Osteonecrosis is also associated with cancer, lupus, sickle cell disease, HIV infection, Gauchers disease, and Caisson disease (dysbaric osteonecrosis). The condition may also occur without any clear reason.Bisphosphonates are associated with osteonecrosis of the mandible. Prolonged, repeated exposure to high pressures (as experienced by commercial and military divers) has been linked to AVN, though the relationship is not well understood.In children, avascular osteonecrosis can have several causes. It can occur in the hip as part of Legg–Calvé–Perthes syndrome, and it can also occur as a result after malignancy treatment such as acute lymphoblastic leukemia and allotransplantation. Pathophysiology
The hematopoietic cells are most sensitive to low oxygen and are the first to die after reduction or removal of the blood supply, usually within 12 hours. Experimental evidence suggests that bone cells (osteocytes, osteoclasts, osteoblasts etc.) die within 12–48 hours, and that bone marrow fat cells die within 5 days.Upon reperfusion, repair of bone occurs in 2 phases. First, there is angiogenesis and movement of undifferentiated mesenchymal cells from adjacent living bone tissue grow into the dead marrow spaces, as well as entry of macrophages that degrade dead cellular and fat debris. Second, there is cellular differentiation of mesenchymal cells into osteoblasts or fibroblasts. Under favorable conditions, the remaining inorganic mineral volume forms a framework for establishment of new, fully functional bone tissue. Diagnosis
In the early stages, bone scintigraphy and MRI are the preferred diagnostic tools.X-ray images of avascular necrosis in the early stages usually appear normal.
In later stages it appears relatively more radio-opaque due to the nearby living bone becoming resorbed secondary to reactive hyperemia. The necrotic bone itself does not show increased radiographic opacity, as dead bone cannot undergo bone resorption which is carried out by living osteoclasts. Late radiographic signs also include a radiolucency area following the collapse of subchondral bone (crescent sign) and ringed regions of radiodensity resulting from saponification and calcification of marrow fat following medullary infarcts. Types
When AVN affects the scaphoid bone, it is known as Preiser disease. Another named form of AVN is Köhler disease, which affects the navicular bone of the foot, primarily in children. Yet another form of AVN is Kienböcks disease, which affects the lunate bone in the wrist. Treatment
A variety of methods may be used to treat the most common being the total hip replacement (THR). However, THRs have a number of downsides including long recovery times and short life spans of the hip joints. THRs are an effective means of treatment in the older population; however, in younger people, they may wear out before the end of a persons life.Other techniques such as metal on metal resurfacing may not be suitable in all cases of avascular necrosis; its suitability depends on how much damage has occurred to the femoral head. Bisphosphonates which reduce the rate of bone breakdown may prevent collapse (specifically of the hip) due to AVN.