Page 66 - WSAVA2018
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 25-28 September, 2018 | Singapore
Lifetime studies on the hip status of dogs show that maintaining a lean body condition produces overall better hip confirmation and reduced hip arthritis. Restricted calorie loads in “large-breed puppy foods” promote a more uniform growth rate where the boney and soft tissue components can develop and mature
in unison. Excessive compaction on the hips (jumping and landing with full body weight on the hind limbs) should be avoided in immature dogs when the skeletal components of the hip are still cartilaginous and liable to deformation.
HEREDITY OF HIP DYSPLASIA
The evolutionary development of breeds has produced some with higher and lower liability for developing hip dysplasia, based on which dysplasia liability genes they have lost or retained over time. Different studies find that hip dysplasia is 20% to 40% heritable. This means that 20 to 40% of the variability of dysplastic development
is due to genetic factors, and the rest of the variability is due to environmental factors. This classifies hip dysplasia as a moderately heritable disorder, comparable to other complexly inherited traits such as egg production in poultry, and milk production in cattle. Proper selection against hip dysplasia should result in a reduction of the frequency of affected dogs.
The inheritance of hip dysplasia is polygenic, meaning that the action of several genes must combine together to produce the disorder. The specific combination of genes that produce liability to dysplastic development will vary between breeds, familial clusters, and between individual dogs. Environmental variables that can alter the expression of the disorder can include dietary load and degree of activity/mechanical stress.
Genetic studies into hip dysplasia have broken down the phenotypic liability into several components that appear to be inherited separately. Some of these variables include; joint laxity, age of ossification, depth of the acetabulae and liability for osteoarthritis.
Breed differences in prevalence of hip dysplasia often have to do with breed defining characteristics. Breeds that were established on a racing phenotype had extensive selective pressure for good hip conformation. Those who did not excel were not used for breeding. Other breed differences have to do with conformational morphology. Lighter-boned tight-muscled breeds have a lower prevalence of HD compared to heavier-boned course-muscled breeds.
Chondrodystrophic breeds and dogs have in general poorer radiographic hip joint conformation. However, their lower hip scores do not necessarily correlate
to increased clinical disease. In a study of Pembroke Welsh Corgis, all dogs showed radiographic signs
of hip dysplasia, but this was not correlated to their susceptibility to develop later osteoarthritis.
Studies on the genetic control of polygenically inherited traits show that selection based on phenotypic measurements of individuals show less improvement when compared with selection based on familial data. OFA data show that hip conformation scores are directly correlated to the scores of the parents, grandparents, and their siblings. Combined parent hip scores are linearly correlated to the production of offspring with hip dysplasia - showing its inheritance as an additive (quantitative) trait.
Familial data can also be computed as estimated breeding values (EBVs), based on the phenotype of the parents, siblings, siblings of parents, offspring, and other relatives. By utilizing phenotypical depth and breadth
of pedigree, EBVs utilize information that can more accurately reflect the cumulative genetic influences passed down to the individual dog.
An issue with the accuracy of calculating EBVs involves dogs with missing phenotypes – as most breeds
have less than 10% of breeding dogs or their siblings evaluated. To provide the most power, EBVs require data on all normal and abnormal sibs within litters. Without this, the accuracy and precision of EBVs is low. In an applied setting, dogs with high EBVs may also become popular sires thus putting pressures on gene pools
that can affect genetic diversity. EBVs for hip dysplasia have been developed for several breeds in the UK by Dr. Lewis at the Kennel Club, in the US by Dr. Todhunter at Cornell University, and by the Australian Kennel Club. EBVs should include power estimates based on pedigree completeness.
Genomic breeding values (GBVs) are based on
DNA markers that segregate with hip dysplasia in experimental populations. These markers may or may not be correlated to specifically identified dysplasia liability genes. Todhunter’s group at Cornell and Dr. Distl’s group in Hanover, Germany are working on GBVs. At this time breed-specific genetic marker panels are specific
to the populations being studied, but do not accurately predict phenotypic liability in larger populations of the same breed or in different breed populations. Therefore, current commercial hip dysplasia liability DNA marker panels should be viewed with caution as they may not correlate to other populations within the same breed, or other breeds.
GBVs have greater promise in producing improvement with hip dysplasia as they avoid the issues of missing phenotypic information required for EBVs, as well as phenotypic variation caused by environmental influence. However the development of accurate GBVs requires full extended pedigree phenotypic information. While EBVs and GBVs appear to hold the most promise for improved genetic selection against hip dysplasia, their specific clinical use and validation are a work in progress.
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43RD WORLD SMALL ANIMAL VETERINARY ASSOCIATION CONGRESS AND 9TH FASAVA CONGRESS











































































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