Radiation Effects on Bone

Abstract

Several recent articles (3–7) have again called attention to the importance of radiation effects upon growing and adult bone. Whereas it was formerly thought that adult bone is one of the most radioresistant of normal tissues, it is now recognized that it is the soft-tissue components of the bone, such as the terminal blood vessels of the haversian and Volkmann's canals, which may be particularly affected by hyperemia and later by obliterative endarteritis. Another reason for the interest in this subject is the present tendency toward the use of higher and higher voltages for therapy, with delivery of increasing amounts of radiation to the deeper tissues. In spite of the fact that there is less differential absorption by bone from these higher voltages, nevertheless fractures have occurred following such irradiation just as with conventional cross-fire therapy, regardless of whether or not lateral pelvic portals were used. It should be remembered that the blood supply to the femoral head and neck comes from the deep pelvic arteries, whose caliber may be reduced by heavy irradiation aimed at controlling a neoplasm of the pelvic contents. Repetitive treatment tends to produce damage out of proportion to the amount given, probably because recuperative capacity is diminished by previous irradiation. Although there may be direct radiation effects on osteoblasts and osteoclasts, the vascular changes are equally important and probably account for fractures in those bones subjected to stress and strain. In other bones the roentgen appearance and clinical course suggest disintegration of bone substance on a basis of aseptic necrosis from partial reduction of blood supply, and perhaps a relatively poor collateral circulation. A possible explanation for the bone changes which follow irradiation is the production of hyperemia and osteoclastic activity. Hyperemia is followed by widening of the haversian and Volkmann's canals from persistent dilatation of the vessels and, if absorption becomes great, rarefaction or osteoporosis will result. The osteoporosis described by the pathologist, however, is an earlier phase than that seen by the radiologist. The femoral neck is porotic and brittle even though it looks strong roentgenographically, but any sudden strain or unusual stress may produce a fracture. The delay in the appearance of roentgen alterations may be due to the fact that bone is dense and shows a definite lag in its response to associated pathologic conditions, with respect to both degenerative changes and reparative processes. Osteoclasts probably play a secondary part, since it is likely that decalcification must first occur before the osteoclast can exert its phagocytic action. Decalcification is a poorly understood physiochemical phenomenon brought about by the tissue juices, or possibly by the indirect effect of the osteoclasts themselves.