Hip dysplasia affects man and all other domestic mammals. In man, 1.3 children in 1000 are affected. In dogs the prevalence may run over 50% in large dogs if control measures have not been practiced. Few data are available on the prevalence of hip dysplasia in other mammals, but it is thought to be low. The disease is undoubtedly rare in undomesticated animals. No specific genetic pattern of inheritance has been demonstrated in this variable disease. It has been demonstrated that both genetic and environmental influences contribute to development, regardless of the species affected [5, 9, 20, 21, 26, 47, 50]. Consequently, the disease has been designated as polygenic or multigenic. There is no evidence that a primary defect of bone exists but rather the disease is a failure of the muscles and other soft tissues to hold the hip joint in full congruity [20, 21]. This is further supported by the fact that bony dysplasia can be increased, decreased, or prevented by controlling the degree of joint instability and incongruity [35]. No other malformations are associated with the disease [52], which signifies that hip dysplasia is ‘many diseases that end up with common degenerative lesions of the hip joint’ [51]. Inborn metabolic errors of chemical and hormonal origin are not evident [34, 58]. The quantity of hormones needed to produce hip dysplasia experimentally far exceeded those that could be produced by any biological system [34, 36, 57]. A causal relationship between muscles and soft tissue defects or pathological changes other than lack of muscle mass or strength has not been established [25, 26]. Experimentally, hip dysplasia may be produced in many ways [27, 36, 47, 50, 58, 59]. These include any circumstances that contribute to an unstable hip joint, that is, adductor forces, lack of muscle strength, chemical relaxation of the pelvic soft tissues, traumatic injury to the hip joint, and overloading of the joint by weight. Hip dysplasia is a concentration of factors from a pool of genetic weaknesses and environmental stresses that fall into a programmed pattern of progressive remodelling and degenerative joint disease.