Erosion is a common phenomenon in the general population of developed countries. However, due to variations in indices, sample sizes and general study designs, it is difficult to compare the various studies and to estimate actual global prevalence. Therefore, the aim of this present paper is to give a narrative overview on the data available on the global prevalence of erosion. Information on prevalence is not available from each country; in particular, data from Asia, Africa, South America, North America and large parts of South-Eastern Europe are unavailable. There is a large variation in global prevalence ranging between 0 and 100%. Calculating a rough mean from the data available, a mean prevalence in deciduous teeth between 30% and 50% and in permanent teeth between 20% and 45% can be estimated. There seems to be a gender difference and an increase in prevalence with age. Prevalence studies on erosion risk groups show comparable variation. Only in patients with gastro-oesophageal reflux disease (GORD) and eating disorders associated with vomiting can a clear impact on erosion prevalence be found. In people who consume acidic foods and drinks, a higher risk can be found for some specific comestibles. However, there is a lack of controlled epidemiological studies, making it difficult to generalise. There is a clear need for well-designed studies on this issue.
Resistance against radio(chemo)therapy-induced cell death is a major determinant of oncological treatment failure and remains a perpetual clinical challenge. The underlying mechanisms are manifold and demand for comprehensive, cancer entity- and subtype-specific examination. In the present study, resistance against radiotherapy was systematically assessed in a panel of human head-and-neck squamous cell carcinoma (HNSCC) cell lines and xenotransplants derived thereof with the overarching aim to extract master regulators and potential candidates for mechanism-based pharmacological targeting. Clonogenic survival data were integrated with molecular and functional data on DNA damage repair and different cell fate decisions. A positive correlation between radioresistance and early induction of HNSCC cell senescence accompanied by NF-κB-dependent production of distinct senescence-associated cytokines, particularly ligands of the CXCR2 chemokine receptor, was identified. Time-lapse microscopy and medium transfer experiments disclosed the non-cell autonomous, paracrine nature of these mechanisms, and pharmacological interference with senescence-associated cytokine production by the NF-κB inhibitor metformin significantly improved radiotherapeutic performance in vitro and in vivo. With regard to clinical relevance, retrospective analyses of TCGA HNSCC data and an in-house HNSCC cohort revealed that elevated expression of CXCR2 and/or its ligands are associated with impaired treatment outcome. Collectively, our study identifies radiation-induced tumor cell senescence and the NF-κB-dependent production of distinct senescence-associated cytokines as critical drivers of radioresistance in HNSCC whose therapeutic targeting in the context of multi-modality treatment approaches should be further examined and may be of particular interest for the subgroup of patients with elevated expression of the CXCR2/ligand axis.
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