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Genetic Welfare Problems of Companion Animals

An information resource for prospective pet owners

German Shepherd Dog (Alsatian)

German Shepherd Dog (Alsatian)

Hip Dysplasia (HD)

Related terms: Coxofemoral joint laxity, Hip joint arthritis, Coxofemoral joint arthritis, osteoarthritis of the hip

Outline: As a result of selection of particular features during the breeding of German Shepherd dogs, they are commonly affected with a hip disease characterised by excessive laxity in the joint (the ball moves too much within its socket) or excessive shallowness of the hip socket joint. In time this leads to painful arthritis.

Summary of Information

(for more information click on the links below)

1. Brief description

Hip dysplasia (HD) is a complex condition where the hip joints of a growing puppy develop abnormally. The primary reason for this abnormal development is hip joint laxity ie the joint is too loose; leading to the two articulating parts of the joint of the pelvis – the femoral head and the acetabulum (which form the ball-and-socket of the joint) - moving abnormally relative to one another; the femoral head subluxating (partly dislocating) from the acetabulum. This leads to abnormal stresses and strains on the joint and leads to inflammation and degeneration of the joint tissues. Ultimately, permanent osteoarthritis develops in the joints. These changes produce pain and disability for the dog which may show up in a number of ways, such as lameness, abnormal gait (movement), stiffness, reluctance to get up and move and difficulty in running and playing.

Both genetic and environmental factors play a part in the development of hip dysplasia.

2. Intensity of welfare impact

Hip dysplasia (HD) has a major welfare impact for many dogs with the condition. Though it may initially cause intermittent disease, hip dysplasia develops into a persistent condition causing chronic joint pain and progressive disability due to joint deformation. Chronic joint pain can be severe and debilitating and may need long-term medication to control. Control of the secondary osteoarthritis can be difficult and euthanasia is common.

3. Duration of welfare impact

For some dogs, signs of hip dysplasia will develop whilst they are still immature (less than a year old), for others signs can develop at any age after maturity. Once present it remains throughout life, unless major surgical interventions are undertaken.

4. Number of animals affected

Hip dysplasia is common in large dogs. UK VetCompass data for dogs overall, showed that 7.2 dogs per 1000 dogs from a random sample of 3884 dogs were diagnosed with hip dysplasia between 2009 and 2013 (O Neill et al 2014). Figures for the proportion of German Shepherds affected vary from study to study but range from 18-49%, and the breed appears to have significantly higher risk of hip dysplasia than Dobermanns, Labradors and Rottweilers.

5. Diagnosis

A diagnosis of hip dysplasia is made by a veterinary surgeon examining the dog and taking x-rays of its hip joints. For a formal diagnosis, the radiographs are submitted to a panel for evaluation.

6. Genetics

German Shepherd dogs have a known predisposition to hip dysplasia. Hip dysplasia in dogs is a polygenic, multifactorial disease; thus many genes are thought to play a role in its development, along with significant influences from environmental factors.

7. How do you know if an animal is a carrier or likely to become affected?

The general advice is to choose a puppy whose parents have been screened for hip dysplasia and have healthy hips. However, this does not definitely preclude any of their puppies developing hip dysplasia, so an alternative approach is to choose a dog that is old enough to have its hip joint laxity assessed via the PennHIP scheme in the USA. There is limited access to this scheme outside the USA and dogs need to be 4 months or over for this assessment.

All potential breeding animals should be assessed according to a recognised hip dysplasia control scheme prior to breeding and the scheme’s guidance should be followed. It is currently not straightforward to identify dogs which carry genes predisposing to hip dysplasia – see additional details below.

8. Methods and prospects for elimination of the problem

As hip dysplasia is a multifactorial disease caused by multiple genes combined with the effects of environmental factors, its elimination is also not straightforward. Currently, various schemes to assess hip traits exist around the world, including the British Veterinary Association/ Kennel Club hip dysplasia scheme in the UK. Slow progress has been made on decreasing the prevalence of hip dysplasia. The possibility of generating breeding values for individual dogs based on multiple hip traits plus knowledge of the health of their ancestors and progeny may increase the rate of elimination of this disease and, in future, genetic tests may become available to help.

For further details about this condition, please click on the following:
(these link to items down this page)

1. Clinical and pathological effects

Hip dysplasia (HD) is a disease of the hip (coxofemoral) joints. Dysplasia means abnormal development. Both hips are usually affected (Brass 1989). It is a complex disease that results from a combination of genes that predispose a dog to developing hip dysplasia interacting with environmental factors that lead to its full development and expression (Riser 1993). It is characterized by hip joint instability which, if compounded by environmental factors, then results in secondary osteoarthritis and the clinical signs of hip dysplasia which include pain, lameness and disability (Zhang et al 2009).

To fully understand hip dysplasia, it is necessary to understand the structure of the hip joint. The hip joint is the joint at the top of the hind leg, where it articulates (forms a joint) with the pelvis. It is described as a ball and socket joint, as in normal hips the ball-shaped head of the femur (the thigh bone) fits perfectly into a cup-shaped socket in the pelvis, the acetabulum. The head of the femur (femoral head) and the acetabulum are normally covered with cartilage which produces a smooth, low friction surface. Within the joint there is also a fine layer of synovial fluid that acts as a lubricant between these cartilaginous surfaces. This thin layer of synovial fluid, along with the round ligament (a ligament that runs round the edge of the acetabulum – between the acetabulum and the femur), keeps the two cartilaginous surfaces together by creating a suction-like effect. The ligaments and the joint capsule also help to hold the ball and socket closely together. Keeping the femur ‘ball’ and acetabulum ’socket’ intimately connected but moving smoothly over each other enables a healthy hip joint to undertake many different movements and a healthy dog to run, jump and change direction quickly etc. (http://www.bva.co.uk/Hip_Scheme.aspx). In newborn puppies, because the bones are soft and not fully ossified (turned into bone) as they need to grow and develop, they are still deformable if abnormal movements or stresses and strains occur in them. Riser (1993) suggests that, in a normal six month old individual, ossification of the bones and soft tissue strength (the strength of the surrounding ligaments, joint capsule and muscles) have developed enough to prevent hip dysplasia .

Hip dysplasia is described as a biomechanical disease. The hips appear normal at birth. However, in affected individuals, the hips develop abnormally due, at first, to joint instability (sometimes called joint laxity) (Riser 1993). This means that the developing femoral head and acetabulum are not held constantly, closely together, and can move into abnormal positions relative to one another. This puts abnormal stresses and strains on the joint. Riser (1993) states this is due to the soft tissues, such as ligaments and muscle, not being strong enough to maintain congruity between the articular surfaces of the femoral head and the acetabulum ie the constant contact between the surfaces of the bones is not maintained.

Joint laxity (the looseness of the joint, allowing abnormal movements of the parts relative to one another) can lead on to joint subluxation (partial dislocation of the joint on movement) that in turn causes flattening of the acetabular cup and femoral head (Shell & Harasen 2007). The pathological changes seen due to the joint instability are progressive inflammation and degeneration of the tissues that together form the joint.

Brass (1989) details the following changes in the joint: The joint capsule can become thickened and the round ligament can become stretched or ruptured leading to additional, excessive movements. The synovial fluid increases in volume and changes in nature, due to inflammation, this pushes the joint surfaces apart. The cartilage on the bone surfaces gets worn away exposing subchondral bone (the layer of bone beneath the surface cartilage). Unlike cartilage, bone contains nerve endings and such exposure will commonly cause pain. The rim of the acetabulum becomes damaged and flattened and later new bone starts to grow here as the body tries to stabilize the joint. The femoral head becomes deformed and flattened and also grows abnormal bone (called exotoses or osteophytes). This changing of the shape of the joint with new bone growing in abnormal positions, and being lost in others, is called joint remodelling.

The signs that are seen with hip dysplasia can vary hugely in their severity, the age at which they first appear and their progression. In mild cases dogs can be free from clinical signs for years; however, for more severely affected individuals, signs of pain can develop whilst they are still immature (less than a year old)

Signs include acute pain, particularly after strenuous exercise or movement. This may show as lameness or reluctance to jump, to go for walks, climb steps or move at all if really severe. The pain may be worse in cold, wet conditions (Brass 1989). Dogs may be stiff after rest and have difficulty rising (Shell & Harasen 2007), or show other gait abnormalities such as swaying of the hips or a “rolling hindleg gait” (Bennett & May 1995), or they may not pick their feet up properly when walking, leading to scuffing of nails (Brass 1989). Sometimes affected animals bunny hop, moving their hind legs together (Shell & Harasen 2007). These signs may start intermittently, but over time can become constant. Muscle wastage is often seen in the hindlegs (Brass 1989).

There appears to be little correlation between the severity of pain shown by the dog and physical abnormalities felt on examination by a vet or revealed on an x-ray (Brass 1989) ie some dogs can be in severe pain but have few changes on x-rays and vice versa. This is typical of any joint disease.

The environmental factors that are known to affect the development of hip dysplasia include the dog’s weight and age ie the heavier and older the dog is the more likely it is to have hip dysplasia (Runge et al 2010). Controlling food intake during growth has been shown to decrease hip dysplasia in Labradors ie by reducing excessive energy intake and therefore excessive weight gain during growth (Kealy et al 1997). High calcium intake during growth has been shown to delay maturation of the skeleton and increase the risk of hip dysplasia in Great Danes (Hazewinkel 2004). It is thought that controlling the amount and form of exercise during development may also help (Corr 2007). Bennett and May (1995) suggest excessive exercise during development can lead to hip dysplasia.

Treatment for hip dysplasia is complex; many surgical interventions have been developed to prevent signs appearing in young animals with high joint laxity and to treat dogs with severe osteoarthritis. All need specialist surgeons. Various medications to aid pain relief are also available, along with recommendations to reduce the effect of environmental factors.

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2. Intensity of welfare impact

Though some dogs may be mildly affected, for many German Shepherd dogs with hip dysplasia, the impact of the condition is major and life changing. These animals suffer pain that is severe and debilitating, leading them to be in pain even with small everyday movements such as standing up. Their quality of life is severely affected so that they are unable to enjoy normal canine behaviours such as walking and running. It is not uncommon for dogs to be euthanased due to the pain and disability of arthritis associated with hip dysplasia.

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3. Duration of welfare impact

Hip dysplasia is a progressive disease with signs seen from any age. For some dogs pain starts before a year of age. Signs may be intermittent to start with but often progress to be constant. Medical treatment and advice can help control pain and possibly slow progression, though a cure can only be obtained with major surgical intervention in dogs that are considered suitable candidates for such surgery.

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4. Number of animals affected

Hip dysplasia is the most common joint problem of large dogs (Smith et al 2001). UK VetCompass data for dogs overall, showed that 7.20 dogs per 1000 dogs from a random sample of 3884 were diagnosed with hip dysplasia between 2009 and 2013 (O Neill et al 2014; see also: http://www.rvc.ac.uk/vetcompass/learn-zone/infographics/canine). In this sample, diagnosis of conditions affecting the pelvis (eg hip dysplasia) did not significantly differ between purebred and crossbred dogs.

Figures vary greatly for how frequently German Shepherds are affected by hip dysplasia, depending on the method by which they have been screened and the database reviewed. The frequency is likely to vary for geographically different populations of the same breed (Brass 1989).Using the OFA (Orthopedic Foundation for Animals) database in the USA (1974-2015), 20.4% German Shepherd dogs had hip dysplasia (23,650 of 115,933 dogs screened). Of German Shepherd dogs born between 2011 and 2015, the prevalence of hip dysplasia was marginally lower, at 18% (1009 of 5607 dogs screened). However, Paster et al (2005) suggested that the OFA population was biased, as it is not compulsory for radiographed dogs to have their x-rays submitted to the OFA scheme so some owners may have had dogs pre-screened and only submitted apparently non-dysplastic ones for consideration and scoring.

In a Swedish study using 5-point severity scoring of pelvic radiographs, 49% of German Shepherd dogs tested had hip dysplasia (188 of 402 dogs), and had a significantly greater risk compared to other breeds (relative risk: 1.85; Martin et al 1980). In one study of Italian purebreds, the prevalence of hip dysplasia (scores C, D and E) in German Shepherd dogs was 26.62% (4977 of 18,696 dogs; Sturaro et al 2010). In this study, German Shepherd dogs had a higher odds ratio of hip dysplasia occurrence than Dobermanns, Labradors and Rottweilers, indicating that the breed is at a significantly higher risk of hip dysplasia development.

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5. Diagnosis

For a young dog suspected of hip dysplasia, a diagnosis can be made on the clinical signs shown at home and on examination of the dog, including assessment of joint laxity and joint pain plus evaluation of radiographs (x-ray pictures) of the hip joints (Corr 2007). Assessment of the joint laxity and radiographs may need to be performed by a specialist vet who is used to checking for this condition. For a formal diagnosis, the radiographs are usually submitted to a panel for evaluation. There are three methods of assessing joint laxity. Corr (2007) favours the Ortolani Test, the others being the Barlow Test and the Bardens Test (Corr 2007). For a dog over two years of age, with appropriate signs, diagnosis is made on examination of the dog for lameness and muscle wastage, manipulation of the hip joints, checking for decreased range of hip movement, crepitus (a feel of abnormal grating within the joint) and/ or pain, plus radiographs of the hip joints. Radiographs and assessment of joint laxity need to be performed under heavy sedation or anaesthesia (Corr 2007).

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6. Genetics

Hip dysplasia in dogs is a polygenic disease; many genes are thought to play a role in its development. Most of these genes probably have small additive effects (quantitative, polygenes) and some probably have larger effects (Zhang et al 2009). For example, one study identified 5 single nucleotide polymorphisms associated with hip dysplasia in German Shepherd dogs, and the genotype effects of these explained 20-32% of the phenotypic variation in hip dysplasia seen in the German Shepherd dogs tested (Fels & Distl 2014).

Heritability estimates are used to demonstrate how much variation in a phenotypic trait is due to genetic variation among individuals in a population. Using hip scores published by the British Veterinary Association, heritability for hip scores of German Shepherd dogs was 0.30±0.02, which suggests moderate genetic variation (Wilson et al 2012). 

Genes are not solely responsible for whether a dog with the genetic potential for hip dysplasia develops the condition. Environmental factors play an important part. They are discussed in the clinical and pathogenic effects section above. However, there are significant breed predispositions to this condition and the German Shepherd dog is one of the breeds affected.

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7. How do you know if an animal is a carrier or likely to become affected?

There are a number of breeding schemes around the world developed to decrease the incidence of hip dysplasia in dog breeds. These schemes assess potential breeding animals in somewhat different ways. All aim to give breeders and owners a strong indication of which dogs are likely to produce healthy offspring and which should not be bred. However, this is by no means straightforward for hip dysplasia as it is a polygenic condition in which the genetics are poorly understood and which is also affected by environmental factors in a major way. This lack of clarity has produced much debate over the best way to assess potential breeding dogs.

A brief summary of the various schemes follows including some current evidence for their benefits.

  • UK and Australia: BVA/KC Hip Dysplasia Scheme (started 1984)
    This scheme is a mandatory scheme for Kennel Club Assured Breeders of German Shepherd dogs. The scheme consists of scoring the dog’s extended hip radiograph (EHR) by a panel of veterinary specialists. All dogs must be at least 12 months of age. There are nine radiographic features which are scored, including the Norberg angle (NA - a measurement for hip laxity taken from the EHR) and each dog is given a score out of 53 for each hip (total of up to 106 for both). A low score indicates healthy hip joints (eg Greyhounds would score 0, as is not seen in this breed) and a higher score indicates worse hip dysplasia. The scheme records all scores and publishes a median for each breed (http://www.bva.co.uk/Hip_Scheme.aspx). Breeders are recommended to only breed from animals with a score lower than the breed medianscore e.g. for German Shepherd dogs  the breed median score is currently 11, so only dogs with hip scores lower than this should be bred from (http://www.bva.co.uk/Hip_Scheme.aspx).
  • USA: OFA’s (Orthopedic Foundation for Animals) scheme (started in 1960’s)
    This is the oldest hip-improvement scheme in the world. It is also based on an extended hip radiograph (EHR), which is then graded by three independent experts to give an overall grade. All dogs must be over 2 years of age to be assessed. There are seven possible grades for the radiograph: excellent, good, fair, borderline, mild, moderate or severe hip dysplasia. Dogs with hips that are assessed excellent, good or fair on radiograph are certificated for breeding purposes (http://www.offa.org/hipproc.html).The OFA’s website also recommends consideration of the ancestry and the progeny of breeding dogs along with their EHR grade. Such guidance to breeders includes: “breed normals to normals, breed normals with normal ancestry, breed normals from litters (brothers/sisters) with a low incidence of hip dysplasia, select a sire that produces a low incidence of hip dysplasia , replace breeding dogs with dogs that are better than the breed average” (http://www.offa.org/hipguide.html).
  • Fédération Cynologique Internationale’s (FCI) scheme
    This scheme is used in much of Europe and also other parts of the world. Again, it is based on an EHR and the NA is measured as part of the grading system. Dogs must be between 1 and 2 years of age and the radiograph is graded by someone appointed by each breed club – they do not have to be an expert. Grades include: A- no signs of hip dysplasia, B – near normal hip joints, C – mild hip dysplasia, D – moderate hip dysplasia, E – severe hip dysplasia. Older dogs can be assessed but the likelihood of more secondary osteoarthritic changes is taken into account.
  • USA: PennHIP scheme
    This is a relatively new scheme, developed by the University of Pennsylvania, USA. Dogs from 4 months of age can be assessed. It involves the assessment of three different radiographic views of the hip joints called the distraction view, the compression view and the EHR. The EHR view is looking for secondary osteoarthritic changes in the joint, the distraction view is to provide a quantitative measurement of joint laxity called the Distraction Index (DI) and the compression view is to assess joint congruity (http://info.antechimagingservices.com/pennhip/). The radiograph must be taken by a vet who is registered with the scheme and the radiographs are assessed by vets at the PennHIP Analysis Center. Dogs with a DI lower than 0.3 are considered to have normal joint laxity and have an extremely low risk of developing hip dysplasia. Dogs with increasing DI values over 0.3 up to 0.7 have increasing joint laxity and increasing likelihood of developing hip dysplasia A.

Advocates of the PennHIP method like it because it accurately identifies individuals who have hip laxity - the primary phenotypical abnormality that predisposes dogs to hip dysplasia. The other schemes only look at the EHR and though the NA can be measured from this, the NA has been shown to be an inaccurate method to assess hip laxity (Culp et al 2006). Much of what is assessed on the EHRs are secondary arthritic changes, these are not specific to hip dysplasia and are affected by many environmental factors. Recently, researchers from the University of Pennsylvania have confirmed that the Distraction Index DI is a significant risk factor for the development of hip dysplasia. In other words, DI scores give a very good indication of the likelihood of osteoarthritic changes, due to hip dysplasia, developing in the future (Smith and others 1993, 1995, 2001, Smith 1997, Runge et al 2010). These and other researchers argue that the other schemes are not as good at detecting animals that have hip dysplasia as the PennHIP method and, despite older schemes existing for over 40 years, little improvement has been seen in  hip dysplasia in the general pet population (Corley 1992, Kaneene et al 1997, Leppanen et al 2000, Paster et al 2005). In fact, one recent study looking at a database of over 1,240,000 dogs found an increase in the prevalence of hip dysplasia (Witsberger et al 2008). Hou et al (2010) found that the heritability of EHR scores from the OFA scheme was 0.21 ie only 20% of the result could be put down to the effects of genes and 80% were due to environmental factors. However EHR scores were found to have a much higher heritability (0.76) in another study and this study also found the heritability of DI to be relatively high at 0.61 (Zhang et al 2009). Heritability studies are difficult to compare between different populations with different environmental influences. To improve the gene pool, phenotypic traits that can be easily detected with strong links to the genotype (genetic make-up) of animals have to be found.

Ideally, any potential pet would have had its hip joints assessed by one of the above schemes prior to purchase, although this is often unhelpful, as most pets are purchased as young puppies. Ideally, all puppies’ parents will be certified to have better than average (for the breed) hip joints. Unfortunately, this does not guarantee all their offspring will be free from hip dysplasia.

Certainly any potential breeding animal should be assessed prior to breeding using an appropriate scheme. The scheme’s guidelines should be followed and further veterinary advice sought if necessary.

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8. Methods and prospects for elimination of the problem

Hip dysplasia is a complex trait which involves multiple unknown genes and environmental factors. Eradication schemes have been running in some countries for decades and still it is commonplace. Thus prospects for its quick elimination are low. The OFA scheme to control hip dysplasia relies on one single phenotypical hip trait – the score from an EHR. The PennHIP scheme uses two traits, those of the EHR and DI to determine breeding potential and the FCI and BVA/Kennel club schemes also use two traits: the EHR including the NA. In a recent study, Zhang et al (2009) suggested that using scores from four hip traits combined to create a breeding value for each animal would help speed up elimination of the condition. This combined score would provide more information about a dog’s genetic potential than information about one single trait such as the EHR. They felt that information on the single joint trait EHR (eg the OFA scheme) gave insufficient information to provide the basis for breeding decisions.

Zhang et al’s (2009) breeding values were calculated from four traits: the EHR, DI, and NA already discussed, plus the dorsolateral subluxation score (DLS). The DLS is a measurement made from an x-ray taken in a weight-bearing position to measure the subluxation of the femoral head (Farese et al 1998). In this study on two populations of dogs where environmental factors were strictly controlled, heritabilities for all these traits were found to be relatively high eg heritabilities were 0.61 for DI, 0.54 for DLS score, 0.73 for NA and 0.76 for EHR (Zhang et al 2009). The researchers suggested these heritabilites were higher than expected due to the controlled environmental conditions. Zhang et al (2009) suggested an improved way for selectively breeding out hip dysplasia would be if breeders could be given breeding values derived from the four traits for each potential breeding animal, plus a measurement of the inbreeding of any potential mating eg the inbreeding coefficient. This way, they suggest, inbreeding can be avoided and only animals with phenotypes strongly indicative of healthy hip joint genes would be bred from. This scheme is a more organised form of others that have suggested using a combination of breeding values determined from pedigree information and phenotype score (Ginja et al 2008, Hou et al 2010) .

As described by Bell (2005), when breeders are prioritising raising dogs that have good hip dysplasia genotypes for future breeding the phenotype has to be used as a marker for the genotype. Although the diagnostic signs can be affected also by environmental factors such as feeding and exercise regimes. It is important that the puppies are raised in a standard and not excessively protective way. Otherwise, dogs that would normally have developed radiographic signs of hip dysplasia will have this masked and their genes will be perpetuated.

Future development of genetic tests to help identify some of the hip dysplasia genes, along with more use of pedigree data that includes the health of ancestors and progeny (for clinical signs of hip dysplasia and also for other inherited defects of German Shepherd dogs), may well help to improve methods used to eliminate this condition. Currently we have to continue to rely on choosing phenotypical traits which apparently indicate the presence of healthy genes.

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9. Acknowledgements

UFAW is grateful to Rosie Godfrey (BVetMed MRCVS), David Godfrey (BVetMed FRCVS), Dr Emma Buckland (BSc PhD), Dr David Brodbelt (MA VetMB PhD DVA DipECVAA MRCVS) and Dr Dan O’Neill (MVB BSc MSc PhD  MRCVS) for their work in compiling this section.

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10. References

Bell J (2005) Managing polygenic disease: canine hip dysplasia as an example. Tufts’ Canine and Feline Breeding and Genetics Conference, Sturbridge, Massachusetts September 30 – October 1, 2005

Bennett D and May C (1995) Joint diseases of dogs and cats. In Ettinger S and Feldman E (Eds) Textbook of Veterinary Internal Medicine. Philadelphia: WB Saunders Company

Brass W (1989) Hip dysplasia in dogs. Journal of Small Animal Practice 30: 166-170

BVA (No date) Hip dysplasia scheme. (On-line website) Available at http://www.bva.co.uk/Hip_Scheme.aspx. Accessed 5.8.10.

Corley E (1992) Role of the Orthopedic Foundation for Animals in the control of canine hip dysplasia. Veterinary Clinics of North America: Small Animal Practice 22: 579-593

Corley E and Hogan P (1995) Trends in hip dysplasia control: analysis of radiographs submitted to the Orthopedic Foundation for Animals, 1974 to 1984. Journal of American Veterinary Medical Association 187(8): 805-809

Corr S (2007) Hip dysplasia in dogs: treatment options and decision making In Practice 29: 66-75

Culp W, Kapatkin A, Gregor T, Powers MY, McKelvie PJ and Smith G (2006) Evaluation of the Norberg angle threshold: a comparison of Norberg angle and distraction index as measures of coxofemoral degenerative joint disease susceptibility in seven breeds of dogs. Veterinary Surgery 35(5): 453-459

Farese J, Todhunter R, Lust G, Williams A and Dykes N (1998) Dorsolateral subluxation of hip joints in dogs measured in a weight-bearing position with radiography and computed tomography. Veterinary Surgery 27: 393–405

Fels L and Distl O (2014) Identification and validation of quantitative trait loci (QTL) for canine hip dysplasia (CHD) in German Shepherd Dogs. PloS one 9, e96618. doi:10.1371/journal.pone.0096618

Ginja M, Gonzalo-Orden J, Melo-Pinto P, Bulas-Cruz J and Orden M (2008) Early hip laxity examination in predicting moderate and severe hip dysplasia in Estrela mountain dog. Journal of Small Animal Practice 49: 641–646

Guillard (Date unknown) Hip Scoring (On-line website page) Available at http://www.nantwichvetgroup.co.uk/103/hip-scoring. Accessed 9.8.10.

Hazewinkel H (2004) Nutritional Influences on Hip Dysplasia. WSAVA World Conference Proceeding 2004, (On-line). Available at http://www.vin.com/proceedings/Proceedings.plx?CID=WSAVA2004&PID=8727&O=Generic. Accessed 6.8.10.

Hou Y, Wang Y, Lust G, Zhu L, Zhang Z and Todhunter R (2010) Retrospective Analysis for Genetic Improvement of Hip Joints of Cohort Labrador Retrievers in the United States: 1970–2007. PLoS ONE 5(2) e9410. doi:10.1371/journal.pone.0009410

Jessen C and Spurell F (1973) Heritability of canine hip dysplasia. Proceedings of the Canine Hip Dysplasia Symposium. USA, pp 53-61

Kaneene J, Mostosky U and Miller R (2009) Update of a retrospective cohort study of changes in hip joint phenotype of dogs evaluated by the OFA in the United States, 1989-2003. Veterinary Surgery 38(3): 398-405

Kaneene J, Mostosky U and Padgett G (1997) Retrospective cohort study of changes in hip joint phenotype of dogs in the United States. Journal of the American Veterinary Medical Association 211: 1542-1544

Kealy R, Lawler D, Ballam J, Lust G, Smith G, Biery D and Olsson S (1997) Five-year longitudinal study on limited food consumption and development of osteoarthritis in coxofemoral joints in dogs. Journal of the American Veterinary Medical Association 210: 222–225

Leppanen M, Maki K, Juga J and Saloniemi H (2000) Factors affecting hip dysplasia in German Shepherd dogs in Finland: efficacy of the current improvement programme. Journal of Small Animal Practice 41: 19-23

Martin S, Kirby K and Pennock P (1980) Canine hip dysplasia: breed effects. Canadian Veterinary Journal 1980, 21: 293–296

O Neill DG, Church DB, McGreevy PD, Thomson PC and Brodbelt DC (2014) Prevalence of disorders recorded in dogs attending primary-care veterinary practices in England. PloS one 9, e90501. doi:10.1371/journal.pone.0090501

OFA (Orthopedic Foundation for Animals (2016) Hip Dysplasia by breed (On-line website) Available at http://www.ofa.net/stats_hip.html. Accessed 28.04.16.

Paster E, LaFond E, Biery D, Iriye A, Gregor T, Shofer F and Smith G (2005) Estimates of prevalence of hip dysplasia in Golden Retrievers and Rottweilers and the influence of bias on published prevalence figures. Journal of the American Veterinary Medical Association 226(3): 387-392

PennHIP organisation (no date) Owner and Breeder information about PennHIP (On-line website) Available at (http://research.vet.upenn.edu/pennhip/OwnerBreederInformation/SelectiveBreeding/tabid/3350/Default.aspx.  Accessed 9.8.10.

Riser WH (1993) Canine hip dysplasia. In Bojrab M (Ed) Disease mechanism in Small Animal Surgery. 2nd Ed. London: Lippincott, Williams and Wilkins.p797-803

Runge J, Kelly S, Gregor T, Kotwal S and Smith G (2010) Distraction index as a risk factor for osteoarthritis associated with hip dysplasia in four large dog breeds. Journal of Small Animal Practice 51: 264–269

Shell L and Harasen G (2007) Hip Dysplasia. (On-line webpage). Available at
http://www.vin.com/Members/Associate/Associate.plx?DiseaseId=1227. Accessed 2/8/10.

Smith G (1997) Advances in diagnosing canine hip dysplasia. Journal of the American Veterinary Medical Association 210: 1451-1457

Smith G, Gregor T, Rhodes W and Biery D (1993) Coxofemoral joint laxity from distraction radiography and its contemporaneous and prospective correlation with laxity, subjective score, and evidence of degenerative joint disease from conventional hip-extended radiography in dogs. American Journal of Veterinary Research 54: 1021-1042

Smith G, Mayhew P, Kapatkin A, McKelvie P, Shofer F and Gregor T (2001) Evaluation of risk factors for degenerative joint disease associated with hip dysplasia in German Shepherd Dogs, Golden Retrievers, Labrador Retrievers, and Rottweilers. Journal of the American Veterinary Medical Association 219(12): 1719-1724

Smith G, Popovitch C, Gregor T and Shofer F (1995) Evaluation of risk factors for degenerative joint disease associated with hip dysplasia in dogs. Journal of the American Veterinary Medical Association 206: 642-647

Sturaro E, Menegazzo L, Piccinini P, Bittante G, Carnier P and Gallo L (2010). Prevalence and genetic parameters for hip dysplasia in Italian population of purebred dogs. Italian Journal of Animal Science 5: 107–116. doi:10.4081/ijas.2006.107

Wilson BJ, Nicholas FW, James JW, Wade CM, Tammen I, Raadsma HW, Castle K and Thomson PC (2012) Heritability and phenotypic variation of canine hip dysplasia radiographic traits in a cohort of Australian German shepherd dogs. PloS one 7: e39620. doi:10.1371/journal.pone.0039620

Witsberger T, Villami J, Schultz L, Hahn A and Cook J (2008) Prevalence of and risk factors for hip dysplasia and cranial cruciate ligament deficiency in dogs. Journal of the American Veterinary Medical Association 232: 1818-1824

Zhang Z, Zhu L, Sandler J, Friedenberg S, Egelhoff J, Williams A, Dykes N, Hornbuckle W, Krotscheck U, Moise S, Lust G and Todhunter R (2009) Estimation of heritabilities, genetic correlations, and breeding values of four traits that collectively define hip dysplasia in dogs. American Journal of Veterinary Research 70: 483-492

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