The Dysplastic Joint

Hip Dysplasia is a terrible genetic disease because of the various degrees of arthritis (also called degenerative joint disease, arthrosis, osteoarthrosis) it can eventually produce, leading to pain and debilitation.

The very first step in the development of arthritis is articular cartilage (the type of cartilage lining the joint) damage due to the inherited bad biomechanics of an abnormally developed hip joint. Traumatic articular fracture through the joint surface is another way cartilage is damaged. With cartilage damage, lots of degradative enzymes are released into the joint. These enzymes degrade and decrease the synthesis of important constituent molecules that form hyaline cartilage called proteoglycans. This causes the cartilage to lose its thickness and elasticity, which are important in absorbing mechanical loads placed across the joint during movement. Eventually, more debris and enzymes spill into the joint fluid and destroy molecules called glycosaminoglycan and hyaluronate which are important precursors that form the cartilage proteoglycans. The joint's lubrication and ability to block inflammatory cells are lost and the debris-tainted joint fluid loses its ability to properly nourish the cartilage through impairment of nutrient-waste exchange across the joint cartilage cells. The damage then spreads to the synovial membrane lining the joint capsule and more degradative enzymes and inflammatory cells stream into the joint. Full thickness loss of cartilage allows the synovial fluid to contact nerve endings in the subchondral bone, resulting in pain. In an attempt to stabilize the joint to decrease the pain, the animal's body produces new bone at the edges of the joint surface, joint capsule, ligament and muscle attachments (bone spurs). The joint capsule also eventually thickens and the joint's range of motion decreases.
          
No one can predict when or even if a dysplastic dog will start showing clinical signs of lameness due to pain. There are multiple environmental factors such as caloric intake, level of exercise, and weather that can affect the severity of clinical signs and phenotypic expression (radiographic changes). There is no rhyme or reason to the severity of radiographic changes correlated with the clinical findings. There are a number of dysplastic dogs with severe arthritis that run, jump, and play as if nothing is wrong and some dogs with barely any arthritic radiographic changes that are severely lame.

         









Normal Hip Conformation          



Breeders and the OFA
          
Progress in hip joint phenotype of dogs in the United States between the 1970's and early 1990's has been shown through results of a retrospective study using the OFA data base. This improvement was evident as an increase in the percentage of dogs classified as having excellent hip joint phenotype and a decrease in the percentage of dogs classified as having hip dysplasia (HD). The increase in percentage of dogs classified as having excellent hip joint phenotype was greater for German Shepherd dogs, Golden Retrievers, Labrador Retrievers, and Rottweilers than for all dog breeds combined. In addition, the submission screening rate for these four breeds was higher than the screening rate for all dogs. Within these four breeds, the improvement was greatest for Rottweilers, which also had the highest screening rate.

Overall, low screening rates for breeds found in this study offer some insight into the problems involved with reducing the incidence of HD. The typical dog breeder is involved in breeding dogs for about five years. Thus, informed, experienced breeders are continually replaced with uninformed, inexperienced breeders who may not be as aware of the problems associated with HD or of the importance of participating in a screening program. In addition, many breeders choose which dogs they breed on the basis of the hip phenotype of individual dogs without knowledge of the phenotype of related dogs or previous offspring. It can be very difficult to get hip information on siblings and previous offspring due to the overall low number of dogs radiographed in a given litter (most dogs in a litter end up in pet homes). This is the slowest method of reducing the incidence of an undesirable trait or increasing the incidence of a desirable trait. The use of preliminary radiographs as early as 4 months of age can be used by breeders to add valuable information on the hip status of dogs they choose to use in a breeding program.

What can breeders do?
Hip dysplasia appears to be perpetuated by breeder imposed breeding practices, but when breeders and their breed clubs recognize HD as a problem and establish reduction of HD as a priority, improvement of the hip status can be accomplished without jeopardizing other desirable traits. Prospective buyers should check pedigrees and/or verify health issues with the breeder. If suitable documentation is not available, assume the worst until proven otherwise.

Do not ignore the dog with a fair hip evaluation. The dog is still within normal limits. For example; a dog with fair hips but with a strong hip background and over 75% of its brothers and sisters being normal is a good breeding prospect. A dog with excellent hips, but with a weak family background and less than 75% of its brothers and sisters being normal is a poor breeding prospect.

OFA's Recommended Breeding Principals

Breed normals to normals
Breed normals with normal ancestry
Breed normals from litters (brothers/sisters) with a low incidence of HD
Select a sire that produces a low incidence of HD
Replace dogs with dogs that are better than the breed average

*Above information from the OFA web site