Differential diagnosis

Reactive, regenerative or reparative squamous epithelium, for example in response to trauma, inflammation, irradiation or ulceration, may manifest atypical cytology or architectural disturbance. Nutritional deficiencies such as iron, folate, and vitamin B12, can also simulate dysplasia. Such lesions are not considered precursor lesions and should be distinguished from them. Clinical history is helpful and morphological changes suggestive of the inciting event, such as ulceration, inflammation, haemorrhage, radiation-induced mesenchymal and/or endothelial nuclear enlargement and hyperchromatism, may be present. The epithelial changes in these cases are generally less pronounced than in dysplasia. Relevance of dysplasia. I t is reasonable to assume that the changes described in dysplasia are due to genetic changes in the epithelium occur, but it is unlikely that the mutations involved are the same ones as are associated with development of malignancy. More severe dysplasia has been traditionally believed to be associat ed with a greater likelihood of progression to malignancy. This might indicate that the greater the accumulation of mutations in tissue, the greater the chance that the critical mutations for malignancy will be present. The corollary is also true in that malignancy can arise from non-dysplastic epithelium {2493} presumably because these critical mutations can be present in the absence of the mutations causing dysplasia.

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