Genetic predisposition, infection releasing cytotoxic factors,  trauma, or emboli could result in vascular damage to the coxofemoral joint.  The interuption in blood supply could result in death of the osteocytes and bone resorption. This decreases the cross-sectional area producing a location of stress concentration.  Stress concentration at the periphery produces a fracture through the cancellous bone that follow the junction of living "repair bone" and devascularized trabeculae. Fibrous tissue or fibrocartilage fills the fracture gap and begins to replace the remaining devascularized bone within the femoral head. These portions of the femoral head are mechanically weak and may collapse under loads producing articular incongruities and pain.