Dog Hip Dysplasia
Dysplasia (Greek. Dys – prefix, meaning a deviation from the norm, Greek. Plasis – formation, formation, dysplasia – developmental disruption). Hip dysplasia (TPD) is a common disease. It was first discovered in dogs in the United States more than 50 years ago. A few years later, it was proved that dysplasia is caused by hereditary factors inherent in many breeds. Hip dysplasia is more common in large fast-growing dogs, which are characterized by a large mass and powerful physique. Both sexes are equally affected by this disease, St. Bernards, Newfoundlands, Molosses, Bernese Shepherds, Rottweilers, German Shepherds and Boxers are especially prone to dysplasia. According to statistics, this pathology is widespread, and in the absence of control measures, the frequency of its occurrence can reach 70% among these breeds.
Currently, this pathology is assessed from the standpoint of the integration effect of exo- and endogenous factors, among which the leading role is played by a genetic predisposition that determines the defective histogenesis of bone and cartilage tissue.
Hip dysplasia is a polygenically inherited disease characterized by a loss of correspondence between articular surfaces and leading to dislocation or arthrosis. TPA is a flattening of the acetabulum and subsequent deformation of the femoral head, expressed to a greater or lesser extent. The disease is accompanied by smoothing of the acetabulum, insufficient coverage of the femoral head with the upper edge of the cavity and, as a result, joint looseness, which allows the femoral head to slip out of the cavity partially or completely. In this case, the femoral head, continuously slipping, is damaged, is erased to a flattened surface and a flattened hip joint appears, which most closely corresponds to the picture of subluxation.
The next reason is a violation of the formation of the proximal femur (i.e., deformity of the head), which again leads to hip dysplasia. In addition, ectonic changes in the anatomical structure of the lumbar vertebrae lead to TPA: sacralization (lat. Sacralisatio) – fusion of the last lumbar vertebra with the sacral bone, caused by a change in its transverse processes, or lumbarization (lat. Lumbalisatio) – developmental anomaly, separation of the first sacral vertebra from the rest of the sacrum mass.
The etiology is not clear to the end, but it is believed that various factors influence the development of the disease: genetics, growing and maintenance conditions, and excessive nutrition. In the process of numerous disputes, two theories about the hereditary nature and mechanism of inheritance of TPA have become most widespread among scientists. The greatest number of geneticists are inclined to the theory of additive inheritance, i.e. the actions of genes involved in the final formation of the hip joint.
The second theory comes from the premise that the genes responsible for the final formation of the hip joint influence each other and their mutual actions are combined in various ways, which means that the hereditary nature of the defect is much more complicated than in the first case.
Among some geneticists, there is a third theory, which is a combination of the first two: the action of the genes responsible for the formation of joints can, on the one hand, add up, and on the other hand, individual genetic pairs can affect each other in different ways.
Specialists came to the conclusion that TPA is a classic example of a quantitative trait due to many genes (polygeny), and in this case many environmental factors influence the final result of the formation and manifestation of the trait. One of the factors that spread dysplasia in the population, experts consider the use of close inbreeding in breeding dogs that are not tested for dysplasia. In addition, the dog’s pursuit of “ideal” angles of the hind limbs and long legs is correlatively associated with a concomitant change in the hip joint, provoking this defect. Not all animals with hip dysplasia show clinical impairment, but it cannot be considered that apparently clinically healthy dogs are free of dysplasia. When selecting valuable genotypes, it is necessary to use an analysis of the pedigree, in which ancestors suffering from TPA are necessarily noted. It should be borne in mind that this pathology can be transmitted through 14 generations. When mating “defective” parents, the probability of getting sick offspring increases by 2 times.
The first clinical signs of the disease are observed between the ages of 4-12 months and include reduced locomotor activity, lameness, worse after exercise, swaying and unstable gait, difficulty climbing and jumping. The chest limbs develop more intensively, sometimes hypertrophy of the muscles of the forelimbs develops, since the main load transfers to them, sparing the pelvic. In the hind limbs from…