Hip Dysplasia and Quantitative Genetics

This passage was written by Miroslaw Redlicki and translated from Polish to English by Emilia Peek-Kwasniewska.

"About dysplasia or quantitative genetics".

Almost every breeder has heard about x-rays and exclusion of dogs with dysplasia from breeding. These measures are supposed to lead to the elimination of the disease. Meanwhile, the matter is not so simple at all.

What is dysplasia?

In the simplest terms, hip dysplasia is an abnormal formation of these joints. The entire joint is looser (which is probably due to loosening of the tendons, about which little is known), the head of the femur is not well aligned with the flattened acetabulum, and the result of this mismatch is friction and damage to the joint surface.

Symptoms of dysplasia, depending on its severity, range from reduced activity to severe lameness, significantly limiting freedom of movement. However, it is an indisputable fact that most dogs diagnosed with dysplasia by X-ray do not betray any clinical signs.

Two points of view

In discussions about dysplasia and how to control it, two different positions clash. Advocates of one believe that dysplasia is largely genetic. If this is the case, it is possible to achieve improvement within the breed when selection is applied - the more severe, the faster improvement will occur. According to the most extreme concepts, if all dysplastic dogs were eliminated from breeding, regardless of the degree of dysplasia, the problem would cease to exist after just a few generations. As we already know, such a course of action is not possible (even if it were to be effective), because it would dramatically reduce the breed's gene pool.

The opposing viewpoint emphasizes the role of environmental factors in the development of dysplasia. During the growth period, the hip joint is a delicate, ever-changing structure, sensitive to environmental influences. A puppy that is properly fed, kept on proper bedding and not pushed excessively will not develop dysplasia, even with an inherited predisposition.

Genetics of dysplasia.

Unlike the hereditary diseases mentioned in the previous section, dysplasia is conditioned not by a single pair, but by an unknown but most likely significant number of genes. Such a trait is called quantitative (because the value it achieves can be measured), in contrast to traits conditioned by a single pair of genes, called qualitative. Qualitative traits manifest themselves in the form of two mutually exclusive opposites - a dog is short-haired or long-haired, black or chocolate, has PRA or does not have it. These traits are essentially unaffected by the environment. What is different is the quantitative traits. As I mentioned, their value can be measured. With a sufficient number of measurements, you will find that the value of each trait falls within a range, the boundaries of which are defined by the lowest and highest value. In the case of dysplasia, ideal hip joints can be considered the lowest value, and their severe deformity the highest.

In the system of grading dysplasia in degrees (from A to E) used in Poland, this is not as evident as in the British system, where it is graded by points. The scores obtained there range from 0 (perfect joints) to 108 (most severe deformity). The values collected for the quantitative trait can be graphically represented in the form of the so-called Gauss curve.

The Polish system of evaluating dysplasia, by the way, has proved to be justified. This is because the latest research, based on a complex statistical analysis of several thousand results collected over the years for German Shepherds, has shown that the large group of genes responsible for dysplasia is "dictated" by a few so-called majors (probably three) with more pronounced effects - and they determine the degree of dysplasia.

Type of construction

It is generally accepted that dogs are descended from the domesticated small, light-bodied Asiatic wolf from Central Asia. The pug, dachshund, yorkshire terrier, dog and Irish wolfhound are all descendants of him. But as we know them today, they have existed for a short time. Do wolves, jackals and wild dogs have dysplasia? We don't know, because no one has conducted such research. Certainly, they are perfectly adapted animals, fit and efficient in their struggle for survival. To what extent do changes in conformation, weight and proportions in dogs favor the development of dysplasia? It can be assumed (although this is not an iron rule) that among heavier breeds dysplasia is more common than in light breeds. It is possible that by selecting different breeds for their distinctive conformation characteristics, we are simultaneously "promoting" dysplasia.

After all, it is known that the same genes can affect many different traits. In addition, there may be correlations between different traits. So maybe for many breeds what we arbitrarily define as dysplasia is the norm? It is quite possible, then, that the effective elimination of dysplasia would lead to all dogs becoming like their ancestor again!

Environment

In an adult dog, the hip joint is a strong and durable structure. This is different during the growth period, when the bones are soft and unmineralized, and the various components of the joint grow at different rates. Small wolves remain on a meat diet during the growth period; domestic dogs get foods with a high mineral content, which causes bones to grow faster than muscles and tendons. This can be compounded by being overweight, lack of exercise or over-exercising the growing dog. Puppies are reared on smooth, slippery surfaces like linoleum or ceramic tiles. All of these can cause changes in the developing joint, regardless of genetic predisposition.

Inheritance and selection

The contribution of genetic factors to the development of dysplasia varies from one population to another - it may be different, say, for German Shepherds in Poland and quite different in Sweden. The finding that dysplasia is, at least in part, genetically determined prompted breeding selection to eliminate it. The first comprehensive selection system was introduced in Sweden (1959), followed by the UK (1960), Switzerland (1965), the US (1966) and West Germany (1967), first for German Shepherds, then also for other, more numerous breeds. At first it seemed that selection was effective (although not in all countries; depending on the sharpness of the criteria adopted), but after forty years it can already be said that the effect is much less than expected. In German Shepherds, the incidence of dysplasia has decreased by several percent, but already in Newfoundlands practically none.

It also turned out that even using only dysplasia-free dogs in breeding does not at all guarantee that such will be the offspring. In a certain study, the results of the progeny of 8 sires of German Shepherds (free of dysplasia) were presented, each of which gave more than 100 puppies. Percentage of dysplasia-free

puppies ranged from 80 to just 30, while the ninth dog, itself with mild dysplasia, produced 50 percent dysplasia-free puppies.

Conclusions

In light of what is known about the inheritance of dysplasia, the selection system adopted in most European countries, which eliminates unconditionally from breeding all animals with a score worse than arbitrarily considered borderline, is not justified. The result of the test should be one of the information about the dog, and should not decide its to be or not to be. Dysplastic dogs outstanding in exterior or performance should be allowed to breed, only that it is safer to mate them with individuals free of the disease.

The way puppies and young dogs are reared may be more important to the development of dysplasia than genetic factors.

The breeder's responsibility for the fact that puppies bred by him have dysplasia is limited.

Author: Miroslaw Redlicki