Delayed Radiation Injury (Soft Tissue and Bony Necrosis)

John J. Feldmeier, D.O. and Luis A. Matos, M.D.


Radiation injuries should be differentiated as acute, sub-acute or delayed complications (1). Acute injuries are due to direct cellular toxicity caused by free radical-mediated damage to cellular DNA and are usually self-limited and treated symptomatically. However, they can be very debilitating during their duration. Sub-acute injuries are typically identifiable in only a few organ systems, e.g. radiation pneumonitis following the treatment of lung cancer with an onset typically 2 to 3 months after completion of irradiation. These, too, are generally self-limited but occasionally evolve to become delayed injuries. Delayed radiation complications are typically seen after a latent period of six months or more and may develop many years after the radiation exposure. Often, they are precipitated by an additional tissue insult such as surgery within the radiation field. Although the etiology of delayed injuries may vary somewhat among organ systems, the hallmark of delayed radiation injury is endarteritis with tissue hypoxia and secondary fibrosis (2). Recently, it has become apparent that the evolution of radiation injury is a continuum of events rather than several discrete occurrences (3-5). The elaboration of fibrogenic cytokines begins at the time of irradiation. This recognition may permit the development of predictive assays to identify those patients at high risk for radiation injury prior to its manifestation and permit prophylactic intervention prior to its expression. Such intervention might include Hyperbaric Oxygen Therapy.

Hyperbaric oxygen (HBO2) has been utilized effectively for manifest chronic radiation injuries for many years. The site to which it has been applied for the longest period of time and with the most publications supporting its application is the mandible (6-24). The success in treating mandibular osteoradionecrosis has led researchers to apply HBO2 to radiation injuries at other sites involving other organ systems.

Hyperbaric oxygen has been shown to induce neovascularization and increased cellularity in irradiated and other hypoxic tissues. Marx and co-workers have shown in both an animal experimental model and with serial transcutaneous oxygen measurements in clinical subjects that HBO2 does increase vascular density and resultant tissue oxygen content (16,20,25). Feldmeier and colleagues have shown with several assays in an animal model that tissue fibrosis can also be reduced with the application of HBO2 given in a prophylactic mode (26,27). Marx had previously established the principle of prophylactic intervention in the setting of tooth extractions and alveoloplasty from heavily irradiated mandibles (28). Dental extractions or other surgical procedures are fraught with high complication rates when done in heavily irradiated tissues without the benefit of preoperative HBO2 therapy (29-33).1


1 Hyperbaric Oxygen 2003: Indications and Results, The Hyperbaric Oxygen Therapy Committee Report by John J. Feldmeier, D.O., Chairman and Editor. Copyright 2003, Undersea and Hyperbaric Medical Society, Inc., Kensington, MD.