The mechanisms of acceleration of repopulation in squamous epithelia during daily irradiation.

Recent experimental data relating to the mechanisms of accelerated repopulation during daily fractionated irradiation are reviewed. There is evidence indicating that acceleration of repopulation is an active response towards the progressively accumulating radiation damage which is characteristic for squamous cell carcinomas and their tissue of origin, i.e. normal squamous epithelium. Whereas little is known about the mechanisms in tumours, various aspects of the trigger and the biological mechanisms have recently been elucidated in normal squamous epithelium. It is reasonable to expect that some of them might also operate in squamous cell carcinomas. Acceleration is due to the loss of asymmetry of stem cell divisions. This may be associated with changes in the keratinocyte differentiation pattern leading to a functionally defective, parakeratotic and hyperproliferative epithelium. This occurs at a certain level of tissue injury. Although related to the time of incipient erythema, the trigger is not the inflammatory response itself or the functional insufficiency of the irradiated epithelium. Rather, the trigger is directly related to the progressive hypoplasia which causes changes in intercellular communication. There is also evidence that acceleration is modulated by signalling processes between the effector keratinocytes and various mesenchymal cells in the irradiated tissue.