CHD has been called inherited, a developmental disease, and most accurately in the author's opinion, a "moderately heritable
disease". CHD is a multifactorial disease with part of its cause being from genetic influences (estimated at 25%-80%) and
part from environmental influences. The specific gene(s) involved have not been identified, although karyotyping for dogs
is actively progressing. Controlled breeding studies have shown that breeding phenotypically normal dogs will result in fewer
offspring with clinical CHD than breeding an affected dog to a phenotypically normal dog, or by breeding two affected dogs.
Despite controlled multi-generation breeding programs, selective breeding alone has not been able to eliminate CHD from any
group of dogs. Less controlled breeding programs such as those promoted by Kennel Clubs of a specific breed have been somewhat
effective. The percentage of affected dogs presented to the OFA for evaluation from 24 breeds for the time period 1972 to
1980 was compared to 1981 to 1988. Of the 24 breeds, 14 breeds had a reduction in the % of CHD ranging from 10% to 40.5%,
and 5 breeds had a reduction ranging from 2.9% to 10%. Four breeds had an increase ranging from 1.1% to 9.7% and one breed
had no change. Although the OFA is a good indicator, the % of dysplastic dogs reported by the OFA is an underestimation of
dysplasia in the general population since radiographs from many dogs with obvious hip dysplasia are not sent to OFA for evaluation.
Body size and type, directly related to genes, are important risk factors for CHD. All breeds and size dogs have been reported
to have hip dysplasia. Large and giant breeds of dogs are perceived by the lay public to be at greatest risk. The OFA indicates
that many relatively small dogs (e.g. American Water Spaniel) have a very high incidence of CHD, while some large dogs (e.g.
sight hounds) have very low incidences of CHD. Clinical signs of CHD and DJD are exacerbated in heavier dogs, which partially
explains the public perception of CHD being a large breed disease. In addition to size, body type is important. Giant breeds
with acromegally characteristics (e.g. Saint Bernard) are at greatest risk for CHD. Giant breeds at high risk for CHD are
stocky, clumsy, have soft ill-defined muscles, and have 5% to 10% fat in the soft tissues of the hind quarters. Athletic
dogs (e.g. Greyhound) have a lower prevalence of CHD and tend to be coordinated, have well defined and firm muscles, tightly
adherent skin with 1% to 2% fat in the soft tissues of the hindquarters.
Environmental factors influencing the phenotypic expression of CHD include exercise and nutrition. A major factor in CHD
is laxity between the femoral head and the acetabulum. In puppies that exercise heavily the laxity is exacerbated and the
joint is traumatized by the abnormal motion and impact of repeated subluxations and reductions. This trauma is further exacerbated
by increased body weight, causing the joint to withstand even more force. Therefore, clinically significant CHD is most prevalent
in large and giant breed dogs, especially of non-atheletic breeds. Also, within a litter the fastest growing, most active
dogs have a greater tendency toward CHD. In a study of 222 German Shephards, the 111 dogs that weighed more than the group
mean at 2 months old had a 63% incidence of CHD at a year of age, compared to 37% of the dogs weighing less than the mean.
The major nutritional factors promoting CHD are rapid weight gain (as promoted by excessive calories and ad libitum feeding)
and excessive calcium supplementation. Slower rates of weight gain in puppies does not affect their adult size since the
physes do not close until later in dogs with slower weight gain rates. Other factors have not been shown to have a significant
influence on the development of CHD.