Authors

Judith E Raber-Durlacher

DDS, PhD

Department of Periodontology, Academic Centre of Dentistry Amsterdam, University of Amsterdam and VU University, Amsterdam, The Netherlands

Articles by Judith E Raber-Durlacher

Crispian Scully

CBE, DSc, DChD, DMed (HC), Dhc(multi), MD, PhD, PhD (HC), FMedSci, MDS, MRCS, BSc, FDS RCS, FDS RCPS, FFD RCSI, FDS RCSEd, FRCPath, FHEA

Bristol Dental Hospital, Lower Maudlin Street, Bristol BS1 2LY, UK

Articles by Crispian Scully

Article

Oral mucosal keratinocytes have a high mitotic rate and are, like cancer cells, targets of RT and cancer cytotoxic CTX agents. Mucosal damage is one of the most common adverse effects of CTX and of RT to the head and neck, with a prevalence ranging from 10–100%. Cancer therapy thus produces collateral damage. Mucositis is the result of a complex series of biological events that ultimately lead to ulceration and is often a dose-limiting toxicity. Thus, while other toxicities of cancer therapy may be declining following, for example, the introduction of Intensity Modulated Radiation Therapy (IMRT), mucositis remains an area of concern to both patients and clinicians. Even newer agents may produce oral ulceration or enhance toxicity of RT and of CTX. These include:

RT is most often administered in small fractions over several weeks and to a localized area. Radiation-induced mucositis is invariable within the radiated field of mucosa and typically begins at cumulative doses of about 15 Gy (ie after around 10 days) and reaches full severity at 30 Gy, persisting for weeks or months (Figure 1). Tissues such as the soft palate, and the lateral borders and ventral surface of the tongue and floor of the mouth, which have a good vascular supply or a higher cell turnover rate, are more susceptible to radiation mucositis. Risk factors for radiation mucositis, apart from the radiation dose and fractionation include:

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