For the past two years, patients in the group have been asking me if hip dysplasia can cause femoral head necrosis. Strictly speaking, these are two different diseases and therefore are not usually confused. However, some diagnoses intentionally or unintentionally confuse the two, which makes patients more ambiguous about their disease and leads to the phenomenon of seeking medical help in a hurry. The bony structure of the hip joint consists of the femur, the acetabulum, and the cartilage tissue covering both sides. The osteoclastic structure of the femur and acetabulum provides effective support for the cartilage and ensures that the cartilage does not undergo significant deformation when subjected to stress, while the cartilage covering the osteoclastic structure provides lubrication and load absorption for the bone tissue during activity. Femoral head necrosis, as the name implies, occurs when the normal blood supply to the bone tissue of the femoral head is destroyed due to trauma to the hip joint, rheumatism, hematologic disease, diving disease, burns, etc., or when the circulation is impaired, resulting in the high pressure in the hip joint capsule due to the obstruction of venous return to the femoral head, resulting in a continuous decrease in the blood supply to the bone cells, continuous necrosis of the bone tissue, and a significant decrease in new bone growth or no new bone production. The blood supply to the osteocytes decreases continuously and the bone tissue becomes necrotic. Then the reduced bone tissue cannot provide effective support for the cartilage, resulting in distant cartilage collapse. Osteoarthritis of the hip joint, a disease that accumulates both cartilage and bone tissue, is usually characterized by inadequate cartilage repair or massive damage to the cartilage, resulting in impairment of normal joint lubrication and load absorption, causing pain or discomfort during activity; distal cartilage damage to the surface is exhausted and begins to destroy bone tissue, resulting in persistent pain. At the same time, the bone tissue is stimulated to proliferate, most significantly in the most unstable locations, and new bone tissue is formed – the so-called bone spurs. Therefore, in patients with hip dysplasia, osteoarthritis occurs later due to accelerated cartilage wear and insufficient cartilage repair caused by poor cartilage coverage. The main site of the lesion is in the cartilage in the first place, and thus there is generally no possibility of fast death of the femoral head.