When we deal with the "Sporting Group" or Gundog breeds such as retrievers, setters, and others, we must not limit our concern over orthopedic disorders to hip dysplasia (HD or CHD for "canine HD"). After all, there are serious problems involving other joints in our gun dogs such as ruptured cruciate (knee) ligaments. However, HD is by far the most commonly encountered bone/joint disease in the field (and stream) breeds as well as in all others; thus, it deserves much attention. While there may be degenerative joint disease (DJD) in several joints, people are most familiar with that seen in the hips.
As in almost any disorder, there is a genetic component. Because of the layman’s misunderstanding of the word "heritability", a misconception has arisen about how much of HD "is" genetic and how much "is" environmental. As our president explained, it depends on what your definition of "is" is. You can be certain that except for the extremely rare case of dysplasia (if at all existent) supposedly resulting from severe trauma such as being hit by a car, HD is 100% genetic in its transmission. That is, you can’t get what isn’t there; you need "bad genes" to produce bad hips. Where the confusion comes in, is the fact that environmental forces can influence the expression (though not the presence) of those genes. The greatest influence is through nutrition, and a minor effect is had by exercise. Still, "overnutrition" (a diet too high in calories and/or calcium) will only affect the hips of dogs who are genetically predisposed toward some grade of hip dysplasia. Their parents have bequeathed them too many defective genes to allow them to escape it.
Even if you have a dog with very low risk of HD, it is possible to damage other developing joints by feeding ad libitum, or more than they need for optimum health and growth. Again, genes play the greatest role, but if you raise roly-poly puppies, you may be flirting with disaster or deformity. Imbalance in calcium and other minerals, coupled with high-energy diets for the fastest growth, can cause changes in the growth plates, which are temporary cartilage dividers between growing bone centers at the ends of the long bones of the legs. This cartilage is supposed to change into bone cells at a reasonable rate. If disrupted, one of the two bones in the lower foreleg, for example, may grow at a different rate and to a slightly wrong length. Certain disorders result at least in part to this inequality, such as slipped kneecaps (luxated patellas) and FCP (one of the elbow dysplasias). Mineral imbalance is also thought to be a key factor in knee, shoulder, and hock problems known as OCD (osteochondritis dissecans). Labrador Retrievers are frequent victims of OCD in these joints, as well as of HD; Golden Retrievers very commonly have OCD in the shoulder joint. While HD is a different disorder, all of these seem to be related to some extent. Therefore, the club or breeder that makes an effort to reduce HD incidence usually finds a reduction in frequency of the other manifestations of what some call "generalized osteochondrosis". This very well could be largely a matter of general good breeding practice rather than so much of an inter-relationship.
An excellent article by Jerome Robinson, author of "Training the Hunting Retriever", appeared in the January 2000 issue of Field & Stream, a magazine probably read by many UKC sporting-dog owners, if only in the barber shop or the hunting-clubhouse. But there may be some misinterpretations or erroneous inferences. Technically, a pup is not "born with" HD, at least not clinical, radiographic, or histological (autopsy, surgery) signs. It is, however, born with the genes that can produce this progressive, developmental disease. Even if the expression of the several responsible genes is suppressed by keeping the pup lean with a calorie-restricted diet, or if the lower number of genes or other factors allow the pup to grow up with few or no signs, it still will pass those genes to the next generation. And in most cases, there will be pups that are much worse than the parents, and can cost the owner much grief and money.
Some breeds have very low incidence of HD. The racing dogs are genetically programmed for tighter ball-and-socket hip joints. However, even in these breeds, you can develop more HD than normally is found, simply by neglect. Conversely, the breeder of competition racing Greyhounds, Borzois, etc., will have a better chance of totally escaping HD in his lines than will the breeder of such breeds destined only for a show-ring or home life. Hypothetically, and possibly in reality, the show-only breeder will find more HD than will the person who refuses to breed dogs that do not win races. Putting demands on performance tends to mimic natural selection. Nature weeds out dysplastic Dingoes, wolves, and other wild predators by keeping them from being the first at the kill and therefore the only ones in the pack to exercise dominance in other area, such as breeding. Likewise, any joint disease in the caribou tends to affect its chances of escape.
Nevertheless, genetically superior (tighter) hip joints in breeding partners is the best route to orthopedic soundness in the offspring. The questions then arise: How can I tell how tight my dog’s hip joints really are? And how early? How can I relate that information to the number of good versus bad genes he might pass along? Why have we breeders reached a plateau in our ability to reduce or eliminate HD, after 35 years of "control registries"?
The answer to that last question is partially non-compliance by too many fellow breeders, but also the inherent insufficiency of the traditional evaluation in determining true looseness of the joints. Since OFA teaches us that tighter joints mean better dogs (as does every other orthopedic disease registry in the world), we who breed dogs should demand the best diagnostic techniques, the most precise and accurate means of determining that looseness (called laxity or subluxation). After all, it has been long known that the greater the laxity, the greater the risk of later degenerative joint disease and the pain of arthritis.
Now, there is another "great leap forward" in regard to diagnosing HD more accurately and earlier than ever before. It is called PennHIP, an acronym for (U. of) Pennsylvania Hip Improvement Program. Researchers at that university’s small animal division found that if the dog were to be radiographed (X-rayed) in a neutral-natural position nearly identical to its most relaxed stance, only upside-down on a table, they could demonstrate laxity by pushing the upper part of the thighs apart. This distraction method prevents laxity from being undetected. In the former method, still used by OFA and other groups, the dog is on its back, with legs pulled down so it resembles the stance of an upright human.
However, in dogs do not extend their legs that way in a relaxed mode, so this position artificially winds up and tightens the tissues around the joint capsule: ligaments, tendons, and muscles. This means that many loose hips are hidden; it’s like the twisting of a rubber band or tourniquet that makes something loose appear tight. The PennHIP protocol removes that "false negative for HD" because laxity cannot hide from the distraction technique the way it can from the hip-extended view. Years of testing and follow-up have shown that once a certain level of laxity is objectively measured (the PennHIP DI or Distraction Index is the number used) at ages as low as 4 or 5 months, it does not materially change. Therefore, you can test your 4-month-old pup and have high confidence it will read the same when he is mature. Most of the damage to joints is done during this fast-growth period before skeletal maturity.
When this discovery was made and published in veterinary journals, the OFA reacted and unfortunately put out non-peer-reviewed publicity claiming the leg-extended view also could now be accurate to as young as 4 months. Of course, breeders find that hard to swallow, because scientific studies sponsored or reported by OFA have always shown that there is an uncomfortable number of dogs that look good as puppies (even up to a year of age) that later develop HD: 30% in many breeds.
The good news is the "new" news. Although PennHIP started more than 15 years ago, the early years were those of building data. Now, this latest and greatest advance in the diagnosis of hip dysplasia has the statistical foundation that qualifies it for the description of "good science". It is much more objective than previous methods (laxity is measurable), much more precise and repeatable, and can be used to accurately predict at much younger ages the relative risk of a dog developing DJD. Veterinarians are being trained and certified at a few conferences each year, and a list can be found on either http://synbiotics.com or http://www.vet.upenn.edu/researchcenters/pennhip/. Breeders now can utilize a system that gives much better clues as to the genetic make-up of their dogs and the likelihood of producing dysplasia-free or at least low-risk pups. The "ultimate breeder" will use as many tools as possible to increase the odds that the young retrievers, pointers, or hounds that he sells will live long and useful lives, and serve their new sportsmen owners with pleasure, not pain. The same is true for dogs working in other fields, and those simply intended to be no more and no less than companions.
The hip-extended view, used by all hip registries and in all countries, allows for much laxity to go undiscovered, but is the best position for seeing DJD. Most are "closed registries", meaning that only those dogs adjudged to have "normal" hips will be on any lists available to the people looking for dogs to buy, or for information on their dogs’ families. There are very few open registries, listing all dogs regardless of hip quality. The most notable is the Institute for Genetic Disease Control (GDC) at <http://www.vetmed.ucdavis.edu/gdc>. If your dog or its near-relatives are listed with GDC, anyone can get a better picture of their probable genetic quality than is possible with the closed registries such as OFA, OVC, and those many others. Late news, 2002: GDC, forced by lack of enough participation to make its database meaningful, merged with OFA. Whether this will help anybody is doubtful.
Mr. Robinson wisely advised breeders to "identify dogs with normal hip ancestry, select sires that produce a low incidence" of HD, and use dogs with "better hips than the breed average". Although he was under the impression that OFA enabled breeders to do this, technically OFA does not publish any sort of real breed average. It is PennHIP that develops such information; every dog radiographed must be entered into the database. In Germany, some breed clubs are starting to use progeny results to give breeding dogs a "Breed Value" (BV), and they have made another forward step in the battle against HD. Not as great a leap as PennHIP allows us to take, but an improvement, anyway.
In my mind, these are the best tools for the breeder, especially in combination:
Use PennHIP for early accurate assessment of orthopedic (hip) disease risk
If the dog is over 12 months, have your PennHIP vet send a copy of the "standard position" (hip extended) X-ray picture to GDC for another permanent record that is accessible to all other breeders. Contact GDC first to see if they are still operating. GDC will confirm PennHIP’s evaluation of DJD; If the dog is over 24 months, you can choose between the fully open GDC registry or the semi-closed OFA one
Progeny testing: find out what the record is regarding hip production of your dog, its parents, and its siblings
Show preference for dogs that fit the above picture in addition to having the looks and working qualities you want.
note: Fred Lanting, author of Canine Hip Dysplasia", lives next to a hunting preserve in Northern Alabama. He lectures and judges shows worldwide. He judges all breeds for UKC and other U.S. and foreign registries, and has many years’ experience as an SV and AKC judge. He can be reached email@example.com