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What is HD - Canine hip dysplasia (HD)
The following article provides an insight into the problems of hip dysplasia (HD) in dogs. As you read it, it becomes clear that HD can only be combated in the long term by carefully selecting suitable breeding dogs. The success depends very much on the impartial cooperation of the breeders and the dog owners. It is entirely up to you to further reduce the percentage of dogs with HD.
What is HD What are the signs of HD?
We understand hip dysplasia (HD) to be a malformation of the hip joints. The two joint-forming bones, the joint socket and the femoral head do not fit together correctly. The malformation usually occurs on both sides and can vary in severity. HD develops in the first 15 months of a dog's life, later only the extent of the osteoarthritis changes. Young dogs with pronounced HD mainly show pain as a result of the unusually strong looseness of the hip joints. In older dogs, the pain predominates as a result of wear and tear (osteoarthritis) of the hip joints. In milder forms of HD, signs of illness may be absent as long as the dog is not put under heavy strain. The pain perception between the individual dogs is also quite different: While one dog with mild HD is already limping, the other dog with advanced osteoarthritis has developed a special movement technique to avoid pain, so that the owner may not even notice the disability.
What is causing HD?
The cause of the HD has not yet been conclusively uncovered. The latest research results, however, allow the conclusion that the stability of the hip joint and thus the correct development of the connective tissue that forms the joint capsule is of crucial importance. The most important basis for HD lies in a dog's genetic make-up. Which genes play a role has not yet been conclusively clarified.
How does a dysplastic hip joint develop?
The development of the hip joints is significantly influenced by two components:
- through hereditary disposition and
- through the dog's diet.
Hereditary factors: It has been proven that HD often manifests itself in the form of excessive looseness or instability of the hip joint, which favors the development of osteoarthritis. Just as we soon catch blisters or sore muscles when we wear shoes that are too big, the hip joint is also damaged if the head of the femur keeps sliding around in the socket. In technical terms, a loose hip joint experiences the same changes as a loose wheel bearing: it is knocked out. In young dogs, therefore, the greatest changes are seen in the joint socket: it widens and flattens out. This means that the head of the femur is no longer guided correctly and osteoarthritis develops. A tight joint does not develop HD.
Regarding nutrition: Feeding that makes the dog grow very quickly and, in particular, quickly gain weight, has been shown to promote the faulty development of the joints if the dog has a tendency to HD due to its genetic makeup. A dog with a predisposition to HD can actually eat the osteoarthritis of the hip! In theory, this knowledge is of great benefit to a breeder. By overfeeding his dogs, he could discover those who develop good joints despite excessive weight gain, i.e. are genetically less heavily burdened with HD genes. Because a genetically HD-healthy dog will hardly ever develop HD even through improper feeding.
Conversely, in a dog with a predisposition to HD, it is possible to alleviate the extent of the disease through a low-calorie and balanced diet. It has been proven that slow-growing dogs are less likely to develop HD than their faster-growing and therefore heavier littermates. It is particularly important to avoid an oversupply of calcium (feed lime) in the feed. Today's ready-made feed contains enough calcium so that no feed lime should be added. Hazewinkel considers 0.8% calcium on a dry weight basis (0.76 g calcium per 400 kcal. Or 1700 kJ.) To be sufficient. The calcium / phosphorus ratio should be around 1: 1 (quoted by Wess). Optimized feeding helps that a single dog has a greater chance of developing acceptable hip joints and leading a largely normal and pain-free life, despite unfavorable genetic makeup. However, this tactic is not suitable for future breeding animals, as the genetic burden for HD cannot be uncovered with it. If dogs raised in this way but hereditary problems are used for breeding purposes, the predisposition to HD is passed on to the next generation. The result is that dysplastic offspring will occur among the offspring of dogs with good hip joints.
It is believed by breeders that the puppies' youthful activity could cause HD. To date, this theory has not been proven. A healthy hip joint is not damaged by normal movement or playing with other dogs. It is certainly sensible to avoid massive overuse of the still immature skeleton of the young dog, since a bone is less resilient as it grows than the skeleton of an adult animal.
What are the consequences of HD?
When moving, the hip joints are regularly subjected to cyclical loads. A stable joint can withstand this lifelong stress without any problems, it remains healthy. Regular exercise is even necessary to nourish the joint cartilage. In the case of an unstable or malformed hip joint, however, the recurring improper loading leads to strains of the joint capsule, the ligaments and damage to the articular cartilage and the bones involved in the joint. Bony formations and deformations develop on the joint, which are visible on the X-ray as permanent osteoarthritis. The consequences are pain in the hip joint. The dogs try to relieve the hind limbs. These two mechanisms lead to muscle wasting, which further promotes osteoarthritis because the muscles in the hip joint lose their supportive function. Dogs with moderate to severe HD are therefore usually less active. They often lie down, have trouble getting up and are lame in their hindquarters, especially after lying down for long periods of time. In the early stages of the disease, the lameness may go away after the first steps. Later on, dogs plagued by dysplasia show more and more signs of lameness during physical activity. It is not uncommon for the dog to change its character under chronic pain. The happy companion can become a disgruntled, sometimes even biting, contemporary.
How is the diagnosis of HD made?
The diagnosis of HD can be made using x-rays of the hip joint. Visible changes can occur in the acetabulum, the femoral head, or both bones. Occasionally, only a noticeably loose hip joint can be observed in young dogs, in which the femoral head is not correctly positioned in the socket.
There are five degrees of severity of HD based on the changes on the x-ray.
|HD grade (FCI)|
|A = HD-free|
|B = transitional form|
|C = mild HD|
|D = moderate HD|
|E = high level HD|
How common is HD in the dogs examined?
Between 1991 and 1994 3749 dogs were examined by the two HD commissions. The HD results are shown in Figure 6. HD occurred equally frequently in males and bitches, so the occurrence does not depend on the sex of the animal. A quarter of the dogs examined were assessed as HD-free, and a third as a transitional form. This means that almost 60% of the dogs belonged to the two grades that can be used for breeding with a clear conscience. More than a quarter of the dogs were rated as slightly dysplastic (HD grade C); they should not be used for breeding or only in justified cases. Around every 7th dog even fell into HD grades D and E with pronounced joint changes. Such animals are excluded from breeding.
The more recent data from the HD Commission Zurich from 1995 to 2000 show a clear decrease in the frequency of HD and also in the degree of severity (Figure 6). Around 70% of the dogs can be recommended for breeding. Only every 11th dog still suffers from moderate or severe HD, which is still too much. The longstanding efforts of dog owners and breeders are still beginning to bear fruit!
Does HD appear equally in all races?
The proportion of dysplastic dogs is very different in the different breeds, the distribution is shown in Figure 7. The Siberian Husky had the best hip joints, followed by the Collies and the Belgian Shepherds. Around two thirds of all Hovawarts, Flat Coated Retrievers, Leonberger and Rottweilers, over half of the Labrador Retrievers and Bernese Mountain Dogs, half of the Golden Retrievers, Newfoundland dogs and German Shepherds, but less than half of the boxers examined were free of dysplasia. In St. Bernard dogs, as well as English and Gordon setters, the HD rate was a shockingly high 60-70%. Due to the intensive efforts of breeders in recent years, the number of dysplastic dogs, especially among the St. Bernard dogs, has fallen sharply.
Why are there such racial differences in HD frequency?
In various breeds, the disease was rare even at the beginning of the HD control. Sled dogs or hunting dogs in particular, which have always been bred for lifelong performance, hardly show any HD; Dogs that became lame after strenuous work were not used for breeding in the first place. At the Hovawart, many dogs were free of dysplasia even before the introduction of the HD control, which is why a strict selection has always been carried out.
The most important reasons for the high proportion of HD in various breeds are the use of dysplastic parent animals (HD grade C) for breeding and the extensive lack of a progeny control. The St. Bernard took revenge on the fact that the breeding animals had not been examined for HD for years and that dogs were used for breeding despite pronounced HD. For many breeds, when choosing breeding dogs, too much importance was attached to the conformation and the fighting instinct. Health aspects were hardly taken into account. Due to the intensive educational work, however, this perspective has changed significantly, and today more attention is paid to the health of animals.
The proportion of dysplastic dogs is probably higher than the figures in Figure 6 reflect. X-rays of severely dysplastic dogs are rarely sent in for official assessment, as breeders fear for their good reputation as an HD-free kennel. Images of dysplastic animals, which are X-rayed for movement disorders before the licensing, are hardly ever evaluated. This procedure hampers progress enormously, as it is not possible to check the breeding successes and to adapt the breeding regulations. In addition, calculations on the heritability of HD are falsified. The breeders and dog owners cheat themselves out of their efforts to sustainably reduce the HD frequency.
Why is HD still common?
If a disease is to be controlled in a breed, carriers of the disease must not be used for breeding. The use of dysplastic animals for breeding is therefore irresponsible. It contradicts the idea of animal welfare, which says only breeding animals that are free from diseases that limit the quality of life. This includes the painful HD. Every buyer of a pure-bred dog is basically entitled to a healthy and therefore dysplasia-free dog. However, as long as C dogs are declared fit for breeding, the HD frequency in the offspring cannot be further reduced. To make matters worse, the breeding value of an animal for the trait HD does not only depend on the quality of its own hip joints, but also on that of its close relatives such as parents and siblings. Only if their HD results are also taken into account can the hip joint quality of the offspring be estimated.
How can HD be prevented?
In the case of an individual dog, every breeder and dog owner can have a direct influence on the development of the hip joints by carefully feeding the young dog. It has been proven that gaining weight too quickly in the first 10 months of life promotes joint development. Excessive amounts of calcium in the feed have been shown to favor the development of HD. Presumably too large feed rations are also disadvantageous. If an HD-endangered dog is put under excessive strain as it grows, the HD can get worse. On the other hand, neither the dog's final height nor the final body weight seem to have a significant influence on the hip joints. However, being very overweight in a dysplastic dog makes the pain worse.
Many "secret recipes" are circulating among dog owners that promise a cure. Unfortunately, these promises almost always turn out to be ineffective. For example, vitamin C cannot prevent HD. Most common feed additives also have no verifiable effects on a dysplastic joint. Supplementary feeding of glucosamine sulphate can relieve the pain in certain dogs, but the osteoarthritis cannot be cured. The substance does not work equally well in all dogs or in all of them. Side effects are not known According to the latest findings, gold implants around the hip joints are also ineffective. In the best case, gold can alleviate the inflammation, but not the existing changes. Larger, serious double-blind studies have not yet been carried out.
The most effective long-term measure to reduce HD is the introduction and enforcement of Pairing restrictions. The proportion of healthy offspring increases if not only the HD level of the animal itself (the so-called personal performance), but also the HD results of its siblings and, in particular, of its already-born offspring are taken into account. With the help of such a Breeding value estimation the breeder could choose a suitable partner for his breeding animal without having to remove his dog from breeding due to HD exposure from the outset. This concept is called strategic pairing and has the goal of only breeding puppies that have a below average risk have developed HD. The breeding license is no longer made dependent on the HD result of the individual animal, but on the HD risk for the offspring of a mating. This method of breeding selection has proven to be extremely successful in livestock breeding. It has been introduced by many dog breed clubs in recent years. In Germany, more than 50 pedigree dog clubs have already followed this path. Success depends on the disease to be combated. The strategic mating is only successful if a clear breeding strategy has been worked out beforehand and the mating restrictions are consistently adhered to.
Recently, approaches to the molecular genetic elucidation of HD have moved into the center of interest. Countless gene markers (so-called microsatellites) are recorded and analyzed with the help of the so-called Single nucleotide polymorphism (SNPs). Preliminary results show that the development of the hip joint in dogs is influenced by many genes located on different chromosomes. Certain genes seem to have a significantly greater influence on joint development than others. They are known as the dominance genes. The aim of these studies is to base the decision as to whether an animal can be used for breeding no longer solely on the X-ray findings of the adult animal, but also on its genetic characteristics, i.e. its genomic breeding value to determine. Since the genes are invariable at birth, puppies of any age could be examined for this. The breeder would no longer have to wait for the X-ray results to find out which of his animals will probably later be suitable for breeding (at least as far as HD is concerned). If the prognoses are correct, such tests should be available shortly. However, they have to be developed separately for each breed, which is associated with some financial effort. Molecular genetic analyzes are also becoming increasingly important in human medicine, less to verify our "ancestry" and more to determine the risk of developing a certain disease and to determine individual drug sensitivity. And since the pharmaceutical industry sees a huge profit potential in this for us western people of civilization, the progress in the meaning of the above mentioned SNP will not be long in coming.
Back to the x-ray of the hip joints. The transition from the lumbar spine to the sacrum can also be seen on a correctly created image. At this transition, deformities in the form of a switching vortex or transition vortex occur in 0-20% of the dogs.It has been shown that such switching vortices significantly increase the risk of later damage to the nerves in the spinal cord. An uneven development of the hip joints is also associated with it. It is therefore worthwhile to evaluate this area in the future and to record it in the findings sheet. Details will follow in a further article.
The strongest incentive to improve the HD situation among pedigree dogs will undoubtedly come from the critical and demanding buyer. It is becoming less and less acceptable that one in six dogs in certain widespread breeds is affected by advanced HD. In the case of dysplastic animals, he demands a reduction in the purchase price and the assumption of the treatment costs or even demands the full purchase price back from the breeder or seller. A breeder drives cheaper if he introduces an effective breeding plan than continuing to mate dogs at his own discretion and turning a blind eye to the poor results. It is extremely detrimental to the health of a breed not to officially assess the x-rays of dysplastic dogs, but simply to let them disappear. The owner is not only cheating the breeder out of years of efforts to improve, his behavior leads to the fact that the HD statistics are completely wrong and thus largely worthless. The suggestions of the breeding commissions derived therefrom are of course ineffective. Even worse damage to their breed is caused by those breeders who use an unapproved male for breeding and indicate another as sire. In doing so, they are clearly making themselves liable to prosecution. In addition, the years of development work of the other breeders is damaged. The Shepherd Dog Club has found out about such black sheep and therefore requires proof of parentage by means of a blood test (DNA analysis) of the breeding dogs.
Finally, the legislature can trigger beneficial changes in breeding behavior through an effective animal protection law. Furthermore, the breed clubs are called upon to abolish the nonsensical honoring of a single Champion of Champions and to reward those breeders who breed healthy and long-lived dogs that meet a reasonable breed standard. It is not a lonely top dog that guarantees a healthy breed, but a broad base of healthy and well-balanced animals.
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