Histologic and angiographic studies of femoral heads with osteonecrosis have identified consistent involvement of the superior retinacular and lateral epiphyseal vessels. Some attempt at vascular repair can be seen with ingrowth of new vessels from the stumps of occluded vessels and from other vessels in the region. However, this process is usually limited and is often blocked by the presence of necrotic material and collapsed bone (personal observation, MES).

Within hours of the vascular insult, death of marrow elements can be seen. Death of bone also takes place, but cannot be identified histologically until several days later when disappearance of osteocytes from their lacunae is noted (Fig. 7.2). Osteoclasts and phagocytic cells infiltrate the margins of the necrotic region and begin to remove dead tissue. This process is accompanied by the release of lysosomal enzymes. This is followed by the arrival of osteoblasts which attempt to repair the damage by laying down new bone directly upon the surface of dead trabeculae (Fig. 7.3). This composite of living and dead bone results in markedly thickened trabeculae which appear as radiodense or “sclerotic” regions at the margins of the infarct (Fig. 7.4). Adjacent areas from which dead bone has been removed become filled with fibrous tissue and amorphous debris, appearing as radiolucent or “cystic” areas.

(We use the University of Pennsylvania Classification of Osteonecrosis—Table 7.1). Within the first 2–3 weeks after the vascular insult, X rays appear normal but changes can usually be detected on MRI (Stage I) (Fig. 7.5a, b). However, they do not appear on routine radiographs until several weeks to months later (Stage II) (Fig. 7.6). The processes of osteolysis and bone resorption and bone repair continue, during which the affected area steadily loses mechanical strength. Because the superior retinacular and lateral epiphyseal vessels, which supply the antero-superior aspect of the femoral head, are primarily involved, and since this is also the area of maximal weight bearing, collapse of subchondral trabeculae gradually develops in this region. This often takes place before the articular surface itself is affected and may appear as a radiolucent “crescent sign” (Stage III). This stage is not always seen as collapse of the articular surface with the subchondral bone may occur more or less simultaneously. If the necrotic region is small and not close to an area of major weight bearing, the situation may stabilize and the repair process may provide it with sufficient strength so that it does not collapse. It may persist as an area of radiodensity, although occasionally it is resorbed and disappears from radiographs. This corresponds with the clinical observation that very small lesions, especially those located medially, have a good prognosis. However, less than 5 % of lesions meet these criteria [15, 16]. It has also been observed that the prognosis for sclerotic lesions is better than for lesions which appear cystic. This is most likely due to the fact that sufficient new bone has been formed to provide mechanical strength to the region and hence decrease the incidence of collapse [17].

With progressive collapse of subchondral trabeculae, the unsupported articular surface eventually begins to flatten. This represents an irreversible stage in the pathogenesis, Stage IV (Fig. 7.7). The articular cartilage is attached to the subchondral plate and remains viable, since it is nourished by diffusion from the synovial fluid and not by the vascular supply to the femoral head itself. However, the attached bone plate becomes necrotic (Figs. 7.8 and 7.9).

Radiographs of the hip continue to show a normal appearing acetabulum for quite some time after femoral head collapse. This can be misleading as histological changes in the articular cartilage are already taking place. In a study of 41 hips with ON which underwent total hip replacement despite a radiographic diagnosis of a “normal acetabulum,” 40 hips showed gross changes in the acetabular cartilage, and all 41 showed histologic degeneration [18]. It is important to keep this in mind when considering a hemi-arthroplasty involving only the femoral head with the assumption that the acetabulum is “normal.”

Progressive degenerative changes take place in the acetabulum secondary to the abnormal mechanical stresses imposed by the collapsed femoral head. Initially they involve only the articular cartilage as indicated by radiographic narrowing of the joint line. Later the underlying bone becomes affected and radiolucent and sclerotic regions appear in the roof of the acetabulum, often accompanied by marginal osteophyte formation. This represents Stage V radiographically. In a small number of cases this process continues until the joint is almost completely obliterated, which represents Stage VI [19].