Half a Century with Canine Hip Dysplasia
Tufts' Canine and Feline Breeding and Genetics Conference, 2013
Åke A. Hedhammar, DVM, MSc, PhD, DECVIM (Companion Animals)
Department of Clinical Sciences, Swedish University of Agricultural Sciences, Uppsala, Sweden

Malformations of the hips in dogs was described by Dr. Schnelle already in 1937, but it was not until about a century ago that it was made evident that it was a widely spread entity affecting not only German shepherds.

Since then, great attention and efforts have been paid worldwide by researchers as well as breeders to reveal the mechanisms behind it and to decrease its prevalence.

The following is an attempt to briefly review knowledge attained and achievements made over these years.

The perspective is from a veterinarian, neither a surgeon nor radiologist nor a geneticist. It's the perspective of someone involved in some research on the effect of genes and environment and as consultant to the Swedish Kennel Club in the institution of screening and breeding programs to assist in the selection of suitable breeding stock. Neither surgical nor medical treatment will be covered. With reference to lectures to follow by Drs. Keller, Lewis and Todhunter on the OFA database, genetics, and genomic tools, respectively, those aspects will not be covered very extensively.

Etiology and Risk Factors

Definition of CHD

"Varying degree of laxity of the hip joint permitting subluxation during early life, giving rise to varying degrees of shallow acetabulum and flattening of the femoral head, finally inevitably leading to osteoarthritis."

Contrary to human hip dysplasia, it soon became evident that canine hip dysplasia (CHD) is a developmental and degenerative disease rather than congenital/present already at birth.


We have learned that its structural and functional properties during its development and its clinical course by degenerative processes are affected by genes as well as environmental factors.


Based on that knowledge, we have got various tools to handle genetic as well as environmental factors in individuals and breed populations.

To Be Further Known and Achieved

The true etiology by genes involved and their expression is still to be revealed as well as the interaction between genes and environmental factors.

Screening Procedures and Registries

Screening for early signs of CHD have been proven to predict clinical outcome as well as genetic transmission (disposition for early signs as well as clinically manifest CHD).


Various screening methods have been investigated and validated for its purpose. Radiographic methods in standardized stressed or non-stressed positioning have proven to be more useful than palpation as practiced in human HD. The outcome of any radiological screening is strongly affected by age at screening, positioning and level of sedation calling for standardizations of these parameters.


Based on that knowledge, screening programs have been extensively established by various bodies worldwide.

Registries on results from these programs nowadays most commonly contain positive as well as negative results on permanently identified individuals, are open to the public and accessible online and supporting computerized information on national breed populations.

To Be Further Known and Achieved

Earlier and more simple and inexpensive screening methods would enhance a more extensive usage. An ongoing dispute regarding the value of different screening methods hampers the inclination to screen by any method. By computerization of results from many individuals, the prediction of the genotype is much more accurate than any screening of an individual dog.

Exchange of results from national registries is hampered by differences in procedure and recordings and calls for an international harmonization.

Epidemiology and Prevalence

CHD do affect almost all large-sized breeds to variable extent and not just purebred/pedigree dogs. The prevalence is affected by type of dogs, mollosoid dogs to high extent and scent hounds to less than other.


The prevalence is known and documented in populations with extensive screening but most commonly is restricted to clinically unaffected animals at age of screening.


A decreased prevalence is proven to be achieved in populations in which breeding stock routinely have been selected for hip status by standardized measures.

To Be Further Known and Achieved

The prevalence in most populations - pedigree and non-pedigree - is still unknown and scarce regarding clinically affected individuals.

Genetics and Breeding Programs

Based on known genetics and established screening programs, structured breeding programs have been instituted in a couple of countries on national breed populations.


The advancement of tools in both population genetics and molecular genetics has enhanced our knowledge on how to handle the selection of breeding stock with reference to CHD.


Structured breeding programs have proven to be very effective in purpose-bred populations of dogs for police, armed forces, and as guide dogs, as well as in national populations on condition that a significant fraction of the population is screened and that the result is taken into account.

To Be Further Known and Achieved

Breed-specific breeding programs would beneficially account for breed variations in prevalence, population structure, and other traits to take into account.

The extent of breeding programs - not just screening - is needed to significantly affect the true prevalence in most national breed populations. International breeding programs would enhance the effect by exchange of results from different screening programs.

Nutritional Impact

The detrimental effect of overnutrition, i.e., excessive amounts of food (overfeeding) and excessive amounts of specific nutrients (oversupplementation), has been proven for many orthopedics conditions in large-sized breeds, including CHD.


Already at an early stage it was proven how ad lib feeding increases prevalence and severity of skeletal disorders including CHD. Contrary to earlier belief, no specific nutrient can prevent CHD by given in excessive amounts.


Feeding practices of large-sized dogs have to some extent changed from "the more-the better" to feeding moderate amount of complete and balanced diet resulting in optimal skeletal conformation rather than maximal rate of growth.

To Be Further Known and Achieved

Despite extensive promotion of chondroprotective products, very little is still known on how to prevent from arthritis in developmental disorders as CHD.

Summing Up

By attention and efforts by researchers as well as cynological organizations and breeders worldwide, extensive knowledge has been accumulated and effective tools have been developed to control for CHD. The full effect of this is, however, hampered by lack of a wider implementation.

A wider implementation of current screening methods and thereon based breeding programs is much more important than any refinement to reveal more of the phenotypic expression of CHD.


1.  Schnelle GB. Congenital dysplasia of the hip in dogs. J Am Vet Med Assoc. 1959;135(4):234–235.

2.  Henricson B, Olson SE. Hereditary acetabular dysplasia in German shepherd dogs. J Am Vet Med Assoc. 1959;135(4):207–210.

3.  Hedhammar Å, Wu Fu-ming, Krook L, Schryver HF, Lahunta A, Whalen JP, et al. Overnutrition and skeletal disease. An experimental study in growing Great Dane dogs. Cornell Vet. 1974;64:Suppl 5.

4.  Kasström H. Nutrition, weight gain and the development of hip dysplasia. Acta Radiol. 1975;344 Suppl:135–179.

5.  Hedhammar A, Olsson SE, Andersson SA, Persson L, Pettersson L, Olausson A, Sundgren PE. Canine hip dysplasia: study of heritability in 401 litters of German Shepherd dogs. J Am Vet Med Assoc. 1979;174(9):1012–1016. www.ncbi.nlm.nih.gov/pubmed/570968

6.  Swenson L, Audell L, Hedhammar A. Prevalence and inheritance of and selection for hip dysplasia in seven breeds of dogs in Sweden and benefit: cost analysis of a screening and control program. J Am Vet Med Assoc. 1997;210(2):207–214. www.ncbi.nlm.nih.gov/pubmed?cmd=Retrieve&db=PubMed&list_uids=9018354&dopt=Abstract

7.  Hedhammar A. Activities by Federation Cynologic International (FCI) to combat elbow and hip dysplasia. International Elbow Working Group. 1998. www.vet-iewg.org/joomla/index.php/archive/13-1998-bologna/20-hedhammar-1998

8.  Hedhammar A, Swensson L, Egenwall A. Elbow arthrosis and hip dysplasia in Swedish dogs as reflected by screening programmes and insurance data. Europ J Comp Anim Pract. 1999;9:2.

9.  Hedhammar A. Nutrition and selection of breeding stock with reference to skeletal health in large growing dogs - Swedish experiences over 25 years. In: IAMS Large Breed Health Care Symposium, Venice, Italy. November 17th, 2001.

10. Sallander M, Hedhammar Å, Trogen M. Diet, exercise and weight as risk factors in hip dysplasia and elbow arthrosis in Labrador retrievers. J Nutr. 2006;136:2050S–2052S. http://jn.nutrition.org/content/136/7/2050S.full.

11. Malm S, Strandberg E, Danell B, Audell L, Swenson L, Hedhammar A. Impact of sedation method on the diagnosis of hip and elbow dysplasia in Swedish dogs. Prev Vet Med. 2007;78(3–4):196–209.

12. Hedhammar A. Canine hip dysplasia as influenced by genetic and environmental factors. Europ J Comp Anim Pract. 2007;17(2):141–143. www.docstoc.com/docs/80460727/Canine-Hip-Dysplasia-as-influenced-by-genetic-and-environmental

13. Comhaire FH, Snaps F. Comparison of two canine registry databases on the prevalence of hip dysplasia by breed and the relationship of dysplasia with body weight and height. Am J Vet Res. 2008;69(3):330–333.

14. Malm S, Fikse F, Egenvall A, Bonnett BN, Gunnarsson L, Hedhammar A, Strandberg E. Association between radiographic assessment of hip status and subsequent incidence of veterinary care and mortality related to hip dysplasia in insured Swedish dogs. Prev Vet Med. 2010;93(2–3):222–232.

15. Wilson B, Nicholas F, Thomson P. Selection against canine hip dysplasia: success or failure? Vet J. 2011;189:160–168. http://actualidadveterinaria.files.wordpress.com/2011/08/selection-against-canine-hip-dysplasia-success-or-failure.pdf

16. Dennis R. Interpretation and use of BVA/KC hip scores in dogs. In Pract. 2012;34:178–194. 

17. Fikse WF, Malm S, Lewis TW. Opportunities for international collaboration in dog breeding from the sharing of pedigree and health data. Vet J. 2013 Aug 8. pii: S1090-0233(13)00197-4. doi: 10.1016/j.tvjl.2013.04.025. [Epub ahead of print].

18. Hazewinkel HAW, Goedegebuure SA, Poulos PW, Wolvekamp WThC. Influences of chronic calcium excess on the skeletal development of growing Great Danes. J Am Anim Hosp Assoc. 1985;21:377–391.

19. Lavelle RB. The effects of overfeeding of a balanced complete commercial diet to a group of growing Great Danes. In: Burger IH, RiversJPS, eds. Nutrition of the Dog and Cat. Cambridge: Cambridge University Press; 1989:303–314.

20. Comhaire FH, Snaps F. Comparison of two canine registry databases on the prevalence of hip dysplasia by breed and the relationship of dysplasia with body weight and height. Am J Vet Res. 2008;69(3):330–333.


Speaker Information
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Åke A. Hedhammar, DVM, MSc, PhD, DECVIM (Companion Animals)
Department of Clinical Sciences
Swedish University of Agricultural Sciences
Uppsala, Sweden

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