Avascular Osteonecrosis and Bone Infarction

Pathologically, osteonecrosis may be defined as the devitalization of osteocytes and cellular bone marrow elements. A single decisive factor that may lead to osteonecrosis is vascular deprivation with resultant ischemia. The causes vary, but they can be divided into definite and probable associations (Ficat and Arlet 1980). The definite causes include trauma, fracture, irradiation, sickling, electrical damage, freezing damage, and caisson disease. Although de batable, trivial trauma, alcohol indulgence, chemotherapeutic agents, corticosteroids, gout, rheumatoid arthritis, and connective tissue disorders are considered the probable causes. Avascular osteonecrosis associated with Legg-Calve-Perthes disease and some other osteo-chondroses constitutes the third distinct group as discussed under the respective entries. Of many causes mentioned, femoral neck fracture, steroid-induced osteonecrosis, and osteone-crosis related with renal transplantation are probably most common. Osteonecrosis due to alcoholism, which typically affects the femoral head, is also common (Jones 1971; Jones 2001).

Both anatomical and radiographic studies have indicated avascular osteonecrosis and bone infarction to occur almost invariably within the fatty bone marrow of adult long bones (Resnick and Niwayama 1988). Avascular necrosis has a strong predilection for the long bone epiphysis and is painful in the acute phase, whereas bone infarction predominantly affects the meta-diaphysis of long bones and is easily transformed into the chronic form, which is silent. The femoral head is the most frequently affected site of avascular necrosis and the femoral condyles and small rounded bones in the wrist and ankle are also frequently affected. Bone infarction is typically multifocal, involving many long bones on both sides of the body and is rarely transformed into sarcoma with a prevalence rate of less than 1%.

Radiography is not regularly used in the early or preclinical stage of avascular bone necrosis and infarction. In established cases, however, plain radiography plays a decisive role, often needing no further diagnostic tests. Avas-

Multifocal Osteonecrosis

Fig. 14.1A-F Sensitive and specific diagnosis of avascu-larity and revascularization in avascular osteonecrosis. A-C Serial anteroposterior radiographs of the right hip in a 60-year-old male alcoholic with osteonecrosis show slowly progressive flattening and bony condensation over a period of 6 months (arrows). D-F Serial anterior pinhole scintigraphs show initial photon defect and reactive hypervascularity in the femoral head followed by gradual revascularization (open arrows)

Fig. 14.1A-F Sensitive and specific diagnosis of avascu-larity and revascularization in avascular osteonecrosis. A-C Serial anteroposterior radiographs of the right hip in a 60-year-old male alcoholic with osteonecrosis show slowly progressive flattening and bony condensation over a period of 6 months (arrows). D-F Serial anterior pinhole scintigraphs show initial photon defect and reactive hypervascularity in the femoral head followed by gradual revascularization (open arrows)

cular necrosis manifests as subchondral crescent lucency, an admixture of irregular lucency and sclerosis, and bone flattening or collapse, which are virtually pathognomonic (Fig. 14.2A). The adjacent articulation is usually unaltered unless attended by secondary or preexisting os-teoarthritis, and the "sagging rope" sign appears in occasional cases (Apley and Wientroub 1981; Clarke et al. 1983). In contrast, bone in farctions, seen most typically in dysbaric necrosis in the metadiaphyses of the long bones, manifest as irregular mottled, curly, or smoke-like mineralization (Figs. 14.3 A and 14.4A). Idiopathic infarctions show basically the same radiographic changes in the long-bone metadia-physes. When bone infarction is transformed to sarcoma, geographic osteolysis occurs with ballooning and cortical disruption (Fig. 14.5A).

Ischemic Necrosis Bone

Fig. 14.2A, B Ischemic bone necrosis. A Anteroposterior radiograph of the right hip in a 55-year-old man with Chandler's disease reveals an ovoid, condensed bone in the femoral head top (n) bordered by a crescent lucent zone (large arrowheads), sclerosis, the collapse and flattening of the head, and a linear density in the head's base ("sagging rope" sign; small arrowheads). B Anterior pinhole scan shows a photopenic defect in the condensed bone of the femoral head top bordered by intense tracer uptake (open arrows), the collapse of the head, and bandlike tracer uptake across the head's base. The last-mentioned is the scintigraphic version of the radiographic "sagging rope" sign that is the projection of the drooping head (arrows)

Fig. 14.2A, B Ischemic bone necrosis. A Anteroposterior radiograph of the right hip in a 55-year-old man with Chandler's disease reveals an ovoid, condensed bone in the femoral head top (n) bordered by a crescent lucent zone (large arrowheads), sclerosis, the collapse and flattening of the head, and a linear density in the head's base ("sagging rope" sign; small arrowheads). B Anterior pinhole scan shows a photopenic defect in the condensed bone of the femoral head top bordered by intense tracer uptake (open arrows), the collapse of the head, and bandlike tracer uptake across the head's base. The last-mentioned is the scintigraphic version of the radiographic "sagging rope" sign that is the projection of the drooping head (arrows)

The concurrence of other mineralized infarctions in the adjacent bones, often across the joint, is an extremely helpful finding.

Scintigraphically, avascular osteonecrosis is indicated by a photon defect. As mentioned above, bone scintigraphy is not only specific but also highly sensitive in diagnosing avascu-lar necrosis. Actually, it is not rare that an obvious photon defect can be shown in the absence of radiographic change (Fig. 14.6). Typically, such a photon defect is sharply demarcated caudally by intense uptake in the reparative and reactive zone that extends to the neck. It is of differential diagnostic interest to note that, unlike the poor caudal definition of reparative uptake, the demarcation of neck fracture uptake is very sharp so that it can clearly be distinguished from accompanying avascular necrosis in the femoral head (Fig. 14.7). In chronic avascular osteonecrosis, pinhole scintigra-phy reveals the combination of four different findings: a "cold" area in the top of collapsed head, intense uptake along the lower border of the cold area in the top, mottled uptake in the remainder of the head, and lace-like uptake across the neck, the "sagging rope" sign (Fig. 14.2B). These four scan signs appear to be roughly correlated, respectively, with avascular osteonecrosis, reparative bone interface, reactive hyperemia, and bone reinforcement or microfractures of the overhanging anterior lateral edge of the femoral head that is drooping.

On the other hand, bone infarctions intensely accumulate tracer when the lesions are relatively fresh and mineralization is partial and modest (Figs. 14.3B and 14.4B). It appears that relatively fresh infarctions with active osteoge-nesis avidly accumulate tracer while densely calcified, aged infarctions accumulate little or no tracer. Sarcomatous transformation is indicated by bubbly photon defects with ballooning and irregular tracer uptake in ruptured or actively invaded borders (Fig. 14.5B).

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  • VERDIANA
    What is small bone infarct?
    4 years ago

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