[1] Although the definitive pathologic process is poorly understood, there are several hypotheses: 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.

This process takes place over months to years and eventually causes disabling arthritis, particularly of the femoral head (hip).

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.

Microscopic cysts form, fill with necrotic material and there is massive necrosis with replacement by cancellous bone with collapse of the lesions.

[citation needed] Prompt treatment of any symptoms of decompression sickness (DCS) with recompression and hyperbaric oxygen also reduce the risk of subsequent DON.