Background: Osteoradionecrosis of the jaw (ORNJ) is a well-recognized complication of radiotherapy. The purpose of this study was to assess predictive factors for the development of ORNJ.

Three types of stimulus, chemical, physical and viral, are known to be carcinogenic to susceptible animals. This review considers these stimuli and their possible mechanisms in general terms and their possible relevance to the induction of oral mucosal carcinoma in particular.

No abstract

A number of changes occur in preneoplastic and neoplastic cells as they progress towards a greater degree of malignancy. These alterations include genetic changes, epigenetic changes, surface alterations and alterations in intercellular interactions. In some instances, these changes are contributing factors to the degree of pathology noted, whilst others are resultant. In many situations, the relationship between these changes and the progression towards neoplasia is not understood. Nevertheless, it seems probable that these changes are ultimately involved in driving cells further along the path to neoplastic transformation. It is the purpose of this review to consider the changes which occur as cells progress from normality to being neoplastic, with particular reference to the cells of the oral mucosa, and the use to which detectable changes can be used as prognostic indicators.

Precancerous lesions and squamous cell carcinomas (SCCs) were induced in the oral mucosa of outbred male Sprague-Dawley rats by repeated application of the carcinogen 4-nitroquinoline-1-oxide. Temporal alterations in the pattern of cytokeratins expressed by epithelial cells in these developing neoplasms were investigated by means of one- and two-dimensional polyacrylamide gel electrophoresis and by probing electrophoretic blots of these gels with anticytokeratin antibodies. Progressive diminution in the expression of a 58.3 kDa cytokeratin was detected in moderately dysplastic epithelium and subsequent lesions, as was reduced expression of a 53.5 kDa cytokeratin after a stage of severe dysplasia had been induced. Analysis of two-dimensional electrophoretograms indicated an alkaline shift of acidic variants of a 49.0 kDa cytokeratin in moderately dysplastic epithelium; this shift was more pronounced in the induced, severely dysplastic epithelium and SCCs. The latter finding of an alkaline shift in cytokeratins of dysplastic epithelial cells has not been previously reported in preneoplastic lesions.