Ischaemia of bone.

Abstract

In recent years bone necrosis has become of increasing significance and has stimulated much interest amongst clinicians, radiologists and pathologists. It is now an important cause of disability because it commonly complicates intracapsular femoral neck fracture which is frequent in aging populations (Barnes et al, 1976; Graham and Wood, 1976). It is a hazard not only to tunnellers working in compressed air(MRCDecompression SicknessPanel Report, 1971) but also to divers whose numbers and activities are ever expanding with the exploitation of North Sea oil (Lancet, 1974; Davidson, 1976). It gives rise to articular symptoms in some patients receiving therapeutic steroids (Fisher and Bickel, 1971; Park, 1976) and particularly in those on the high dosages and prolonged administration associated with immunosuppression following organ transplant. In addition to necrosis associated with these and other well accepted causes, so-called idiopathic or spontaneous necrosis may occur, especially in the femoral head (table I). The predisposing causes of such 'idiopathic' necrosis are currently the subject of intensive investigation (Zinn, 1971a and b) (table II). Unfortunately the clinical diagnosis ofbone necrosis is not easy. There are usually no signs to indicate an ischaemic episode until many months have elapsed and necrotic bone shows no radiological change unless the part is immobilized, then the dead bone may appear denser than the adjacent viable, porotic bone. A true increase in radiological density may result from laying down of new bone during repair, from compaction of trabeculae or from calcification within living or dead tissue (Johnson, 1964). Diagnosis may thus be difficult and caution is required in inferring underlying tissue changes even from well recognized radiological patterns. The widespread use of prosthetic replacement of bone and joints has provided the pathologist with the opportunity of studying more rewarding material than the small biopsy or the end-stage necropsy specimen, and there is now fairly general agreement on the pattern of morphological changes following necrosis (Catto, 1976): the sequence of events which brought these changes about is, however, open to more than one interpretation. In many conditions the pathogenesis of necrosis is controversial and is not always accepted as being primarily vascular (table I). Many questions remain unanswered, including one of major clinical importance; why is revascularization so often arrested and incomplete? The purpose of this paper is to indicate how bone necrosis may be recognized, to describe in a general way the main morphological features, and to point out areas of difficulty and controversy. Many topics, and particularly the osteochondritides of childhood, are omitted since it is rare for the pathologist to obtain material from them.