Abstract
Radionecrosis is still one of the major complications following the use of radiotherapy in the treatment of malignant tumors [1–7]. Because of the late effects of radiation, soft tissue and bone changes as obliterative endarteritis and fibrosis occur [8–11]. These changes may, in a small percentage of the patients, lead to bone and/or soft tissue necrosis. The histopathological sequence of events after exposure of normal tissue to radiation can be divided into four phases [12]:
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Phase I:
Characterized by the development of acute damage to cells and tissues. Initial damage to small blood vessels and connective tissue.
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Phase II:
Characterized by processes of recovery from acute damage. There may be some persisting evidence of cell necrosis or tissue hypoplasia and evidence of beginning of chronic or permanent tissue damage. Replacement fibrosis may already be evident. Atypical repair processes representing the beginning of an increase in arteriocapillary fibrosis.
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Phase III:
An intermediate phase with little or no change in parenchymal cellularity. Degenerative changes in fine vascularity and interstitial fibrosis may progress slowly.
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Phase IV:
Delayed or late parenchymal degeneration, either in the form of gradual premature involution of tissues, with hypoplasia, atrophy, and replacement fibrosis, as in premature aging, or in the form of a more rapid breakdown or necrosis of tissues.
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© 1996 Springer-Verlag Italia, Milano
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van Merkesteyn, J.P.R., Bakker, D.J., Kooijman, R. (1996). Radionecrosis. In: Oriani, G., Marroni, A., Wattel, F. (eds) Handbook on Hyperbaric Medicine. Springer, Milano. https://doi.org/10.1007/978-88-470-2198-3_11
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