The morphogenesis, remodeling, and degeneration of diarthroidial joints are directly under the control of the loading histories created by the musculoskeletal system during development and aging. The altered loading histories in individuals with cerebral palsy (CP) lead to aberrations in joint morphogenesis and an acceleration of joint degeneration. To understand this process in the hip, the normal ontogeny of the hip joint is reviewed with special attention to the mechano-biological factors associated with joint morphogenesis, endochondral ossification, and cartilage degeneration. A contrast is then made with the mechano-biological alterations observed with CP and the consequent influence on joint destruction. The features of the pathogenesis are: (1) altered muscular activity and restricted range of motion result in abnormal joint morphology, subluxation, and poor coverage of the femoral head; (2) joint incongruities created in early development cause local stress concentrations that can mechanically damage the articular cartilage; (3) the reduced magnitudes of muscular forces reduce the contact pressures at the joints, creating thinner cartilage and osteopenia; and (4) the thinner cartilage degenerates early, and subchondral bone collapse further contributes to the mechanical destruction of the remaining cartilage.