Dysbaric osteonecrosis or DON is a form of avascular necrosis where there is death of a portion of the bone that is thought to be caused by nitrogen (N₂) embolism (blockage of the blood vessels by a bubble of nitrogen coming out of solution) in divers. Although the definitive pathologic process is poorly understood, there are several hypotheses:

Dysbaric osteonecrosis is associated with exposure to large ambient pressure changes, but the underlying etiology remains uncertain. Dysbaric osteonecrosis is radiologally indistinguishable from similar lesions not associated with pressure changes.

The prevalent hypothesis is that gas bubbles which block the flow of blood are the cause, but there is not always symptomatic decompression sickness recorded in bones where dysbaric osteonecrosis later occurs. It is therefore considered possible that there may be other factors increasing the effects of gas bubbles on the affected bone. It has been suggested that rapid compression may impede intramedullary venous drainage and increase the risk of DO.

The lesion begins as a localised area of infarction, usually without symptoms. Early identification of lesions by radiography is not possible, but over time areas of radiographic opacity develop in association with the damaged bone. Symptomatic lesions usually involve joint surfaces, and fracture where attempted healing occurs. This process takes place over months to years and eventually causes disabling arthritis, particularly of the femoral head (hip).

Dysbaric osteonecrosis lesions are typically bilateral and usually occur at both ends of the femur and at the proximal end of the humerus. Symptoms are usually only present when a joint surface is involved, which typically does not occur until a long time after the causative exposure to a hyperbaric environment. The initial damage is attributed to the formation of bubbles, and one episode can be sufficient, however incidence is sporadic and generally associated with relatively long periods of hyperbaric exposure, and aetiology is uncertain.

The diagnosis is made by x-ray/MRI appearance and has five juxta-articular classifications and forehead, neck, and shaft classifications indicating early radiological signs.

Early on there is flattening of articular surfaces, thinning of cartilage with osteophyte (spur) formation. In juxta-articular lesions without symptoms, there is dead bone and marrow separated from living bone by a line of dense collagen. Microscopic cysts form, fill with necrotic material and there is massive necrosis with replacement by cancellous bone with collapse of the lesions.^{[clarification needed]}

The following staging system is sometimes useful when managing lesions.