Patient care and ethics. VIII. Ethics education in dental education in the United States

Dental ethics with its specific aspects has obtained a distinct profile during the past ten years. This article presents a recent impression of courses in dental ethics at a number of dental schools in the USA. Some reflections are given about the continuing development of dental ethics.     

Patient care and ethics. VII. Ethics education in the university dental curriculum in the Netherlands

Dentistry, which has developed independently alongside medicine for more than a hundred years now in the Netherlands, is rooted in a type of natural scientific and technological thinking that gained wide acceptance in the middle of the last century. This type of thinking has had far-reaching consequences for the whole field of medicine, including the independent development of dentistry. The social science side of dental training and the normative aspects of clinical practice have long been seriously neglected as a result of the dominance of the natural sciences. This article surveys development in medicine and dentistry since the middle of the last century. It then examines recent developments in medicine and dentistry and concludes by describing the current status of education in ethics in the dentistry curriculum.     

A prospective,double-blind,randomized, placebo-controlled study on the efficacy and safety of influenza vaccination in myasthenia gravis

Objective

To investigate the efficacy and safety of an influenza vaccination in patients with myasthenia gravis with acetylcholine receptor antibodies (AChR MG).

Effectiveness of a combined exercise training and home-based walking programme on physical activity compared with standard medical care in moderate COPD: a randomised controlled trial

Objective

To estimate the effectiveness of a 10-week combined exercise training and home-based walking programme on daily physical activity (PA) compared with standard medical care in patients with moderate chronic obstructive pulmonary disease (COPD).

Multi-modular bone healing assessment in a randomized controlled clinical trial of root-end surgery with the use of leukocyte- and platelet-rich fibrin and an occlusive membrane

Clinical Oral Investigations - The aim of this study was to assess in a multi-modular manner the bone healing 1 year post root-end surgery (RES) with leukocyte- and platelet-rich fibrin...     

The selective p38 inhibitor SB-239063 protects primary neurons from mild to moderate excitotoxic injury

Inhibition of the p38 mitogen-activated protein kinase (MAP Kinase) pathway reduces acute ischemic injury in vivo, suggesting a direct role for this signaling pathway in a number of neurodegenerative processes. The present study was designed to evaluate further the role of p38 MAP Kinase in acute excitotoxic neuronal injury using the selective p38 inhibitor SB-239063 (trans-1-(4hydroxycyclohexyl)-4-(fluorophenyl)-5-(2-methoxy-pyrimidin-4-yl) imidazole). Unlike the widely used p38 inhibitor, SB-203580 (4-(4-Fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imidazole), this second generation p38 inhibitor more selectively inhibits p38 MAP Kinase without affecting the activity of other MAP Kinase signaling pathways and provides a more accurate means to selectively assess the role of p38 in excitotoxicity that has not been previously possible. SB-239063 provided substantial protection against cell death induced by either oxygen glucose deprivation (OGD) or magnesium deprivation in cultured neurons. The ability of this compound to block excitotoxicity was not due to direct inhibition of N-methyl-D-aspartate (NMDA) receptor-mediated currents as SB-239063 did not alter NMDA electrophysiological responses. SB-239063 did not protect against a severe excitotoxic insult induced by 60-min exposure to NMDA. However, when tested against a less severe, brief (5 min) NMDA exposure, p38 inhibition provided substantial protection. These data demonstrate that inhibition of p38 MAP Kinase can confer neuroprotection in vitro against mild but not severe excitotoxic exposure, and suggests that other additional pathways/mechanism(s) may be involved in severe excitotoxic cell death.     

Corticotropin-releasing factor (CRF) and related peptides confer neuroprotection via type 1 CRF receptors

Corticotropin-releasing factor (CRF) receptors are members of the superfamily of G-protein coupled receptors that utilise adenylate cyclase and subsequent production of cAMP for signal transduction in many tissues. Activation of cAMP-dependent pathways, through elevation of intracellular cAMP levels is known to promote survival of a large variety of central and peripheral neuronal populations. Utilising cultured primary rat central nervous system neurons, we show that stimulation of endogenous cAMP signalling pathways by forskolin confers neuroprotection, whilst inhibition of this pathway triggers neuronal death. CRF and the related CRF family peptides urotensin I, urocortin, and sauvagine, which also induced cAMP production, prevented the apoptotic death of cerebellar granule neurons triggered by inhibition of phosphatidylinositol kinase-3 pathway activity with LY294002. These effects were negated by the highly selective CRF-R1 antagonist CP154,526. CRF even conferred neuroprotection when its application was delayed by up to 8 h following LY294002 addition. The CRF peptides also protected cortical and hippocampal neurons against death induced by beta-amyloid peptide (1-42), in a CRF-R1 dependent manner. In separate experiments, LY294002 reduced neuronal protein kinase B activity while increasing glycogen synthase kinase-3, whilst CRF (and related peptides) promoted phosphorylation of glycogen synthase kinase-3 without protein kinase B activation. Taken together, these results suggest that the neuroprotective activity of CRF may involve cAMP-dependent phosphorylation of glycogen synthase kinase-3.     

Lipocortin-1 is an endogenous inhibitor of ischemic damage in the rat brain

Lipocortin-1 (annexin-1) is an endogenous peptide with antiinflammatory properties. We have previously demonstrated lipocortin immunoreactivity in certain glial cells and neurons in the rat brain (Strijbos, P.J.L.M., F.J.H. Tilders, F. Carey, R. Forder, and N.J. Rothwell. 1990. Brain Res. In press.), and have shown that an NH2-terminal fragment (1-188) of lipocortin-1 inhibits the central and peripheral actions of cytokines on fever and thermogenesis in the rat in vivo (Carey, F., R. Forder, M.D. Edge, A.R. Greene, M.A. Horan, P.J.L.M. Strijbos, and N.J. Rothwell. 1990. Am. J. Physiol. 259:R266; and Strijbos, P.J.L.M., J.L. Browning, M. Ward, R. Forder, F. Carey, M.A. Horan, and N.J. Rothwell. 1991. Br. J. Pharmacol. In press.). We now report that intracerebroventricular administration of lipocortin-1 fragment causes marked inhibition of infarct size (60%) and cerebral edema (46%) measured 2 h after cerebral ischemia (middle cerebral artery occlusion) in the rat in vivo. The lipocortin-1 fragment was effective when administered 10 min after induction of ischemia. Ischemia caused increased expression of lipocortin-1 around the area of infarction as demonstrated by immunocytochemistry. Intracerebroventricular injection of neutralizing antilipocortin-1 fragment antiserum increased the size of infarct (53%) and the development of edema (29%). These findings indicate that lipocortin-1 is an endogenous inhibitor of cerebral ischemia with considerable therapeutic potential.     

Regenerative endodontic procedure of an infected immature permanent human tooth: an immunohistological study

Objectives

An immunohistological study of an infected immature permanent human tooth after a regenerative endodontic procedure (REP) was conducted in order to determine the histologic outcome of this procedure. Besides observed signs of angiogenesis and neurogenesis, repair and/or regeneration of the pulp-dentin complex was also investigated.

Materials and methods

A REP was performed on tooth 45 of a 10-year-old girl. Eleven months post-treatment, the tooth had to be removed for orthodontic reasons. The following investigations were performed: immunohistology and radiographic quantification of root development. After hematoxylin-eosin (HE) staining, the following immunomarkers were selected: neurofilament (NF), pan cytokeratin (PK), osteocalcin (OC), and CD34.

Results

The REP resulted in clinical and radiographic healing of the periradicular lesion and quantifiable root development. The HE staining matches with the medical imaging post-REP: underneath the mineral trioxide aggregate a calcified bridge with cell inclusions, connective pulp-like tissue (PLT) with blood vessels, osteodentin against the root canal walls, on the root surface cementum (Ce), and periodontal ligament (PDL). The PDL was PK⁺. The blood vessels in the PLT and PDL were CD34⁺. The Ce, osteodentin, and stromal cells in the PLT were OC⁺. The neurovascular bundles in the PLT were NF⁺.

Conclusions

Immunohistologically, REP of this infected immature permanent tooth resulted in an intracanalar connective tissue with a regulated physiology, but not pulp tissue.

Clinical relevance

REP of an immature permanent infected tooth may heal the periapical infection and may result in a combination of regeneration and repair of the pulp-dentin complex.

     

Sulphasalazine-induced reversible male infertility

A male patient suffering from ulcerative colitis, presented with primary infertility due to sulphasalazine therapy. Sulphasalazine was discontinued and the patient was treated with a 5-aminosalicylic acid preparation (Salofalk) in the form of an enema. After 3 months, the semen quality was dramatically improved and a successful pregnancy ensued. The sulphapyridine moiety of sulphasalazine seems to be responsible for male infertility and depressed semen quality. The metabolite 5-aminosalicylic acid is proposed as a suitable alternative to sulphasalazine in cases of male infertility.