Hip dysplasia is not a genetic malformation of the hip socket, as commonly thought, but rather a weakness in the ligaments that support the hip joint. This allows the ball of this ball-in-socket joint to bang away at the joint surface, preventing the socket from forming properly. In other words, the instability created by weak supportive ligaments keeps the body from being able to manufacture a deep, smooth hip socket for the ball to fit snuggly into, resulting in the flattening of the acetabulum (hip socket) and a squaring of the femoral head (the ball). The sockets are shallow because of repetitive trauma to the developing bone (micro-fractures), which prevents the weight-bearing surface of the hip joint from forming properly. These changes worsen drastically as the cartilage covering of the joint wears away and bone-on-bone contact occurs, leaving them with the characteristic signs of the osteoarthritis we see in radiographs of affective dogs.
This may sound like a radical idea but there have been veterinary studies that strongly suggest this for years and years, beginning with those done by orthopedic surgeons and radiologists who developed a technique for measuring joint laxity in Labradors. They took 2 sets of X rays of the hip one with the ball forced deeply into the socket and one with the ball distracted as much as possible, measuring the differential and trying to use those measurements as a predictor hip dysplasia in the individual. Read entire article HERE