Multiple factors cause the hip displaia as genetic, environmental and nutritional elements are involved, which influence its occurrence and severity.

It is considered a hereditary disease. Unlike in humans, it is not congenital. This implies that the disease can be transmitted to descendants, but it is not common to be present at birth, since it develops during the growth stage. The responsible gene or genes have not been identified yet.

Heredity is considered to be quantitative with continuous variations. It can only be estimated through methods of population genetics.

Environmental conditions of breeding must also be considered.

At this point, we include health, parasitic load and diseases which may weaken the general state of the puppies.

Nutrition plays a major role in the development of the disease.

It is clearly seen that an increase in weight, caused by an excess of nutrients, proteins, energy, and calcium, contribute to the occurrence of this pathology.
Overfeeding stimulates skeleton growth, bone remodelation and weight increase in breeds with intrinsic capacity for fast growth.

Excessive nutrition causes a disproportion between body weight and skeleton growth, which leads to an overload of skeleton structures.
It negatively affects both the joint components and its bio-mechanical function.

This combination of fast growth and remodeling weakens the sub-chondral region of the joint in its support to the cartilaginous area, and creates a spongy osteopenic sub-chondral area with bio-mechanical weakness. There is an inappropriate support to the joint cartilage. The increase in body mass applies excessive bio-mechanical forces on the joint cartilage and promotes side disturbances in nutrition, metabolism and chondro-cellular feasibility.

The nutrition of the pregnant bitch participates in the development of the joint disease. In puppies weaning, and the phase of growth to approximately 8-9 months are fundamental to the skeleton integrity in adults.

There is evidence which implies specific elements such as calcium. Giant breeds may be limited to face the excess of mineral, such as the excess of Ca.. Thus, the results are an abnormal development of the bones and skeleton pathology.

Excessive Ca intake is expressed as a delay in bone maturing, inhibition of osteoclastic activity and delay in cartilage maturing. Vit. C could contribute to the disease. (not proved yet).

Nutritional handling per se would not be enough to treat evolutionary osteopathies. However, adequate diets of optimized nutrients can help to prevent their development.

Excessive phisical exercise at an early age has a negative effect at joint level and so has early training.
Swimming is an appropriate exercise, since it exercises all the muscles without bearing body weight.

CV Dra. M.Durán EspañolEnglish