On our page regarding hip and bone disorders, we discuss many things that can cause hip dysplasia as well as other bone ailments that can appear to be HD. Sometimes, a canine owner is told by a veterinarian that their young puppy may have HD, when in fact....they may not. The OFA board themselves, will not permit any radiographs to be presented to them until the canine is at least 2 years of age. The reason for this is because the canine is still considered to be growing. When
radiographs (X-rays) are taken, there are factors to be considered:
The HD radiograph: What is to be considered?
We have listed the two most important points that should be considered for canine radiographs:
Following statements must be on the film at time of exposure:
Tattoo number (2 letters/4 numerals) or micro-chip number
Complete name (example: Visum vom Arminius). Labeling with stickers or markings after developing the film is not accepted as proof of identification! Any received without proper identification are returned.
Asymmetrical pictures (poor positioning) are unfortunately a frequent quality problem. Avoid sending such films if possible. If a canine is not under anesthesia at the time of taking x-rays, it is nearly impossible to get a true reading.
Early X-ray
While early x-rays can be used to help show a change, if any, in the latter x-rays, Goldendoodles can not be properly addressed for HD under the age of 12 months. A definite finding can not be determined by the OFA board until they are 24 months.
The early result is not of interest to the OFA board, however; therefore no such preliminary HD-exam stamp will be placed on their pedigree. Also no OFA diagnostic report can be created. Such x-rays are not received or accepted by the OFA board. The OFA board has its own radiograph specialists who determine the findings upon canine x-rays when submitted to them for such and providing that the canine is at least 2 years of age. To increase the accuracy of a correct diagnosis, it is recommended to repeat the radiographs at a later date (usually 6 months). This allows the radiologist to compare the initial film with the most recent film over a given time period and assess for progressive arthritic changes that would be expected if the dog was truly dysplastic. Most dogs with this grade (over 50%) show no change in hip conformation over time and receive a normal hip rating; usually a fair hip phenotype.
Any Goldendoodle owner who has been told by their vet that their puppy or doodle dog has HD, may find the book below of help:
**Canine HD and Other Orthopedic Disorders by Fred Lanting**
It covers all joints plus many bone disorders and includes genetics, diagnostic methods, treatment options, and the role that environment plays. This new "Hip Dysplasia and Other Canine Orthopedic Disorders" book is a comprehensive (nearly 600 pages!), amply illustrated, annotated, monumental work that is suitable as a coffee-table book, reference work for breeders and vets, and a study adjunct for veterinary students, for the dog trainer and the general dog owner of any breed.
MORE ABOUT GENETICS AND THE CANINE:
by John Armstrong © Copyright June, 2004 - 2006
Many people label any problem that appears to be inherited a "genetic disease." However, though there are legitimate genetic diseases, there are also a variety of problems that have an inherited component but are of a fundamentally different nature. Dealing effectively with any genetic problem requires an understanding of the relationship between the genes (genotype) and the phenotype. In many cases this is lacking. In this article, I would like to describe some of the differences, in order to give breeders and owners a better understanding of what they are dealing with.
Inborn Errors of Metabolism: The true "genetic diseases"
The first clearly-described relationship between genotype and metabolic deficiencies is credited to Sir Archibald Garrod, an English physician. In 1901, he showed that the inherited disease alkaptonuria results from an inability to metabolize certain amino acids, leading to the accumulation of homogentisic acid. Some of this compound accumulates in skin and cartilage (the latter leading to arthritis). The rest is excreted in the urine, turning it black. Garrod suggested that the metabolic block was caused by an enzyme deficiency, though this was not confirmed until the enzyme (homogentisic acid oxidase) was characterized in 1958.
Since Garrod's time, many other inherited metabolic diseases have been discovered. Some can be managed by careful attention to diet; others cannot. A particularly nasty example is Tay-Sachs disease, which involves an enzyme important in lipid metabolism. Individuals homozygous for a deficiency in this enzyme accumulate a compound called a ganglioside in the nervous system. They appear normal at birth, but progressively lose motor function and die around three years of age. There is no treatment.
Most of these conditions involve mutations that lead to the production of a nonfunctional enzyme, or one that is totally absent. In heterozygotes, the single good copy of the gene is generally able to produce sufficient enzyme to handle the normal workload. However, in a few cases, carriers as well as affected individuals have to be careful about their diet or may exhibit less severe phenotypic effects.
Example of inherited metabolic diseases in dogs include phosphofructokinase deficiency in Cocker and Springer Spaniels, and pyruvate kinase deficiency in Basenjis.
Not all mutations involve metabolic pathways. Some involve proteins that have structural roles in cells and tissues. Others involve regulatory genes that control the correct sequence of events during development. These may lead to such problems as septal defects in the heart or the failure of the embryonic kidney to develop into the adult form. Nevertheless, all can legitimately be considered genetic diseases, as there is a direct one-to-one relationship between a single mutated gene and a particular problem.
Problems such as bloat (gastric dilatation-volvulus, or GDV) and hip dysplasia clearly have a genetic component, but also an environmental component and, perhaps, a behavioral one, as well (which also may be determined partially by the genes).
Bloat is not a "genetic disease" in the same sense as the metabolic and other disorders described above, and it seems unlikely that a single gene is responsible for bloat. One might better compare a bloat attack to a bad case of indigestion in a human. Some people are more prone to such attacks than others, and there may well be an inherited component, but other factors also come into play. Research into bloat suggests that diet, behavior, and conformation may all play a role.
Leaving aside the question of the role of genetics in behavior, the results suggest that the incidence of bloat increases with the size of the dog and the depth-to-width ratio of the chest cavity. This is a conformational problem, not a genetic disease. Certainly, the overall conformation is, ultimately, determined by the genes, but not by a single gene. There are probably dozens or hundreds of genes that go into determining the shape and size of the head, trunk, and limbs. Wherever there is genetic variability, one can select for larger, smaller, narrower, wider, etc. If the fancy as a whole decides that a taller, narrower dog looks more "refined," more of that description will be kept for breeding purposes, and the population will be shifted toward a more bloat-prone conformation.
When it comes to the question of correcting this problem, the solution, in theory, is simple. We stop breeding for a bloat-prone conformation and select for a slightly smaller dog with a chest cavity that is not so deep or narrow. Some may regard this as a retrogressive step, but we have to decide which we want to sacrifice.
I do not rule out the possibility that two dogs of identical conformation may have one or more genes that lead to one being more bloat-prone than the other. If we could identify these genes, we might be able to reduce the incidence of GDV somewhat while retaining some of the desired "refinement."
While it may be argued that there is nothing wrong with a tall, narrow dog aside from the greater risk for bloat, selecting for a conformation that is not functionally sound is a recipe for disaster. Wild canids do not move awkwardly. Any that did would be eliminated by natural selection. After thousands of years of evolution, the musculoskeletal system of the average wolf has found a combination that works efficiently. Because there is diversity in the gene pool, there is always the possibility of a chance combination of genes that produces an individual that can move more quickly and efficiently. There is also the possibility that a less efficient combination may arise, but it is not likely to be favored.
In the artificial world of the show dog, one can insulate an individual from natural selection and favor a conformational extreme, because the breeder or the public thinks it looks more attractive or just different. Two such extreme dogs, bred together, may lead to something even more extreme and more popular. However, the changes in one component must be accompanied by changes in others, or the result, from a structural standpoint, may impose stresses that the components are not designed for. The result will be components easily damaged or deformed while the puppy is still growing.
In such a case, one may not be dealing with genes that are "bad" and make a nonfunctional or defective product, just with a bad combination of genes. But if, during this "unnatural selection," the genes necessary to make a good combination have been discarded, where does this leave the breed?
While many people assume that the best way to treat hip dysplasia is to try and prevent it, until DNA genetic markers are available for the Golden Retriever and the Poodle, it is impossible to know whether either parent for Goldendoodles is a carrier for the defective, polygenic gene that can help cause hip dysplasia. Many people place too much emphasis on asking breeders if their breeding dogs have been tested for hip dysplasia before buying a puppy. Certified-free parents are not guaranteed to have dysplasia-free pups.
Some veterinarians postulate that if more than 25 percent of the pup's ancestors developed hip dysplasia, it is more likely to develop the disease. In our own Poodles' pedigree that dates back to the 1930s, that we researched over a period of several years, showed over 400 OFA good Champion ancestors. This extensive information was not made available on the pedigrees for our Goldens....but we were able to see many OFA good Champions dating inside of their lineage. While this in itself does not guarantee that our Goldendoodle puppies would be free of developing hip dysplasia, it does show that the risk of our Goldendoodle puppies developing HD is very low. Because we have completed extensive Pedigree research on our breeding dogs, we do know that our percentage of having dysplastic Goldendoodles is very low and approx. the same percentage, if not less than, that of a breeder who has had their breeding stock tested. We continue to keep an eye out for VETGEN to come up with genetic DNA markers to rule out the silent canine carriers of HD so that we ...as well as all breeders...will know 100% which dogs to keep out of their breeding programs.
New evidence shows that hip dysplasia can be delayed or prevented by restricting the growth rate of susceptible puppies. Dogs predisposed to hip dysplasia may benefit from a conservative diet until 2 years of age. One study showed that feeding a 24 percent smaller ration to puppies, beginning at 8 weeks of age, resulted in a 46 percent lower occurrence of hip dysplasia. Check with your veterinarian for an appropriate diet. Boisterous play can aggravate dysplastic joints. Keep your puppy from any kind of jumping or sustained activity until it is 1 year old. Thereafter, avoid activities involving strenuous jumping or sudden momentum changes. Swimming, which puts little stress on the joints, is recommended.
Once a diagnosis of hip dysplasia is made, there are several options for the dog and owner. In "mild" cases, no treatments may be indicated. One of the "nutriceuticals" (products used in treatment which are not considered drugs) such as Glycoflex, Inflammex, glucosamine sulfate, chondroitin sulfate or Cosequin may be recommended. This class of products is claimed to increase joint fluid viscosity and provide nourishment for the joint surfaces. Until recently no controlled studies had been done to document the effectiveness of the nutriceuticals. A study of a similar injectable product (Adequan) suggested marked improvement in the joints of dogs treated versus the untreated control group. I have been very impressed with the effects of Glycoflex in particular in reducing or alleviating the symptoms of discomfort associated with joint problems. Another option available is the use of non-steroidal-antiinflammatory drugs. This category of medication includes aspirin, phenylbutazone, Rimadyl, Etogesic, Arquel and other drugs. While they may give relief from the symptoms of joint pain, they do not improve the joint in any way. A third choice is steroids such as prednisolone and methylprednisolone. Steroids are, for me, the drug of last resort for joint pain. Like the non-steroidals, these drugs do nothing to improve the joint. They are strictly used to reduce inflammation. Long term use of either steroidals or non-steroidals may actually contribute to degeneration of the joint.
While the exact mode of inheritance is unknown, osteochondrosis is considered to be an inherited disease. In affected individuals there is a disruption in ossification of the cartilage mold beneath the articular cartilage of the joint. This results in aseptic necrosis and when the weakened area collapses, the articular cartilage fractures resulting in lameness.
