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.

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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.

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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.

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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

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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.

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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.

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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.

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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.

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The authors assess the Pros and Cons of Standard diagnostic methods for hip dysplasia

This is the third 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.

This third article deals with the abnormal hip and how to diagnose it. Though CHD can afflict all breeds, it is more common in the large and giant breeds. There is far more to a proper diagnosis than first meets the eye. Anecdotal evidence has shown that canine hip dysplasia is one of the most over-diagnosed and misdiagnosed problems afflicting dogs. Many clinicians may depend too often on only subjective radiographic interpretation in the diagnosis of CHD. Physical examination techniques are helpful, and one can often pick up on concurrent conditions that could be otherwise overlooked. Initially, this article will focus on the clinical signs of hip dysplasia, the specific methods used by the experienced practitioner to make the diagnosis and the problems associated with the classic hips-extended, Orthopedic Foundation for Animals-approved X-ray positioning for radiographic study. The latter part of the article will be devoted to important new developments that hold promise for predicting the probability of phenotypic expression of CHD.

In the second article in the series, we said that canine hip dysplasia can be conveniently categorized into two major types. The first is severe and is seen early in the afflicted dog's life. The second, and far more common type, is the insidious chronic form that develops over a period of time. It is therefore useful to separate dogs by age classification when describing the clinical signs of hip dysplasia. A reasonable classification that takes into account maturity, puberty and attaining adult height, if not near adult weight, would be dogs less than one year in age and those more than one year in age. This gives time for atrophy and extraordinary musculature to develop as clinically recognizable signs. In the young dog, the first symptoms appear to be decreased activity, sometimes accompanied by joint pain. ¹ If a young dog is found to have a swaying or unsteady gait, or runs with both hind legs moving together - often referred to by breeders as the "bunny hop" - it is worth further investigation. Acute episodes of lameness with both or only one side affected can also occur after exercise or minor trauma. These signs can also be the result of infections in joints, lack of synovial fluid or the result of trauma. As CHD progresses, the dog may also have difficulty rising from a lying or sitting position and will frequently balk at going up or down stairs.

Two clinical signs that most often appear together in the older dog are well-developed muscles in the forelimbs and shoulders due to shifting weight forward. ² As the disease progresses, hypertrophy (over-development) of the front end is accompanied by symmetrical or non-symmetrical atrophy of the pelvic muscles. Such animals appear weak in the pelvic region, are reluctant to exercise, generally prefer sitting to standing and exhibit extreme discomfort when their forelimbs are lifted off the ground.

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Remember also that the affected dog may exhibit none of these symptoms. A substantial number of dogs with radiographic signs of hip dysplasia show no clinical signs of the disease. Explanations of this phenomenon are as varied as they are controversial. Quite a few practitioners believe that a dog radiographically positive for hip dysplasia but clinically negative for signs is just a dog in an intermediate stage of the disease progression. This period may last for months, even years, until the onset of substantial degenerative joint disease. It is not uncommon for an afflicted (genetically predisposed) dog to die of old age before any non-radiographic signs develop.

We repeat again the warning issued in the preceding articles: You cannot tell if a dog is genetically predisposed to hip dysplasia by its movement. Reject the false wisdom of the old-time breeder who emphatically states that if his or her dogs had hip dysplasia he or she would be able to see it. Hip dysplasia is a polygenic, multifactorial disease.

Before a definitive diagnosis of CHD can be made, other problems must be ruled out. ³ Thorough medical, orthopedic and neurological examinations must be made in order to rule out other disorders of the hip and spine. Multiple joint involvement may be the case. The following is a condensed list of some of the more common conditions that mimic or may be concurrent with canine hip dysplasia:

• Physical disorders of the stifle-ruptured or torn cranial cruciate ligaments; luxating patellae; meniscus tears in the knee.
• Diseases of the joints-rheumatoid arthritis; metabolic bone disease; polyarthritis from Lyme and other infectious disease; panosteitis (bone inflammation).
• Nutritional bone disease-chronic subclinical scurvy.
• Spinal disorders-ruptured vertebral disease; degenerative spinal disease; lumbosacral instability.
• Neurological conditions-trauma; poisoning (lead, etc.);infections; neural lesions; proprioception (posture sense).

An example of another condition masquerading as hip dysplasia is the all-too-common spinal degenerative myelopathy in German Shepherd Dogs. After reading the preceding list, you should realize that CHD is not an easy condition to diagnose with great surety unless a full examination is conducted. If you do not find radiographic signs, that still does not preclude some of the problems mentioned above.

Dr. William Inman a clinician in Washington state feels that canine hip dysplasia is the most over-diagnosed and misdiagnosed condition in the veterinary medical practice. 4 While he feels that hip dysplasia is genetically predisposed, he remains puzzled by finding in his practice clinically dysplastic dogs with radiographically normal hips and symptom-free dogs with coxofemoral joints that look "like a bomb went off in them." Inman states, "Curiously, in all the young dogs we see with hip dysplasia signs in the 5 to 18-month range, we always find a subluxation at T8-T10 [dislocation of the Thoracic vertebra 8 through Thoracic vertebra 10]." This is a potentially important finding because the T8 to T10 area "innervates the peraspinal muscles and the iliopsas muscle, which attaches to the femoral head and pulls it forward. Subluxation leads to muscle spasming, which causes continued anterior traction of the femur on the hip socket, flattening the Joint... reduction of this subluxation reverses the progression of hip dysplasia by curing the musculo-skeletal dysfunction." Inman has relieved the symptoms of more than 3,500 dogs with his procedure.

The conclusion that Inman has drawn from his practice is that the T8-T10 subluxation is a physical condition that, unless dealt with immediately, will progress to the joint capsular fibrosis and muscle stricture associated with decreased range of motion. The subsequent skeletal changes that follow can only be addressed surgically. He recommends early intervention in dogs thus afflicted to halt this insidious process.

Inman's theory appears radical, but it is not contrary to the concepts previously presented. He does not maintain that a genetic disease is not associated with hip dysplasia, only that a misdiagnosed physical condition mimics the disease process. Thus, the incidence of CHD may be lower than previously thought by other researchers.

Given that many other processes may be at play, the following are some of the physical techniques used in the diagnosis of CHD. While a tentative diagnosis can be made on the basis of history, clinical signs and the various palpation methods, standard veterinary practice requires radiographic signs of CHD. Diagnostic methods fall into two general categories: subjective and quantitative. We have found no method, subjective or quantitative, that is without its detractors or without serious controversy.

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SUBJECTIVE METHODS OF DIAGNOSIS

Observation

The first step in the diagnosis of a suspected case of CHD is orthopedic examination, which should include observation of the dog at rest, walking, running and a re-examination of the dog the day following vigorous exercise.5, 6 Observation and neurologic examination should be conducted before administering any drugs, and especially before sedation or general anesthesia, which can significantly alter the dog's neurologic status.

Range of motion

In an anesthetized dog, the coxofemoral joint's range of motion is approximately 110 degrees. ⁷  With pathology, this range of motion can be reduced to as little as 45 degrees. When following a chronic patient, the clinician uses changes in the range of motion to quantify the progress of the disease and as an aide when determining treatment options. Figure 1 is a table of the clinical categories by range of motion.

Changes in gait patterns

A shortened length of stride is associated with a loss in range of motion. There is a considerable variance among animals, but as a general rule, shortened stride length does not appear until fully extended movement is painful for the dog. This is the case with severe degenerative joint disease. Similarly, this type of gait abnormality can occur if the joint capsule has become fibrous. The many shapes and sizes of dogs make it impossible to describe all the potential gait changes. However, the bunny hop, left to right shift of the pelvis or an elliptical swing of the leg and hip are common gait problems encountered.

Forced extension

Affected dogs will not only exhibit discomfort with forced extension of the hip, but will try to return the limb to a more relaxed position. Depending on the temperament of these animals, they may also vocalize or exhibit aggressive behavior in response to pain. Be aware that the fighting dogs and the Northern breeds tend to have high pain tolerance levels and are generally stoic with respect to pain.

Downward pressure on the rear limb

When force is applied to the hips of a standing animal, the affected animal will show little or no resistance to the pressure, and will assume a sitting position. Several factors may simultaneously be involved and interrelated, such as pain, muscle weakness or atrophy.

Palpation

In humans, the most popular and reliable palpation maneuver used to identify congenital dislocation of the hip determines the presence or absence of the Ortolani sign. "A positive Ortolani sign confirms the diagnosis of coxofemoral subluxation in newborns prior to development of clinical signs or radiographic changes." ⁸  Many veterinarians feel that the techniques have too much subjectivity and variance to be of much use. Nonetheless, the Ortolani sign still figures prominently in the literature. ^9-14  Animals to be examined must be anesthetized past the point where there is still a palpable response. Two basic approaches are used: dorsal recumbency and lateral recumbency, with dorsal recumbency being preferred for large dogs. Downward pressure is applied down the axis of the femur until the femoral head subluxates. The leg is slowly abducted while holding the stifle firmly. If the joint is loose, a distinct clicking may be felt and in some cases will be audible.

Other palpation methods have been proposed by Barlow and Bardens. ^15,16 Barlow's Sign is essentially the first half of the Ortolani Test. Downward axial pressure is applied on the femur without abducting the leg. The Bardens' Test places the dog on its side, and the leg is held perpendicular to the spine. Lifting pressure is applied to the femoral shaft without abduction. The examiner's finger is placed on the greater trochanter. Any movement of the finger by more than one-fourth inch is considered a positive sign for a loose joint. Palpation has shown diagnostic use in human neonates, but is controversial and may have little diagnostic or prognostic utility in the dog. A caution: In human infants, it has been suggested that repetitive Barlow tests, and presumably Ortolani and Bardens as well, are capable of making infant hips unstable, thus giving a false-positive result. ¹⁷

The Neurologic exam

During a normal physical examination, the clinician will observe both the posture and movement of the dog. Of the two observations (gait and posture), how the animal stands or its ability to return to a normal stance tells more about the neurological status. Some breeds have been selectively bred for a characteristic gait. Thus gaits may vary tremendously among breeds. A Borzoi moving as a Bulldog would be one sick Borzoi. A poor postural response may indicate a proprioceptive deficit.

Proprioception, or posture sense, is the ability to recognize the location of limbs in relation to the rest of the body without visual clues. An abnormally wide stance is one indication of a possible problem. The simplest method of evaluation is to bend the paw so the back of the foot is bearing the dog's weight. The normal response is to immediately reposition the paw correctly. A problem in proprioception positioning is often an early indication of neurological problems, and most often precedes motor dysfunction (gait anomalies).

When evaluating the dog specifically for hip dysplasia, one needs to rule out deficits in the spinal-reflex arc. An example of the spinal-reflex arc where the neural response is not transmitted to the brain but returned (arcs back) is the familiar tap on the knee with a rubber hammer. (The neural response travels from the muscle to the spine and returns to the muscle, without traveling to the brain.) The absence of an involuntary response or an exaggerated response are indications of neurologic problems. Some variance among breeds is noted, as large dog responses tend to be less rapid than those in smaller breeds.

Routinely, the "knee jerk" (quadricep reflex) is tested first with the normal reaction being a single quick extension of the stifle. Next, the flexor reflex is evaluated by gently pinching the toes. The normal dog should pull the entire limb (hip, stifle and hock) up toward the belly. Although not strictly analogous, the extension toe reflex has been compared to the Babinski reflex in humans. The examiner will hold the hock and gently stroke the back surface from the hock down toward the pad. The normal animal will either exhibit no response or a slight flexion of the toes. The abnormal reaction is the extension and spreading of the toes. These tests, by no means comprehensive or exhaustive, constitute the minimal examination to rule out spinal problems in a dog being evaluated for hip dysplasia. ^₁₈

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SUBJECTIVE DIAGNOSTIC RADIOGRAPHIC METHODS

Hip-extended radiographic method

This traditional X-ray position has been the standard position, which has the dog sedated, on its back, with legs fully extended and patella facing upward, became the standard of the American Veterinary Medical Association Panel on Hip Dysplasia in 1961, and was adopted by the Orthopedic Foundation for Animals in 1966. University of Pennsylvania studies have been conducted that show interpretations are not highly consistent among radiologists, and are not highly consistent when the same radiologist reads the same deck of X-rays in shuffled order.¹⁹  OFA scores (excellent, good, fair, borderline, mild, moderate and severe) have wide acceptance but as subjective interpretations not readily repeatable with the same animal , nor likely to be interpreted consistently by different radiologists. At first it appeared that the seven-point scale was more discrete than diagnostic protocol warranted. When the seven-point scale was collapsed to a three-point scale (normal, borderline, dysplastic) agreement improved. The hips-extended positioning has come under criticism because it masks joint laxity. This positioning masks joint laxity in two ways both involving the joint capsule. With the hip extended, the fibers of the joint capsule tighten in such a way as to push the femoral head into the acetabulum. This position also leads to a lowering of the intra-articular pressure, which combined with the fixed synovial fluid volume causes invagination of the joint capsule. These two conditions limit the amount of sideways movement of the femoral head. Similarly, unsedated positioning may further mask joint laxity.

Norberg Angle method

The Norberg Angle radiographic method of determining joint laxity (subluxation) has been used more in Europe than in the United States. The standard OFA hip-extended radiographic projection is used (see figure 3). Norberg angles typically range from 55 degrees to 115 degrees, with the smaller numbers representing looser hips. Unfortunately, there is no common agreement as to what constitutes a normal angle, though 105 degrees may be used as a point estimate for normal joint laxity. Correlation with OFA interpretations is poor, which is one reason the Norberg Angle method is not well accepted as a diagnostic tool and is considered subjective at this time.

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QUANTITATIVE DIAGNOSTIC RADIOGRAPHIC METHOD

Compression/Distraction method

This new stress radiographic method originated at the University of Pennsylvania School of Veterinary Medicine and is currently marketed by PennHIP®. What started as a look at the role of passive hip laxity in CHD has become a quantitative diagnostic protocol referenced to an extensive data base. In recent years joint laxity has been established in the literature as prognostic for degenerative joint disease. Initially, however little statistical evidence supported this contention. Now that a major data base has been developed for purposes of comparison and for determining probabilities, joint laxity can be used as an indirect variable with which to predict the probability of eventual phenotypic expression of CHD.

Unfortunately for breeders, deep sedation is required in the compression/distraction method. The traditional OFA positioning was found inadequate. In the stress radiographic method, the dog is laid on its back with its hips at a neutral flexion/extension angle. A compression view is taken with the femoral heads seated tightly in the acetabula congruency between the two joint surfaces. A second, or distraction, view is taken showing the maximum separation distance of the femoral head center from the acetabular center A special device is used to force the femoral head away from the acetabulum for the distraction view. This protocol has been shown at University of Pennsylvania to reveal 2.5 times more joint laxity than the standard hip-extended radiograph.

The power of this method lies both in the new positions and in the statistical significance of the compression index (CI) and the distraction index (DI) as supported by a data base. 20 The indices range from 0 to 1, with "0 being a fully congruent hip (as seen in the compression radiographic view) and 1 representing the most extreme joint laxity as might be seen in the distraction view of hips that are virtually luxated." 21 The OFA scoring method is an ordinal scale, the Norberg Angle method is an interval scale and the DI is a ration scale. Thus the DI is intuitive in its meaning: A hip with a DI of 0.5 has twice the laxity of a hip with a DI of 0.25. Similarly a DI of 0.5 can be thought of as a hip 50 percent luxated. The DI ratio scale is far more useful a rating than the Norberg Angle. See figure 2 for a comparison of scales.

Breeders are always looking for earlier detection of CHD, the earlier the better for determining which animals to keep and classify as show and breeding hopefuls. Compression and distraction evaluations have been done on a sample of 8-week-old German Shepherd Dog puppies without the results being conclusive. At 16 weeks, this method becomes useful. Dr. Gale Smith, et. al., at the University of Pennsylvania Hip Improvement Program (PennHIP) recommended that dogs not be evaluated before 16 weeks and that follow-up radiography should be done at 6months or 1 year of age. ²²  In later articles in this series we will address the utility of the PennHIP protocol for prognosis.

Genetic (blood-based) diagnostic test

At this time, no biomechanical or metabolic differences have been identified in the dysplastic dog. Extensive work continues for an early blood marker for the condition. Finding such a marker would be ideal, as it would both allow the breeder to definitively screen breeding stock, and help the clinician identify appropriate treatment protocols. Parallel work is being done in determining genetic factors in humans for rheumatoid arthritis and osteoarthritis. Restriction Fragment Length Polymorphism (RFLP) linkage analysis has been used to identify genes associated with those diseases. Since there appears to be a strong genetic base for CHD, restriction fragments in the white blood cell DNA should correspond to the dysplastic phenotype. ^{23, 24}

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Conclusions:

Canine Hip Dysplasia can be difficult to diagnose. Other orthopedic, neurological, autoimmune/infection and metabolic problems may mimic CHD or may be concurrent with CHD. Numerous palpation techniques (Ortolani, Bardens, Barlow) have been proposed; however, they remain subjective nonquantitative methods that rely heavily on the skill of the clinician. The standard in current veterinary practice is to confirm CHD radiographically. The traditional American Veterinary Medical Association and Orthopedic Foundation for Animals hip-extended radiographic view distorts the amount of joint laxity present by forcing the femoral head deeper into the acetabular cup, thus understating the amount of laxity present. University of Pennsylvania (PennHIP) protocols for stress radiography are coming to the forefront as a more definitive way of visualizing hip joint laxity. Canine hip dysplasia remains a polygenic, multifactorial disease.

The next article in this series will discuss the various hip dysplasia registries, their approaches to the problems of canine hip dysplasia and the importance of having a "tamper-proof" identification system.

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CREDITS

References

1. Bardens JW Hardwick H. "New Observations on the diagnosis and cause of hip dysplasia." Vet Med Small Anim Clin,63:238, 1968.

2. Bar ARS, Denny HR, Gibbs C. "Clinical hip dysplasia in growing dogs: The longterm results of conservative management." J Sm Anim Pract,28:243, 1987.

3. Brinker WO, Peirmattei DL, Flo GL. "Physical examination of lameness." In Handbook of Small Animal Orthopedics and Fracture Treatment, ed 2. Philadelphia, WB Saunders, 1990, p. 267.

4. Personal communication with Dr. William Inman, Lake City Animal Hospital, 13045 Lake City Way N.E., Seattle, WA 98125; (206)362-0909.

5. Brinker WO, Peirmattei DL, Flo GL. "Physical examination of lameness." In Handbook of Small Animal Orthopedics and Fracture Treatment, ed 2. Philadelphia, WB Saunders, 1990, p. 341.

6. Lust G, Rendano VT, Summers BA. "Canine hip dysplasia: Concepts and diagnosis." J Am Vet Med Assoc, 187:638, 1985.

7. Riser WH, Newton CD. "Canine hip dysplasia as a disease." In Bojrab MJ (ed). Pathophysiology in Small Animal Surgery.Philadelphia, Lea & Febiger, 1981, p. 618.

8. Chalman JA, Butler HC. "Coxofemoral joint laxity ant the Ortolani sign." J Am Animal Hosp Assoc, 21:671, 1985.

9. Fry TR, Clark DM. "In canine hip dysplasia: Clinical signs and physical diagnosis." Vet Clinics No Am Sm Anim Prac, Vol 2, No. 3, pp., 554-557, 1992.

10. Ibid.

11. Ortolani M. "The Classic: Congenital hip dysplasia in the light of early and very early diagnosis." Clin Orthop, 119;6-10, 1976.

12. Bardens JW. "Palpation for the detection of dysplasia and wedge technique for pelvic radiography." In proceedings, 39th Annual Meet Am Anim Hosp Assoc 1972;468-471.

13. Wright PJ Mason TA. "The usefulness of palpation of joint laxity in puppies as a predictor of hip dysplasia in a guide dog breeding programme." J Smal Anim Prac, 1077;18:5513-5522.

14. Dixon RT. "Some experimental observations of the detection and demonstration of coxofemoral subluxation in the dog." Aust Vet Prac, 1975;55:220-226.

15. Bardens JW Hardwick H. "Observations on the diagnosis and cause of hip dysplasia." Vet Med Small Anim Clin,63:238-245, 1968.

16. Barlow TG. "Early Diagnosis and treatment of congenital dislocation of the hips." J. Bon Joint Surg, 44-B:292-301 1968.

17. Fry TR, Clark DM. "In canine hip dysplasia: Clinical signs and physical diagnosis." Vet Clinics No Am Sm Anim Prac, Vol 2, No. 3, pp., 554-557, 1992.

18. Oliver JD, Lorenz MD. Handbook of Veterinary Neurology. 1993,W.B. Saunders, pp. 3-45.

19. Smith GK, Gregor TP Biery DN 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, CO, 1992, p.20.

20. Smith GK Biery DN Gregor TP. "New concepts of coxofemoral joint stability and the development of a clinical stress-radiographic method for quantitating hip joint laxity in the dog." i>J Am Vet Med Assoc, 1990; 196:59-70.

21. Smith GK. "Diagnosis of Canine Hip Dysplasia." Adapted from Smith GK: Current Concepts in the Diagnosis of Canine Hip Dysplasia, in Bonagura JD (ed): Kirk's Current Veterinary Therapy XII: Small Animal Practice. Philadelphia, W.B. Saunders, 1995, p. 16.

22. Ibid, p.18.

23. Sinha AA Lopez MT, McDevitt HO. "Autoimmune diseases: The failure of self tolerance." Science, Vol. 248, June 15, 1990, pp. 1380-1387.

24. Tod JA, Acha-Orbea H, Bell, Chao N, Froneck Z, Jacob CO, McDermott M Sinha AA, Timmerman L, Steinman L, McDevitt HO. "A molecular basis for MHC Class II-Associated Autoimmunity." Science, Vol. 240, May 20, 1988, pp. 1003-1009.

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Causative Factors of Canine Hip Dysplasia

This is the second 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. 

In this article we will address the issue of genetic, nutritional and environmental factors. We hope to debunk some of the myths and introduce some recently developed theories. 

Other diseases, infections or trauma can produce clinical signs suggestive of canine hip dysplasia. In some breeds the animals learn to live with pain and are stoic about letting anyone know of their pain. This stoicism seems to be especially prevalent in terriers and northern breeds and is the case - not the exception - in the fighting breeds. Those fanciers who participate in pulling, freighting, carting or sledding events with their dogs should always be aware that tendonitis or pulled muscles can cause a gait change reminiscent of hip dysplasia. Anyone involved in lure chasing or coursing for real needs to understand that on occasion, an animal will twist or turn the wrong way while in full chase. In the older dog, trauma from younger years may manifest itself as arthritic deterioration. A little bit more unusual is to have viral penetration of the joint capsule with resultant damage to articular cartilage, or the epiphyseal surfaces of the femur. Absent such unusual occurrences, the reality of hip dysplasia is that it is a genetically linked condition--always was, always will be.

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THE ROLE OF GROWTH

In the first article we said that the first six months of a puppy's life seem to be a critical time of development. The rate of growth can be astonishing. When one thinks of the number of things that could go wrong as an Akita puppy, for instance, goes from a birth weight of slightly more than 1 pound to 60 to 70 pounds in six months and then adds another 30 to 40 pounds by year end, it is amazing that most dogs mature without serious problems. It is during this period that dogs are most active. There is evidence to suggest that exercise is necessary to retain the depth of the acetabulum. How much exercise and of what type is unknown. 

One Norwegian anecdotal study published in England in 1991 concluded that German Wirehaired Pointer, English Setter, Irish Setter, Gordon Setter and Labrador Retriever puppies growing up during the spring and summer had a lower incidence rate of hip dysplasia than puppies growing up during autumn and winter. Oddly enough, Golden Retrievers and German Shepherd Dogs did not manifest the same seasonal pattern of incidence of hip dysplasia. ¹ 

While this study may lack strict experimental protocol, it raises many questions. The first question is whether there was an exercise differential between the dogs due to weather in Norway. The second question was whether there was different availability of sunlight necessary for vitamin D production and utilization. The list of questions could go on, but this study is brought up to show that there may be exercise and diet factors at play, and that various breeds may respond to these factors in different ways. It would be reasonable to conclude that there is probably an amount of exercise during a genotypically dysplastic puppy's rapid growth period where phenotypic expression is mitigated, delayed, or both. Without taking the time, cost and effort to conduct a rigorous scientific study, it is still sometimes possible to glean valuable information from existing, i.e., available data. Therefore, do not shy away from creating working hypotheses from anecdotal studies; conversely, do not lock their findings in concrete as inviolate fact. 

With respect to the published scientific literature, we found nothing in Medline (an online listing of medical and biological articles) referencing any journal article addressing the subject of surfaces and their effects on the incidence of hip dysplasia. While we know of breeders who write into their sales contracts that animals must be kept on a specific surface and fed a specific feed, these demands seem to be without scientific basis.

There is some evidence that preventing rapid growth reduces the extent to which the adult dog will manifest hip dysplasia. Decreasing the dog's food consumption during its growth period seems to correlate well with normal hips. ² The Kealy study published in 1992 was based upon 48 8-week-old Labrador Retriever puppies. These puppies were sex-matched littermates randomly assigned to two groups: the first group was fed ad libitum (as much as they wanted, when they wanted to eat); the second group was fed the same feed until they were 2 years old, but in amounts of only 75 percent of what the first group consumed ad libitum. Thus for every puppy fed ad libitum, there was a same-sex littermate on a restricted diet. This rigid protocol gives this study great respectability and credence. The accompanying chart gives the findings in tabular form. Note the tremendous increase in normal animals at two years of age when kept on a restricted diet for those two years. This ought to more than suggest that overweight animals are at risk for phenotypic expression of canine hip dysplasia.

Many researchers conclude that early fusion may lead to bone and cartilage deviations which then could predispose the animal to future dysplasia. An important point that these studies illustrate is that it is possible to improve the individual phenotype of dogs whose parents carried the gene for hip dysplasia (genotypically dysplastic).

In the first article we alluded to joint laxity as being present whenever there is canine hip dysplasia. Given that joint laxity is at least one of the factors governing the onset of hip dysplasia, then any process that retards this condition could possibly minimize the severity of the disease. It also is conceivable that retardation of joint laxity could delay the onset of the physical appearance of the disease.

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FEED FOR HEALTH

A recent study (1993) showed that coxofemoral joint stability was improved in dogs that were fed increased levels of chloride and decreased levels of sodium and potassium. ³ In the eight-part "Feed That Dog!" series (Dog World, July 1993 through February 1994) we emphasized repeatedly the importance of the ratio of sodium and chlorine, with a ratio of 1.5 sodium to chlorine being accepted as the dietary requirement. ⁴ We noted also that "sodium chloride deficiency is manifested by fatigue, decreased utilization of protein, decreased water Intake, inability to maintain water balance, retarded growth, dryness of skin and loss of hair." ⁵ Potassium deficiency " results in poor growth, restlessness, muscular paralysis, a tendency toward dehydration, and lesions of the heart and kidney." ⁶ We cautioned that "prednisone, a steroid commonly prescribed for various skin allergies, causes a loss of potassium and retention of sodium, and retention of sodium can cause further loss of potassium." ⁷

Calcium (Ca), sodium (Na), and potassium (K) are the electrolytes considered most important, as they are necessary to many biological functions. Electrolytes are atoms or molecules that carry either a negative or a positive charge. Anions have an extra electron, and thus carry a negative charge. Cations are missing an electron, thus they carry a positive charge. In the study cited, Kealy et. Al. Introduced the theory of "dietary anion gap" or DAG. ⁸ The researchers explained DAG as the amount of chloride ion subtracted from the sum of sodium ion and potassium ions:

DAG = [(K⁺ + Na⁺) - Cl^-]

This experiment, consisting of the raising of 167 puppies, included puppies from five different breeds. They were placed on three different diets tat varied only in their DAG content. Examples of low DAG ingredients are rice with a DAG of 6 and corn gluten meal with a DAG of 5. The result of this experiment showed that except for some breed-specific exceptions, those dogs that were fed a lower DAG diet had better hips at 30 weeks than those fed a diet with a higher DAG content. Differences in DAG balance did not result in different rates of weight gain. This is important, for it allowed elimination of weight gain as a Causative factor in the study. Hips were evaluated by their degree of subluxation as measured by the Norberg angle. The Norberg angle is the "angle included between a line connecting the femoral head centers and a line from the femoral head center to the crainiodorsal acetabular rim." ⁹ The greater the Norberg angle, the less the subluxation. Norberg angles are commonly measured as <90 degrees for loose hips and >105 degrees for tight hips. Those dogs with better hips at 30 weeks also had good hips at 2 years of age.

Unfortunately, the researchers were unable to explain the mechanism or the "why" of how they got the results they did. One of the theories proposed was that a lower DAG somehow affected the pH or "acidity" of the synovial fluid. This in turn affected the osmolality or "thickness" of the synovial fluid. The osmolality of a fluid depends upon the number of dissolved particles in it, and is the measure of the osmotic pressure. In previous studies, a higher osmolality was associated with the greater synovial fluid volume found in dysplastic dogs. Note, of course, that there is a normal range of DAG values in a balanced diet. Leaving that range while formulating a dog food, for example, could cause serious problems.

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CALCIUM

The question of calcium supplementation while controversial among breeders, is fairly easy to answer: don't do it. It is not necessary to add extra calcium to your dog's diet. Not only is calcium an essential skeletal component, it is also necessary for blood coagulation, hormonal release and muscle contraction. The three biological systems involved in controlling The amount of calcium in the blood are bones, kidneys, and the intestine.

Calcium is constantly being recycled in and out of living bone. In the adult dog, under balanced conditions, both accretion (calcium uptake) and resorption (calcium loss from bone) values vary from 0.1 to 0.2 mmol per kilogram of body weight per day. [A millimole is a minute measure of molecular weight.] For the rapidly growing puppy these values are at least 100 times higher. ¹⁰ Another difference between an adult dog and a puppy is their relative abilities to absorb calcium from the food they ingest. In the adult dog, the percentage of calcium assimilated from food varies from 0 to 90 percent, depending upon the composition of the food and its calcium content. ¹¹

A 1985 study which examined the physical, biochemical and calcium metabolic changes in growing Great Danes, showed that young puppies do not have a mechanism to protect themselves against excessive calcium feeding. Under the influence of certain hormones, the calcium excess is routed to the bones. This results in severe pathological consequences for the patterning for the growing skeleton and the subsequent impairment of gait. Strongly correlated with high calcium intake is disturbed enchrondral ossification (growth plate anomalies) causing the clinical appearance of radius curvus syndrome and osteochondrosis (a disturbance of bone formation within the cartilage, occurring during periods of maximum growth). ¹² Chronic, high calcium intake in large breed dogs has also been associated with hypercalcemia, elevation of the liver enzyme alkaline phosphatase, retardation of bone maturation, an increase in bone volume, a decrease in the number of bone resorption cells, and delayed maturation of cartilage. ¹³ We can safely conclude that calcium plays a significant role in skeletal disease. The giant breed dogs, because of their rapid and intense growth, are sentinels for nutritionally influenced diseases. These changes, while exaggerated in the giant breeds, are just as real-though they may be slower to surface and not as easily identified-in the smaller breeds.

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VITAMIN C

Vitamin C (L-ascorbic acid) has frequently made it into the literature along with calcium. At one time or another vitamin C has been touted by somebody as a cure-all for virtually any malady known to man and beast. This is not discount the requirements for vitamin C, for it is absolutely necessary. Fortunately for dogs, they produce an enzyme called L-gulonolactone oxidase, which allows them to synthesize vitamin C from glucose without having access to a dietary form of vitamin C. (A deficiency could only be the result of either a problem with absorption or an increased need.) Interestingly, canines produce only 40mg of ascorbate per kilogram of body weight, which is far less than other mammals with the ability to synthesize their own vitamin C. There is no established minimum daily requirement for vitamin C in canine nutrition. That said, let's look at the function of the vitamin C the dog manufactures.

Vitamin C figures prominently in the biosynthesis of collagen. ¹⁴ Collagen is an important structural protein in the body. There are different types of collagen, but it is Type I collagen that appears most often in connective tissue, particularly in bone and ligaments. Vitamin C adds an -OH group to the two amino acids proline and lysine. Without this functional group there is a decrease in the number of cross-links in collagen. Without this cross-linking, the melting temperature of the protein is reduced from about 39 degrees to 23 degrees centigrade. In other words, without the cross-links this protein can be denatured at body temperatures.

There is experimental evidence that vitamin C may play a role in bone mineralization by stimulating bone resorption. What has been shown by one researcher to be efficacious in treating the physical manifestations of canine hip dysplasia (CHD) is a form of vitamin C called polyascorbate. ¹⁵ Calcium ascorbate, used in conjunction with vitamin E, also is considered helpful in reducing the inflammatory processes that accompany the disease. In this form, vitamin C is taken up by the bone along with calcium, and this acts like a time release factor that keeps the blood plasma concentration high and the cells constantly "bathed" with vitamin C.

With all the continuing fuss about vitamin C in the fad literature, it was inevitable that it would be tried for treatment of hip dysplasia. Belfield (1976) conducted a somewhat anecdotal study on eight German Shepherd Dog litters of puppies from dysplastic parents or parents known to have produced dysplastic puppies. ¹⁶ Megadoses of ascorbate were given to dams (2 to 4 grams of sodium ascorbate crystals per day) and to the pups (birth to 3 weeks-calcium and vitamin E supplement; 3 weeks to 4 months-500 grams ascorbate per day; 4 months to 1.5 to 2.0 years-1 to 2 grams ascorbate per day). Belfield claimed that none of the pups developed hip dysplasia, and breeders involved with the research were so convinced that they guaranteed dysplasia-free puppies if the ascorbate therapy was followed by the new owner. It is significant to note that no follow-up studies were published. While this is interesting, there is little accepted hard evidence to suggest that supplementation with ascorbate can prevent or ameliorate canine hip dysplasia. Readers are cautioned that large doses of vitamin C are not considered mainstream prophylaxis or therapy. The truth of the matter is that it is in the genes, not the diet, though diet may play a minor part.

A recent study (1993) observed that synovial fluid volume as related to osmolality correlated highly with the incidence of hip dysplasia. ¹⁷ This suggested that the swelling of the joint capsule from excess fluid pressure might be forcing the femoral head out of position in the acetabulum.

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TISSUE CHANGES

Before any radiographic indications appear, there are structural changes at the tissue level of muscles, ligaments and cartilage. Cellular changes and molecular changes occur both in the joint capsule and in the synovial fluid. One study suggested that one of the first observable changes of the disease process is hypertrophy or swelling of the pectineus muscle fibers. ¹⁸ This hypertrophy is thought to be a compensatory adaptation to extreme contractile tensions and may be the result of the muscle mass trying to hold the acetabulum and the femoral head in the proper position.

Another study showed that the composition of the pectineus muscle was significantly different between 2-month-old puppies that eventually developed normal hips, and those that were dysplastic by 24 months. ¹⁹ The two groups differed by the size of the muscle fibers, but this time, the dysplastic animals had smaller than normal muscle fibers (hypotrophy) and the ratio between contractile tissue and non-contractile tissue was lower. Thus, not only did the affected animals have diminished capacity to contract their muscles, their muscles were also less elastic. This study begs the question of joint laxity: Once stretched, would the muscles tend to remain stretched, thus resulting in a looser hip joint? Unfortunately, it cannot be said with any certainty whether these differences are causal or correlative.

It is certain, however, that hip dysplasia is characterized by joint laxity. ^{20,21,22,23,24} Whether such laxity is the result of the pathological processes involved in the disease, or whether the laxity is the cause of the disease, cannot be determined. Remember, however, that loose joints and hip dysplasia are found together. We will be coming back to this point in later articles. There is a little twist to what we find: All dogs that have hip dysplasia have loose hips, but not all dogs with loose hips have hip dysplasia. It is not known which comes first: remodeling of the bony surfaces leading to abnormal wear of articular surfaces and joint instability or vice versa. It may very well be that both processes are concurrent and/or iterative processes.

Other changes that can precede either clinical signs, like pain and gait abnormalities, or radiographic evidence of hip dysplasia include thickening of the joint capsule and swelling of the round ligament. Subtle and early changes in articular cartilage structure also precede clinical signs. Specifically, in affected animals, the ratio between Type A cells and Type B cells differs from the norm. Type A cells are macrophages, i.e., large mononuclear cells produced by the immune system which ingest damaged cells and blood tissue. Type B cells are fibroblasts which are precursors of connective tissue. In one study, the population of Type A cells increased. ²⁵ Conceptually this makes sense, as the function of macrophages is to scavenge damaged cells, which would be the case if articular cartilage is being damaged. Note that these changes can only be observed after dissection and examination under an electron microscope. While diagnostic and predictive, such examination is without use to the clinician who is trying to diagnose the disorder. What is important to remember is that these changes are found in dogs whose x-rays showed them to be perfectly normal at the time of radiographic study. As a concerned breeder or fancier of dogs, this should alarm you. Do not be too alarmed, however, because there is hope for predictive techniques. These will be covered in later articles in this series.

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SIGNIFICANT STUDIES

The major study demonstrating the polygenic and multifactorial aspects of canine hip dysplasia is probably the 1991 German study an German Shepherd Dogs. ²⁶ Unfortunately this article is in German and we know of no translations available. While this poses no problem for co-author Thorpe-Vargas, as she used to be at the Max Planck Institute in Germany, it is a real problem for co-author Cargill, as he has to take her word for it, supported only by Medline abstracts in English! The importance of this study is that it covered 10,595 dogs. Furthermore, this study attempted to quantify both environmental influences and genetic influences on the frequency of hip dysplasia. Models were developed using the following variables-independent random variables: age at X-raying, birth year, season, litter size, percent of X-rayed dogs in each litter and sex ratio of litter; independent fixed variables: sire and dam.

Through multiple linear and non-linear regression methods it was shown that sire, dam, sex and age at X-raying all showed statistically significant influence on the occurrence of hip dysplasia. The heritability indices (H²) were-Relationship: full siblings, H² = 0.30; maternal half-siblings, H² = 0.48; and paternal half-siblings, H² = 0.11.

The researchers' caveat at the end of the study was that only the paternal half siblings' heritability index should be accepted because kennel and breeder effects are confounded with the dam effect. Their overall conclusion was that the frequency of hip dysplasia could be reduced if selection for breeding based upon the estimation of breeding values (H²) with respect to the frequency of hip dysplasia in all relatives was implemented.

Many of the world's militaries are good sources of information on German Shepherd Dogs. The goals of such organizations have been to improve behavioral traits and to reduce the frequency of CHD. One of the more interesting studies in the literature is the one based uopn information provided by the US Army's division of Biosensor Research on the German Shepherd Dogs bred between 1968 and 1976.²⁷ Detailed records were available for 575 animals representing 4 years, 18 sires, 71 dams and 48 human handlers. Variance component estimates were made, which allowed estimates of the heritabilities for both temperament and CHD scores to be made. The heritability index (H²) for temperament was 0.51 and for CHD was 0.26. Interestingly, in this population the genetic correlation between good temperament and bad hips was -0.33. Given the selection process of the U.S. Army, it was not surprising to find that dogs with good temperaments also had good hips. Because of the extremely high heritability index for temperament, records of the animal being evaluated can be used for repeat breeding selection rather than the records of the progeny.

A 1993 Austrian dissertation looked at a population of 10,750 Hovawarts from 1962 to 1988, out of which CHD findings were available for 4,387 dogs. ²⁸ The goal of the dissertation was to statistically calculate two parameters. The first was a prediction coefficient based upon the CHD findings of all the ancestors of a specific animal. The second was a "taint" coefficient calculated on the basis of the CHD findings of all ancestors as well as of the individual CHD finding as well as those of any offspring already checked for CHD. The conclusions of this dissertation were that both the "prediction" and "taint" coefficients were useful in calculating the relative CHD risk of the prospective offspring when selecting breeding partners. A connection was found between the CHD findings and the inbreeding level of an animal as calculated from the "ancestor loss coefficient" and Malecots "coefficient de parente." Thus, increasing levels of inbreeding increase the risk of CHD. There was no difference between males and females for risk of CHD. Detailed coverage of the various genetic coefficients is beyond the scope of this article. Readers are directed to modern comprehensive texts, dissertation abstracts and the like in genetics should more than a passing familiarity with the intricacies of these coefficients be required.

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Conclusions:

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 that are exercised regularly and to avoid breeding any 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 tat 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. Let your conscience and your veterinarian be your guides in supplementing with vitamin C. Fortunately, large doses of vitamin C are readily excreted, but it is still possible to cause untoward side effects with megadoses.

The next article in the series will address the abnormal hip, to include differential diagnosis, observation, palpation fluid sampling and sedated and unsedated radiographic studies.

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CREDITS

References

1. Hanssen I. "Hip Dysplasia in dogs in relation to their month of birth." Vet Rec. 1991 May 4;128(18):425-6.

2. Kealy R.D., Olsson S.E., Monti K.L., Lawler D.F., Biery D.N., Helms R.W., Lust G., Smith G.K. "Effects of limited food consumption on the incidence of hip dysplasia in growing dogs." J Am Vet Med Assoc. 1992 September 15;201(6):857-63.

3. Kealy R.D., Olsson S.E., Monti K.L., Lawler D.F., Biery D.N., Helms R.W., Lust G., Smith G.K. "Effects of dietary electrolyte balance on subluxation of the femoral head in growing dogs." Am J Vet Res. 1993 April:54(4):555-62.

4. Cargill J.C. "Feed That Dog! Part II." Dog World. 1993 August;75(8):12.

5. Ibid.

6. Ibid.

7. Ibid.

8. "Effects of dietary electrolyte balance." Pp. 555-62.

9. Smith G.K., Gregor T.P., Rhodes W.H. Biery D.N. "Coxofemoral joint laxity from distration 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 July;54(7):1023.

10. Hedhammer A., Wu F.M., Krook L., Schryver H.F., de Lahunta A., Wahlen J.P., Kallfelz F.A., Nunez E.A., Hintz H.F., Sheffy B.E., Ryan G.D. " Overnutrition and skeletal disease. An experimental study in growing Great Dane dogs." Cornell Veterinarian 1974;64 supp15:11-160.

11. Hedhammer A., Krook L., Schryver H.F., Kallfelz F. " Calcium balance in the dog." In "Nutrition of the Dog and Cat" ed. Anderson R.S.; Pergamon Press, Oxford 1980:119-27.

12. Hazewinkle H.A.W. "Influence of different calcium intakes on calcium metabolism and skeletal development in young Great Danes." PhD Thesis Utrecht State University 1985.

13. Hazewinkle H.A.W., Goedegbuure S.A. Poulos P.W., Wolvekamp W.ThC. "Influences of chronic calcium excess of the skeletal development of growing Great Danes." J Am An Hosp Assoc. 1985;21:377-91.

14. Berg R.A., Prockop B.J. "The thermal transition of a non-hydroxilated form of colagen: Evidence for a role for hydroxiproline in stabilizing the triple helix of collagen." Bio Chem Bio Phys Res Commun. 1973; Vol. 52:115-129.

15. Berge, G.E. "Polyascorbat, et behandlings-alternativ ved kroniske forandringer I stotte og bevegelsesapparetet hos hund" ("Polyascorbate, an interesting alternative by problems in the support and movement apparatus in dogs.") Norsk Veterinaertidsskrift (Norwegian Vet J),August/September 1990;102:581-582.

16. Belfield, W.O. "Chronic subclinical survey in canine hip dysplasia." Vet Med Sm An Clin. 1976; Vol. 71:1399-1403.

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. Cardinet, G.H. III, Wallace L.J., Fedde M.R. "Developmental myopathy in the canine." Arch Neurol. 1969, 21:620-630.

19. Lust G., Craig P.H., Ross G.E. "Studies on pectineal muscles in canine hip dysplasia." Cornell Vet. 1972, 62:628-645.

20. 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.

21. 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." 1990 January 1;196(1):59-70.

22. "Coxofemoral joint laxityPp.1021-1042.

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

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

25. Greisen H.A., Summers B.A., Lust, G. "Ultra Structure of the Articular Cartilage and Syunovium in the Early Stages of Degenerative Joint Disease in Canine Hip Joints." Am J Vet Res. 1982; 43:pp. 1963-1971.

26. Distl O., Grussler W., Schwarz J., Karusslich H. "Analyse umweltbedingter un genetischer Einflusse auf die Haufigkeit von Huftgelenksdysplasie beim Deutschen Shaferhund." ("Analysis of environmentally conditioned and genetic influences on the frequency of hip joint dysplasia in German Shepherd Dogs"). Zentralbl Veterinarmed A. 1991 Jul;38(6):460-71.

27. Mackenzie S.A. "Inheritance of temperament and hip dysplasia scores in German Shepherd Dogs." 1984 March; Dissertation Abstracts International-B 44/09, p.2652.

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

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To understand this genetically transmitted disease, we must first
understand the workings of the normal canine hip.

This is the first in a series of articles addressing 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 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.

Hip dysplasia is one of the most controversial and widespread problems in the dog fancy. So many old-wives tales, anecdotes, misconceptions and even lies abound that one of the goals of this series of articles must be to lay things out to the reader as they are, supported with some scientific basis.

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Let's start with a hypothetical scenario, but one which too many of us have faced:

He's major-pointed; he moves like a dream; that head piece may just be the best you have ever bred. In short, this boy typifies everything that is good about your breed and is the culmination of many years of hard work, hopes, tears, frustration and all the ups and downs, joys and heartaches common to the fancy. Now it is time to X-ray his hips so that you can not only use him in your breeding program, but advertise him at stud. This is one boy that is going to make it, and we are talking national specialty here.

Problem - the radiographic results come back with a diagnosis of canine hip dysplasia-severe. What should you do?

More among us than will admit have had this experience, and most of those who haven't have seen it happen to other breeders concentrating on similar bloodlines. Now back to our hypothetical scenario:

You never suspected a thing. The dog never appeared to be in pain and his gait was what won him his major points. You have invested time, money and your hopes on this animal, and it all has been for naught! Now is the time for hysteria and self-blame:

• What went wrong?
• Could this have been prevented?
• Was he not fed correctly?
• Was he kept on an improper surface growing?
• What is this disease that keeps reappearing in the most conscientious of breeding programs, and which frustrates our attempts to eradicate it?

The first step in understanding canine hip dysplasia is to recognize it as not just one disease but many diseases, which together result in degenerative effects on the hip joint. An extremely complex disorder, hip dysplasia is now thought by some to be the most noticeable manifestation of a systemic condition that can affect not only the hip joints but also those of the elbow, shoulder and event the joints between the vertebrae ¹. Whatever else might result from the systemic conditions of this polygenic and multifactorial disease, hip dysplasia remains a common, usually painful and often debilitating disease. "Efforts by dog breeders and veterinarians to reduce the prevalence of the disorder have proven marginally effective." ²

While there is much that we do not know we do know that canine hip dysplasia is a genetically transmitted disease. If you need to, or if you disagree at this point, please re-read that statement. We will be repeating it throughout this series of articles, and this concept is the basis for determination of fitness for breeding. The genetic concept of heritability is a complicating factor and is one reason why hip dysplasia remains so controversial. So often when you breed you get more than you see. Without resorting to too much math, heritability is equal to the statistical variance due to genetic influence divided by the sum of the statistical variance due to the genetic influence plus the variance due to the environmental influence. It is easier to comprehend the mathematical notation than the statement of the equation:

H ² = heritability index
V_genetics = variance due to genetics
V_environment = variance due to environmental influences

Thus, heritability is defined as an estimate of how much environmental factors play in the expression of the inherited genes. A high heritability index means that environmental considerations are not as important as genetic elements. The numerical value or heritability index is a function not only of breed type but of the population from which the data is extracted. "Studies of hip dysplasia genetics have indicated that the disease is polygenic and multifactorial, with estimates of heritability index in the range of 0.2 to 0.3"³

For instance, in a 1986 Swedish study, the heritability of hip dysplasia in German Shepherds was 0.40 in Sweden, but only 0.25 in the British Isles during the same time period. The difference between breeds may also reflect their levels of inbreeding. The more inbreeding, the lower the heritability index because inbreeding reduces the total genetic variability-that is, the gene pool is smaller. Inbreeding is not a bad word. It only becomes problematic when undesirable genetic traits are concentrated within the gene pool. By definition, every purebred dog of any given breed is highly inbred, or else it would look like a feral dog. We frequently hear that the problem with the American Kennel Club purebred dogs is that they are inbred. We should hope so, otherwise we could never fix type to the point where there were discernible differences between breeds. On the other hand, we would hope that the concentrated gene pools for the various breeds would have been concentrated from stock exhibiting only desirable genetic traits. We would hope that our field, bench and obedience champions would be fit to contribute to the gene pool. Of course, we know that is not true, or there would be no purpose in writing this article. ^4,5,6

(diagram based on reprint from the Journal of the American Veterinary Association, Vol.196, No.1,pp.59-70. "New concepts of coxofemoral joint stability and the development of a clinical stress-radiographic method for quantitating hip joint laxity in the dog," by Gail K. Smith, V.M.D., Ph.D.; Darryl N. Biery, D.V.M.; and Thomas P. Gregor, B.S.)

 To further complicate matters is the fact that the pattern of inheritance indicates that more than one gene is involved. Hip dysplasia is polygenic (involves many different genes) and multifactorial (influenced by many non-genetic factors). This makes sense when you think of the complexity of the various structures involved. Every cell in the body, except for sex cells, carries two copies of each gene and each gene codes for a specific characteristic. One very simple example is eye color:

If the cell's two sets of genes for a specific characteristic are exactly alike, then the animal is homozygous for that characteristic.

If the two genes are different, i.e., heterozygous, then one copy of the genes could code for blue eyes and the other could code for brown eyes.

Let's complicate the matter even further. If the animal carries two different copies of the same gene for eye color, only one copy can be expressed in any given eye. Closer to home, in humans for example, a child born to parents heterozygous for eye color (both parents have a blue-eyed gene and brown-eyed gene) will have a one-in-four chance of having blue eyes. This is because the gene for blue eyes is recessive and both copies for that code for blue eyes must be present before that characteristic can be expressed. On the other hand, if the child has brown eyes, we don't know what type of genes for eye color he or she has. This is because the gene for brown eyes is dominant and is able to "mask" the physical expression of the blue-eyed gene. Alternatively, the child could have only the genes that code for brown eyes. It is beyond the scope of this article to address the various "odd" eye color combinations, but co-dominance and variable penetrance may be what we are dealing with in canine hip dysplasia.

What you have just read is an example of phenotype vs. Genotype. Phenotype is the physical expression of a genetic characteristic. Genotype is genetic composition of the organism. Using our eye-color example, the child with two different copies of the gene will express the brown-eyed phenotype, but his or her genotype will be heterozygous.

Let's add to the complexity once again. Co-dominance of genes is a situation where neither gene is dominant. A clear example illustrating the concept of genetic co-dominance is flower color. A snap dragon homozygous (both copies of color genes exactly alike) for white petals crossed with a snap dragon homozygous for red petals will produce a flower with pink petals, not a flower with either white or red petals or a mixture of red and white petals. Many researchers feel that hip dysplasia may be a mixture of dominant, recessive and co-dominant genes. Quite probably, this is one of the reasons why isolation of the causative genetic factors of canine hip dysplasia has been so elusive.

The concepts that you need to be clear on as we leave this mini-course on genetics are: heritability index; genetic and environmental variability; dominant vs. Recessive genes; homozygous vs. heterozygous; genetic co-dominance; and most importantly that hip dysplasia is genetically inheritable and is polygenic and multifactorial. In short, you can get it in your breeding program when you bred from animals that did not show it.

Before we can discuss an abnormal process (disease), we need to first understand the normal process. In this case, we must be able to answer the question, "What is a normal hip, what makes it normal, and how does it get that way?"

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First, what is the hip? The hip joint is a main weight-bearing joint consisting principally of a ball and socket. This joint connects the pelvis to the lower extremities. The ball is on the end of the femur (thigh bone) and the socket (acetabulum) is part of the pelvis. Note from figure 1 how the femoral head fits into the acetabulum in the normal hip joint. This will be key to all our discussions from this point forth. A true ball-and-socket joint has three degrees of freedom, that is, it supports rotation about three different axes. The canine hip joint is unusual as a ball-and-socket joint in that it has a fourth degree of freedom. The femoral head may be displaced laterally from the acetabulum. While this is the genius of this joint, allowing the attached appendage a full range of motion, it can also create a problem if there becomes too much laxity in the joint. Note the fourth degree of freedom in Figure 2, which provides for the femoral head (ball) to move directly away from the acetabulum (socket). From Figures 1 and 2, it should be obvious that much lateral displacement of the femoral head from its seat in the acetabulum will produce high joint stresses during weight bearing. This joint laxity will be a major consideration for the changes it causes in the joint mechanics as we progress through this series of articles.

The acetabulum is formed from the embryonic process of fusion of the ilium (top of the hip), the ischium (lowest part of the hip) and the pubis (below the ilium but above the pubis) and the acetabular bone. Most researchers feel that normal development requires close conformity (close, tight fit) between the acetabulum and the femoral head throughout their growth period. In other words, the joint must fit tightly, deeply and snugly. This is how a puppy's hip starts out-dysplastic and non-dysplastic puppies' hips are indistinguishable. The first six months of life seem to be the most critical growth period when the depth of the socket must be maintained. It is believed that the depth of the socket in the growing puppy may be in part a function of the amount of stress the femoral head can produce on the immature acetabulum. Think of it as a thumb pushing into a ball of clay. The harder the thumb pushes, the deeper the indentation in the clay. Much as a knife edge concentrates force onto a relatively small surafce area (and a pin of a diameter equal to the width of the knife edge even more), the two phenotypic traits that maximize the forces between these two developing bony structures are a small femoral head and a long femoral neck. Note, however, that the normal acetabulum is well-formed in utero, thus the stress may only serve to maintain that socket depth.

To cushion the force between these two bony surfaces, there is a truly remarkable substance called articular cartilage. This cartilage is similar to a hard sponge with a slick hard surface facing the interior of the joint. In the normal joint, articular cartilage is able to change its shape slightly when force is applied to it, thus spreading and distributing force more evenly into the subchrondal bone directly beneath the articular cartilage. This is of major importance to the long-term integrity of the joint.

Holding everything in place is another structure that does more than just enhance the stability of the joint. The joint capsule is a fibrous structure filled with synovial fluid that surrounds, isolates and protects the joint. This joint capsule is essential to proper development and functioning of the joint. This structure is similar to the rubber grease bladder around a ball joint in the front suspension of your car. The cushioning effect of the grease with the fluid pressure of the grease and the elasticity of the bladder helps to stabilize the joint. The bladder helps keep out contaminants. This function becomes even more important as the joint ages and surfaces become worn. The joint capsule contains the all-important synovial fluid, the most important ingredients of which are nutrients, which diffuse into the joint from the blood supply, and hyaluronic acid (HA). The tissues within the joint extract nutrients from the synovial fluid in which they are bathed.

Hyaluronic acid has a critical function: to provide lubrication. This slippery and viscous substance prevents rapid erosion of the articular cartilage and the surfaces of the femoral head and the acetabulum. A membrane called the synovial membrane lines the inside of the joint capsule, providing further isolation of the joint space. Should the synovial membrane become injured or ruptured, white blood cells release enzymes and oxygen radials (free radicals) that attack and destroy hyaluronic acid. When this occurs, the loss of HA reduces the lubrication that prevents friction and limits erosion of the articular cartilage. Even worse, loss of HA allows the enzymes from white blood cells to join forces with oxygen free radicals and attack the articular cartilage. Free radicals play a major role in degenerative arthritis.

The ball-and-socket (coxofemoral) joints of an affected puppy radiographically appear to be structurally and functionally normal at birth. The hips of an affected puppy are indistinguishable from a normal puppy at birth. This is an important point to remember. As an affected puppy grows, the hip joint undergoes severe structural alterations. The changes result from joint laxity and adulteration/destruction of the constituents of the synovial fluid and subsequent loss of lubrication and nourishment, which serve to reduce the regenerative and elastic (force-absorbing and distributing) properties of the articular cartilage. The normal joint retains its tightness and close fit. Whereas in the genetically dysplastic-to-be puppy, the acetabular rim and femoral head become eroded.

Remember that the acetabular depth is partially a function of the small "footprint" of the femoral head which concentrates force into a small surface area. As the femoral head is flattened, the coxofemoral joint no longer fits snugly. Excessive force is applied unevenly, especially at the edges of the flattened femoral head. Visualize this joint looseness as the difference between the impact of a boxer's fist when the punch is thrown with the glove already in contact with the opponent's jaw as contrasted with an initial stand-off distance of say 20 inches. In the first case, little impact force is transmitted and no damage is done; in the second, there may be a knock-out. In the joint, the increase in stress results not only in abnormal wear of the articular cartilage, but causes tiny micro-stress fractures to appear in the subchondral bone. The body attempts to heal these fissures, causing the acetabulum to become filled in, i.e., made shallower. It is this cycle of damage and repair (osteophyte formation) that leads to deformation of the joint, and degenerative hip disease.

Conclusions: Hip dysplasia is not something a dog acquires; a dog either is genetically dysplastic or it is not. Initially, the hips of affected and normal puppies are indistinguishable. Later in life, an affected animal can exhibit a wide range of phenotypes, all the way from normal to severely dysplastic and functionally crippled. You should take away from this article the idea that hip dysplasia is genetically inherited. Never believe a fellow breeder or fancier who claims there is no hip dysplasia in his or her line. Never believe breeders who claim that if their breeding lines carried the genes for hip dysplasia they would be able to see it in their animals' gaits. This just is not true.

Although work has been started to find the genetic markers for the disease, we have as yet no method of genetic analysis that can tell breeders whether their dogs are dysplastic or not. We only have physical expression of the disease, and an effort to "back door" into clear stock for breeding purposes. Breeders must come to understand that the only way to reduce the incidence of hip dysplasia is by trying to breed from as few animals that have progenitors, siblings, get, or get of siblings that had clinical manifestations of hip dysplasia. Obviously, a great amount of information is lacking to make a rational breeding choice. These are hard words to have read, but much of our problem has come from thousands of years of less than natural selection resulting from the domestication of the dog.

In our second article in this series we will address in greater detail the parts nutritional, environmental and other factors play in mitigating or increasing the physical expression of canine hip dysplasia.

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CREDITS

References

1. Olsewski J.M., Lust G., Rendano B.T., et al. "Degenerative joint disease: Multiple joint involvement in young and mature dogs." Am J Vet Res. 1983; vol 44:1300-1308.

2. Smith G.K., Biery D.N. "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;196:59-70.

3. Ibid., p. 59.

4. Cargill J. "Truth in advertising: breeder self-regulation I." Dog World. 1990(Jul);75 No.7:38-82.

5. Cargill J. "Truth in advertising: breeder seregulation II." Dog World. 1990(Aug);75 No.8:111-116.

6. Cargill J. "What should 'champion' mean?" Dog World. 1993(Feb);78 No.2:34-35.

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