Ask about our Early Bird Special on all unborn litters!!
I have had a lot of recent emails asking me about pricing on my upcoming litters.
This is for color pure breeding only .
We will be making another list for off color and carriers.
7/8 European or Full European Puppies
Color Limited Reg. (Pet) Full Reg. (Breeding Rights)
Harlequin 1500.00 2000.00
Mantle 1400.00 1900.00
Merle Mantle 1300.00 1500.00
Merle 1300.00 1500.00
Merlequin 1300.00 1500.00
Black/white 950.00 1450.00
1/2 European Puppies
Color Limited Reg. (Pet) Full Reg. (Breeding Rights)
Harlequin 1200.00 1500.00
Mantle 900.00 1200.00
Merle Mantle 750.00 900.00
Merle 750.00 900.00
Merlequin 750.00 900.00
Black/White 700.00 850.00
Full American Puppies
Color Limited Reg. (Pet) Full Reg. (Breeding Rights)
Harlequin 1000.00 1300.00
Mantle 900.00 1200.00
Merle Mantle 600.00 800.00
Merle 600.00 800.00
Merlequin 600.00 800.00
Black/white 500.00 700.00
Information about Great Danes
When reading the below, remember that all pups follow their own guide, and grow at their own rate--other guides (listed below chart), are better for knowing what is "right" than just ht/wt data.
That said, here is a general guide:
Birth weight: 1-2 lbs
Week 1: 2-3 lbs
Week 2: 3-5 lbs
Week 3: 4-7 lbs
Week 4: 5-8 lbs
Week 6: 12-20 lbs
Month 2: 18-27 lbs (13-17")
Month 3: 30-45 lbs (17"-22")
Month 4: 50-65 lbs (21"-25")
Month 5: 65-85 lbs (25"-30")
Month 6: 70-100 lbs (27-32")
Month 7: 75-110 lbs (27-33")
Month 8: 80-115 lbs. (27-34")
Month 9: 85-120 lbs. (28-34")
One year: 90-135 lbs (28-36")
Full grown: 100-190 lbs (28"-38")
For males, 140-170 lbs. & 33-36" is typical;
for females 110-140 & 30-33" is typical.
NOTE: Some danes may actually weighless/be smaller a bit less than this chart indicates, a few may weigh more--but more in this case is probably an indication the pup is being overfed & growing too fast (or the dog in question is too fat). If not, he is likely overboned-so he *really* then needs to stay slim, as heavy boned dogs are more prone to joint & bone problems.
**Remember the only requirement under the standard is 28" for females & 30" for males (and that was generally intended to apply specifically to adult danes).** When there was a weight guide in the standard, that 28" female was expected to weigh 100 lbs. & that 30" male 120 lbs. Balance is what the standard calls for!
Take a look at your dog. You can see quite a few things about her. You can tell what her coat color is, if her hair is long or short, what her eye color is. You can even "look" through the use of x-rays and laboratory tests, to determine if her hips are sound, and if her thyroid gland it working properly. All of these things make up the dog's phenotype.
Your dog's genotype refers to what is actually present in her DNA, whether or not that has transferred to her appearance, build, how her body functions. Each dog has two full sets of genetic information, one from each parent. So each locus (genetic unit) has a pair of genes. This pair of genes can be either homozygous meaning that both of the genes in the pair are identical or heterozygous meaning that the two genes are different. There may only be two options for a particular locus, or there may be many options. Any single trait may be controlled by a single locus, a single pair of genes, or it may be controlled by the combination and interaction of many pairs of genes. The available genetic options at each locus are called alleles.
Dominant and recessive refer to the gene's behavior if they are different. In simple terms, if the two genes at a locus are different, the dominant gene will determine the dog's phenotype, what you see. A dog will only show a recessive trait if BOTH genes at a locus are the recessive allele. Both dominants or one dominant and one recessive will result in the dominant phenotype. Dominant and recessive DO NOT mean "good" and "bad." In fact, many desirable traits in Great Danes are the result of recessive genes. However, it is easier to "breed away" from a bad dominant gene--if the gene is there, you see it, and you can choose not to breed the animal displaying the trait. A recessive trait can be carried, hidden, for many generations, and will never display the trait unless it gets paired up with another matching recessive gene from the other side of the family.
Unfortunately, not everything works as a simple dominant/recessive. At some loci, the different alleles may have a relationship of incomplete dominance. That is, if both genes are recessive, the trait coded by the recessive will be displayed. If the locus is heterozygous, the phenotype will show a "halfway in between" appearance. Only when the locus is homozygous for the dominant will the appearance show the dominant gene.
In a simple case, there are only two alleles that can appear there. That locus will either be homozygous for the dominant, heterozygous, or homozygous for the recessive. Homozygous dominant, the dominant trait will appear. Likewise if it is homozygous recessive, the recessive trait will appear. In the heterozygous case, you will see either the dominant phenotype (if the alleles have simple domiant-recessive relationship) or a phenotype that is halfway in between (if there is an incomplete dominance relationship.) At some gene loci, there are several genes that can appear there. Many times, we can rank these allelles in order of dominance. Since only two allelles will be present in any one dog, we can still use the dominant-recessive idea to see what will or could be produced.
Primary Coat Color
First, we’ll look at the different loci that affect coat color in the Great Dane.
In each series, the possible alleles will be listed in terms of dominance, with the more dominant genes at the top, ranging to the most recessive at the bottom. The usual convention is to have the dominant gene capitalized, with recessive genes in lower case letters.
To begin, we'll touch on three series, the A-series, the E-series and the D-series. While all three do affect coat color in Great Danes, my intention here is to discuss primarily the Black, Harlequin, Mantle, Merle and White colors. All of these colors are AA, EE, and DD.
A-series: This determines the "base" color of the coat. Dogs have two forms of melanin in their coats. One, eumelanin, is dark. It varies in color due to variations in the protein that forms the framework of the pigment granule. The base form of eumelanin is black. Eumelanin can also be brown (also called chocolate or liver) or blue-gray. The other pigment, phaeomelanin, ranges from pale cream through shades of yellow, tan and red to mahogany.
The available alleles are:
- A Dominant Black, eumelanin can appear everywhere. A is seen in Black, Blue, Merle, Harlequin, and White Great Danes.
- ag Agouti or wolf gray (not present in Great Danes) Each hair is banded with eumelanin and phaeomelanin.
- ay Sable Each hair is the phaeomelanin color with eumelanin only at the tip. The ay genotype (always homozygous in Great Danes, acts, IN DANES as a simple recessive to A) is responsible for the base color in Fawn and Brindle Danes. Modifiers can increase or reduce the amount of black tipping. In Great Danes, we have selected for modifiers to reduce this tipping, although it is still often visible at the base of the tail and around the ears.
- at Tanpoint, Doberman and Rottweiller color (not present in Great Danes) Eumelanin color with only phaeomelanin at the "points" on the face, legs, under the tail.
- as Saddle, more tan than tanpoint, seen in German Shepherd Dogs (not present in Great Danes) As tanpoint above, but with far larger areas of phaeomelanin only.
- a Recessive black (not present in Great Danes)
E-series: The E-series is poorly understood and very controversial. In the simplest form, E=can produce eumelanin, and e=only phaeomelanin is produced (regardless of the A-series genes, and ee dog will show ONLY the yellow/red pigment, as is seen in yellow Labradors and Irish Setters.)
There are some theories that Masking (as on our Fawns) and Brindling are also on the E-series. Other research indicates that one or both of these traits are at a different locus altogether. In any case, all Great Danes can produce black pigment.
For now, I'm assuming (only further research will allow us to know for sure) that Brindling is on separate locus, that I'll call Br=Brindle, br=not-brindle. What is clear is that Brindle is dominant to Not-Brindle.
D-series: This determines whether the recessive gene that makes the eumelanin Blue instead of Black is present. There are only two alleles.
- D Normal (Black) pigment
- d Blue dilution. All areas that the A-series codes as Black will be Blue in color. Note that dd can affect the mask and/or stripes in Fawns and Brindles.
Other loci that affect coat color in dogs, but do not enter into discussion of the Great Dane are:
- C albino series. All Great Danes are C, no albino traits. Other more recessuve alleles range from slight to full fading of color.
- G graying The dominant G causes puppies that are born dark, with the color fading as they mature. All Great Danes are gg, no graying.
- T ticking series. The dominant T produces individual pigmented hairs through spots of colored hair in otherwise white areas on the dog. All Great Danes are tt, no ticking.
- B brown The recessive causes the eumelanin to be red/brown in color. The recessive b should not be present in Great Danes, although there is some chance that it is. The homozygous recessive bb produces red Dobermans and chocolate Labradors. If present, it could produce chocolate Danes, "red merle" Danes, or a brown mask and/or stripes on Fawns and Brindles.
So, the Black, Harlequin, Merle, Mantle, and White Great Danes are ALL AAEEDDCCggttBB. To simplify discussion, we will ignore these genes in the rest of our discussion, as all loci are homozygous for a particular gene, these alleles will not vary from individual to individual.
From the series previously discussed, we now are left with solid Black dogs. Three gene series are responsible for creating the wide range of colors/patterns seen in the Harlequin color-group of Great Danes.
M-Series: merle. This gene is an incomplete dominant. There are two alleles:
There are thus three possible combinations of the above in any one dog:
H-series: Harlequin gene. This too is an incomplete dominant, but with some additional complications. The two alleles are:
The dominant gene H ONLY has an effect of the phenotype in combination with the Merle gene. If a dog is mm (not-merle) the H gene may very well be present, but will have NO effect on the dog's appearance. As with Merle, there are three possible combinations of these genes, but only two appear in dogs.
Looking only at the above two genes, we have the following possible combinations:
S-Series: White Spotting. There are several alleles at this locus. Although ranked by dominance, all show a pattern of incomplete dominance, with the resulting pattern being in between the two alleles in a heterozygous dog. The pattern seems to lean a bit more in the direction of the dominant of the two alleles, but still is in between the patterns coded by each of the two genes that is present in the individual dog. There are also plus and minus modifiers that affect somewhat the amount of white, meaning that each genetic combination will show variation. Between the effect of each gene being varied by the plus and minus modifiers, and the incomplete dominance action of these alleles, guessing S-series patterning from looking at a dog (rather than also examining the parents and offspring) can be difficult.
Now let's look at the appearance of some of the heterozygous possibilites.
Although the white patterns are easily visible on Black and Merle Danes, there are obvious complications in determining the white pattern on a Harlequin, due the impossibility of distinguishing white caused by the H-series from white caused by the S-series.
Breeding-Where do Deaf Whites Come From?
We've now covered the genetics that make up Black, Harlequin, Merle and (double merle) White. Let's take a look at what we get when we start breeding these dogs. For now, let's disregard S-series white spotting. We'll take a look at it again later. For Black and White Danes, I'll use BlackH and WhiteH if these dogs are carrying the H gene. Please note that these percentages are theoretical, given that HH is lethal. However, MMHh is also a sub-lethal, in that some MMHh dogs also do not develop, so the WhiteH numbers stated are HIGHER than would actually be expected in actual puppies born. While it may be possible to distinguish WhiteH from White because the WhiteH, while rarer, should show only black patches on the few areas of pigment, whereas a White (not carrying Harle) can show Merle and Black patches. There is no way to visually distinguish between Black and BlackH.
!=will produce double-merle white puppies, *=will produce Harlequin
|Black x Black||mmhh x mmhh||100% Black|
|Black x BlackH||mmhh x mmHh||50% Black, 50% BlackH|
|Black x Merle||mmhh x Mmhh||50% Black, 50% Merle|
|Black x Harlequin||mmhh x MmHh||25% Harle, 25% Merle, 25% Black, 25% BlackH|
|Black x White||mmhh x MMhh||100% Merle|
|*||Black x WhiteH||mmhh x MMHh||50% Merle, 50% Harle|
|BlackH x BlackH||mmhh x mmHh||50% Black x 50% BlackH|
|*||BlackH x Merle||mmHh x Mmhh||25% Black, 25% BlackH, 25% Merle, 25% Harle|
|*||BlackH x Harlequin||mmHh x MmHh||33%BlackH, 16.7%Black, 33%Harle, 16.7% Merle|
|*||BlackH x White||mmHh x MMhh||50% Merle, 50% Harle|
|*||BlackH x WhiteH||mmHh x MMHh||33% Merle, 67% Harle|
|!||Merle x Merle||Mmhh x Mmhh||25% Black, 50% Merle, 25% White|
|!*||Merle x Harlequin||Mmhh x MmHh||25% Merle, 25% Harle, 12.5% Black, 12.5% BlackH, 12.5% White, 12.5% WhiteH|
|!||Merle x White||Mmhh x MMhh||50% Merle, 50% White|
|!*||Merle x WhiteH||Mmhh x MMHh||25% Merle, 25% Harle, 25% White, 25% WhiteH|
|!*||Harlequin x Harlequin||MmHh x MmHh||8.3% Black, 16.7% BlackH, 33.3% Harle, 16.7% Merle, 16.7% WhiteH, 8.3% White|
|!*||Harlequin x White||MmHh x MMhh||25% Merle, 25% Harle, 25% White, 25% WhiteH|
|!*||Harlequin x WhiteH||MmHh x MMHh||33.3% WhiteH, 16.7% White, 33.3% Harle, 16.7% Merle|
|!||White x White||MMhh x MMhh||100% White|
|!||White x WhiteH||MMhh x MMHh||50% White, 50% WhiteH|
|!||WhiteH x WhiteH||MMHh x MMHh||66.7% WhiteH, 33.3% White|
Hypertrophic Osreodystrophy (HOD)
Who gets hypertrophic osteodystrophy?
HOD is a disease of young, rapidly growing dogs. It usually strikes puppies between the ages of 3 to 6 months. It is primarily a disease of large or giant breeds of dogs, although there can be exceptions to this rule. As with most of the young, large breed bone disorders, it affects males more commonly than females. There does not appear to be an increased incidence in any one large or giant breed. There does not appear to be a strong inherited or genetic link.
What are the symptoms of hypertrophic osteopathy?
Dogs that are stricken with HOD often show symptoms of mild to moderate painful swelling of the growth plates in the leg bones. It most commonly affects the ends of the radius, ulna, (long bones from the elbow to the wrist) and tibia (long bone from the knee to the hock). The dogs may show lameness and a reluctance to move. They may be lethargic and refuse to eat. A fever may come and go rising as high as 106 degrees. The disease usually affects both legs at the same time. The symptoms may wax and wane and resolve on their own or if the fever is very high for long periods and the bony involvement severe, the dogs may suffer permanent structural damage or even die.
How is hypertrophic osteodystrophy diagnosed?
Diagnosis is based on the history, symptoms, physical exam showing pain and swelling at the growth plates, and with x-rays. The x-rays will show a thin radiolucent (dark) line at the metaphysis (growth plate) in the end of the ulna, radius, or tibia. Bony inflammationand bone remodeling may also be seen at these sites. Occasionally, there may be involvement and changes in the skull and teeth. Dogs often have a fever and occasionally a high white blood cell count.
What is the treatment?
The treatment is generally supportive. Since this is a very painful condition anti-inflammatories and painkillers such as buffered aspirin or carprofen (Rimadyl) are given. (Do NOT give your cat aspirin unless prescribed by your veterinarian.) In addition, the animals are usually given a broad-spectrum antibiotic. Strict rest on a comfortable warm bed is recommended. Feeding a nutritious, highly palatable food will help to encourage some dogs to eat. In severe cases steroids may need to be given to control the pain, but because of the possibility of this being a bacterial disease their use may be contraindicated due to their immunosuppressive qualities. Vitamin C is often supplemented though its benefit may be questionable.
What causes it and how is it prevented?
The prevention lies in understanding what causes this disease. Unfortunately, there is currently no agreement on the cause of this disease. One possible cause may be a bacterial infection. The bony changes and high fever support this possibility. The difficulty in obtaining a bacterial culture from the site and the sometimes-poor response to antibiotic therapy may fuel the argument against this possible cause.
Another suspect in the disease is vitamin C. It has been shown that dogs with this disease show very similar symptoms and bony changes as people with scurvy (vitamin C deficiency). In addition, these dogs often have a lowered blood vitamin C level. However, dogs synthesize their own vitamin C and do not have a nutritional requirement for this vitamin. In several studies and in practice, feeding affected dogs high doses of vitamin C does not always alter or cure the disease. Some researchers therefore speculate that the low blood level of vitamin C may be a result of the disease, not the cause.
Another possible cause of the disease may be nutritional. It has been suggested that several bone diseases in young puppies are linked to an excess of protein and caloriesin the diet leading to the development of these problems. The studies have not been done that confirm this, though many owners of large and giant breed puppies are currently feeding a diet lower in fat and protein to try to encourage moderate steady growth instead of rapid growth. It is possible that this disease may be caused by several factors. At this time, however, we do not know the cause or how to prevent it. Hopefully future studies will give us more information on the cause and prevention of this painful and debilitating disease.
References and Further Reading
Bloomberg, M; Taylor, R; Dee, J. Canine Sports Medicine and Surgery. W.B. Saunders Co. Philadelphia, PA; 1998.
Brinker, W; Piermattei, DL; Flo, GL. Handbook of Small Animal Orthopedics and Fracture Treatment. W.B. Saunders Co. Philadelphia, PA; 1983.
Ettinger, S. Textbook of Veterinary Internal Medicine. W.B. Saunders Co. Philadelphia, PA; 1989.
Veterinary & Aquatic Services Department, Drs. Foster & Smith, Inc.
Canine hip dysplasia is a very common degenerative joint disease seen in dogs. There are many misconceptions surrounding it. There are many things that we know about hip dysplasia in dogs, there are also many things we suspect about this common cause of limping, and there are some things that we just do not know about the disease. We will cover all of those here and hope to separate out fact, theory, hypothesis, and opinion.
What is hip dysplasia?
To understand what hip dysplasia really is we must have a basic understanding of the joint that is being affected. The hip joint forms the attachment of the hind leg to the body and is a ball and socket joint. The ball portion is the head of the femur while the socket (acetabulum) is located on the pelvis. In a normal joint the ball rotates freely within the socket. To facilitate movement the bones are shaped to perfectly match each other, with the socket surrounding the ball. To strengthen the joint, the two bones are held together by a ligament. The ligament attaches the femoral head directly to the acetabulum. Also, the joint capsule, which is a very strong band of connective tissue, encircles the two bones adding further stability. The area where the bones actually touch each other is called the articular surface. It is perfectly smooth and cushioned with a layer of spongy cartilage. In the normal dog, all of these factors work together to cause the joint to function smoothly and with stability.
Hip dysplasia results from the abnormal development of the hip joint in the young dog. It may or may not be bilateral, affecting both right and left sides. It is brought about by the laxity of the muscles, connective tissue, and ligaments that should support the joint. Most dysplastic dogs are born with normal hips but due to genetic and possibly other factors, the soft tissues that surround the joint start to develop abnormally as the puppy grows. The most important part of these changes is that the bones are not held in place but actually move apart. The joint capsule and the ligament between the two bones stretch, adding further instability to the joint. As this happens, the articular surfaces of the two bones lose contact with each other. This separation of the two bones within a joint is called subluxation and this, and this alone, causes all of the resulting problems we associate with the disease.
What are the symptoms of hip dysplasia?
Dogs of all ages are subject to the symptoms of hip dysplasia and the resultant osteoarthritis. In severe cases, puppies as young as five months will begin to show pain and discomfort during and after vigorous exercise. The condition will worsen until even normal daily activities are painful. Without intervention, these dogs may be unable to walk at all by a couple years of age. In most cases, however, the symptoms do not begin to show until the middle or later years in the dog's life.
The symptoms are typical for those seen with other causes of osteoarthritis. Dogs may walk or run with an altered gait, often resisting movements that require full extension or flexion of the rear legs. Many times, they run with a 'bunny hopping' gait. They will show stiffness and pain in the rear legs after exercise or first thing in the morning. Most dogs will warm up out of the muscle stiffness with movement and exercise. Some dogs will limp and many will decrease their level of activity. As the condition progresses, the dogs will lose muscle tone and may even need assistance in getting up. Many owners attribute the changes to normal aging but after treatment is initiated, they are shocked to see much more normal and pain-free movement return.
Who gets hip dysplasia?
Hip dysplasia can be found in dogs, cats, and humans, but for this article we are concentrating only on dogs. In dogs, it is primarily a disease of large and giant breeds. The disease can occur in medium-sized breeds and rarely even in small breeds. It is primarily a disease of purebreds although it can happen in mixed breeds, particularly if it is a cross of two dogs that are prone to developing the disease. German Shepherds, Labrador Retrievers, Rottweilers, Great Danes, Golden Retrievers, and Saint Bernards appear to have a higher incidence, however, these are all very popular breeds and may be over represented because of their popularity. On the other hand, Greyhounds and Borzois have a very low incidence of the disease.
What are the risk factors for the development of hip dysplasia?
Hip dysplasia is caused by looseness in the hip joint. The looseness creates abnormal wear and erosion of the joint and as a result pain and arthritis develops. The disease process is fairly straightforward; the controversy starts when we try to determine what predisposes animals to contract the disease. Almost all researchers agree that there is a genetic link involved. If a parent has hip dysplasia, then the offspring are at greater risk for developing hip dysplasia. Some researchers feel that genetics are the only factor involved, where others feel that genetics contribute less than 25% to the development of the disease. The truth probably lies in the middle. If there are no carriers of hip dysplasia in a dog's lineage, then it will not contract the disease. If there are genetic carriers, then it may contract the disease. We can greatly reduce the incidence of hip dysplasia through selective breeding. We can also increase the incidence through selectively breeding. We cannot, however, completely reproduce the disease through selective breeding. In other words, if you breed two dysplastic dogs, the offspring are much more likely to develop the disease but will not all have the same level of symptoms or even necessarily show any symptoms. The offspring from these dogs will, however, be carriers and the disease may show up in their offspring in later generations. This is why it can be difficult to eradicate the disease from a breed or specific line.
Nutrition: Experimentally, we can increase the severity of the disease in genetically susceptible animals in a number of ways. One of them is through obesity. It stands to reason that carrying around extra weight will exacerbate degeneration of the joint in a dog with a loose hip. Overweight dogs are therefore at a much higher risk. Another factor that may increase the incidence is rapid growth in a puppy during the ages from three to ten months. Experimentally, the incidence has been increased in genetically susceptible dogs when they are given free choice high protein and high calorie diets. In a large study done in 1997, Labrador Retriever puppies fed a high protein, high calorie diet free choice for three years had a much higher incidence of hip dysplasia than their littermates who were fed the same high calorie, high protein diet but in an amount that was 25% less than that fed to the dysplastic group. As might be expected, however, the free choice group was significantly heavier at maturity and averaged 22 pounds heavier than the control group. Because obesity is also a risk factor, this study may be difficult to interpret.
There have also been studies looking into protein and calcium levels and their relationship to hip dysplasia. Both of these studies were able to increase the level of hip dysplasia by feeding increased amounts of calcium and protein. But once again, the studies of puppies fed greatly increased amounts over normal recommended values and compared them to animals fed decreased amounts. They failed to compare puppies fed a normal amount of food that had the recommended amount of protein, fat, and calcium to those fed a diet with slightly less protein, fat, and calcium (similar to those 'large breed puppy foods' that are now flooding the market). We have yet to see a study that links an increased incidence in hip dysplasia in dogs fed a normal diet of commercial puppy food versus a specialty diet formulated just for large breed puppies.
Exercise: Exercise may be another risk factor. It appears that dogs that are genetically susceptible to the disease may have an increased incidence of disease if they over-exercised at a young age. But at the same time, we know that dogs with large and prominent leg muscle mass are less likely to contract the disease than dogs with small muscle mass. So exercising and maintaining good muscle mass may actually decrease the incidence of the disease. Moderate exercise that strengthens the gluteal muscles, such as running and swimming, is probably a good idea. Whereas, activities that apply a lot of force to the joint are contraindicated. An example would be jumping activities such as playing Frisbee.
How is hip dysplasia diagnosed?
Diagnosis of hip dysplasia in dogs that are showing clinical signs of arthritis and pain is usually made through the combination of a physical exam and radiographs (x-rays). If a dog is showing outward signs of arthritis, there are usually easily recognized changes in the joint that can be seen on radiographs. In addition, the veterinarian may even be able to feel looseness in the joint or may be able to elicit pain through extension and flexion. Regardless, the results are straightforward and usually not difficult to interpret.
However, about half of the animals that come in for a determination on the health of their hip joints are not showing physical signs, but are intended to be used for breeding. The breeder wants to ensure that the animal is not at great risk for transmitting the disease to his or her offspring. There are two different testing methods that can be performed. The traditional and still most common is OFA testing. The other newer technique is the PennHip method.
OFA: The method used by the Orthopedic Foundation for Animals (OFA) has been the standard for many years. The OFA was established in 1966, and has become the world's largest all-breed registry. The OFA maintains a database of hip evaluations for more than 475,000 dogs. Radiographs are taken by a local veterinarian under specific guidelines and are then submitted to the OFA for evaluation of hip dysplasia and certification of hip status. Since the accuracy of radiological diagnosis of hip dysplasia using the OFA technique increases after 24 months of age, the OFA requires that the dog be at least two years of age at the time the radiographs are taken. They also recommend that the evaluation should not be performed while the female is in heat. To get the correct presentation and ensure that the muscles are relaxed, the OFA recommends that the dog be anesthetized for the radiographs. OFA radiologists evaluate the hip joints for congruity, subluxation, the condition of the acetabular margins and acetabular notch, and the size, shape, and architecture of the femoral head and neck. The radiographs are reviewed by three radiologists and a consensus score is assigned based on the animal's hip conformation relative to other individuals of the same breed and age. Using a seven point scoring system, hips are scored as normal (excellent, good, fair), borderline dysplastic, or dysplastic (mild, moderate, severe). Dogs with hips scored as borderline or dysplastic are not eligible to receive OFA breeding numbers.
The OFA will also provide preliminary evaluations (performed by one OFA radiologist) of dogs younger than 24 months of age to help breeders choose breeding stock. Reliability of the preliminary evaluation is between 70 and 100% depending on the breed. Results published by the OFA suggest that the incidence of hip dysplasia in certain breeds has decreased as a result of selective breeding programs. When dogs born in 1972 to 1980 were compared with dogs born in 1989 and 1990, 60% of the breeds demonstrated a statistically significant decrease in hip dysplasia. At the same time, 68% of breeds had a statistically significant increase in the number of hips scored as excellent. This information may suggest progress is being made to decrease the frequency of hip dysplasia, but it may simply be that only radiographs from dogs thought to have normal hips are being submitted to the OFA, while those with dysplasia are being screened out by referring veterinarians.
PennHIP: The diagnostic method used by the University of Pennsylvania Hip Improvement Program (PennHIP) uses distraction/compression radiographic views to more accurately identify and quantify joint laxity. Radiographs of the hip joints are taken with the dog under heavy sedation. Two views are obtained with the hind limbs in neutral position to maximize joint laxity. Weights and an external device are used to help push the head of the femur further into or away from the acetabulum. The amount of femoral head displacement (joint laxity) is quantified using a distraction index (DI). The DI ranges from 0 to 1 and is calculated by measuring the distance the center of the femoral head moves laterally from the center of the acetabulum and dividing it by the radius of the femoral head. A DI of 0 indicates a very tight joint. A DI of 1 indicates complete luxation with little or no coverage of the femoral head. A hip with a distraction index of .6 is 60% luxated and is twice as lax as a hip with a DI of .3. When the DI was compared to the OFA scores for 65 dogs, all dogs scored as mildly, moderately, or severely dysplastic by the OFA method had a DI above .3.
Hip joint laxity as measured by the DI is strongly correlated with the future development of osteoarthritis. Hips with a low DI are less likely to develop osteoarthritis. Hips with a DI below .3 rarely develop osteoarthritis visible on radiographs. Although hips with a DI above .3 are considered "degenerative joint disease susceptible" not all hips with a DI greater than .3 eventually develop osteoarthritis. It is known that some hips with radiographically apparent laxity do not develop osteoarthritis. A means of differentiating lax hips that develop osteoarthritis from those that will not is important in developing a prognosis and making treatment recommendations. In one study, the DI obtained from dogs at four months of age was a good predictor of later osteoarthritis, though the 6 and 12-month indices were more accurate.
To assure quality and repeatability among diagnostic centers using the PennHip technique, veterinarians must take a special training course to become certified. As this technique gains popularity more and more veterinarians are becoming certified.
How is hip dysplasia treated surgically?
There are several surgical procedures available depending on the age and the severity of the joint degeneration.
Triple Pelvic Osteotomy (TPO): TPO is a procedure used in young dogs usually less than 10 months of age that have radiographs that show severe hip laxity, but have not developed severe damage to the joints. The procedure involves a surgical breaking of the pelvic bones and a realignment of the femoral head and acetabulum restoring the coxofemoral weight-bearing surface area and correcting femoral head subluxation. This is a major surgery and is very expensive, but the surgery has been very successful on animals that meet the requirements.
Total Hip Replacement: may be the best surgical option for dogs that have degenerative joint disease as a result of chronic hip dysplasia. Total hip replacement is a salvage procedure that can produce a functionally normal joint, eliminate degenerative changes, and alleviate joint pain. The procedure involves the removal of the existing joint and replacing it with a prosthesis. To be a candidate for this procedure, the animal must be skeletally mature and is usually performed on dogs weighing at least 20 pounds. There is no maximum size limit. If both hips need to be replaced, there is a three-month period of rest recommended between the surgeries. As with the TPO surgery, this is a very expensive procedure but has had some very good results.
Femoral Head and Neck Excision: Femoral head and neck excision is a procedure in which the head of the femur is surgically removed and a fibrous pseudo-joint forms. This procedure is considered a salvage procedure and is used in cases where degenerative joint disease has occurred and total hip replacement is not feasible. The resulting pseudo-joint will be free from pain and allow the animal to increase its activity, however, full range of motion and joint stability are decreased. For best results, the patient should weigh less than 45 pounds, however, the procedure may be performed on larger dogs.
Juvenile Pubic Symphysiodesis: A new, less invasive surgery for treating hip dysplasia, called Juvenile Pubic Symphysiodesis, is currently being evaluated. This surgery prematurely fuses two pelvic bones together, allowing the other pelvic bones to develop normally. This changes the angle of the hips, lessening the likelihood of arthritis. Early diagnosis is critical, since the procedure must be done before 20 weeks of age, preferably 16 weeks.
Pectineal Myectomy: This is a somewhat controversial treatment for patients with chronic hip dysplasia. The pectineus is one of the muscles attaching the femur to the pelvis. By cutting and removing this muscle, the tension on the joint and joint capsule are reduced. This offers some pain relief for some patients, but does not slow the progression of the disease. There are possible complications with this procedure and with the introduction of the newer, better procedures. This surgery is rarely performed anymore.
How is hip dysplasia treated medically?
Medical treatment of hip dysplasia and osteoarthritis has greatly improved in the last several years thanks to the introduction and approval of several new supplements and drugs. Because hip dysplasia (and other types of dysplasias) are primarily inherited conditions, there are no products on the market that prevent their development. Through proper diet, exercise, supplements, anti-inflammatories, and pain relief, you may be able to decrease the progression of degenerative joint disease, but the looseness in the joint or bony changes will not change significantly.
Medical management is indicated for both young dogs with clinical signs and for older dogs with chronic osteoarthritis. Because of the high cost involved with many surgeries, medical management is many times the only realistic option for many pet owners. Medical management is multifaceted. For the best results, several of the following modalities should be instituted. For most animals, veterinarians begin with the first recommendations and work their way down this list as needed to control the pain and inflammation associated with degenerative joint disease.