The Role of Orthopedic Registries in Fighting Canine Hip Dysplasia

This is the fourth part in a series on canine hip dysplasia. What follows is written from the perspective that the readers of the series are conscientious breeders who are the guardians of the genetic pools that constitute their breeds. While this series of articles will not replace a stack of veterinary medical texts, it is a relatively in-depth look at the whole problem of a canine hip dysplasia. Furthermore, the series is designed to be retained as a reference. When you finish reading it you will have a sufficient background to make rational breeding choices and will be able to discuss the subject from an informed basis with your veterinarian. You may not like what you read, but you will be more competent to deal with the problem.

Conclusions from Part I:

Genetics is the foremost causative factor of canine hip dysplasia. Without the genes necessary to transmit this degenerative disease, there is no disease. Hip dysplasia is not something a dog gets; it either is dysplastic or it is not. An affected animal can exhibit a wide range of phenotypes, all the way from normal to severely dysplastic and functionally crippled. Hip dysplasia is genetically inherited.

Conclusions from Part II:

While environmental effects, to include nutrition and exercise, may play a part in mitigating or delaying the onset of clinical signs and clinical symptoms, hip dysplasia remains a genetically transmitted disease. Only by rigorous genetic selection will the incidence rate be reduced. In the meantime, it makes sense to have lean puppies and to avoid breeding animals from litters that showed signs of hip dysplasia. It is probable that even normal exercise levels may increase the phenotypic expression of CHD of a genetically predisposed dog. Stay away from calcium supplementation of any kind; all it can do is hurt. There is no conclusive evidence that vitamin C can prevent hip dysplasia, but there is some evidence that vitamin C may be useful in reducing pain and inflammation in the dysplastic dog.

Conclusions from Part III:

Canine hip dysplasia can be difficult to diagnose, as a number of other orthopedic neurological, autoimmune and metabolic problems may mimic it. Controversy surrounds the question of positioning for hip X-rays and what part joint laxity plays in hip dysplasia. Hip dysplasia may be more common in large and giant breeds and is one of the most over-diagnosed and misdiagnosed conditions.

In this article we address the issue of orthopedic registries. Given the widespread incidence of canine hip dysplasia, registries are not just nice to have; they are essential until we have a DNA or other genetic test available for screening and breeding.

The name of this article might well have been titled "Hip Dysplasia: The Controversy." We find that the various registries and the various diagnostic bodies have their own separate agendas, much of which seem to be mutually exclusive. The reader must understand that there are few definitive answers concerning hip dysplasia, and those that are more definitive than others are so only through the power of statistics and at the expense of the other theories. Generally accepted practices, and widespread acceptance of many popular beliefs and status of a given registry, seem to have little scientific basis.

The reality is this: Canine hip dysplasia is a polygenic and multifactorial disease that is closely associated with selection for breeding. There is a host of entrepreneurs ready in the wings, or already established, with many a system of registry or diagnostic and identification method to purvey to the dog breeder. The chaff greatly outnumbers the wheat. The focus of this article is to examine several registries, their practices, their strong points and their shortfalls. In so doing, we recognize we will be speaking unfavorably about some well-established "cash cows" from which many draw their livelihood. We recognize that along with "God, Country and Corps" there is the American Kennel Club, the Orthopedic Foundation for Animals and each of the breed clubs. In this article we will be taking several sacred institutions to task.

Back to top

THE AKC'S STANCE

The traditional stand of the AKC is that it is a registry for purebred dogs of breeds that have petitioned through their breed clubs to have their stud books accepted. The AKC has resisted requests to perform the wider task of registering the results of genetic screening, leaving that matter up to the breed clubs. A bench championship means no more than your dog amassed the necessary 15 points with two majors in shows sanctioned by the AKC. The "you breed them, we register them" mentality means that there is no warranty, expressed or implied, that such animals are fit for any task, function or for breeding. It is possible to register an animal that is a carrier or which is phenotypic for any genetically transmittable disease. So if the AKC in the United States is not going to stand for genetic screening, who is? The AKC has suggested that since the breed clubs set their rules and standards, they should also set the rules for their breeds genetic screening. This is what is done in Germany, for example. As of this writing, our attempts to discuss this stance with the AKC have gone unanswered.

Back to top

THE ROLE OF OFA

The grandfather of orthopedic registries in the United States is the powerful and prominent Orthopedic Foundation for Animals. Beyond a shadow of a doubt, the OFA is the world's largest all-breed orthopedic registry with more than 475,000 cases from 221 breeds on file evaluated between January 1, 1974 and January 1, 1995. ¹

Your vet anesthetizes your dog, shoots the X-rays in the hip-extended, American Veterinary Medical Association-approved position, and the film is sent to OFA for evaluation by three veterinary radiologists. These OFA-licensed veterinary radiologists evaluate the film based upon the hip-extended position. Your vet collects a fee; OFA collects a fee; if the hips pass, you get a number. This is the number much like an AKC registration number. The AKC number has so little value that the Canadian government does not currently allow importation of commercially bred dogs under the age of ten months if the dubious claim is made that because they are AKC-registered they are purebred. AKC registration is based on the honor system, and not all breeders or puppy mills have been honorable. The AKC is a cash cow catering to the puppy mills and breeders from which they draw significant revenue. The AKC has announced it is putting OFA numbers on registrations. Thus, for a little bit-or not so little bit-of money you can have two numbers of dubious value associated with your dog. This is only where the hip dysplasia controversy begins, not where it ends.

The problem with many closed(confidential) orthopedic registries is that they can become self-serving, self-selecting and, if they pass the test of time, self-perpetuating. While we authors have both separately done preliminary X-rays on young dogs, and later sent in X-rays for formal evaluation by a registry both in the United States and in Europe, we also have not bothered to spend money for formal evaluation when the local preliminary evaluation was "junk." We suspect that this is more common than not. We suspect that more dysplastic dogs are not evaluated by a registry than those that are. As we shoed in the earlier articles in this series, when a disease is polygenic and multifactorial, the best possible prediction is made by knowing about parents, siblings and progeny. ² Here is where most registries fall down. There is no requirement for filing of pedigrees and having all get in a litter evaluated. The OFA position is that the frequency of hip dysplasia in the general population is not that essential to know, but the frequency in the breeding population is. ³ The premise is that:

• Occurrence of HD in the progeny is significantly less when both parents are considered phenotypically normal. The reduction in occurrence of HD is even greater if there is pedigree depth and breadth for normal animals.

• Occurrence of HD in the progeny significantly increases when normals are mated with dysplastics and increases even more when dysplastics are mated with dysplastics.⁴

Taking a priori (beforehand-speculation) approach, one would predict that if a fledgling registry became established and self-perpetuating, it would be used for demonstrating that a given animal was in fact sound at the time of evaluation. Thus, the self-selection process would predominate, the percentage of animals with "excellent" hips would increase over time and the percentage of dysplastic animals would decrease. This has been the case with the OFA registry.⁵ All it means is that the registry is now catering to owners who wish to demonstrate the soundness of some of their dogs. Before OFA, there was no good public vehicle for doing this. Unfortunately, soundness of an individual animal means little genetically. One needs to know the soundness of siblings, parents and siblings of the parents. Unfortunately, hips which are sound at 24 months of age may be dysplastic later in life. The chronic (most common) form of hip dysplasia is insidious and may not show up radiographically for some time; however, radiographic signs are usually in evidence by 12 months of age.

Back to top

HAS OFA REDUCED DYSPLASIA?

Perspective in understanding this phenomenon is necessary if one is to draw appropriate conclusions about correlation and causation. The question before the dog fancy is whether OFA has in any meaningful manner contributed to the reduction of hip dysplasia. The answer is a resounding "No." Each year more than 2 million new dogs are registered with AKC. Over the period January 1974 to January 1995, this amounts to 40 million dogs. OFA evaluated only 475,000 dogs. This amounts to about 1 percent of the new dogs registered. The modest decrease in the self-selected dysplastic evaluations is but a drop in the bucket compared with the number of new AKC registrations. Thus the impact of the registry on hip dysplasia has been negligible.

A quick survey of various breed publications reveals that some breed followers are very much into thyroid and von Willebrand's tests and OFA and Canine Eye Registration Foundation (CERF) registry of hips and eyes, respectively. On the other hand, followers of other breeds are reluctant to advertise such results. Hip dysplasia is with us now as it was before. What we have been doing is not the answer. Until the time that provisional non-breeding registrations are given, and until proof is presented of the animal being clear of hip dysplasia, it is doubtful that the situation will much change. There have been limited efforts by breed clubs to reduce problems, but the examples are few and far between. Two stand out immediately for their success: When achondrodyplasia (dwarfism) was recognized in the Newfoundland, the parent club took immediate steps to require test breedings based upon pedigree research and virtually eliminated the problem within a few generations. ⁶ Similarly, the Malamute club is having success in ferreting out dwarfism and eliminating it from the gene pool. Without grassroots action by parent clubs supported by policies of the main registry (AKC), little can be expected. ^7-14

Back to top

DYSPLASIA TESTING ABROAD

In Germany, as in Japan, the breed clubs are very powerful and dictate to their members pretty much how things are going to be. Using Rottweilers in Germany as an example, pups are tattooed in their right ears at 8 weeks by a "breed warden." At 18 months of age they are X-rayed by a veterinarian licensed by the breed club, and the X-rays are interpreted by veterinary radiologists at the university clinic at Gottingen, also licensed by the breed club. The breed club then maintains a registry of the results. Currently, three ratings are given: HD free, HD+/-, and HD+, with the Norberg Angle used in making the determination. Progeny can only be registered from animals rated HD free or HD+/-.

By way of contrast, the Hovawart breed club follows a similar process of using club-licensed veterinarians to take the X-rays and to interpret them. However, only progeny from HD free parents are admitted to the registry. Remember, the subjectivity of legs-extended X-ray determinations and the lack of correlation between OFA and the Norberg Angle. ¹⁵

Persons we have interviewed report there have been instances where animals that scored well in Germany did less well under OFA scoring and vice versa. In the United Kingdom, the British Veterinary Association got together with the Kennel Club. English breed clubs were encouraged to establish standards for their own breeds and several have. However, in the absence of such a breed standard (and most clubs have not established a standard), the system is this: The lower the score, the less the degree of hip dysplasia. The minimum score for each hip is 0 and the total score of 0-4 with not more than 3 for one hip may be regarded to the "pass certificate" of old. A score of not more than 6 for one hip equates to a "breeder's letter" under the old system. ¹⁶

The scores are derived by deducting points corresponding to faults differing from a concept of perfect hips. From the limited experience author Cargill has had with only one dog (Ch. Kobu's K.O.) having been evaluated under both the OFA and BVA/KC systems, and they appear to be comparable. An OFA "excellent" or "good" should still show up as a score less than 8 in England, consistent with the subjectivity of interpretation discussed in the third article in this series. The British Veterinary Association informs the Kennel Club periodically of registered dogs that have obtained a score of 8 or less, with not more than 6 on one hip, and their names are published in the Kennel Gazette, the official publication of the Kennel Club.

Back to top

THE QUESTION OF JOINT LAXITY

Time for more controversy: joint laxity. The findings of research reported in the first three articles of this series indicate that hip dysplasia may be predicted by joint Laxity determined through stress radiography. ^17-23 The OFA rejects this hypothesis on the basis of "lack of standard pressure for the fulcrum and lack of pathologic evidence of secondary changes." ²⁴ Thus the conclusion drawn concerning the efficacy of joint laxity measurements made from stress radiography (as being propounded by Penn-HIP/ICG) being prognostic indicators of future phenotypic expression of canine hip dysplasia are rejected out of hand by OFA. Both OFA and Penn-HIP/ICG claim the other's methods are subjective and not reliable as predictors of future phenotypic expression of hip dysplasia.

Back to top

Conclusions:

Sadly, no breed registry in the United States requires genetic screening of parents as a prerequisite for litter registration, or even offers a "fitness for breeding" certification. The current The current registries for hip dysplasia (and other genetically transmitted problems) cover so little of the AKC-registered dog population that their impact so far has been minimal. The tools we need are there. Joint responsibility for failing to use the tools at hand lies with the AKC, United Kennel Club, parent clubs and individual breeders. Until this is done, we, the dog fancy, are wasting our time, and any breed registry such as the AKC, must be known as a "registry of sick dogs."

The next article in the series will cover the OFA vs. PennHIP controversy, and the requirement and desirability of an evaluation method that is not only diagnostic but also prognostic with an ability to predict the probability of phenotypic expression of hip dysplasia. Hand in hand with these methods goes the requirement for positive identification rather than the honor system currently in place and the concept of "open" genetic registries.

Back to top

CREDITS

References

1. Corley, E.A., Keller, G.G. "Hip Dysplasia: A progress report and update." 1993 Supplement.Orthopedic Foundation for Animals. p.1.

2. Cargill, J.C., Thorpe-Vargas, S. "Canine Hip Dysplasia Parts I & II." DOG WORLD. May and June 1995.

3. Corley, E.A., Keller, G.G. "Hip Dysplasia: A progress report and update." 1993 Supplement.Orthopedic Foundation for Animals.

4. Ibid.,p.2.

5. Ibid.,p.6.

6. Cargill, J.C. "What should 'champion' mean?" DOG WORLD. February 1993. Vol. 78, No. 2, p. 34.

7. Cargill, J.C. "Truth in advertising: breeder self-regulation Part I." DOG WORLD. July 1990. Vol. 75, No.7.

8. Cargill, J.C. "Truth in advertising: breeder self-regulation Part II." DOG WORLD. August 1990. Vol. 75, No.8.

9. Cargill, J.C. "Genetic Screening Essential." Pure-Bred Dogs/Am Kennel Gazette. January 1991, pp.68-72.

10. Jolly, R.D., Dodds, W.J., Ruth, G.R., Trauner, D.B. "Screening for genetic diseases: principles and practice." Adv. Vet. Sci. Comp. Med. 25:245-276, 1981.

11. Dodds, W.J. "Protect the health and longevity of purebred dogs through genetic screening for blood and thyroid diseases." Teaching syllabus. 1988.

12. Dodds, W.J. "Detection of genetic defect by screening programs." Pure-Bred Dogs/Am Kennel Gazette. June 1982. Pp.56-60.

13. Dodds, W.J. "An effective mass screening program for animal models of the inherited bleeding disorders." Prog. Clin. Biol. Res. 94:117-132. 1982

14. Dodds, W.J. "Genetic screening for inherited bleeding disorders. " Kal-Kan Forum. 1:52-28. 1982.

15. Smith, G.K., Gregor, T.P., Biery, D.N., et. al. "Hip dysplasia diagnosis: A comparison of diagnostic methods and diagnosticians." Proceedings of the 1992 Annual Scientific Meeting of the Veterinary Orthopedic Society, Keystone, Colorado, 1992. P.20.

16. British Veterinary Association. New BVA/KC Hip Dysplasia Scoring Scheme. February 1988.

17. Lust, G., Beilman, W.T., Rendanom, V.T. "A relationship between degree of laxity and synovial fluid volume in coxofemoral joints of dogs predisposed for hip dysplasia." Am J Vet Res.1980, 41:55-60.

18. Henricscon, B., Norberg, I., Olsson, S.E. "On the etiology and pathogenesis of hip dysplasia: a comparative review." J Small Anim Pract. 1966;7:673-687.

19. Smith, G.K., Biery, D.N., Gregor, T.P. "New concepts of coxofemoral joint stability and the development of a clinical stress-radiographic method for quantitating hip joint laxity in the dog." J Am Vet Med Assoc. 1990 Jan 1;196(1):59-70.

20. Smith, G.K., Gregor, T.P., Rhodes, W.H., Biery, D.N. "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." Am J Vet Res. 1993 Jul; 54(7).pp.1021-1042.

21. Morgan, S.J. "The pathology of canine hip dysplasia." Vet Clin N Am Sm Anim Prac. 1992 May;22(3):541-50.

22. Alexander, J.W. "The pathogenesis of canine hip dysplasia." Vet Clin N Am Sm Anim Prac. 1992 May;22(3):503-11.

23. Potscher, L.A. "Selktion gengen hueftgelenksdysplasies (HD) in einer Hovawart popuulation" [Selection criteria concerning hip dysplasia (HD) in a Hovawart population]. 1993 Winter; Dissertation Abstracts International-C 54/04, p.1069.

24. Corley, E.A., Keller, G.G. "Hip dysplasia: A progress report and update." 1993 Supplement.Orthopedic Foundation for Animals. p.17.

Back to top