Should Dental Schools Invest in Training Predoctoral Students for Academic Careers? Two Viewpoints: Viewpoint 1: Dental Schools Should Add Academic Careers Training to Their Predoctoral Curricula to Enhance Faculty Recruitment and Viewpoint 2: Addition of Academic Careers Training for All Predoctoral Students Would Be Inefficient and Ineffective.

This Point/Counterpoint considers whether providing dental students with academic career training and teaching experiences during their predoctoral education would be valuable to recruit dental academicians. While training the next generation of dentists continues to be the primary focus for dental schools, the cultivation and recruitment of dental faculty members from the pool of dental students remain challenges. Viewpoint 1 supports the position that providing dental students with exposure to academic career opportunities has positive value in recruiting new dental faculty. The advantages of academic careers training as a required educational experience in dental schools and as a potential means to recruit dental students into the ranks of faculty are described in this viewpoint. In contrast, Viewpoint 2 contends that such career exposure has limited value and argues that, across the board, allocation of resources to support preparation for academic careers would have a poor cost-benefit return on investment. Adding a requirement for educational experiences for all students would overburden institutions, students, and faculty according to this viewpoint. The authors agree that research is needed to determine how and where to make predoctoral curricular changes that will have maximum impact on academic recruitment.

Acetaldehyde activates Jun/AP-1 expression and DNA binding activity in human oral keratinocytes.

Oral cancer is a significant health problem, particularly among individuals that ingest alcohol in combination with the use of tobacco products. The enhanced development of tobacco-initiated oral cancers by ethanol suggests that ethanol or one of its metabolites may act as a type of tumor promoter. Nevertheless, the mechanisms underlying the ability of ethanol to enhance oral carcinogenesis remain unclear. We hypothesize that acetaldehyde, the first metabolite of ethanol, may activate the expression and/or activity of Jun/AP-1 in oral keratinocytes analogous to the phorbol ester TPA and other tumor promoters in epidermal keratinocytes. To test this hypothesis, we treated HPV immortalized, non-tumorigenic human oral keratinocytes with acetaldehyde at various concentrations and for various times and measured several parameters of Jun/AP-1expression and function. Our results indicated that c-Jun mRNA and protein levels increased in the acetaldehyde treated cells compared to untreated control cells. Moreover, Jun/AP-1 DNA binding activity was rapidly activated by acetaldehyde in a dose-dependent fashion. The increases in Jun protein and AP-1 DNA binding activity were accompanied by increased transactivation of an AP-1 responsive reporter construct as well as increased transcript levels of a candidate AP-1 responsive gene, stromelysin 3. The levels of acetaldehyde employed were minimally toxic to the cells as determined by MTT assays. Thus, acetaldehyde was found to activate the expression and activity of an oncogenic transcription factor in HPV-initiated cells. Taken together, these results suggest that acetaldehyde may participate, at least in part, in the promotion stage of oral carcinogenesis.