip dysplasia. The profound impact of limited energy consumption was demonstrated in a study comparing 2 groups of 8 week old Labrador retriever pups from a dysplastic breeding line. Starting at 8 weeks of age and continuing to 2 years of age, 1 group was fed ad lib and the second group was fed 25 % less. Radiographs at 2 years showed significantly less hip dysplasia in the limit-fed dogs. Continued restriction substantially reduced the prevalence and severity of hip dysplasia at 5 years of age.

Hip joint laxity is also an essential component to hip dysplasia. It is not yet clear exactly how abnormal endochondral ossification and hip joint laxity result in hip dysplasia. Dogs that develop hip dysplasia are born with apparently normal hip joints, but after they have reached a few weeks of age, joint laxity can be demonstrated. Joint laxity is thought to be heritable. Joint laxity may occur due to an accumulation of excessive joint fluid. When the hip is in a neutral position, it is primarily stabilized by a vacuum effect. Any increase in synovial fluid can disturb the vacuum effect and allow for subluxation of the joint. The early signs of hip dysplasia in dogs include effusive synovitis and accumulation of synovial effusion and there is a close association between the volume of synovial fluid and degree of hip laxity. Subluxation induces abnormal mechanical stress on the dorsal acetabular rim which contributes to degenerative change and conformational changes.