Abstract

The mechanism of the medium-voltage x-ray effect on bone is apparently as follows: On contacting bone, much of the primary beam is converted to photoelectrons which are especially concentrated in the first 5 mm. of bone. The range of these electrons is short, about 50 to 100 microns. This does not permit extensive travel in calcified bone. However, the lacunae containing osteocytes are about 25 to 50 microns long, 6 to 14 microns wide, and 4 to 9 microns thick. Consequently, the photoelectrons easily traverse this distance, rebounding off the walls of the lacuna and ionizing the cellular elements within. Likewise, irradiation developing on the inner wall of a Haversian canal may readily cross its 22 to 110 microns, affecting the vessels and tissue within. Larger areas, such as the marrow cavity, are not greatly affected by short-range “scatter” from the wall. Since the osteocyte does not undergo mitosis, death of the cell with evacuation of the lacuna is the usual effect of its ionization. Devitalized bone must be resorbed and replaced by living tissue. These processes are ordinarily accomplished by (1) the cellular elements from the periosteum, either on the external surface of the bone or within the Haversian canals, or (2) by the endosteum. It was previously believed that irradiation had its initial effect on the blood vessels within the Haversian canal and that damage to the vessel wall was accompanied by thrombosis. The bone died as a result of this altered blood supply. According to recent observations, 11 the primary damage is to the osteocyte. The blood vessels respond more slowly, with a thickening of the walls of arteries and arterioles. The decreased nutritional supply is a factor during long survival periods when the osteocytes which have been injured but not destroyed are attempting to recover. However, the damage to the osteocyte is often so severe that its death is rapid and nutritional factors are a secondary concern. The periosteum within the Haversian and Volkmann canals is also readily affected by rebound across these structures. Severe injury or death of these cellular elements of the periosteum will seriously delay healing of the irradiated area. Apparently this was the situation which developed in the case reported here. There was an appreciable layering effect on the surface of the cortex, so that the back scatter contributed to the skin damage. The deeper-penetrating x-rays of the low-voltage therapy produced enough internal rebound to cause cessation of root growth in the irradiated area as well as alteration of the growth potential of the developing maxilla and mandible. Unquestionably, in the case reported here the patient received an excessive x-ray dosage (3,500 r) as far as growth was concerned but only moderate dosage from the aspect of skin irradiation. In the jaws, where bone is interposed between the soft tissues of the cheek and the pharynx, the maximum medium-voltage x-ray radiation of bone should not exceed 35 per cent of the skin dosage that is tolerated elsewhere. The precise quantity of irradiation which stops tooth development or alters growth of the maxilla or mandible is still unknown. However, it appears to lie somewhere between 800 r and 1,500 r, depending upon the age and physical characteristics of the individual patient.

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