FRIENDS OF THE ALASKAN MALAMUTE CLUB

HIP DYSPLASIA IN SOUTH AFRICA

by Robert M Kirberger BVSc MMedVet (Rad), Section Radiology, Department of Surgery, Faculty of Veterinary Science, University of Pretoria (South Africa)

Hip dysplasia is a developmental, multifactorial, genetically influenced condition that is characterized by ill-fitting or loosely-fitting hip joints and the development of secondary degenerative joint disease (arthrosis). The word dysplasia is derived from the Greek "dys" meaning abnormal and "plassein" meaning to form. As hip dysplasia is a developmental disease, it only manifests itself radiologically after the age of about 6 months. There is no doubt about the fact that the tendency to develop hip dysplasia is inherited but environmental factors like excessive protein intake and excessive strenuous exercise at a very young age play a role in the degree of dysplasia that is eventually manifested. Genetically susceptible dogs become dysplastic when the primary muscle mass that supports the joint fails to mature at the same rate as the skeletal structures. The resultant disparity between soft tissue strength and biomechanical forces during skeletal growth is manifested as a loss of congruency between the articular surfaces of the acetabulum and the femur head. This results in joint laxity and eventual hip arthrosis.

Hip dysplasia was first described in 1935 by Dr G B Schnelle but it was only in the 1950s that significant research results started appearing in the scientific literature and the seriousness of the condition became a widespread concern to breeders and veterinarians alike as it became known as an inherited disease. Since the 1950s hundreds of scientific articles have been published and many hours of research spent in trying to come to grips with this condition. Much has been learnt over the past 40 years, but as yet minimal progress has been made in preventing the occurrence of this potentially devastating disease. In the 1960s control programmes were set up in different countries by applying genetic principles and breeding programmes. Hopefully, after this discussion, breeders will have a greater understanding of the complexities of the condition and be able to make more knowledgeable decisions when breeding their dogs.

The need for a greater understanding of hip dysplasia by dog breeders, owners and veterinarians alike is highlighted below in Table 1 which shows data from the Orthopaedic Foundation for Animals (OFA) in the United States. Only breeds found commonly in South Africa have been extracted from the data.

DIAGNOSIS

The diagnosis of hip dysplasia is usually made after the dog has shown clinical signs of the conditions or after radiograhic examination to evaluate the suitability of a dog's hips for breeding purposes.

Clinical examination
Hip dysplasia is the most common orthopaedic problem affecting larger breed dogs with a prevalence of up to 43%. Lameness in the hind quartes is the most common clinical complaint. In dogs less than a year old, the clinical signs tend to be a result of the loosely fitting joint (laxity). This results in stress on the joint capsule and round ligament as well as injury to the cartilaginous acetabular rim and micro-fractures. Both hind limbs, rarely only 1 limb, show episodes of lameness, usually exacerbated by exercise. Other signs seen may include difficult in rising, walking, running and stair climbing and occasionally bunny-hopping. Once the dogs are mature, clinical signs often improve until the dogs develop servere degenerative joint disease (arthrosis). These dogs may show muscle wasting, a waddling gait, appear weak in the hind quarters, are reluctant to exercise, and prefer sitting to standing.

Hip dysplasia is not the only possible cause of the above clinical signs. A thorough clinical examination by a veterinarian as well as appropriate radiographs are required to confirm the condition and to rule out other or concomitant diseases. A complicating factor is that the severity of radiographic changes is poorly correlated to the clinical signs. A dog with grade 3 or 4 hip dysplasia may walk normally and a dog with grade 1 hip dysplasia may show marked clinical signs. This is most likely due to differing pain thresholds or compensatory mechanisms in the dogs but makes if very difficult for the veterinarian to convince a breeder not to breed with a grade 3 hip dysplasia dog if the dog appears quite normal to the owner.

The Ortolani test is a common physical examination manipulation that may be used to diagnose instability of the hip joint, and thus hip dysplasia. It usually requires general anaesthesia. Pressure is applied via the femoral shaft towards the hip joint to subluxate the lax femoral head. On further manipulation, the head pops back into the socket resulting in a click behing felt or heard. The procedure should be repeated a few times to confirm a negative Ortolani test. A false-positive Ortolani sign occurs occasionally but false-negatives are fairly common, particularly up to 18 weeks of age. Some older dogs with hip dysplasia may not demonstrate a positive Ortolani test due to extensive fibrosis (scar tissue) around the joint or the hip being totally luxated.

Ultrasound examination
Recent research work has shown a statiscal correlation between dynamic ultrasonographic measured maximum distraction distance and stress-radiographic techniques in 6-8 weeks old puppies. As the technique is very operator dependent, further data are required to determine if this will become a clinically useful diagnostic or prognostic test.

None of the above examinations are definitive diagnostic methods for hip dysplasia and pelvic radiographs are required to confirm the diagnosis or to evaluate the hips for the dog's breeding potential.

Radiographic examination (X-ray examination)
Radiological examination is the only definitive method of determining the presence of hip dysplasia. In severe cases, definite radiological changes confirming the condition will be present at the age of about 6 months or even earlier, but routine radiographic examination for the purpose of certification is delayed until skeletal maturity has been reached. There is a 5% possibility that hips that are normal at the age of 12-13 months can still develop a mild degree of dysplasia. It is of course also possible that many, or all, of these cases that develop hip dysplasia subsequently were not diagnosed originally due to incorrect positioning, poor quality radiographs (X-rays), or unfamiliarity with the early radiological signs. A certain degree of deterioration (about one degree) is quite possible between the ages of 1 to 2.5 years in cases showing radiological signs at the age of one year. Theoretically it should therefore also be possible to develop a grade 1 dyplasia in that time if the hips appeared to be normal at the age of one year. Although extremely rare, the reverse, namely improvement in the laxity of the hips, is also possible in cases subject to regular exercise to strengthen the muscles responsible for holding the femoral head firmly in position. Radiographic evidence of hip dysplasia is a phenotypic expressions of the condition. Normal radiographs does not necessarily mean that the dog is genotypically negative for hip dysplasia. This is part of the problem of controlling this condition and will be discussed later. In South Africa official certification is done at 12 months or older and at 18 months in the Rottweiler. Giant breeds currently have no hip dysplasia requirements but it is advisable to wait until 18 months of age before making radiographs. In the United States official radiographs can be made in younger dogs purely for diagnostic reasons but will have to be redone at the correct age for certification purposes.

Radiographing dogs that are pregnant or in oestrus is a contentious issue. A recent study by Hassinger showed that there was no statistically or clinically significant change in hip joint laxity in bitches studied during the various stages of the oestrus cycle. However the OFA recommends that radiographs be made one month after weaning of pups or one month before or of after a heat cycle and where possible this is probably still the safest route to follow.

Evaluation and grading
Unfortunately, there is no standard international grading scheme (see Table 2 below) and this has led to much confusion amongst breeders, particulary if wishing to import or export dogs or semen. The Federation Cynologique Internationale (FCI), as well as the World Small Animal Veterinary Association, have attempted since 1974 to standardise grading schemes without much success. They have however standardised terminology and set guidelines which include:

a) Minimum age of examination is 1 year with 1 1/2 years for giant breeds.

b) Dogs should be positively identified (tattoo or microchip) and this information to be present on the pedigree certificate and on the radiographs.

c) Left and right sides must be marked on the radiographs as well as the date of examination.

d) A central evaluation panel and method of appeal must be available.

To complicate matters further, in individual countries, certain breed societies still have their own grading schemes which differ from the above basic standards of A-E or 0-4. In the United Kingdom a completely different grading scheme is used (Table 1). The same general interpretation principles apply but they give a score of 0-6 for 8 individual radiographic characteristics and 0-5 for additional characteristic. The score for each hip can thus theoretically range from 0-53. The same scheme is used in Australia and New Zealand.

A certain degree of subjectivity is built into the radiological diagnosis of canine hip dysplasia, irrespective of which of the above grading schemes is used. The subjectivity can be minimised by using scoring panels where consensus is obtained by using only qualified specialist veterinary radiologists. In the USA and UK the hip dysplasia schemes have a panel of eight or more specialists who can be called upon to evaluate radiographs. In South Africa, with its relatively small population of veterinarians, there are currently two registered small animal radiologists and a specialist veterinary surgeon who evaluate radiographs in their private capacity for the various organisation controlling dog breeding in South Africa. Control schemes are usually run by the major dog controlling bodies in tandem with the national veterinary associations. In South Africa, due to lower numbers, these organisations do not have the financial muscle that their sister organisations in the larger countries have and this, together with the lack of specialist radiologists, makes if very difficult to run similar schemes to those in place overseas.

Reference Material:
Proceedings: Hereditary Conditions in Dogs, Dog Breeders' / Owners' Symposium Presented by Faculty of Veterinary Science, University of Pretoria in association with SA Veterinary Foundation and S.A Breed Registry Body.

Procedure for Scoring

It's a must that the dog's Microchip Number should be recorded on the radiograph.

It is essential that your dog be given a general anaesthetic for the radiographs as the dog must be correctly positioned on its back with hind legs extended and parallel to each other. The entire pelvis and hind legs to the stifles must be included and the legs held as close to the x-ray plate as possible. Obviously even the quietest dog would be difficult to restrain in this position without an anaesthetic.

Any tilting of the pelvis is undesirable as it usually improves the appearance of one hip and makes the other look worse than it actually is, making accurate assessment difficult.

The radiograph and completed form are submitted to the Onderstepoort Institute Office with a fee and stamped addressed envelope should be included so that the results maybe forwarded to the issuing veterinarian. All radiographs are retained for research purposes.

Scoring is done to the BVA/GSDL scoring system and the scoring sheet will be sent to your veterinarian who will interpret the results for you.

The pedigree information gathered is summated to give an overview of the situation in the major breeds and reports will be presented annually to veterinarians.

A detailed account of the method of scoring is most necessary for this discussion, however a brief description of the major points taken into account may help the breeder understand the significance of the figure which has been arrived at.

Each hip joint is assessed separately using nine features shown in the below diagram. Each feature is assessed according to written guidelines and given a number from 0 to 6 being grossly abnormal and 0 normal. The addition of these figures for both hips results in a score between 0 and 106. Therefore, from this it can be seen that the higher the score, the more abnormal the hips are.

The nine features looked at are designed to indicate the degree of subluxation of the joint (ie. how unstable the joint is) and the severity of the degenerative changes to all parts of the joint. See above diagram.

When the overall score is arrived at, more weight is given to the degenerative changes as these are considered to be more significant in the disease.

Cause

Hip dysplasia is a developmental disorder affecting the coxofemoral (hip) joints in dogs. The problems associated with hip dysplasia stem from an imbalance in the muscle mass and mechanical forces which are centered on the hip joint. This imbalance is associated with excessive laxity (looseness) which is usually the result of a shallow acetabulum (cup). When the hip joints exhibit laxity, the ball of the femur rides on the edge of the socket rather than gliding smoothly in the socket. This results in pain and eventually to the formation of abnormal calcium deposits, bone spurs and/or arthritis. Eventually, some hip joints will suffer either a partial or complete luxation. Continued use of the affected joint causes abnormal wear on the joint ’s cartilage surfaces leading to further damage and a self-perpetuating degenerative process ensues. Abnormal bony development of the hip joint often results, and inflammation and irritation (arthritis) ultimately cause mild to severe lameness. The joint capsule becomes inflamed and a subsequent increase in synovial fluid in the joint exacerbates the laxity. These physiological changes should be dealt with early (between 4 and 8 months) to attempt to reduce the progress toward degenerative joint disease. The hallmark sign of degenerative joint disease is articular cartilage damage. This results in the exposure of subchondral bone and pain nerve fibers resulting in significant joint pain. Once degenerative joint disease is present, there are fewer treatment options available.

Hip dysplasia is a congenital disease that affects mostly large breed dogs. It causes weakness and lameness to the rear quarters, and eventually leads to painful arthritis. This arthritis goes by several names; degenerative joint disease, arthrosis, osteoarthritis. 

Many factors work together to cause this disease, which is a combination of a dog genetically inclined to get this disease interacting with environmental factors that bring about the symptoms. These environmental factors excess calcium in the diet of puppy food for large breed dogs, along with obesity, high protein and calorie diets, and a lack of or too much exercise. The breeding of dogs that already have hip dysplasia is one of the primary reasons the disease is still present. A dog that has hip dysplasia in one socket is prone to having a problem with the ligaments of the knee in the other leg (anterior cruciate rupture).

Pathophysiology

During the degenerative process the cartilage that lines the hip joint, called hyaline cartilage, is damaged. The damage results from the abnormal forces on the cartilage from the deformed hip socket. Small fractures can occur in the cartilage also. Eventually an enzyme is released that degrades the joint further and decrease the synthesis of an important joint protectant called proteoglycans. The cartilage becomes thinner and stiffer, further compromising its ability to handle the stresses of daily movement and weight bearing. As the problem progresses more enzymes are released, which now affect the precursors to proteoglycans, molecules called glycosaminoglycans and hyaluronate. Lubrication is negligible, inflammation occurs, and the joint fluid can no longer nourish the hyaline cartilage. This viscious cycle continues until pain occurs. The body attempts to reduce this pain by stabilizing the hip joint. New bone is deposited at the joint, both inside and out, along with some of the ligaments and muscle attachments to the area. This causes thickening and a decrease in the range of motion. This is the actual arthritis noted on a radiograph, which will not go away and will continue to progress.

The heritability of hip dysplasia has been firmly established. Several genes have been found to contribute to the ultimate size,shape,strength and growth potential of the hip joint. Furthermore, hip dysplasia is a genetically additive disease; the severity of the affliction is largely the result of a number of disease-related genes present in a particular animal. The multitude of genetic and environmental factors that influence the transmission and development of hip dysplasia make it difficult to predict how the disease will be expressed.It is safe to say that breeding dogs between phenotypically normal dogs will generally result in more normal puppies than will breeding a dysplastic and normal dog or two dysplastic dogs to each other. However,studies have shown that even when both parents are phenotypically normal they can still produce offspring that are phenotypically dysplastic [1]. In spite of careful breeding efforts and the use of classifications from the Orthopedic Foundation for Animals (OFA),such as breeding animals whose parents and grandparents were normal,the progress toward eradication of this disease has been frustratingly slow.

Five misconceptions about Canine Hip Dysplasia From the John M. Olin Laboratory for the Study of Canine Bone and Joint Diseases & James A. Baker Institute for Animal Health, College of Veterinary Medicine, Cornell University

1.  Only hip joints and surrounding tissues are affected. Rather, evidence now indicates that the shoulder and knee joints and some intervertebral joints may show similar changes: the loss of cartilage, inflammation of the joint capsule, bone damage and the growth of spurs at the bone-cartilage interface. Hip dysplasia is simply the most conspicuous -- and most painful -- manifestation of this form of osteoarthritis.

2.  Only dogs suffer hip dysplasia. While 50 percent of some of the larger dog breeds are afflicted, the disease is not unknown in humans. About 1 percent of the general human population suffers hip dysplasia, and the rate for the inherited disease is higher in some populations of American Indians. Many Navajos in New Mexico went through life with hip dysplasia until mothers stopped the traditional practice of strapping infants, straight-legged, to cradle boards and allowed babies to assume the more relaxed, bent-legged position. Replacement of diseased hip joints with artificial joints is one treatment, both for canine and human patients.

3.  The absence of hip dysplasia in canine parents guarantees dysplasia-free pups. Unfortunately, out of 100 matings of "normal" dogs in breeds affected by hip dysplasia, 75 percent of puppies will be "normal" but 25 percent, on average, will have hip dysplasia. Genes for hip dysplasia are believed to be "masked" or hidden in some generations, making the elimination of the disease from breeding stock even more difficult. Canine hip dysplasia was first diagnosed in the 1930s, but probably has troubled domestic and wild canines for centuries.

4.  All large-sized breeds of purebred dogs are candidates for hip dysplasia. Although the disease is particularly common among certain large breeds (from Bernese Mountain Dogs, Bloodhounds and Boxers to Rottweilers, St. Bernards and Welsh Corgis) mixed breeds of all sizes also are subject to hip dysplasia and not even the toy breeds are spared. However, the incidence is lower in small dogs. Large-sized breeds with a relatively low incidence of hip dysplasia include the Alaskan Malamute, Borzoi, Doberman Pinscher, Great Dane, Greyhound, Irish Wolfhound and Siberian Husky.

5.  A hearty diet helps avert hip dysplasia. To the contrary, dogs that are genetically predisposed to hip dysplasia seem to benefit from a lean diet during their first two years. In one study beginning at eight weeks of age, pups that were restricted to a 24-percent smaller ration had a 46-percent lower occurrence of hip dysplasia than pups that could eat freely. Slowing the growth rate during the early months of life, some veterinary nutritionists now believe, can lessen the severity of hip dysplasia and even prevent it.

So Your Dog Has a Hip score - What Now?

The advantage of such a joint scheme is that it allows comparison within the breed and selection of the best hips of that particular breed. Also, due to the previously described genetic nature of the disease, sires and dams with normal hips but which consistently produce offspring with poor hips may be "weeded out".

With the increased awareness of breeders to the problem of hip dysplasia and this standardised scoring system, the future will hopefully see a gradual improvement in hip conformation.

Communication have started with the Breed Registry Body to obtain rating information for all Alakan Malamutes in South Africa and should not be seen as an afford by the Club to "witch hunt" other breeders or their lines.

KUSA SCHEDULE 2:

APPENDIX 'C' - BREED SPECIFIC LITTER REGISTRATION REQUIREMENTS

1. ALASKAN MALAMUTES

1.1 Only Alaskan Malamutes with hip scores of A1, A2, B1 or B2 may be mated to Alaskan
Malamutes with hip scores of C1 or C2. Alaskan Malamutes with hip scores of A1, A2, B1 or
B2 may also be mated to each other.

(The old terms in short were: at worst 0.0 to 1.1 or 0.0 to 0.0)

1.2 All dogs are positively identified by microchip before any X-ray examination is made. The
identification number is included on all developed X-ray film.

1.3 At the time of whelping, the Dam is twenty-two (22) months of age or older.

NO MATING IS ALLOWED WITH ANY DOG SHOWING SCORES OF D1, D2, E1 or E2 WHATSOEVER.
 

For more articles on Hip Dysplasia, follow the links below.