Canine Hip Dysphasia Part II - Causative Factors of Canine Hip Dysphasia

by John C. Cargill MA MBA MS

 

Copyright May, 2000 - 2005

Causative Factors of Canine Hip Dysphasia

 

Owners must separate fact from myth when examining theories on genetic, nutritional and environmental factors that influence CHD.

This is the second part in a series on canine hip dysphasia. 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 dysphasia. 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 dysphasia. Without the genes necessary to transmit this degenerative disease, there is no disease. Hip dysphasia is not something a dog gets; it either is dysphasic or it is not. An affected animal can exhibit a wide range of phenotypes, all the way from normal to severely dysphasic and functionally crippled. Hip dysphasia 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 dysphasia. 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 dysphasia. 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 dysphasia is that it is a genetically linked condition--always was, always will be.

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 dysphasia 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 dysphasia. 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 dysphasic 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 dysphasia. 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 dysphasia. 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 dysphasia.

Radiographic
Evaluation
Method

Group 1
Ad Libitum Feeding

Group 2
75% of Ad Libitum Feeding

Dysplasic Normal % Normal Dysplasic Normal % Normal
OFA
Swedish
16
18
8
6
33%
25%
7
5
17
19
71%
79%

Many researchers conclude that early fusion may lead to bone and cartilage deviations which then could predispose the animal to future dysphasia. 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 dysphasia (genotypically dysphasic).

In the first article we alluded to joint laxity as being present whenever there is canine hip dysphasia. Given that joint laxity is at least one of the factors governing the onset of hip dysphasia, 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.

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.

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.

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 f