![]() It also causes the production of cytokines that contribute to cartilage degradation. Concurrently, inflammation results in an increase in joint fluid volume, contributing further to incongruity of the joint. Repeated subluxation causes cartilage fibrillation and destruction, remodeling of the femoral head and acetabulum, and periarticular new bone formation. Subluxation results in joint capsule stretching, which causes the initial pain and lameness associated with hip dysplasia in young animals. In turn, laxity leads simultaneously to subluxation, inflammation, and periarticular new bone formation. Polygenic and environmental factors contribute in a complex manner to cause laxity via morphologic changes such as joint incongruity or abnormal pelvic musculature, joint capsule, or round ligament. While various etiologies have been proposed, it is generally accepted that coxofemoral joint laxity is a principle component of hip dysplasia at an early stage. ![]() Simplistically, the pathophysiology of hip dysplasia can be described as joint laxity leading to degenerative joint disease. Screening for hip dysplasia in young dogs is important for treating affected individuals as well as for making breeding recommendations for owners. The etiology is multifactorial, having both genetic and environmental components. Large breed dogs are most commonly diagnosed, however small breed dogs and cats also are affected. First described in the 1930's, it continues to affect millions of dogs worldwide. Hip dysplasia is the most common developmental orthopedic disease in dogs.
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