Contemporary educational methods in periodontology.

AIM The 1st European Workshop on Periodontal Education in 2009 made recommendations regarding the scope of periodontal education at undergraduate (UG), postgraduate (PG) and continuing professional development (CPD) levels, defining competencies and learning outcomes that were instrumental at the time in helping to define periodontal teaching curricula. The 19th European Workshop on Periodontology and 2nd European Consensus Workshop on Education in Periodontology (Education in Periodontology in Europe) was held in 2023 to identify changes and future developments in periodontal education (including those informed by the COVID-19 pandemic) and embracing methods and formats of periodontal teaching and training. The aim of this review was to assess current knowledge regarding education methods in periodontology, including traditional face-to-face (F2F) teaching and the move to student-centred methods, virtual learning methods and use of digital technology, as well as blended teaching and learning (including teaching delivery and assessment) at UG, PG and CPD levels. MATERIALS AND METHODS Systematic searches were conducted to identify relevant studies from the literature. Data were extracted and descriptive summaries collated. RESULTS The pandemic was a major disruptor of traditional F2F teaching but provided opportunities for rapid implementation of alternative and supplementary teaching methods. Although online learning has become an integral part of periodontal education, teachers and learners alike favour some form of F2F teaching. Blended teaching and learning are feasible in many areas of periodontal education, both for knowledge and skills acquisition as well as in assessment. Student-centred methods and blended approaches such as the flipped classroom seem highly effective, and online/virtual classrooms with both synchronous and asynchronous lectures are highly valued. Learning with haptic methods and virtual reality (VR) enhances the educational experience, especially when VR is integrated with traditional methods. The quality of the teacher continues to be decisive for the best knowledge transfer in all its forms. CONCLUSIONS Live F2F teaching continues to be highly trusted; however, all types of student-centred and interactive forms of knowledge transfer are embraced as enhancements. While digital methods offer innovation in education, blended approaches integrating both virtual and traditional methods appear optimal to maximize the achievement of learning outcomes. All areas of periodontal education (UG, PG and CPD) can benefit from such approaches; however, more research is needed to evaluate their benefits, both for knowledge transfer and skills development, as well as in assessment

Effects of muscarinic receptor stimulation on Ca2+ transient, cAMP production and pacemaker frequency of rabbit sinoatrial node cells

We investigated the contribution of the intracellular calcium (Cai2+) transient to acetylcholine (ACh)-mediated reduction of pacemaker frequency and cAMP content in rabbit sinoatrial nodal (SAN) cells. Action potentials (whole cell perforated patch clamp) and Cai2+ transients (Indo-1 fluorescence) were recorded from single isolated rabbit SAN cells, whereas intracellular cAMP content was measured in SAN cell suspensions using a cAMP assay (LANCE®). Our data show that the Cai2+ transient, like the hyperpolarization-activated “funny current” (If) and the ACh-sensitive potassium current (IK,ACh), is an important determinant of ACh-mediated pacemaker slowing. When If and IK,ACh were both inhibited, by cesium (2 mM) and tertiapin (100 nM), respectively, 1 μM ACh was still able to reduce pacemaker frequency by 72%. In these If and IK,ACh-inhibited SAN cells, good correlations were found between the ACh-mediated change in interbeat interval and the ACh-mediated change in Cai2+ transient decay (r2 = 0.98) and slow diastolic Cai2+ rise (r2 = 0.73). Inhibition of the Cai2+ transient by ryanodine (3 μM) or BAPTA-AM (5 μM) facilitated ACh-mediated pacemaker slowing. Furthermore, ACh depressed the Cai2+ transient and reduced the sarcoplasmic reticulum (SR) Ca2+ content, all in a concentration-dependent fashion. At 1 μM ACh, the spontaneous activity and Cai2+ transient were abolished, but completely recovered when cAMP production was stimulated by forskolin (10 μM) and IK,ACh was inhibited by tertiapin (100 nM). Also, inhibition of the Cai2+ transient by ryanodine (3 μM) or BAPTA-AM (25 μM) exaggerated the ACh-mediated inhibition of cAMP content, indicating that Cai2+ affects cAMP production in SAN cells. In conclusion, muscarinic receptor stimulation inhibits the Cai2+ transient via a cAMP-dependent signaling pathway. Inhibition of the Cai2+ transient contributes to pacemaker slowing and inhibits Cai2+-stimulated cAMP production. Thus, we provide functional evidence for the contribution of the Cai2+ transient to ACh-induced inhibition of pacemaker activity and cAMP content in rabbit SAN cells

Separation of early afterdepolarizations from arrhythmogenic substrate in the isolated perfused hypokalaemic murine heart through modifiers of calcium homeostasis

In human type 1 diabetes (T1D) and in its murine model, the major histocompatibility complex (MHC) class II molecules, human leukocyte antigens (HLA)-DQ and -DR and their murine orthologues, IA and IE, are the major genetic determinants. In this report, we have ranked HLA class II molecule-associated T1D risk in a two-sided gradient from very high to very low. Very low risk corresponded to dominant protection from T1D. We predicted the protein structure of DQ by using the published crystal structures of different allotypes of the murine orthologue of DQ, IA. We discovered marked similarities both within, and cross species between T1D protective class II molecules. Likewise, the T1D predisposing molecules showed conserved similarities that contrasted with the shared patterns observed between the protective molecules. We also found striking inter-isotypic conservation between protective DQ, IA allotypes and protective DR4 subtypes. The data provide evidence for a joint action of the class II peptide-binding pockets P1, P4 and P9 in disease susceptibility and resistance with a main role for P9 in DQ/IA and for P1 and P4 in DR/IE. Overall, these results suggest shared epitope(s) in the target autoantigen(s), and common pathways in human and murine T1D

Changes in Intracellular Na+ following Enhancement of Late Na+ Current in Virtual Human Ventricular Myocytes

The slowly inactivating or late Na+ current, INa-L, can contribute to the initiation of both atrial and ventricular rhythm disturbances in the human heart. However, the cellular and molecular mechanisms that underlie these pro-arrhythmic influences are not fully understood. At present, the major working hypothesis is that the Na+ influx corresponding to I(Na-L)significantly increases intracellular Na+, [Na]; and the resulting reduction in the electrochemical driving force for Na+ reduces and (may reverse) Na+/Ca2+ exchange. These changes increase intracellular Ca2+, [Ca2+]; which may further enhance I(Na-L)due to calmodulindependent phosphorylation of the Na+ channels. This paper is based on mathematical simulations using the O'Hara et al (2011) model of baseline or healthy human ventricular action potential waveforms(s) and its [Ca2(+)]; homeostasis mechanisms. Somewhat surprisingly, our results reveal only very small changes (<= 1.5 mM) in [Na] even when INa-L is increased 5-fold and steady-state stimulation rate is approximately 2 times the normal human heart rate (i.e. 2 Hz). Previous work done using well-established models of the rabbit and human ventricular action potential in heart failure settings also reported little or no change in [Na] when I(Na-L)was increased. Based on our simulations, the major short-term effect of markedly augmenting I(Na-L)is a significant prolongation of the action potential and an associated increase in the likelihood of reactivation of the L-type Ca2+ current, Ica-L. Furthermore, this action potential prolongation does not contribute to [Na]; increase.This work was supported by (i) the "VI Plan Nacional de Investigacion Cientifica, Desarrollo e Innovacion Tecnologica" from the Ministerio de Economia y Competitividad of Spain (grant number TIN2012-37546-C03-01) and the European Commission (European Regional Development Funds-ERDF-FEDER), (ii) by the Direccion General de Politica Cientifica de la Generalitat Valenciana (grant number GV/2013/119), and by (iii), Programa Prometeo (PROMETEO/2016/088) de la Conselleria d'Educacio Formacio I Ocupacio, Generalitat Valenciana. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.K Cardona; Trénor Gomis, BA.; W Giles (2016). Changes in Intracellular Na+ following Enhancement of Late Na+ Current in Virtual Human Ventricular Myocytes. PLoS ONE. 11(11). https://doi.org/10.1371/journal.pone.0167060S111

Atrio-sinus interaction demonstrated by blockade of the rapid delayed rectifier current

BACKGROUND: Proper pacemaking of the heart requires a specific organization of the sinoatrial (SA) node. The SA node drives the surrounding atrium but needs to be protected from its hyperpolarizing influence, which tends to suppress pacemaker activity. It has been suggested that the hyperpolarizing atrial influence is minimal at the site of the central nodal area. METHODS AND RESULTS: Atrio-sinus interaction was assessed by specific depolarization of the SA node by blocking the HERG-encoded rapid delayed rectifier current (I(K,r)) with the drug E-4031. In the SA node, E-4031 (1 micromol/L) changed action potential configuration drastically but never resulted in pacemaker arrest. In the atrium, E-4031 did not affect the membrane resting potential, thereby leaving the normal hyperpolarizing load on the SA node intact. When the SA node was sectioned into strips and subsequently separated from the atrium, spontaneous electrical activity of the strip containing the primary pacemaker ceased on I(K,r) blockade. When not separated from the atrium, I(K,r) blockade never resulted in pacemaker arrest. A similar effective atrio-sinus interaction was demonstrated in computer simulations. CONCLUSIONS: Our results demonstrate that the atrium provides an effective hyperpolarizing load on the central SA nodal area and is at least one of the controlling mechanisms for normal pacemaking function. The present study can be of help in understanding why patients with long-QT2 syndrome secondary to a mutation in HERG do not show sinus arres