[Biology of the femoral head necrosis. Clinical studies (author's transl)].
From the study of femoral heads either experimental or human it is clear that the clinico-pathological called idiopathic necrosis is due to the death of bone cells, as it is in necrosis after fracture or dislocation. But the cause of cell's death is clearly avascular only in traumatic necrosis: in idiopathic necrosis there is no evidence of arterial alteration or obliteration, whatever condition is associated. In both avascular (traumatic) necrosis, and idiopathic necrosis, the cartilage remains alive: the deformation of the head, secondary rupture and destruction of cartilage and finally osteoarthritis are the consequence not of the death of bone cells (a dead head with living cartilage would work for along time) but of the revascularisation process. This process is different in the two syndrome. In idiopathic necrosis proliferation of living tissues in the head is active, but bone formation is limited, shearing forces create a subchondral fracture in the dead part of the head. In avascular necrosis, after the fracture is united, proliferation invades the dead head, with active osteogenesis. The pathological fracture is between dead and bone and revascularised part of the head. One can suggest as therapeutic measure the prevention of revascularisation.
D002470:Cell Survival; D005271:Femur Head Necrosis / Q000150:complications / Q000503:physiopathology*; D006620:Hip Fractures / Q000209:etiology; D006801:Humans; D009389:Neovascularization, Pathologic; D010003:Osteoarthritis / Q000209:etiology; D010011:Osteocytes / Q000502:physiology*; D010012:Osteogenesis
Biologie de l'ostéonécrose de la tête fémorale chez l'homme. Applications cliniques.