Two-Year Trajectories of Dental Anxiety in Parents and Their Association with Parents' and Children's Oral Healthcare Procedures in FinnBrain Birth Cohort Study.

We aimed to identify parents' dental anxiety trajectories and the association of the trajectories with the number of parents' and their children's oral healthcare procedures in the FinnBrain Birth Cohort Study. Dental anxiety was measured with the Modified Dental Anxiety Scale at gestational weeks (gw) 14 and 34, as well as 3 and 24 months (mo) after childbirth. Oral healthcare procedures from gw14 to 24 mo were obtained from the national patient data register and categorized as preventive and treatment. Trajectories were identified with latent growth mixture modelling for 2068 fathers and 3201 mothers. Associations between trajectories and procedures adjusted for education were analyzed using unordered multinomial logit models. Fathers' trajectories were stable low (80.1%), stable high (3.4%), stable moderate (11.0%), moderate increasing (3.9%) and high decreasing (1.6%). Mothers' trajectories were stable low (80.7%), stable high (11.2%), moderate increasing (5.3%) and high decreasing (2.8%). Mothers with decreasing dental anxiety had a higher number of preventive and treatment procedures. Fathers with decreasing dental anxiety had a higher number of preventive and treatment procedures, while fathers with increasing dental anxiety had fewer procedures. Children of mothers with stable low dental anxiety had higher number of preventive procedures. There seems to be a two-way association between dental anxiety trajectories and oral healthcare procedures.

Concurrent changes in dental anxiety and smoking in parents of the FinnBrain Birth Cohort Study.

We evaluated associations between changes in dental anxiety and tobacco use, adjusted for general anxiety and depressive symptoms. The FinnBrain Birth Cohort Study data, collected at gestational weeks 14 and 34 and at 3 months postpartum, were used. Questionnaires included the Modified Dental Anxiety Scale (MDAS), the Edinburgh Postnatal Depression Scale (EPDS), and the anxiety subscale of the Symptom Checklist-90 (SCL). Smoking was categorized as "stable non-smoking", "started smoking", "quit smoking", and "stable smoking". Changes in smoking and dental anxiety were evaluated "during pregnancy" (i.e., from gestational week 14 to gestational week 34) in 2442 women and 1346 men and "after pregnancy" (i.e., from gestational week 34 to 3 months postpartum) in 2008 women and 1095 men. Changes were evaluated in three smoking categories (stable non-smoking, fluctuating, and stable smoking), using data from all three time-points (1979 women and 1049 men). Modeling used repeated measures analysis of covariance. Stable smoking mothers had statistically significantly higher levels of dental anxiety (mean MDAS 12.3-12.6) than non-smoking mothers (mean MDAS 10.1-10.7) or mothers who smoked at some point during pregnancy (mean MDAS 10.8-11.5). A similar tendency was observed in fathers. However, no systematic change in dental anxiety by changes in smoking habits was observed. Those smoking during pregnancy and with high dental anxiety may need special support for smoking cessation.

Modification of national OSCE due to COVID-19 - Implementation and students' feedback.

AIM: The aims were to describe the development of a modified national online OSCE during COVID-19 and assess related student feedback. MATERIAL AND METHODS: The modified online OSCE comprising of eight question entities was organised simultaneously in all four dental institutes of Finland using the Moodle virtual learning environment. All fourth-year students (n = 179) attended the examination online at home. Student feedback was collected via an anonymous questionnaire with multiple-choice questions and open-ended questions concerning attitudes towards the modified online OSCE, as well as content and usability of the question entities in the examination. Means and standard deviations were calculated for multiple-choice questions. Content analysis was used for open-ended questions. RESULTS: Of 179 students, 119 (66%) consented to the study. Students experienced they had received adequate information (mean 3.8; SD 1.2), had a positive attitude before the examination (4.0; 1.0) and found the practice test useful (3.7; 1.1) (range 1-5). Technical implementation (2.7; 0.7) and the difficulty of the questions (2.9; 0.6) (range 1-4) were found to be good. The teaching students received during their studies was sufficient (3.2; 0.5) (range 1-4). Content (mean 3.2; 0.4) and usability (2.9; 0.4) of the question entities were good (range 1-4). The themes arising from open-ended questions were importance and practicality of the topic (in questions) in relation to the work of a dentist and gratitude for the rapid conversion of the OSCE into an online examination despite COVID-19. The themes arising from negative experiences included difficulties in completing the examination within the time allocated, and dissatisfaction with the model answers provided after the examination. CONCLUSION: The positive student feedback towards the modified online OSCE encourages including an online examination to complement the traditional OSCE.

Estrogen and the selective estrogen receptor modulator (SERM) protection against cell death in estrogen receptor alpha and beta expressing U2OS cells.

In the current work, we compared the ability of 17beta-estradiol (E2) and the selective estrogen receptor modulators (SERMs), tamoxifen (Tam), raloxifene (Ral) and ospemifene (Osp) to promote the survival of osteoblast-derived cells against etoposide-induced apoptosis. In order to compare the roles of the two estrogen receptor (ER) isotypes, we created a U2OS human osteosarcoma cell line stably expressing either ERalpha (ERalpha) or ERbeta (ERbeta). Transfection with either of the ERs was able to render the U2OS cells sensitive to E2. We show that E2 opposed etoposide-induced apoptosis and that the effect was mediated via both ER isotypes. The ER isotype selective agonists propyl-pyrazole-triol (PPT) and diarylpropionitrile (DPN) had the same effect in U2OS/ERalpha and U2OS/ERbeta cells, respectively. Osp also opposed apoptosis at least in U2OS/ERalpha cells. Tam and Ral were not able to protect against etoposide-induced cell death. In order to evaluate the protective effects of E2 and Osp upon etoposide challenge, we studied the expression of two E2-regulated, osteoblast-produced cytokines, IL-6 and OPG in E2 and SERM-treated U2OS/ERalpha and U2OS/ERbeta cells. Etoposide strongly increased expression of IL-6 and decreased that of OPG. E2 opposed IL-6 increase only in U2OS/ERalpha cells and OPG decrease primarily in ERbeta cells. Osp opposed the effect of etoposide on OPG primarily in U2OS/ERbeta cells but interestingly, it had little effect on IL-6 expression. E2, PPT, DNP and Osp also inhibited etoposide-induced death and cytokine changes in SAOS-2 osteosarcoma cells expressing endogenous ERalpha and ERbeta. Collectively, our results suggest that the osteoblast protective anti-apoptotic effects of E2 are mediated by both ERalpha and ERbeta but those of Osp primarily by ERalpha. In addition, E2 and Osp opposed the etoposide-induced increase of IL-6 and decrease of OPG which changes would increase osteoclastic activity. These anti-resorptive effects of E2 and Osp upon etoposide challenge differed from each other and they seemed to be differentially mediated in ERalpha and ERbeta expressing osteoblast-derived U2OS cells.

Tamoxifen-induced rapid death of MCF-7 breast cancer cells is mediated via extracellularly signal-regulated kinase signaling and can be abrogated by estrogen.

Tamoxifen (Tam) is widely used in chemotherapy of breast cancer. It inhibits proliferation and induces apoptosis of breast cancer cells by estrogen receptor (ER)-dependent modulation of gene expression. In addition, recent reports have shown that Tam also has nongenomic effects. We previously reported induction of a rapid mitochondrial death program in breast cancer cells at pharmacological concentrations of Tam. Here we studied the upstream signaling events leading to mitochondrial disruption by Tam. We observed that 5 mum Tam rapidly induced sustained activation of ERK1/2 in ER-positive breast cancer cell lines (MCF-7 and T47D) and that PD98059 (inhibitor of ERK activation) was able to protect MCF-7 cells against Tam-induced death. These data suggest that activation of ERK has a primary role in the acute death response of the cells. In addition, inhibition of epidermal growth factor receptor (EGFR) opposed both Tam-induced ERK1/2 phosphorylation and cell death, which suggests that EGFR-associated mechanisms are involved in Tam-induced death. ERK1/2 phosphorylation was associated with a prolonged nuclear localization of ERK1/2 as determined by fluorescence microscopy with ERK2-green fluorescent protein construct. 17beta-Estradiol was shown to exert a different kind of temporal pattern of ERK nuclear localization in comparison with Tam. Moreover, 17beta-estradiol was found to oppose the rapid effects of Tam in MCF-7 and T47D cells but not in MDA-MB-231 cells, which implies a role for estrogen receptors in the protective effect of estrogen. The pure antiestrogen ICI182780 could not, however, prevent Tam-induced ERK1/2 phosphorylation, suggesting that the Tam-induced rapid cell death is primarily ER-independent or mediated by ICI182780 insensitive nongenomic mechanisms.