Histologically, the area of necrosis is usually much more widespread than is evident radiologically. Necrosis is first recognized by the absence of osteocytes in the bone lacunae. This probably starts within a few hours of infarction.
Revascularization then commences from areas of viable bone to form an area of vascular granulation tissue that extends into the infarcted area. Necrotic trabeculae are effectively thickened and strengthened by this new growth, and some lesions even disappear. The revascularization may be arrested before all areas of necrosis have been invaded. Continuing formation of new bone forms a zone of thickened trabeculae separated from necrotic bone by a line of dead collagen. This area of increased bone bulk is usually the first detectable radiological sign.
The necrotic trabeculae not strengthened by the revascularization process may eventually collapse under a load. It is at this stage that clinical symptoms, not necessarily temporally related to recent hyperbaric exposure, are noted. With lesions near articular cartilage, there is some flattening of the articular surface, and with further load, stress fractures appear in the subchondral bone. The underlying necrosis causes progressive detachment of the articular surface from its bed. This process resembles that of late segmental collapse, as seen in ischaemic necrosis following fractures of the neck of the femur. Secondary degenerative osteoarthritis often develops in affected joints.
Cases of malignant fibrous histiocytoma, superimposed on DON, may develop in conjunction with the prolonged reparative process set in train by the necrosis.