Hip Dysplasia

Definition

Hip dysplasia is a loosening of the ligaments joining the two parts of the hip joint: the head of the femur and the acetabulum. This loosening of the ligaments results in poor pressure distribution in the joint, leading to (very painful) damage to the cartilage and sometimes dislocation of the joint (dislocation of the femoral head from the acetabulum).
The condition was first described in 1935.

Origin

Ligament loosening is a genetic anomaly transmitted by a gene that is probably recessive.
However, this genetic anomaly is only expressed under certain conditions. As a result, 25% of genetically affected dogs show no ligament loosening at all. What's more, 50% of dysplastic dogs (i.e. with ligament loosening) show no clinical signs (lameness, pain). The 92 and 93 World Champion German Shepherd suffered from mild dysplasia without showing the slightest sign.
In fact, other factors can play a role in promoting or masking dysplasia:
- diet: rapid growth favours the appearance of dysplasia,
- weight: excess weight, by placing greater stress on the joint, also favours the appearance of dysplasia,
- musculature: on the other hand, strong pelvic muscles can compensate for weak ligaments and mask dysplasia.

Racial predisposition

All these factors result in greater or lesser susceptibility, depending on the breed. Heavy breeds pay a heavier price for this condition, while light, muscular breeds selected for work are less affected: greyhounds, sled dogs, hunting dogs, Belgian Shepherds (selected for Agility).
Rate over 25% :
Saint Bernard, Bullmastiff, Stafford Shire Terrier.
Rates between 20% and 25% :
Golden Retriever, Mastiff, Rotweiller, Gordon and English Setter, Chow-Chow, Giant Schnauzer, German Shepherd.
Rates between 10% and 20% :
Bouvier des Flandres, Briard, Spaniel Springer, Shar Pei, Boxer, Airedale, Labrador, Border Collie, Irish Setter, Alaskan Malamute, Samoyed, Cavalier King Charles, Medium Schnauzer.
Less than 10% :
Pointer, Cocker, Dalmatian, Afghan Greyhound, Belgian Shepherd, Siberian Husky.

Symptoms

The main symptom is lameness:
appears at the start of exercise (“cold”)
subsides after a few minutes' warm-up
reappears with fatigue.
Over time, as the lesions evolve, the pain reappears more and more quickly during exercise, appearing as soon as the animal warms up. At this stage, the animal is permanently limping.

Treatment

This highly disabling condition can nevertheless be treated. Several techniques are used, depending on the severity of the symptoms.
Mild dysplasia: use of anti-inflammatory drugs in conjunction with cartilage protection factors.
If possible, functional re-education can be combined with weight loss (use of low-fat kibbles) and strengthening of pelvic muscles (regular, moderate exercise, ideally swimming, taking care to dry the dog thoroughly afterwards).
Mild dysplasia with intense pain: pectineal myectomy. In its normal function, the pectineal muscle tends to pull the head of the femur away from the joint, aggravating the dysplasia and leading to dislocation. This muscle is therefore cut to relieve the joint.
Moderate dysplasia with intense pain: in this case, the head of the femur, which is the site of the pain, can be removed. The hip muscles, together with the periarticular envelope, support the femur by creating a pseudo joint, enabling the dog to lead a normal life, although in this case he is unfit for work.
Severe dysplasia: hip prosthesis: defective joints are replaced with biocompatible prostheses. This technique gives the best results, but is very costly. The animal can then work normally, so this technique can be indicated for even mild dysplasia in animals that have invested heavily in training.

Prevention

Prevention consists in preventing the genetically transmitted dysplasia from expressing itself. In puppies, growth should be limited by rationed feeding. Naturally, calcium (250 mg/kg/d) and phosphorus (200 mg/kg/d) intakes must be respected.
Specific foods for large-breed puppies incorporate these two aspects.
Care should also be taken to ensure harmonious development of the pelvic muscles through regular, moderate exercise, including swimming where possible.

Eradication

The only way to eliminate dysplasia is to eliminate from reproduction all individuals carrying this defect. To achieve this, the hips of future breeding stock are x-rayed at 1 year of age.
On the X-ray, the coaptation of the femoral head in the acetabulum (i.e. the way they fit together) is assessed. We also measure the Norberg-Olsson angle (the angle formed by the straight line joining the center of the 2 femur heads with the straight line joining the femur head with its corresponding acetabulum rim).
Stage A: No sign of dysplasia
perfect femoral head/acetabulum coaptation and N-W angle > 105°.
Stage B: Intermediate stage
poor femoral head/acetabulum coaptation and N-W angle > 105°.
or
good femoral head/acetabulum coaptation but N-W angle between 100° and 105°.
Stage C: Mild dysplasia
poor femoral head/acetabulum coaptation and N-W angle between 100° and 105°.
Stage D: Moderate dysplasia
poor femoral head/acetabulum coaptation and N-W angle between 90° and 100°.
signs of arthrosis
Stage E: Severe dysplasia
dislocation or subluxation of femoral head/acetabulum and N-W angle < 90° signs of osteoarthritis
osteoarthritis

Recourse

The law protects buyers against this congenital anomaly (i.e. potentially present at the time of sale).
The law of June 22, 89 makes it a redhibitory defect, which means that in the event of findings before the age of 1 year, the sale is null and void and the buyer can claim reimbursement or exchange of his dog.
If, on the other hand, the buyer considers that his pet is above all a living being that cannot be exchanged, like a vacuum cleaner that has broken down during the warranty period, he can keep it, but will only be entitled to a refund of half its value.
The law also allows recourse on the grounds of latent defect, which presupposes that the seller was aware of the defect at the time of sale. This could be the case of a puppy sold quite late (4 - 5 months) after having been returned by an unsatisfied first owner. In such a case, given the seller's obvious lack of scrupulousness, compensation may be more severe. This procedure must be initiated within 1 month of the defect being detected.
In all cases, it's a good idea to get the seller to sign an attestation to the effect that, to the best of his knowledge, the dog sold does not suffer from dysplasia, and that its parents are free of the condition.