In the early 1980s Marx re-defined the pathophysiology of ORN
by proposing that radiation therapy induces an endarteritis that results
in tissue hypoxia, hypocellularity, and hypovascularity which
in turn causes tissue breakdown and chronic non-healing wounds.1
In 1990, Bras et al. reported their study in which sequestrectomy
and resection specimens from mandibles diagnosed with ORN
were compared with both non-irradiated and irradiated nonosteoradionecrotic
mandible specimens.9 The histopathologic
findings suggested that the radiation induced obliteration of the
inferior alveolar artery was the dominant factor leading to ischemic
necrosis of the mandible